cxEPA
United Stales
Environmental Protection
Agency
Office of
Toxic Substances
Washington DC 20460
EPA 560 11-79-009
July 1979
Toxic Substances
An Assessment of
the Need for Limitations
on Trichloroethylene,
Methyl Chloroform,
and Perch loroethylene
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EPA-560/11-79-009
AN ASSESSMENT OF THE NEED FOR LIMITATIONS ON
TRICHLORQETHYLENE, METHYL CHLOROFORM,
AND PERCHLOROETHYLENE
FINAL REPORT
July 1979
Prepared under
Contract No. 68-01-4121
For
U.S. Environmental Protection Agency
Office of Toxic Substances
401 M Street, S.W.
Washington, D.C. 20460
Dr. Stanley C. Mazaleski
Project Officer
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DISCLAIMER
This report has been reviewed by the Office of Toxic Substances, U.S.
Environmental Protection Agency, and approved for publication. Approval does
not signify that the contents necessarily reflect the views and policies of
the U.S. Environmental Protection Agency, nor does mention of trade names or
commercial products constitute endorsement or recommendation for use.
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PREFACE
This report presents the results of an assessment of production, use, en-
vironmental losses, human health effects, environmental impacts, and environ-
mental levels of trichloroethylene, methyl chloroform, and perchloroethylene.
The study also includes an assessment of needs for regulating production, use,
handling and transport so as to mitigate the human and environmental risks as-
sociated with these chemicals.
This study was performed by Midwest Research Institute under Contract No.
68-01-4121 for the Office of Toxic Substances of the U.S. Environmental Protec-
tion Agency. The Office of Toxic Substances project officers for this study
were: Mr. Edward Brooks, Dr. George Semeniuk, Dr. Patricia Hilgard, and
Dr. Stanley Mazaleski. Principal Midwest Research Institute contributors to
this study included: Dr. Thomas W. Lapp (Project Leader), Senior Chemist;
Dr. Betty L» Herndon, Associate Physiologist; Mr. Charles E. Mumma, Senior
Chemical Engineer; Mr. Arthur D. Tippit, Assistant Environmental Scientist;
and Mr. Robert P. Reisdorf, Assistant Environmental Scientist. This report
was prepared under the supervision of Dr. Edward W. Lawless, Head, Technology
Assessment Section.
Midwest Research Institute would also like to express its appreciation
to the many industrial, university, and government agency personnel who pro-
vided technical input and guidance during the conduct of this study.
Approved for:
MIDWEST RESEARCH INSTITUTE
Q/. I . x&^*~~-*^
L. J.( Shannon, Director
Environmental and Materials
Sciences Division
July 31, 1979
iii
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CONTENTS
Preface iii
Figures ................. vii
Tables ix
1. Introduction 1-1
2. Executive Summary 2-1
3. Market Input/Output Analysis 3-5
3.1 Chemical structure and properties ........ 3-5
3.2 Market data 3-18
3.3 Manufacturing process technology .. 3-32
3.4 Consumption and utilization 3-60
3.5 Future projections 3-79
3.6 Overall materials balance 3-85
3.7 Summary of chemical losses .3-101
References 3-103
4. Alternatives ............. 4-3
4.1 Manufacturing alternatives 4-3
4.2 Use alternatives 4-9
References 4-31
5. Health Impacts 5-7
5.1 Trichloroethylene ..... 5-7
References - Trichloroethylene ..... 5-73
5.2 Methyl chloroform (1,1,1-trichloroethane) .... 5-102
References - Methyl chloroform ............ 5-164
5.3 Perchloroethylene (tetrachloroethylene) 5-176
References - Perchloroethylene .. 5-231
6. Ecological Effects 6-3
6.1 Environmental fate ..... 6-3
6.2 Environmental effects ..... .... 6-20
References 6-34
7. Monitoring Data and Exposure Levels 7-3
7.1 Atmospheric levels 7-3
7.2 Water levels 7-18
7.3 Soil and sediment 7-33
7.4 Food 7-35
7.5 Exposure levels 7-35
References 7-50
v
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CONTENTS (continued)
8. Regulations and Standards ..... 8-3
8.1 Federal, state, local, and other regulations . . . 8-3
8.2 Standards and recommendations 8-15
8.3 Shipping and transportation practices 8-21
References 8-28
9. Solvent Emissions: Control, Recovery, and Disposal .... 9-3
9.1 Metal cleaning industry . 9-3
9.2 Dry cleaning industry 9-12
9.3 Solvent recovery or disposal 9-28
9.4 Container labels 9-34
References 9-39
10. Summary 10-3
10.1 Market input/output analyses 10-6
10.2 Health effects 10-6
10.3 Ecological effects 10-16
10.4 Monitoring data and exposure levels 10-18
10.5 Regulations and standards 10-21
10.6 Solvent emissions 10-23
11. Proposed Regulatory Options .... 11-2
11.1 Review of major findings 11-2
11.2 Options for specific areas 11-5
Appendices
A. Commercial products containing trichloroethylene, methyl
chloroform, or perchloroethylene ... A-l
B. Results of the written questionnaire B-l
C. Statistical analysis of NCI carcinogenesis data
carcinogenesis bioassays of trichloroethylene,
methyl chloroform, or perchloroethylene C-l
Subject Index SI-1
vi
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FIGURES
Production schematic for trichloroethylene based on
ethylene dichloride 3-36
3-2 Production schematic for trichloroethylene from acetylene . 3-38
3.-3 Flow diagram for production of methyl chloroform from vinyl
chloride 3-40
3-4 Flow diagram for production of methyl chloroform from
vinylidene chloride by hydrochlorination 3-42
3-5 Flow diagram for production of methyl chloroform from ethane
by chlorination ..................... 3-44
3-6 Flow diagram for production of perchloroethylene from
propane 3-45
3-7 Flow diagram for production of perchloroethylene from
acetylene . .............. 3-47
3-8 . Flowchart of perchloroethylene production process used by
Diamond Shamrock Chemical Company .. . 3-55
3-9 Input/output summary for trichloroethylene for 1976 .... 3-93
3-10 . Distribution of trichloroethylene emissions from metal
cleaning in 1976 3-95
3-11 Input/output summary for methyl chloroform for 1976 .... 3-96
3-12 Distribution of total methyl chloroform emissions from
metal cleaning in 1976 3-98
3-13 Input/output summary for perchloroethylene for 1976 .... 3-99
3-14 Distribution of perchloroethylene emissions from dry clean-
ing operations in 1976 3-100
5-1 Proposed intermediary metabolism of trichloroethylene ... 5-15
5-2a Exposure to methyl chloroform by inhalation of 250 and 350
ppm in five subjects at rest and during work . 5-105
5-2b Quotient between arterial blood concentration and alveolar
air concentration after 30 min exposure during rest (N=20)
and exercise (N=4-5). The poor solubility of methyl
chloroform is evident 5-105
5-3 Metabolic route suggested for methyl chloroform 5-107
5-4 Increase in urinary excretion of trichloroacetic acid metab-
olite by repeated exposure to vapor 5-112
5-5 Cardiotoxicity of methyl chloroform 5-120
vii
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FIGURES (continued)
Number
5-6 Metabolic route suggested for perchloroethylene ...... 5-180
5-7 Urinary excretion of trichloroacetic acid 5-182
5-8 Tetrachloroethylene expired air concentrations following
vapor exposure .« 5-204
7-1 Sites of surface water sampling .............. 7-25
viii
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TABLES
Number
3-1 Properties of Pure Trichloroethylene, Methyl Chloroform, and
Perchloroethylene 3_7
3-2 Properties of Commercial Chlorinated Solvents ........ 3-3
3-3 Chemical Names, Trade Names, and Synonyms for Trichloro-
ethylene 3-10
3-4 Chemical Names, Trade Names, and Synonyms for Methyl
Chloroform 3-11
3-5 Chemical Names, Trade Names, and Synonyms for Perchloro-
ethylene 3-12
3-6 Phosgene Formation in Thermal Decomposition of Trichloro-
ethylene 3-14
3-7 Domestic Production and Sales of Trichloroethylene ..... 3-20
3-8 Domestic End-Use Patterns for Trichloroethylene 3-21
3-9 U.S. Imports of Trichloroethylene (metric tons) 3-22
3-10 U.S. Exports of Trichloroethylene From 1970 Through 1977
(metric tons) 3-23
3-11 Domestic Production and Sales of Methyl Chloroform 3-25
3-12 Domestic End-Use Patterns for Methyl Chloroform 3-26
3-^13 Export Data for Methyl Chloroform 3-27
3-14 Domestic Production and Sales of Perchloroethylene 3-29
3-15 Perchloroethylene End-Use Patterns in the United States . . . 3-30
3-16 U.S. Imports of Perchloroethylene (metric tons) 3-31
3-17 U.S. Exports of Perchloroethylene 3-32
3-18 U.S. Production Capacity Data for Trichloroethylene 3-32
3-19 U.S. Production Capacity Data for Methyl Chloroform 3-34
3-20 U.S. Production Capacity Data for Perchloroethylene 3-35
3-21 Consumption of Degreasing Solvents in 1974 3-61
3-22 Solvent Cleaning--Room Temperature and Vapor Degreasing--by
SIC 3-64
3-23 Solvent Cleaning—Room Temperature and Vapor Degreasing--by
Geographic Region . 3-64
3-24 Geographical Breakdown of States by Region 3-65
3-25 Geographical Distribution of Vapor Recovery and Control
Systems in 1974 3-66
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TABLES (continued)
Number
3-26 Disposal Method and Quantity of All Solvents Disposed in
1974 3-67
3-27 Usage of Solvents in Metal Cleaning Plants 3-69
3-28 U.S. Government Purchases and Major Uses of Trichloro-
ethylene, Methyl Chloroform, and Perchloroethylene in 1976. 3-71
3-29 U.S. Dry Cleaning Industry - 1972 3-72
3-30 Consumption of Perchloroethylene in Dry Cleaning for 1975 . . 3-75
4-1 Metal Cleaning Solvents 4-10
4-2 Evaluation of Fluorosolvent F-113 as Substitute for Tri-
chloroethylene in Metal Cleaning 4-18
4-3 Evaluation of Methylene Chloride as an Alternative Solvent . 4-20
4-4 Evaluation of Alkaline Cleaning Solutions as Replacement for
Solvent Metal Cleaning . 4-22
4-5 Categories of Metal Cleaning by Process 4-23
4-6 Evaluation of Methyl Chloroform as Substitute for Trichloro-
ethylene 4-25
4-7 Perchloroethylene as a Substitute for Trichloroethylene . . . 4-26
4-8 Commonly Used Dry Cleaning Solvents 4-29
5-1 Occurrence of Trichloroethylene in Human Tissue 5-12
5-2 Concentrations of Trichloroethylene in Tissues of Dogs and
Rabbits 5-14
5-3 Half-Life of Chloral Hydrate 5-18
5-4 Biological Half-Life of Metabolites in the Urine of Human
Subjects Exposed to Vapors of Trichloroethylene 5-20
5-5 Biological Half-Life of Metabolites in the Blood of Human
Subjects Exposed Occupationally or Experimentally to Vapors
of Trichloroethylene 5-21
5-6 Biological Half-Life of Trichloroethylene and Metabolites in
Rabbits 5-22
5-7 Average Metabolite Concentrations in Urine of Workers Exposed
to Various Concentrations of Trichloroethylene 5-26
5-8 Urinary Excretion of Trichloroacetic Acid and Trichloroetha-
nol in Five Subjects During and Following Trichloroethylene
Exposure 5-28
5-9 Time Required for Metabolites to Reach Maximal and Half-Life
Excretion 5-31
5-10 Toxic Effects of Trichloroethylene on Man and Animals .... 5-43
5-11 Comparison of Psychological Performance Tests Between
Solvent-Exposed Groups and Controls 5-46
5-12 Mutagenicity Testing—Trichloroethylene 5-58
5-13 Summary of Carcinogenic Data 5-61
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TABLES (continued)
Number Page
5-14 Absorption of 1,1,1-Trichloroethane 5-103
5-15 Methyl Chloroform Concentrations in Blood 5-104
5-16 Methyl Chloroform Excretion in Exhaled Breath 5-109
5-17 Fate of Methyl Chloroform 5-111
5-18 Liver Effects of Methyl Chloroform and Other Chlorinated
Hydrocarbons 5-122
5-19 Effects on Clinical Chemistry of Methyl Chloroform in Man . . 5-126
5-20 Acute CNS Effects of Methyl Chloroform 5-129
5-21 Toxic Effects of Methyl Chloroform 5-137
5-22 Comparison of the Incidence of Hepatocellular Carcinoma in
Control Group Mice 5-151
5-23 NCI Evaluative Carcinogenesis Bioassay 5-152
5-24 Human Fatalities With Methyl Chloroform 5-155
5-25 Epidemiologic Effects of Methyl Chloroform 5-161
5-26 Comparison of Computer-Read EGG in Methyl Chloroform Exposure
Study 5-162
5-27 Metabolite Concentrations in Urine Samples From Methyl
Chloroform Exposure 5-163
5-28 Excretion of Urinary Metabolites by Humans, Rats, and Mice
After Exposure to Perchloroethylene 5-181
5-29 Human Urinary Excretion of Trichloroacetic Acid 5-183
5-30 Fate of Perchloroethylene 5-185
5-31 The Effect of Exposure of Rats to the Vapor of Perchloro-
ethylene on Liver Lipid Content 5-186
5-32 Effect of Inhalation Exposure of Rabbits to Perchloroethylene
on the Activity of Liver Enzymes 5-187
5-33 24-Hr Median Lethal and Effective Doses of Perchloroethylene. 5-188
5-34 Summary of Toxicological Effects of Perchloroethylene on Man
and Animals 5-198
5-35 Perchloroethylene Inhalation by Rats 5-202
5-36 Effects of Perchloroethylene on Humans 5-206
5-37 Chronic and Some Subacute Inhalation Toxicity of Perchloro-
ethylene to Laboratory Animals 5-207
5-38 Effect of Inhaled Perchloroethylene on the Incidence of Fetal
Anomalies Among Mouse and Rat Litters 5-212
5-39 Summary of Mutagenicity Studies on Perchloroethylene .... 5-215
5-40 NCI Perchloroethylene (C04580) Evaluative Carcinogenesis
Bioassay ......................... 5-219
5-41 Effects of Chronic Exposure to a Solvent Mixture Containing
75% Methyl Chloroform and 25% Perchloroethylene of Labora-
tory Animals 5-222
6-1 Tropospheric Half-Lives 6-12
xi
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TABLES (continued)
Number
6-2 Hydrolytic Half-Life of Trichloroethylene, Methyl Chloro-
form, and Perchloroethylene 6-17
6-3 Evaporation of Chlorinated Hydrocarbons From Water Contain-
ing Various Soil Types 6-18
6-4 Toxicity of Trichloroethylene, Methyl Chloroform, and Per-
chloroethylene to Fresh and Saltwater Fish 6-21
6-5 Comparison of Acute Flow-Through and Static Fish Toxicity
LC50 Values 6-22
6-6 Chlorinated Solvents Flow-Through Fish Toxicity Studies . . 6-24
6-7 Accumulation of Chlorinated Hydrocarbons in Fish 6-25
6-8 Chlorinated Hydrocarbon Concentrations Found in Marine
Algae 6-27
6-9 Chlorinated Hydrocarbons in Marine Organisms 6-29
6-10 Chlorinated Hydrocarbon Levels in Fresh and Saltwater Birds. 6-30
6-11 Concentrations of Chlorinated Hydrocarbons in Mammals . . . 6-30
6-12 Phytotoxicity of Methyl Chloroform and Trichloroethylene . . 6-31
7-1 Ambient Air Measurements at Manufacturing Sites 7-4
7-2 Ambient Air Measurements at Boeing Corporation ....... 7-6
7-3 Solvent Losses to the Atmosphere From Perchloroethylene Dry
Cleaning Plants 7-7
7-4 Plants Equipped With Carbon Adsorber 7-9
7-5 Ambient Air Concentrations in Selected U.S. Cities 7-11
7-6 Typical Levels of Halogenated Halocarbons Under Inversion
Conditions 7-12
7-7 Ambient Air Levels in England 7-14
7-8 Ambient Air Levels in Selected Western European Countries . 7-16
7-9 Concentrations in Drinking Water 7-19
7-10 Nondrinking Water Levels at Producer Sites 7-22
7-11 Concentrations of Chlorinated Hydrocarbons in Liverpool Bay
Seawater 7-27
7-12 Average Levels of Some Chlorinated Hydrocarbons in Waste-
water .......... ......... 7-28
7-13 Chlorinated Hydrocarbons in English Foodstuffs 7-36
7-14 Calculated Levels of Human Exposure Based Upon Air Concen-
tration Data 7-39
7-15 Calculated Exposure to Trichloroethylene From Drinking
Water 7-42
7-16 Calculated Exposure to Perchloroethylene From Drinking
Water 7-44
7-17 Calculated Exposure From Air and Drinking Water 7-44
8-1 Hazardous Waste Classifications 8-5
8-2 Photochemical Reactivity of Volatile Organic Compounds ... 8-6
8-3 Federal Specifications for Methyl Chloroform 8-10
xii
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TABLES (continued)
Number
8-4 Federal Specifications for Methyl Chloroform
8-5 Federal Specifications for Technical Grade Perchloro-
ethylene
8-6 Summary of NIOSH Recommendations for Occupational Health
Standards 8-16
8-7 Threshold Limit Values . . . 8-19
8-8 Workplace Quality Standards in Use in Different Countries . 8-20
8-9 Handling and Shipping Data for Trichloroethylene . . . . . . 8-22
8-10 Handling and Shipping Data for Methyl Chloroform ...... 8-24
8-11 Handling and Shipping Data for Perchloroethylene 8-26
9-1 Cold Cleaning Control Systems 9-7
9-2 Open Top Vapor Degreasing Control Systems 9-10
9-3 Conveyorized Degreaser Control Systems 9-13
9-4 Perchloroethylene Solvent Mileage and Losses 9-17
9-5 Perchloroethylene Mileage Dry-to-Dry Plants ........ 9-23
9-6 Perchloroethylene Mileage--Transfer Machines With Adsorbers. 9-25
9-7 California Class 1 Site Criteria 9-35
xiii
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SECTION 1
INTRODUCTION
Chlorinated hydrocarbons find widespread usage as solvents and cleaning
agents in the industrial sector. Among the most common in the area of metal
cleaning are trichloroethylene and methyl chloroform. Trichloroethylene has
been used successfully, and in large volume, in this area for over 40 years
and methyl chloroform for over 20 years. The later emergence of methyl chloro-
form for vapor degreasing uses was necessitated by the need for a stabilizer
system to prevent solvent decomposition over extended periods of use. Both of
these solvents are now used extensively in numerous segments of industry where
the cleaning of metals or metal components is required. Subsequent to the ini-
tiation of this study, the Environmental Protection Agency (EPA) requested that
a third compound, perchloroethylene, be added to this study. This compound is
not as extensively used as a metal cleaning agent, but it is a widely used sol-
vent in the dry cleaning industry.
The motivation for this study was based on several factors. Two of the
compounds, trichloroethylene and perchloroethylene, are structurally related
to vinyl chloride, a known carcinogen widely used in the plastics industry.
Trichloroethylene had also recently been reported to be a carcinogen in one
strain of mice. Subsequent to the initiation of this study, similar results
were also obtained for perchloroethylene. An additional motivation for this
study is the fact that use of all three of these compounds is worldwide, so
that a potential exists for exposure of large segments of the population by
emissions to the environment.
Another reason for interest in these three compounds is the detection
of measurable quantities of each of the materials in drinking water samples
taken from selected cities throughout the United States.
The objectives of this study were to compile and organize information on
the three subject compounds concerning physical and chemical properties, mar-
ket status and outlook, manufacturing processes, consumption patterns, alter-
native use products, materials balance, and a summary of losses to the envi-
ronment. In addition, human and animal health effects were compiled and an
1-1
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assessment was made of the environmental effects of these compounds. Monitor-
ing and exposure data were compiled and analyzed, and needs for possible regu-
latory actions regarding these three compounds were assessed. The results of
this study are presented in the subsequent 10 sections of this report.
During the course of this study, the following computerized literature
searches were conducted to obtain technical information:
Chemical Abstracts: 1972 - September 1978
Manual search, 1965-1972
Toxline: 1965 - September 1978
Medline: 1969 - September 1978
The EPA library in Cincinnati, Ohio, provided Midwest Research Institute (MRI)
with an SDC international search of the National Technical Information Service
(NTIS) file. Whenever possible, secondary references were not used in order to
avoid the potential for misinterpretation of the original articles.
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SECTION 2
EXECUTIVE SUMMARY
A summary of the results obtained in this study are presented for tri-
chloroethylene, methyl chloroform, and perchloroethylene. This summary con-
sists of a nontechnical discussion directed primarily towards interested per-
sons without a scientific background. A detailed technical summary is presented
in Section 10.
All three of the subject compounds are manufactured in the U.S. in rela-
tively large quantities. In 1978, the estimated production for all three
compounds amounted to 1,645 million pounds. Of this total, perchloroethylene
was produced in the largest quantities, 721 million pounds, followed by methyl
chloroform at 623 million pounds, and trichloroethylene at 301 million pounds.
Each compound is extensively used in either the metal cleaning industry or the
textile cleaning industry. Over 97% of all trichloroethylene (excluding ex-
ports) is used industrially in metal cleaning operations. For methyl chloro-
form, approximately 80% of the annual production (excluding exports) is used
for industrial metal cleaning; use in adhesives and aerosol products accounted
for 14% and 6% was attributed to miscellaneous uses. Perchloroethylene is
used primarily as a cleaning agent in the textile industry and in metal clean-
ing operations. Excluding its use as a chemical intermediate and export quan-
tities, about 77% of the annual production is used by the textile industry and
about 20% for industrial metal cleaning. Small quantities of the three com-
pounds are used directly in consumer products. All of the quantities used in-
dustrially and in consumer products are eventually lost to the environment,
primarily in the form of atmospheric emissions.
All three of the compounds are globally distributed in the troposphere
primarily as a result of emissions by the users. Atmospheric levels are gen-
erally in the low parts per billion (ppb) or parts per trillion (ppt) range.
Trichloroethylene undergoes rapid photochemical decomposition in the troposphere
to produce carbon monoxide, hydrogen chloride, phosgene, and other halogenated
products. Perchloroethylene undergoes a slower photochemical decomposition
into the same products. Methyl chloroform undergoes photochemical decomposi-
tion much more slowly than the other two compounds; however, the products are
essentially the same as for trichloroethylene and perchloroethylene. In
general, tropospheric concentrations of each of the three compounds are of
the order of 1 to 2 ppb or less. Concentrations near production and user sites
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can be higher than the 1 to 2 ppb level. In recent studies, methyl chloro-
form was detected in the stratosphere at an average level of 79 ppt and
perchloroethylene at a level of approximately 6 ppt. These stratospheric
levels are attributable to the low decomposition rates in the troposphere
which allows these two compounds to ascent to the stratosphere. Once in the
stratosphere, the two compounds (primarily the methyl chloroform) can be dis-
sociate to form chlorine atoms which have been proposed to be an integral
factor in the ozone depletion theory. It has been estimated that methyl chloro-
form may result in a steady state depletion of ozone to the extent of about 2070
of that calculated for the chlorofluorocarbons.
All three compounds have been detected in the drinking water in various
cities throughout the United States. The highest trichloroethylene level was
32 ppb, but in 10 of the 14 cities or areas, the levels were 2 ppb or less.
For methyl chloroform, the highest level was 17 ppb; all other 13 cities were
found to have levels of 1 ppb or less. The highest level of perchloroethylene
was 2 ppb; the remaining cities had levels of 0.4 ppb or less. There have
been confirmed reports of contamination due to each of the three compounds in
public wells used for drinking water. The highest reported level was 38 ppm
of trichloroethylene in a well near a user facility.
Levels of trichloroethylene and methyl chloroform in nondrinking water
near manufacturing site outlets ranged from 74 to 535 ppm and 5 to 344 ppb,
respectively. At three dry cleaning plants, perchloroethylene levels in the
wastewater ranged from 6 to 1,010 ppm. For 204 other U.S. sites, 95% of those
sampled showed levels of the three compounds to be less than 6 ppb. The maxi-
mum levels were 188 ppb for trichloroethylene, 8 ppb for methyl chloroform,
and 45 ppb for perchloroethylene.
All three compounds can be absorbed into the human system by inhalation,
oral intake, or dermal exposure, although inhalation has been the cause of the
greatest acute and chronic exposure potential. Absorption of toxic quantities
through intact skin is unlikely, but the dermititis and localized irritation
that occurs from repeated skin contact is a common complaint. Perchloro-
ethylene and methyl chloroform are found unchanged in the breath of man and/or
animals after inhalation, skin contact, or all routes of administration in
animals. Recent work with man has shown that, at high levels, solvent vapors
may penetrate intact skin.
All three solvents are largely excreted unchanged on the breath. For
short-term, low level inhalation exposure in man, the following percentages
of the total dose were excreted unchanged on the breath: 72 to 85% for tri-
chloroethylene and up to 98% for methyl chloroform. A range of 25 to 807, un-
changed pulmonary excretion has been reported for perchloroethylene. Activity
level and repeated exposure can change the value. The quantity remaining in
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the body is rapidly distributed but accumulates in the lipid portions. Per-
chloroethylene is eliminated the most slowly and accumulates in the lipid.
Methyl chloroform shows only modest lipid storage.
Trichloroethylene is apparently metabolized to a greater percentage than
the other two compounds, and a large amount of excretion occurs as two
metabolites in the urine, trichloroacetic acid and trichloroethanol. Per-
chloroethylene and methyl chloroform are also both metabolized to the same
end products of trichloroacetic acid and trichloroethanol, but at lower levels
than for trichloroethylene. One study on perchloroethylene suggested that it
formed an epoxide intermediate, an oxirane with alkylating potential. Such
epoxides, reactive with tissue in an irreversible manner, are considered
potentially mutagenic and carcinogenic. Many factors in addition to metab-
olism, however, are involved in the production of a chemical effect. These
factors include variations in exposure profiles, including different dose
levels, periods of exposure, routes of dosage, and concomitant exposure to
other chemicals modify the metabolism of compounds in the body. High dose
levels given by abnormal routes may lead to atypical metabolities and routes
of metabolism. Complete pharmacokinetic studies on trichloroethylene, methyl-
chloroform, and perchloroethylene have not been reported.
When the compounds are inhaled, the most common exposure route for man,
the minimum fatal dose is about 2,600 ppm for perchloroethylene, 3,500 ppm for
trichloroethylene, and 9,000 ppm for methyl chloroform. Both exposure time
and concentration are important to survival. With methyl chloroform, for
example, no deaths were reported until over 8,000 ppm concentration, but above
that level, deaths were directly related to time of exposure. Data for ex-
perimental animal show that the injected dose that killed half the animals
was: 2,800 to 3 200 mg/kg for trichloroethylene, 4,200 to 5,300 mg/kg for
methyl chloroform and 3,400 to 5,700 mg/kg for per chloroethylene.
When trichloroethylene, methyl chloroform, and perchloroethylene were in-
haled by a species with high target-organ susceptibility (guinea pigs) for
1 to 6 months, no pathology was found at 100, 650, and 100 ppm, respectively.
Target organs for the toxic effects of these compounds to man are the
central nervous system and cardiovascular system, with effects on the liver,
skin, and kidney attributed to exposure. Central nervous system depression
with symptoms of headache, dizziness, fatigue, burning eyes, and vertigo are
often described with exposure to all three compounds. In general, these ef-
fects are allevaited when the subject is removed from exposure or contact.
Peripheral nervous system effects have been reported for both trichloroethylene
and perchloroethylene in cases of prolonged skin contact. Cases of sudden
death have occurred in the workplace and in abuse of the compounds after chronic
exposure. These fatalities could be secondary to the anesthetic properties of
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these three solvents, which depress the central nervous system and the respira-
tory control center at high levels. It is also possible that these deaths
could be attributed to a ventricular fibrillation. Animal toxicity studies re-
port cardiac arrhythmias and primary cardiac standstill after exposure espe-
cially to methyl chloroform, but also trichloroethylene. It has been suggested
that, in man, these solvents produce an increase in the sensitivity of the
heart to epinephrine; in times of physical or emotional stress when the
epinephrine in the body increases, a sensitivity to epinephrine could result
in serious cardiac arrhythmias. At anesthetic levels methyl chloroform produces
electrocardiogram changes.
Liver and kidney toxicity from trichloroethylene, methyl chloroform and
perchloroethylene have been seen in man only after very high, accidental ex-
posure or abuse; however, the effects of chronic, low level exposure have not
been extensively studied and thus are not well characterized A few studies
have implicated long-term workplace exposure to perchloroethylene, in par-
ticular, as a source of nervous system toxicity such as abnormal reflex
activity and chronic headaches. Animal studies have indicated evidence for
slight liver changes, fatty degeneration, and some degenerative effects on bone
marrow after long-term, low level exposure to these solvents. The greater
number of reports on liver necrosis and kidney damage with perchloroethylene
is probably not a result of any greater reactivity of the chemical, but is a
function of the fact that it is retained in the body longer than trichloro-
ethylene and methyl chloroform.
All three compounds have been found weakly mutagenic in at least one
bacterial system, coupled with activation with liver homogenates from special
strains of mice. Both trichloroethylene and methyl chloroform have been sub-
jected to mutagenesis assays in the last 2 years, and much recent and in-press
literature exists. Some studies use stabilized compounds containing up to
3% of chemicals which are known to be much more toxic than the test compounds
themselves. The two in vivo animal studies on mutagenicity, recognized as
producing data most relevant to man, have been performed only on trichloro-
ethylene and methyl chloroform. Neither of these compounds show mutagenesis
in the rat dominant lethal mutation studies. Both, however, produced stimula-
tion and transformation of a rat cell culture line that carried a rat tumor
virus.
The National Cancer Institute conducted carcinogenesis bioassays for all
three compounds. In separate studies, rats and mice were orally administered
trichloroethylene, methyl chloroform, and perchloroethylene five times per week
for 78 weeks. In the trichloroethylene bioassay, rats were administered 1,097
and 549 mg/kg of the compound; more of the control animals developed cancer
than did the test animals. Mice were administered levels of 2,339 and 1,169
mg/kg for males and 1,739 and 869 mg/kg for females. At both dose levels,
over 507« of the males developed cancerous liver tumors, whereas 237o of the
2-4
-------
females at the higher dose and 87o at the lower dose had cancerous liver tumors.
In the methyl chloroform study, rats were administered 1,500 and 750 mg/kg of
the compound and mice were given 5,615 and 2,807 mg/kg for both males and fe-
males. The dose levels administered to both test animals were sufficiently
high so that each group had early death loss; under 4070 of the starting groups
were alive at the end of dosing. Within the surviving group, no consistant
pattern of carcerous tumors was observed. Because of the low survival rate,
statistical analysis could not be performed. For perchloroethylene, mice were
administered 1,072 and 536 mg/kg for males and 772 and 386 mg/kg for females.
Liver cancer was produced in both sexes of the mice at a significant incidence
compared to the control group. Rats used in the bibassay did not show an in-
creased incidence of malignancies. The bioassays received considerable nega-
tive comments because of the very high dose levels employed and the method of
administration of the dose. Studies of all three compounds are being repeated
with a different test protocol which will employ chronically acceptable dose
levels and which will add administration by inhalation, the common route of
human exposure.
Human exposure levels of trichloroethylene, methyl chloroform, and per-
chloroethylene were calculated from monitoring data for ambient air and water.
Data for concentrations in ambient air and water were available for a very
limited number of cities. The calculated exposure levels are only for those
specific cities. For exposure to trichloroethylene from inhalation the maxi-
mum calculated level was 26 /ig/kg of body weight per day (jj,g/kg/day). Levels
for large cities with high population densities were all about 1 /ig/kg/day or
less. For methyl chloroform, levels were above 2 ^g/kg/day in only one city;
in large cities, levels ranged from 1.3 to 0.1 jj,g/kg/day. One of the two
highest levels of perchloroethylene was in New York City (7.8 ^g/kg/day). In
general, the available data show that a relatively small segment of the general
population is exposed to air levels of trichloroethylene or methyl chloroform
that would result in a bodily retention of greater than 1.5 ^g/kg/day.
Relatively few data are available for calculation of exposure levels re-
sulting from ingestion of water. Bodily intake levels from data for most
cities were found to be less than 0.25 ptg/kg/day for trichloroethylene, less
than 0.05 jxg/kg/day for methyl chloroform, and less than 0.02 j^g/kg/day for
perchloroethylene.
2-5
-------
CONTENTS
3. Market Input/Output Analysis 3-5
3.1 Chemical Structure and Properties 3-5
3.1.1 Physical and chemical properties 3-5
3.1.2 Chemical names, trade names, and synonyms . 3-6
3.1.3 Chemical reactivity 3-12
3.1.3.1 Trichloroethylene 3-12
3.1.3.2 Methyl chloroform 3-13
3.1.3.3 Perchloroethylene 3-15
3.1.4 Stabilization of chlorinated solvents . . . 3-17
3.2 Market Data 3~18
3.2.1 Production history of trichloroethylene . . 3-18
3.2.2 End-use patterns of trichloroethylene . . . 3-19
3.2.3 Imports and exports of trichloroethylene . . 3-21
3.2.4 Production history of methyl chloroform . . 3-24
3.2.5 End-use patterns of methyl chloroform . . . 3-24
3.2.6 Imports and exports of methyl chloroform . . 3-26
3.2.7 Production history of perchloroethylene . . 3-27
3.2.8 End-use patterns of perchloroethylene . . . 3-28
3.2.9 Imports and exports of perchloroethylene . . 3-28
3.3 Manufacturing Process Technology 3-32
3.3.1 Production sites and volumes 3-32
o o o
3.3.2 Trichloroethylene production technology . . ->-->->
3.3.2.1 Production from ethylene dichloride . 3~33
3.3.2.2 Production from acetylene 3~37
3-1
-------
CONTENTS (continued)
3.3.3 Methyl chloroform production technology . . 3-39
3.3.3.1 Production from vinyl chloride . . . 3-39
3.3.3.2 Production from vinylidene chloride . 3-42
3.3.3.3 Production from ethane 3-43
3.3.4 Perchloroethylene production technology . . 3-45
3.3.4.1 Production from ethylene dichloride . 3-45
3.3.4.2 Production by chlorination of hydro-
carbons 3-45
3.3.4.3 Production from acetylene via tri-
chloroethylene 3-46
3.3.5 Manufacturing processes by site 3-47
3.3.5.1 PPG Industries, Inc 3~47
3.3.5.2 Dow Chemical Company 3-50
3.3.5.3 Ethyl Corporation 3-52
3.3.5.4 Diamond Shamrock Chemical Company . . 3-54
3.3.5.5 Occidental Petroleum Corporation
(Hooker Chemical Company) 3-56
3.3.5.6 Vulcan Materials Company 3-58
3.3.5.7 Stauffer Chemical Company 3-59
3.3.5.8 E. I. du Pont de Nemours and Company,
Inc 3-60
3.4 Consumption and Utilization 3-60
3,4.1 Solvent metal cleaning ........... 3-61
3.4.1.1 Consumption of degreasing solvents . 3-61
3.4.1.2 Dow Chemical study 3-62
3.4.1.3 Specific site data 3-68
3.4.2 Textile industries 3-72
3.4.2.1 The dry cleaning industry 3-72
3.4.2.2 Consumption of perchloroethylene by
state 3-74
3-2
-------
CONTENTS (continued)
3.4.3 Miscellaneous uses 3-74
3.4.3.1 Trichloroethylene 3-74
3.4.3.2 Methyl chloroform 3-77
3.4.3.3 Perchloroethylene 3-78
3.5 Future Projections 3~79
3.5.1 Trichloroethylene 3~79
O "7Q
3.5.1.1 Metal cleaning applications
3.5.1.2 Other uses 3'80
3.5.1.3 Imports and exports 3~81
3.5.1.4 Production capacity 3~81
O QO
3.5.2 Methyl chloroform J~°
3.5.2.1 Vapor degreasing 3-82
3.5.2.2 Cold cleaning 3.32
3.5.2.3 Miscellaneous uses 3-82
3.5.2.4 Exports and imports 3-83
3.5.2.5 Production capacity 3-83
3.5.3 Perchloroethylene 3-84
3.5.3.1 Textile industry 3-84
3.5.3.2 Metal cleaning 3-84
3.5.3.3 Intermediate chemical 3-84
3.5.3.4 Miscellaneous uses 3-85
3.5.3.5 Exports and imports 3-85
3.5.3.6 Production capacity 3-85
3.6 Overall Materials Balance 3"85
3.6.1 Natural sources 3"85
3.6.2 Manufacturing 3"85
O Qfi
3.6.2.1 Trichloroethylene production ....
3.6.2.2 Methyl chloroform production .... 87
3.6.2.3 Perchloroethylene production ....
3-3
-------
CONTENTS (continued)
Page
3.6.3 Importation 3-91
3.6.4 Consumption 3-91
3.6.5 Distributors 3-91
3.6.6 Exportation 3-92
3.6.7 Final disposal and environmental loss . . . 3-92
3.6.7.1 Trichloroethylene 3-92
3.6.7.2 Methyl chloroform 3-94
3.6.7.3 Perchloroethylene 3-97
3.7 Summary of Chemical Losses 3-101
3.7.1 Atmospheric emissions 3-101
3.7.1.1 Trichloroethylene 3-101
3.7.1.2 Methyl chloroform 3-101
3.7.1.3 Perchloroethylene 3-102
3.7.2 Solid waste disposition 3-102
References 3-103
3-4
-------
SECTION 3
MARKET INPUT/OUTPUT ANALYSIS
This section contains an analysis of the production, consumption, and
disposal of trichloroethylene, methyl chloroform (1,1,1-trichloroethane), and
perchloroethylene (tetrachloroethylene). For each substance, a detailed dis-
cussion is presented for the chemical structure and properties, market data,
manufacturing process technology, consumption patterns and technology, future
projections, overall material balances, and a summary of chemical losses.
3.1 CHEMICAL STRUCTURE AND PROPERTIES
A discussion of trichloroethylene, methyl chloroform, and perchloro-
ethylene regarding their physical and chemical properties; chemical names,
trade names and synonyms; chemical reactivity; and stability is presented in
the following subsections.
3.1.1 Physical and Chemical Properties
Trichloroethylene, methyl chloroform, and perchloroethylene are members
of a family of chlorinated lower aliphatic hydrocarbons that includes methyl
chloride, methylene chloride, chloroform, carbon tetrachloride, and others.
The substitution of chlorine atoms for hydrogen atoms in this series yields a
number of compounds whose unusual properties have made them commercially impor-
tant. Successive substitution lowers the vapor pressure, reduces the flammabil-
ity, and modifies the solvent power (Considine, 197A).
Trichloroethylene (TCE) is a clear, mobile liquid at room temperature with
an ethereal odor. Due to its essentially nonflammable nature in air, volatility,
and low solubility in water, this compound is a very useful solvent (Franklin
Institute, 1975).
Pure trichloroethylene is subject to decomposition from exposure to light,
heat, metals, oxygen and reactive chemicals (Considine, 1974). Stabilizers are
added to the commercial product to offset these deficiencies (see Section
3.1.4). The compound is also photochemically reactive (Waters et al., 1976).
3-5
-------
Methyl chloroform (MC) is a colorless mobile liquid with a characteristic
odor. It is essentially nonflammable, volatile, and has a low solubility in
water (Kirk-Othmer, 1964).
Perchloroethylene is a colorless, clear, volatile, heavy liquid with an
ethereal odor. This chemical, which is nonflammable and noncombustible, is the
most chemically stable (thermally and photolytically) of all chlorinated eth-
anes and ethylenes. Perchloroethylene is only slightly less reactive in terms
of photochemical oxidation than trichloroethylene. In use or storage, the chem-
ical requires very small additions of stabilizers to prevent corrosion problems.
It is an excellent solvent for a. variety of organic substances, which include
fats, oils, tars, rubber and gums. It has substantial vapor pressure and a low
solubility in water. Because of these properties, the atmosphere is expected to
be its primary mode of environmental transport (Puller, I976b).
Perchloroethylene solvent dissolves sulfur, iodine, mercuric chloride,
and aluminum chloride. It also dissolves 0.47o (by weight) ammonia at room tem-
perature and is a solvent for benzoic, cinnamic, phenylacetic, phenylpropionic,
and salicylic acids. It does not, however, dissolve sugar, glycerol, or protein
to an appreciable extent (Fuller, 1976b)»
The properties of pure trichloroethylene, methyl chloroform, and perchloro-
ethylene are shown in Table 3-1 and the composite data tabulated in Table 3-2
shows the properties for the commercial solvent products.
3.1.2 Chemical Names, Trade Names, and Synonyms
A list of names and synonyms for trichloroethylene is given in Table 3-3.
The preferred name in the 9th Collective Index Chemical Abstracts Service (CAS)
is ethene, trichloro-; however, ethylene, trichloro- is the preferred name in
the 8th Collective Index of CAS. A total of 84 brand names and trade names were
identified.
The names and synonyms for methyl chloroform are shown in Table 3-4. The
accepted chemical name is 1,1,1-trichloroethane. A total of 38 trade names or
synonyms were identified.
The names and synonyms for perchloroethylene are presented in Table 3-5.
The accepted chemical name is 1,1,2,2-tetrachloroethylene. Common names are
perchloroethylene, perk, PER, and PCE. Ten trade names or synonyms were iden-
tified.
3-6
-------
TABLE 3-1. PROPERTIES OF PURE TRICHLOROETHYLENE, METHYL
CHLOROFORM, AND PERCHLOROETHYLENE
Methyl
Trichloroethylene chloroform Perchloroethylene
Chemical Abstracts Service
registry number
Molecular formula
Structure
Molecular weight
Composition (% by wt)
Boiling point, C
Freezing point, °C
Flash point
Fire point
Vapor density
Specific gravity
Density, Ib/gal
Specific heat, Btu/(lb)(°F)
Heat of vaporization, Btu/lb
Viscosity, cP at 25°C
79-01-6
C2HC13
H^ Cl
,c=c
/ x
cr ci
131.40
C 18.28%
H 0.77%
Cl 80.95%
87.2
-86.6
None
None
4.53
1.459
12.14
0.22
101.6
0.54
71-55-6
CoHoGl Q
Cl H
Cl-C— C-H
i i
Cl H
133.42
C 18.00%
H 2.27%
Cl 79.72%
74
-37
None
None
4.55
1.320
10.99
0.25
102
0.79
127-18-4
c2ci4
cix ci
,G=C
/ \
cr ci
165.85
C 14.48%
Cl 85.52%
121.2
-22
None
None
5.8
1.623
13.54
-
90.0
-
Sources: Considine (1974); Fuller (1976a; 1976b); Merck Index (1976).
3-7
-------
TABLE 3-2. PROPERTIES OF COMMERCIAL CHLORINATED SOLVENTS
Molecular weight
Melting point, °C
Boiling point, °C
Freezing point, °C
Decomposition temperature, °C
Density, g/cm
Flash point
Relative rate of vaporization
^ Solvent power, Kauri Butanol Value
oo Surface tension, dyne/cm , 20°C
Refractive index D20
Methyl
chloroform
133.41
-50*/
74-761/
-ii i d/
74. 1—
360-440
1.437^
None
5.0
124
25.56
1.43705'
Trichloroethylene
131.39
86. <£7
-86.4-
700
1.467^
None
3.1
129
26.36
1.4760^
Perch lo roe thv 1 ene
165.83
_22c/
12 1^. /
12 1^7 ,
-22. 47
700
1.462-7
None
1.0
92
32.32
1.5056^-'
^£ mm Hg
Vapor pressure
6
10
20
30
40
50
60
70
80
37
62
100
150
240
340
470
600
900
-20
-10.8
0
10
20
30
40
50
60
86.7
3.4
10.8
20.1
35.2
57.8
94
146.8
212
305.7
760
-20.6
+ 2.4
13.8
26.3
40.0
50.0
60.0
70.0
80.0
90.0
100.0
110.0
121.2
1
5
10
20
41
67
104
135.3
266.0
319.2
438.5
591.6
700.0
(continued)
-------
TABLE 3-2. (continued)
\O
Vapor specific gravity
(air - 1)
Viscosity, cps 25°C
Autooxidation
Hydrolysis
Thermal stability (without
stabilizers)
Solubility, water g/100 g H20
Methyl
chloroform
4.55
0.79
None
Sensitive
Good
0.4420
Trichloroethylene
4.55
0.54
Sensitive
Weak
Good
o.n25
0.12560
Perchloroethylene
5.76
0.84
Sensitive
None
Good
0.01525
j/ Aldrich Chemical Company (97% with 3% p-dioxane).
b/ Aldrich Chemical Company (98%).
_c/ Aldrich Chemical Company (spectrophotometric grade).
_d/ Hooker Chemical Company.
Source: Franklin Institute (1975).
-------
TABLE 3-3. CHEMICAL NAMES, TRADE NAMES, AND SYNONYMS FOR
TRICHLOROETHYLENE
Chemical name: 1,1,2-Trichloroethylene; ethene, trichloro-; 1,1-dichloro-
chloroethylene; l-chloro-2,2-dichloroethylene
Common name: Trichloroethylene; ethylene, trichloro-; acetylene trichloride;
ethinyl trichloride; TCE.
Brand and trade names:
Algylen
Alk-Tri
Aramenth
Benzinol
Blacosolv
Cecolene
Chlorylen
Circosolv
Dow-tri
Ex-tri
Fleck-Flip
Gemaegene
Germalgene
Hi-tri
Lanedin
Lethurin
Narcogen
Narcosoid
Neu-tri
Nialk Trichlor MD
Nialk Trichlor MDA
Nialk Trichlor-Extraction
Nialk Trichlor-Technical
Nialk Trichlor-X-1
Perm-A-Chlor NA
Perm-A-Chlor NA-LR
Petzinol
Nialk
Perm-A-Chlor
Perm-A-Clor
Petzinol
Philex
PhiIlex
Stauffer Trichloroethylene
Threthylen
Threthylene
Trethylene
Tri
Triad
Triad-E
Trial
Triasol
Trichlor
Trichloran
Trichlor Type 113
Trichlor Type 114
Trichlor Type 115
Trichlor Type 122
Triclene D
Triclene L
Trielean LS
Triclene MD
Trichloren
Trie lean
Tri-clene
Ethinyl Trichloride
Ethylene Trichloride
Ethyl Trichloroethylene
Trichlorethylene
Trichloroethene
Trielene
Trielin
Trike
Triklone
Trilene
Triline
Triman
Trimar
Trisan
Vestrol
Vitran
Westrosol
Triclene ME
Triclene R
Triclene
Triclene-High
Alkalinity
Triclene-Paint Grade
Trichloroethylene-.
Diral
Trichloroethylene-
Degr. Gen. Solv.
Trichloroethylene-
Extraction Grade
Trichloroethylene-
High Purity
Tri-Paint Grade
Sources: Gardner (1971); Aviado et al. (1976); Merck Index (1976); trade
literature.
3-10
-------
TABLE 3-4. CHEMICAL NAMES, TRADE NAMES, AND SYNONYMS FOR
METHYL CHLOROFORM
Chemical name: 1,1,1-Trichloroethane
Common name: Methyl chloroform, MC
Trade names or synonyms:
Aerothene TT
Axothene No. 3
Barcothene Nu
Blakeothane
Blakesolv 421
CF£ Film Clean
Chlorotnane
Chlorothene (inhibited)
Chlorothene Nu
Chlorothene VG
Chlorten
Dowclene WR
Dyno-Sol
Ecco 1550
Ethyl III Trichloroethane (MPG)
a-Trichloroethane
Insolv Nu
Insolv VG
Kold Phil
Kwik Solv
Lectrosolv 170
Methyl chloroform, Tech.
Nacon 425
One, One, One
Penolene 643
Perm-Ethane D6 (Permathane)
Saf-T-Chlor
Solvent M-50
Solvent III
Sumco 33
Tri-Ethane
Tri-Ethane, Type 314
Tri-Ethane, Type 315
Tri-Ethane, Type 324
Tri-Ethane, Type 339
Triple One
V-301
Vatron III
Sources: Gardner (1971); Aviado et al. (1976); Merck Index (1976); trade
literature.
3-11
-------
TABLE 3-5. CHEMICAL NAMES, TRADE NAMES, AND SYNONYMS FOR
PERCHLOROETHYLENE
Chemical name: Tetrachloroethylene, 1,1,2,2-tetrachloroethylene
Common names: Perchloroethylene, Perk, PER, PCE
Trade names or synonyms:
Carbon dichloride Perchlor HOC
Perclene Dee-Solv
Perclene-D Dow-Per
Tetrachloroethene Percosolv
Perchlor Tetravec
Sources: Gardner (1971); Merck Index (1976); trade literature.
3.1.3 Chemical Reactivity
This subsection presents a brief summary of chemical reactivity of tri-
chloroethylene, methyl chloroform, and perchloroethylene. Additional informa-
tion on the reactions of each of the three compounds in the atmosphere and in
water is presented in Section 6.
3.1.3.1 Trichloroethylene—
In vapor concentrations of a few parts per million, trichlorpethylene may
decompose upon contact with open flames or with hot surfaces to produce hydro-
gen chloride, carbon dioxide, carbon monoxide, and phosgene (Franklin Insti-
tute, 1975).
In the absence of light, unstabilized trichloroethylene is oxidized at
room temperature to dichloroacetyl chloride by air or oxygen. The dichloro-
acetyl chloride readily hydrolyzes to dichloroacetic acid. In addition to the
principal product, traces of carbon monoxide (CO), carbon dioxide (C02), hydro-
gen chloride (HCl), and phosgene (COC^) were also found (Franklin Institute,
1975).
In the presence of glowing charcoal, trichloroethylene yields 12 to 16
mg of phosgene and 350 to 500 mg of hydrogen chloride per gram of substrate.
In contact with a glowing flame, 1 g of trichloroethylene produces 1 mg of
phosgene and 240 to 290 mg of hydrogen chloride (Franklin Institute, 1975).
3-12
-------
When trichloroethylene is heated to 700°C, the vapor decomposes to form
a mixture of dichloroethylene, perchloroethylene, carbon tetrachloride, chloro-
form, and methyl chloride (Kirk-Othmer, 1964).
The formation of hydrogen chloride and phosgene (COC^) during thermal
decomposition of trichloroethylene, with iron as a contact, has been reported
(Franklin Institute, 1975). Phosgene formation increases with temperature to
a maximum of 29 mg/g of trichloroethylene at 500°C and then rapidly decreases
up to 600°C« Hydrogen chloride formation also increases with temperature to a
maximum of 240 mg/g of trichloroethylene at 500°C. Above 500°C, the formation
decreases but much more slowly than for phosgene.
Data on the formation of phosgene by thermal decomposition of trichloro-
ethylene at elevated temperatures and in contact with various metal substances
are shown in Table 3-6 (Noweir et al., 1972). These data show that relatively
large amounts of phosgene (up to 69 mg/g trichloroethylene) can be formed at
temperatures up to 525°C, especially in the presence of zinc, aluminum, or cop-
per.
The strong alkalies react readily with trichloroethylene to form explo-
sive chloroacetylenes. In contrast, sodium carbonate and aqueous ammonia do
not react with the compound. In the presence of soda lime at 37°C, trichloro-
ethylene decomposes readily to form dichloroacetylene, which oxidizes very
rapidly in air to phosgene and carbon monoxide (Franklin Institute, 1975).
Under ambient conditions trichloroethylene resists hydrolysis. Although
the products from dilute solution hydrolysis have not been reported in the
technical literature, it is thought that dichloroacetic acid and hydrogen
chloride are likely hydrolysis products (Dilling et al., 1975).
Trichloroethylene decomposes violently upon contact with hot nitric acid,
but does not react with cold inorganic acids (Franklin Institute, 1975).
3.1.3.2 Methyl Chloroform-
Methyl chloroform is hydrolyzed in an excess of free water at elevated
temperatures and in the gas phase. Hydrolysis occurs at room .temperature to
yield acetic acid in the presence of a catalyst such as ferric chloride. When
the catalyst becomes dehydrated, dehydrohalogenation predominates, yielding
hydrogen chloride and vinylidene chloride (Franklin Institute, 1975). The
hydrolysis reaction, as described by Dilling et al. (1975), is:
0
Water H
GH3CC13 - rr£- — > H2C=CC12 + H3C-C-OH + HCl
catalyst
3-13
-------
TABLE 3-6. PHOSGENE FORMATION IN THERMAL DECOMPOSITION OF TRICHLOROETHYLENE
(jj
1
-p-
Contact
substance
Iron
Copper
Zinc
Aluminum
me Phosgene per e trichloroethylene at various temperatures (°C)
250 290 300 325 350 375 400 425 450
0.1 1 3 5 - 19
0 0.3 - 7
0 0.3 0.4 4 - 22 39 53 69
0 0 0.5 2 - 10 35 -
475 500 525 550 600
14-5 0.1
34 34 3
25 - 25
0.1
Source: Noweir et al. (1972).
-------
When heated between 75 and 160°C in water under pressure, methyl chloro-
form decomposes in the presence of sulfuric acid or metal chlorides, according
to the amount of water present, to form acetyl chloride, acetic acid, or acetic
anhydride.
Methyl chloroform is inert to atmospheric oxidation under normal condi-
tions; however, at temperatures above 370°C, atmospheric oxidation occurs. The
resulting decomposition products are phosgene, 1,1-dichloroethylene, and hydro-
gen chloride (Franklin Institute, 1975).
Methyl chloroform in contact with iron at 402°C, copper at 369°C, zinc
at 338°C, and aluminum at 354°C produces decomposition products containing
0.8, 0.4, 1.9, and 0.3 mg of phosgene per gram of methyl chloroform, respec-
tively (Noweir et al., 1972).
Chlorine reacts with methyl chloroform in sunlight to give 1,1,1,2-tetra-
chloroethane, plus small quantities of penta- and hexachloroethane. Reaction
with anhydrous hydrogen fluoride at 144°C in the absence of a catalyst results
in the formation of 1,1-dichloro-l-fluoroethane and l-chloro-l,l-difluoroethane
(Kirk-Othmer, 1964).
3.1.3.3 Perchloroethylene—
Stabilized perchloroethylene is relatively inert to air, water, light,
and common construction metals at temperatures below 140°C (Franklin Institute,
1975). In the absence of moisture, oxygen, and catalysts, the compound is stable
to about 500°C. At 700°C, it decomposes upon contact with active carbon to yield
hexachloroethane and hexachlorobenzene.
The unstabilized compound also photodegrades on exposure to sunlight with
a half-life of 2 days. Products formed by photolysis include free chlorine,
hydrogen chloride, and trichloroacetic acid. Perchloroethylene is not affected
by oxygen in the absence of light. When exposed to oxygen and irradiated with
ultraviolet light, trichloroacetyl chloride is formed. An intermediate stage
in this reaction is thought to be the synthesis of peroxy compounds (Fuller,
1976b).
2C12C=CC12
I I
A.
4- 0-
CloC -CC1
CloC-CClo
I I
- 0-0 -
0
II
2C13CCC1
2C12CO
3-15
-------
Perchloroethylene in contact with iron at 450°C, zinc at 400oc, and alum-
inum at 400°C gives off 37, 17, and 3 mg of phosgene per gram of perchloro-
ethylene, respectively (Noweir et al., 1972).
Perchloroethylene decomposes to HCl and elemental carbon at 220°C in the
presence of excess hydrogen and a reduced nickel catalyst. Under these condi-
tions, the expected reaction is reduction at the double bond. Under high pres-
sure, perchloroethylene is completely decomposed by ammonia to yield ammonium
chloride and elemental carbon (Fuller, 1976b).
The decomposition rates for trichloroethylene, methyl chloroform, and per-
chloroethylene in the presence of sunlight and in darkness have been deter-
mined. The results show that the decomposition rates for trichloroethylene and
perchloroethylene were slightly greater in sunlight than in the dark. After
12 months, 7570 of the trichloroethylene exposed to sunlight had decomposed as
compared to 547.. for the reaction in the dark. For the same time period, 7570
of the perchloroethylene exposed to sunlight had decomposed compared to 627o
for the reaction in darkness.
The degradation of all three compounds was nearly the same in the light
after 12 months; this decomposition was probably caused by oxidation and was
likely free radical in character. In contrast, sunlight had relatively little
effect on the reactivity of methyl chloroform. The major reaction of methyl
chloroform was probably ionic hydrolysis. The half-lifes for the dark reaction
were 10.7, 6.0, and 8.8 months for trichloroethylene, methyl chloroform, and
perchloroethylene, respectively (Dilling et al., 1975),
Perchloroethylene in contact with butyl lithium in petroleum ether can
result in an explosive reaction; it also reacts explosively with molten potas-
sium. In the presence of dibenzoyl peroxide, perchloroethylene is reported to
yield copolymers with styrene, vinyl acetate, methyl acrylate, and acrylonitrilei
Strong inorganic acids, such as a mixture of sulfuric and nitric acids,
will oxidize perchloroethylene to yield predominantly trichloroacetyl chloride
and some tetrachlorodinitroethane as a by-product (Fuller, 1976b). Similar
yields are also obtained with fuming nitric acid. Nitrogen dioxide reacts read-
ily to yield tetrachlorodinitroethane. Contact with sulfur trioxide at 150°G
results in an oxidation reaction which yields trichloroacetyl chloride.
Perchloroethylene will react rapidly with hydroxyl ions (half-life of 8
days) and slowly with alkyl peroxy radicals and ozone (half-lives of 220 days
and 11 years, respectively). In the presence of ozone, decomposition occurs
to produce a mixture of phosgene and trichloroacetyl chloride (Fuller, 1976b).
Unstabilized perchloroethylene in contact with water for long periods of
time slowly decomposes to yield trichloroacetic and hydrochloric acids. The
reaction at elevated temperature is (Dilling et al., 1975):
3-16
-------
0
C12C = GC12 1500^ C13CC'-OH + HC1
3.1.4 Stabilization of Chlorinated Solvents
All commercial products of the three compounds require stabilization by
chemical additives* Metals, such as iron, aluminum, and zinc, can remove chlo-
rine from the unstabilized compounds to produce metallic chlorides, which are
capable of promoting further degradation of the solvent. These reactions are
sources of hydrogen chloride, which, in the presence of moisture, is very cor-
rosive to metal surfaces. Thus, organic compounds which scavenge hydrogen chlo-
ride, such as organic amines, are effective corrosion inhibitors (Detrex, 1976).
Hydrogen chloride can also be produced by the interaction of chlorinated
solvents with oxygen and moisture. Thus, antioxidants such as phenols and aro-
matic amines are also effective in preventing metallic corrosion. N-alkyl pyr-
role has become the accepted antioxidant (Detrex, 1976).
In addition to the stabilizers incorporated into the solvent by the manu-
facturers, some users also employ additional stabilizers in the solvent for
vapor degreasing to promote better stability of the solvent (Detrex, 1976).
Commercial trichloroethylene stabilizers cover a tremendous variety of
chemicals. Some of these are: acetone, aniline, borate esters, epoxy compounds,
hydroxyanisole derivatives, hydrazones, isocyanates, nitro compounds, phenol,
pyrocolinic derivatives, stearates, and tetrahydrofuran (Franklin Institute,
1975). The following chemicals, mentioned in the patent literature, are com-
monly used in various combinations (Detrex, 1976):
N-methyl pyrrole Epichlorohydrin
Esters such as ethyl acetate Butylene oxide
Three to four carbon alcohols Nitromethane
Aliphatic amines Diisobutylene
Tetrahydrofuran
Normally, these stabilizers are effective at concentrations of less than
1% by weight. With inhibitor addition, trichloroethylene is stable up to a tem-
perature of 130°C in the presence of air, moisture, light, and common construc-
tion metals. At higher temperatures inhibitors are ineffective and corrosion
of the metals occurs (Fuller, 1976a).
Methyl chloroform is sensitive to hydrolysis under usual handling condi-
tions. The commercial product always contains small amounts of stabilizing sub-
stances (Detrex, 1976). The concentration of specific stabilizers which have
been identified in various commercial methyl chloroform products is shown in
the following list (Aviado, 1977; Detrex, 1976):
3-17
-------
Volume 7o
Nitromethane 0.4-1.8
Butylene oxide 0.4-0.8
Dioxane 2.5-3.5
Dioxolane 1.0-1.4
Methyl ethyl ketone 1.0-1.4
Toluene 1.0-1.4
2-Butyl alcohol 0.2-0.3
Isobutyl alcohol 1.0-1.4
Not all of these stabilizers are in every product, and the maximum total
inhibitor package (combinations of stabilizers) appears to be between 7 and 8%
by volume (Aviado, 1977).
The following chemicals are used in various combinations for the purpose
of stabilizing perchloroethylene:
Amines, such as allyl amine Epibromohydrin
Methylmorpholine N-methyl pyrrole
Epichlorohydrin Allyl glycidol ether
The cleaning grades of perchloroethylene contain from 0.01 to 0.1% by weight
of stabilizers, whereas industrial grades contain up to about 0.3570 by weight
of stabilizers (Detrex, 1977).
3.2 MARKET DATA
This subsection provides a technical and commercial history of the sol-
vents of interest with respect to their production, distribution, usage pat-
terns, disposal, and ultimate fate. Factors included are those pertaining to
the overall market and the supply/demand characteristics. All quantities of
compounds are given in terms of millions of pounds and metric tons (MT).
3.2.1 Production History of Trichloroethylene
This compound was first prepared in 1864 by Fischer in the course of ex-
periments on reduction of hexachloroethane with hydrogen. Commercial produc-
tion in the United States dates from 1925 (Kirk-Othmer, 1964).
A long induction period followed the establishment of its manufacture
before the chemical attained industrial significance. This delay was chiefly
attributable to the absence, until the late 1920's, of systematic attempts
to develop applications for the solvent. Small quantities were consumed in
minor extraction processes, and in the formulation of products such as boot
polish and printing ink driers. During the 1920's, several inventions revolu-
tionized the technique of metal degreasing. These inventions and the spread
3-18
-------
of small dry cleaning businesses during the 1930's formed the technological
substrate for the rapid development of trichloroethylene trade in the United
States before World War II. During the war, only small quantities went to sup-
ply civilian needs. In postwar years, the upward trend of prewar demand con-
tinued (Kirk-Othmer, 1964).
Between 1963 and 1967, 85% of the trichloroethylene produced in the United
States was derived from acetylene. From 1968 through 1972, the acetylene pro-
cess accounted for a decreasing amount of the entire production of trichloro-
ethylene: 65% in 1968, 55% in 1969, 51% in 1970 and 1971, and 15% in 1972.
By 1975 only 10% of the total was produced by the acetylene method; about 9070
was derived from ethylene dichloride (Lowenheim and Moran, 1975). A detailed
discussion of production processes is presented in Section 3.3.
Data for domestic production, sales, and prices of trichloroethylene for
the period 1965 to 1977 are presented in Table 3-7. During the period 1965 to
1976, production and sales ranged from a high of 277,148 and 258,097 MT (611
million pounds and 569 million pounds), respectively, in 1970, to a low of
132,768 and 131,635 MT (293 million pounds and 290 million pounds), respec-
tively, in 1975. The U.S. annual production capacity in 1976 was 276,694 MT
(610 million pounds).
The general decline in trichloroethylene production since 1970 is attrib-
utable to the increased usage of methyl chloroform as an alternative cleaning
solvent. This changeover resulted, in part, from the provisions of the Clean
Air Act. In 1975 the general economic depression in the metal fabricating in-
dustries further heightened the decline in trichloroethylene production.
3.2.2 End-Use Patterns of Trichloroethylene
Table 3-8 shows the domestic end-use patterns for trichloroethylene dur-
ing the period 1968 to 1977.
In 1977, about 8770 of total production was consumed in cleaning of fabri-
cated metal parts, as shown in Table 3-8. The .total exports and miscellaneous
uses represented 137o of production during the same year (Chemical Marketing
Reporter, 1978).
The principal current use of trichloroethylene is as a metal cleaning sol-
vent, including both cold cleaning and vapor degreasing. There are a number of
current miscellaneous applications; these include carrier solvent for spotting
fluids, carrier or base for adhesives and lubricants, and a low temperature
heat transfer fluid. Trichloroethylene is used as a solvent in the cleaning
of textiles, in desizing of synthetic fibers, and as an inhalation anesthetic
3-19
-------
TABLE 3-7. DOMESTIC PRODUCTION AND SALES OF TRICHLOROETHYLENE
Total production
Quantity
Year
1965
1966
1967
1968
1969
1970
V 1971
ro
o 1972
1973
1974
1975
1976
1977
1978
(est)
MT
197,088
217,817
222,263
235,462
270,707
277,057
233,512
193,550
204,890
176,041
132,768
143,111
134,946
136,488
106 Ib
434.5
480.2
490.0
519.1
596.8
610.8
514.8
4Z6.7
451.7
388.1
292.7
315.5
297.5
300.9
Capacity
MT
NA^7
256,282
NA
NA
417,309
NA
292,570
244,942
281,230
281,230
276,694
276,694
260,820
106 Ib
NA
565
NA
NA
920
NA
645
540
620
620
610
610
575
Sales
MT
194,185
209,970
214,415
239,318
254,695
258,051
241,495
200,127
210,061
182,618
131,635
135,400
133,993
106 lb
428.1
462.9
472.7
527.6
561.5
568.9
532.4
441.2
463.1
402.6
290.2
298.5
295.4
Approximate
price
10.3
10.5
10.5
9.3
9.0
10.5
8.8
9.8
10.3
12.8
15.0
15.0
16.0
a/ NA = Not available.
Sources: Franklin Institute (1975); U.S. International Trade Commission (1972-1979);
Lowenheim and Moran (1975).
-------
during parturition and in dentistry. It also serves as a terminator for poly-
vinyl chloride production and as a raw material in the production of a fungi-
cide (Difolatan®). Use as an extractant for medicines and foods (e.g., coffee
beans, hops, soya beans, and spices) has been discontinued; methylene chloride
is now being used as the extractant.
TABLE 3-8. DOMESTIC END-USE PATTERNS FOR TRICHLORDETHYLENE
Percent of total consumption
End use
Metal cleaning
Extraction solvent
Exports
Miscellaneous
1968
94
3
|
3
1
1969
95
3
1
1971
84
-
10
6
1972
87
3
8
2
1973
86
3
|
hi
i
1975
86
-
12
2
1977
87
-
J
/1 3
1
Sources: Oil, Paint and Drug Reporter (1969); Arthur D. Little (1975);
Franklin Institute (1975); Detrex (1976); U.S. Bureau of the
Census (1975); Chemical Marketing Reporter (1978).
A list of representative commercial household products containing tri-
chloroethylene is given in Appendix A.
3.2.3 Imports and Exports of Trichloroethylene
Import data for trichloroethylene covering the period 1965 to 1975 are
given in Table 3-9., In 1976 total imports amounted to about 7,056 MT (15.6 mil-
lion pounds), of which Canada supplied about 42%. The original European Economic
Community (EEC) countries supplied 3,086 MT (44%), other (OECD) countries 6 MT,
and Japan 1,011 MT (147o). No further breakdown concerning the specific European
countries was provided. The total importation to the United States has decreased
over the years from a high of about 53,684 MT (119 million pounds) in 1966 to
a low of 626 MT (1.38 million pounds) in 1974.
Data for exports during the period 1970 to 1977 are presented in Table
3-10. The quantity of total exports has generally ranged between 14,000 and
23,000 MT.
3-21
-------
TABLE 3-9. U.S. IMPORTS OF TRIGHLOROETHYLENE (Metric Tons)
N>
to
Country
Canada
United Kingdom
Netherlands
Belgium
France
West Germany
Poland
Italy
Japan
Other
Total
1967
187
6,539
787
1,194
6,906
5,534
2,957
17,144
1,036
0.5
42,284.5
1968
20
3,836
-
-
3,693
3,222
1,820
14,037
-
_
26,628
1969
—
6
-
-
3,059
2,910
-
10.445
8
3
16,431
1970
292
11
-
-
3,597
2,889
-
5,526
1,545
_
13,860
1971
322
15
-
-
189
1,059
-
2,562
21
.
4,168
1972
2,403
4,567
-
•
901
7,986
- -
8,678
3,010
-
27,545
1973
967
-
-
-
1,449
11
-
16,087
3,001
7
21,522
1974
412
-
-
•
126
-
-
- -
-
88
626
1975
822
-
-
-
1,480
-
-
489
993
10
3,794
1976
2,954
-
-
999
-
-
-
2,076
1,011
17
7,057
1977
2,917
-
-
-
-
-
-
5,766
-
13
8,696
Source: U.S. Bureau of the Census (1965-1977).
-------
TABLE 3-10. U.S. EXPORTS OF TRICHLOROETHYLENE FROM 1970 THROUGH 1977
(Metric Tons)
(jj
ro
Country
Belgium
Canada
Mexico
Columbia
Peru
Chile
Brazil
Netherlands
Singapore
Republic of Korea
Hong Kong
Australia
Republic of South Africa
Argentina
Japan
French Pacific Island
Thailand
Taiwan
Nicaragua
Haiti
Venezuela
Malaysia
Indonesia
West Germany
Philippines
France
Other
Total
1970
_
494
4,054
95
87
113
730
7,685
83
124
403
415
236
-
-
-
-
-
-
-
-
-
-
-
-
-
316
14,835
1971
_
2,032
4,819
144
-
77
2,376
12,912
-
123
-
-
416
107
284
-
-
-
-
-
-
-
-
-
-
-
293
23,583
1972
_
2,142
6,080
148
-
155
462
8,409
-
-
-
-
-
60
1,347
90
-
-
-
-
-
-
-
-
-
-
184
19,076
1973
_
1,262
7,292
-
-
-
1,548
6,612
50
41
297
45
-
-
-
158
63
137
-
-
-
-
-
-
-
-
300
17,805
1974
_
717
7,182
100
63
128
1,394
3,318
620
73
506
-
-
125
3,284
80
152
699
30
80
83
137
414
-
225
176
-
19,584
1975
_
3,274
2,669
-
-
-
1,603
2,726
-
-
-
'
-
-
1,581
-
-
-
-
-
128
-
-
1,950
483
-
993
15,409
1976
1,054
201
2,060
-
-
-
2,047
1,490
823
-
468
374
-
-
-
-
-
-
-
-
110
-
-
3,759
-
3,404
332
16,124
1977
.
659
2,172
-
-
-
4,102
2,683
1,643
-
304
944
-
-
-
-
-
211
-
-
-
-
-
3,785
-
4,487
797
21,788
Source: U.S. Bureau of the Census - Exports (1970-1977).
-------
3.2.4 Production History of Methyl Chloroform
Methyl chloroform was discovered by Regnault about 1840 (Considine, 1974).
Some domestic uses were recorded as early as 1874, but extensive commercial
use depended on stabilization of the compound, since the unstabilized compound
can react with certain metals to generate noxious and toxic compounds. Adequate
stabilizers were not developed until 1954.
In 1975, methyl chloroform was produced by three processes: (a) about
60% by production from vinyl chloride; (b) 30% by production from vinylidene
chloride; and (c) 10% by chlorination of ethane (Lowenheim and Moran, 1975).
A detailed discussion of these processes is given in Subsection 3.3.
Data for the U.S. production and sales and prices of methyl chloroform
for the period 1966 to 1977 are shown in Table 3-11. The production and sales
ranged from a low of 110,179 and 113,263 MT (243 and 250 million pounds), re-
spectively, in 1966, to a high of 286,358 and 278,919 MT (631 and 615 million
pounds), respectively, in 1976.
3.2.5 End-Use Patterns of Methyl Chloroform
The domestic end-use patterns for methyl chloroform during the period 1968
to 1976 are shown in Table 3-12.
The use of methyl chloroform as an intermediate for manufacturing vinyli-
dene chloride began in late 1971 with the Dow Chemical Company but has been
terminated. However, Dow also continued to produce vinylidene chloride from
1,1,2-trichloroethane, which is currently the sole method of production.
Currently, the largest use for methyl chloroform is as a solvent in indus-
trial applications including metal vapor degreasing, electrical and electronic
instrument cleaning, and metal cold cleaning. A wide variety of parts from elec-
tronic components, ranging from printed circuit boards to massive parts for the
automotive, aircraft, or railroad industries, are cleaned with methyl chloroform.
Methyl chloroform is also used, with appropriate additives, in high purity clean-
ing applications including vacuum equipment and semiconductor devices.
Current miscellaneous uses for methyl chloroform include:
* A vapor pressure depressant to replace some fluorocarbons in aerosol
products (e.g., spot remover).
* A resin solvent in adhesive formulations for factory-applied adhesives
and as an on-the-job adhesive activator.
* A lubricant carrier to inject graphite, grease, and dry lubricant.
3-24
-------
TABLE 3-11. DOMESTIC PRODUCTION AND SALES OF METHYL CHLOROFORM
Ni
Total production
Quantity
Year
1960-
1965
1966
1967
1968
1969
1970
1971
1972
1973
1974
1975
1976
1977
1978
(est.)
MT
NA^7
110,179
NA
135,808
147,102
166,154
169,919
199,902
248,754
268,350
208,112
286,358
287,945
282,547
106 Ib
NA
242.9
NA
299.4
324.3
366.3
374.6
440.7
548.4
591.6
458.8
631.3
634.8
622.9
Capacity
MT
NA
NA
NA
136,079
NA
NA
256,282
NA
285,766
NA
335,662
312,984
312,984
106 Ib
NA
NA
NA
300
NA
NA
565
NA
630
NA
740
690
690
Sales
MT
NA
113,263
122,335
130,681
135,580
148,508
154,813
176,449
256,827
261,136
216,912
278,919
254,061
106 Ib
NA
249.7
269.7
288.1
298.9
327.4
341.3
389.0
566.2
575.7
478.2
614.9
560.1
Approximate
price
(t/lb)
-
12.8
-
13.0
-
11.3
-
11.8
14.5
18.5
19.3
19.0
20.0
Sources: Franklin Institute (1975); U.S. International Trade Commission (1972-1979); Lowenheim
and Moran (1975); Chmielnicki (1978).
a/ NA = Not available.
-------
* A coolant and lubricant in cutting oil compounds.
* Use in liquid drain cleaner (e.g., Drano®).
* A solvent in shoe polishes, spot cleaners, insecticides, and printing
inks.
* Use in wig cleaning.
* Use in cleaning of motion picture film.
* Use by the textile industry for processing and finishing, primarily
as a spotter for bulk fabric.
TABLE 3-12. DOMESTIC END-USE PATTERNS FOR METHYL CHLOROFORM
End use
Metal cleaning
solvent
Exports
Vinylidene chloride
Miscellaneous
Percent
1968 1971
80 80
13 5
- -
7 15
of total
1973
70
14
8
8
consumption
1975
75
10
12 1
3 )
1976
75
5
20
Sources: A. D. Little (1975); Chemical Marketing Reporter (1971; 1977).
The Food and Drug Administration has reported that no domestic drug manufac-
turers are using methyl chloroform in any of their products (Food and Drug Ad-
ministration, 1977b). A compilation of commercial products containing methyl
chloroform is given in Appendix A.
3.2.6 Imports and Exports of Methyl Chloroform
Imports and exports of methyl chloroform have not been reported separately
by the U.S» Bureau of the Census. Estimated data are shown in Table 3-13.
Since methyl chloroform has generally been in oversupply in the United
States during recent years, it is believed that imports were negligible.
3-26
-------
TABLE 3-13. EXPORT DATA FOR METHYL
CHLOROFORM
Year
MT x 103 106 Ib
1968
1973
1974
1975
1976
18
35
37
21
14
39
77
81
465/
3L5/
_§_/ MRI estimate.
Sources: A. D. Little (1975);
Dow Chemical Company
(1976).
3.2.7 Production History of Perchloroethylene
Perchloroethylene was first prepared in 1821 by Faraday, who obtained it
by thermal decomposition of hexachloroethane. Regnault, in 1840, prepared the
compound by passing the vapor of carbon tetrachloride through a red-hot tube,
and also by reduction of hexachloroethane with alcoholic potassium hydrosul-
fide. In 1887, Combes produced the compound by prolonged heating of chloral
with anhydrous aluminum chloride. In 1894, Meyer isolated it as a by-product
in the industrial production of carbon tetrachloride from carbon disulfide
(Kirk-Othmer, 1964).
Industrial production began in the United States about 1925. Prior to
1970 the compound was produced by several methods. In one process, which used
acetylene as a raw material, pentachloroethane was synthesized and dehydro-
halogenated to the desired product. Another method involved the chlorination
of acetylene. Using tetrachloroethane as raw material, perchloroethylene was
produced either by chlorination (with hydrogen chloride formed as by-product)
or by oxidation (with water produced as by-product). Other methods included
direct chlorination of ethane or ethylene (Fuller, 1976b).
In 1970 most of the U.S. perchloroethylene production was by the thermal
chlorination of propane. The remaining production was by processes using acet-
ylene as starting material. In 1972, after the two major acetylene-based plants
in the United States were closed, only about 5% of production was based on the
use of acetylene (Fuller, 1976b).
3-27
-------
In 1975, the bulk of perchloroethylene output (97%) was derived from the
oxychlorination of ethylene dichloride, or by the simultaneous chlorination
and pyrolysis of hydrocarbons such as propane. A minor amount of perchloro-
ethylene (about 3%) was produced from acetylene (Lowenheim and Moran, 1975)o
A detailed discussion of these production methods is presented in Subsec-
tion 3.3.
Data for domestic production, sales, and prices of perchloroethylene for
the period 1965 to 1977 are presented in Table 3-14. During this period, the
production ranged from a low of 194,775 MT (429.4 million pounds) in 1965 to
a high of 333,122 MT (734.4 million pounds) in 1974. Since 1974, U.S. produc-
tion has been slowly but steadily decreasing in volume.
3.2.8 End-Use Patterns of Perchloroethylene
Table 3-15 shows the domestic end-use patterns for perchloroethylene dur-
ing the period 1965 to 1975.
During the early 1970fs, the relative demand for perchloroethylene in
metal cleaning and as an export material increased significantly. In 1975,
the domestic end-use distribution (excluding exports) consisted of about 63%
to uses in the textile industry, 16% to metal cleaning, 11% to applications
as a chemical intermediate (primarily for production of fluorocarbons, such
as F-113), and 3% to miscellaneous uses (Lowenheim and Moran, 1975).
The current principal use for perchloroethylene is in the textile indus-
try as a dry cleaning agent and as a solvent in textile processing and finish-
ing.
The second largest end-use is for metal cleaning operations including
vapor degreasing and cold cleaning. Perchloroethylene is also used as an inter-
mediate in the synthesis of fluorocarbons F-113, F-114, F-115, and F-116.
Current miscellaneous applications include use as a solvent for silicones
and in aerosol specialty products that compete with enzyme presoak laundry
products.
3.2.9 Imports and Exports of Perchloroethylene
Import data covering the period 1965 to 1975 are shown in Table 3-16.
In 1976, total imports were 28,227 MT (62.2 million pounds); about 79% of these
imports were supplied by the original European Economic Community (EEC) coun-
tries; Japan and Canada supplied 11 and 10%, respectively. During this period,
the total importation to the United States ranged from a high of 38,805 MT (86
million pounds) in 1966 to a low of 10,704 MT (23.6 million pounds) in 1974.
3-28
-------
TABLE 3-14. DOMESTIC PRODUCTION AND SALES OF PERCHLORQETHYLENE
u>
NJ
\O
Total production
Quantity
Year
1965
1966
1967
1968
1969
1970
1971
1972
1973
1974
1975
1976
1977
1978
(est.)
MT
194,775
209,879
241,767
288,715
288,170
320,648
319,650
333,031
320,149
333,124
308,040
303,413
278,556
326,864
10° Ib
429.4
462.7
533.0
636.5
635.3
706.9
704.7
734.2
705.8
734.4
679.1
668.9
614.1
720.6
Capacity
MT
NA^7
NA
NA
NA
NA
NA
489,885
442,257
401,433
462,669
535,244
548,856
557,928
10° Ib
NA
NA
NA
NA
NA
NA
1,080
975
885
1,020
1,180
1,210
1,230
Sales
MT
174,635
192,688
212,681
257,190
277,450
290,393
296,687
332,244
333,122
321,590
267,306
259,686
239,047
10° Ib
385.0
424.8
468.7
567.0
611.6
640.2
653.9
732.4
734.4
708.8
589.3
572.5
527.0
Approximate
price
(
-------
TABLE 3-15. PERCHLOKDETHYLENE END-USE PATTERNS
IN THE UNITED STATES
Percent of total consumption
Textile
End use 1965 1968
industry 90 85
Metal cleaning 10 2
Chemical
intermediate - 8
Exports
5
Miscellaneous
1973 1975
65 63
12 16
8 11
7
15
3
Sources: Faith et al. (1965); A. D. Little (1975); Lowenheim and
Moran (1975).
3-30
-------
TABLE 3-16. U.S. IMPORTS OF PERGHLOROETHYLENE (Metric Tons)
Country
Spain
Sweden
Canada
United Kingdom
Netherlands
Belgium
France
West Germany
Italy
Japan
Other
Total
1967
—
-
2,509
981
1,073
1,156
10,615
2,175
4,063
89
-
22,661
1968
—
-
3,986
1,123
-
-
6,751
1,178
5,822
1,222
-
28,082
1969
<-
-
609
-
-
500
4,439
3,735
3,445
3,022
-
15,750
1970
.
-
36
-
-
3,242
7,268
708
3,318
3,636
-
18,208
1971
.
1,356
379
-
1,919
2,688
7,904
1,949
2,895
1,062
-
28,152
1972
.
2,780
457
-
981
1,006
1,044
4,805
-
1,030
-
12,103
1973
_
2,352
2,493
-
2,302
5,512
7,230
375
-
-
-
20,264
1974
—
6
901
-
1,531
585
6,386
1,295
-
-
-
10,704
1975
.
24
-
-
2,194
3,116
5,862
3,772
-
2,021
-
16,989
1976
.
-
2,833
-
1,054
5,896
9,467
740
5,210
3,026
-
28,226
1977
528
-
8,559
-
-
5,565
6,432
-
5,972
-
8
27,064
Source: U.S. Bureau of the Census (1965-1977).
-------
Information regarding exports of perchloroethylene was not reported sep-
arately by the U.S. Bureau of Census until 1972. Export data for the period
1972 to 1977 are shown in Table 3-17.
TABLE 3-17. U.S. EXPORTS OF PERCHLOROETHYLENE
Year MT 106 Ib
1972 46,681 107.3
1973 36,159 79.7
1974 13,109 28.9
1975 23,859 52.6
1976 22,181 48.9
1977 21,817 48.1
Source: U.S. Bureau of the Census (1972-1977).
3.3 MANUFACTURING PROCESS TECHNOLOGY
A discussion of production sites and volumes, production technology, man-
ufacturing processes by site, and environmental management practices is pre-
sented in the following subsections.
3.3.1 Production Sites and Volumes
In 1977, trichloroethylene was produced domestically by five manufacturers
at five production sites, as shown in Table 3-18.
TABLE 3-18. U.S. PRODUCTION CAPACITY DATA FOR
TRICHLOROETHYLENE
Annual production
capacity
Producer
PPG Industries, Inc.
Dow Chemical Company
Diamond Shamrock
Corporation
Occidental Petroleum
Corporation
Ethyl Corporation
Total
Site
Lake Charles, LA
Freeport, TX
Deer Park, TX
Taft, LA
Baton Rouge, LA
MT
127,000
68,040
24, 948
22,680
18,144
260,812
(x 106 Ib)
280
150
55
50
40
575
% of
total
capacity
48.7
26.1
9.6
8.7
6.9
100.0
Raw
material
Ethylene
Ethylene
Ethylene
Acetylene
Ethylene
Source: Stanford Research Institute, Directory of Chemical Producers (1978).
3-32
-------
Two companies, PPG Industries, Inc., and Dow Chemical, accounted for about 75%
of the total U.S. production capacity. Total production capacity in 1977 was
260,812 MT (575 million pounds). In 1977, the U.S. production of trichloro-
ethylene was 132,768 MT (292.5 million pounds).
During 1977, methyl chloroform was produced by three companies at three
production sites. Production capacity data (1977) are presented in Table 3-19.
Ethyl Corporation was a manufacturer of methyl chloroform but discontinued pro-
duction during the first quarter of 1976. In 1977, two companies, Dow Chemical
and PPG Industries, accounted for about 90% of the total production capacity
of 313,000 MT (690 million pounds).
Completion of a new methyl chloroform production facility in Plaquemine,
Louisiana, by Dow Chemical occurred in early 1978 with a capacity of approxi-
mately 136,000 MT (300 million pounds). This facility will raise Dow Chemical's
capacity for methyl chloroform to about 750 million pounds. PPG Industries in-
creased the capacity of the facility at Lake Charles to 136,000 MT (300 million
pounds) in 1978 (Chemical Marketing Reporter, 1977).
In 1977 perchloroethylene was produced domestically by eight manufacturers
at 11 production sites. Production capacity data are shown in Table 3-20. To-
tal domestic production capacity in 1977 was about 557,930 MT (1,230 million
pounds). Plant capacities are very flexible because in most cases at least one
other product (e.g., trichloroethylene or carbon tetrachloride) can be produced
with the same equipment. The largest producer was Dow Chemical Company, which
accounted for about 24% of the total production capacity. Plant production
capacities range from a low of 9,072 MT (20 million pounds) per year (Dow Chem-
ical Company, Pittsburg, California) to a high of 90,720 MT (200 million pounds)
per year (PPG Industries, Inc., and Diamond Shamrock Corporation).
3.3.2 Trichloroethylene Production Technology
In 1975, about 90% of the commercial production of trichloroethylene was
by the chlorination or oxyhydrochlorination of ethylene to form the intermedi-
ate ethylene dichloride, which was in turn chlorinated and then dehydrochlori-
nated to form trichloroethylene. The remaining 10% was still manufactured by
an older process which involves chlorination of acetylene in the presence of
a catalyst, followed by. dehydrochlorination of the 1,1,2,2-tetrachloroethane
intermediate.
3.3.2.1 Production From Ethylene Dichloride—
A typical process for the manufacture of trichloroethylene and perchloro-
ethylene from ethylene dichloride is shown in Figure 3-1. There are several
other commercial processes based on ethylene dichloride.
3-33
-------
TABLE 3-19. U.S. PRODUCTION CAPACITY DATA FOR METHYL CHLOROFORM
UJ
Methyl chloroform
producer Site
Dow Chemical Company Freeport, TX
PPG Industries, Inc. Lake Charles, LA
Vulcan Materials Company Geismar, LA
Total
Annual production
capacity
MT (x 106 Ib)
204,100 450
79,400 175
29,500 65
313,000 690
% of
total
capacity
65.2
25.4
9.4
100.0
Raw material
Vinyl chloride
Vinylidene chloride
Ethane
Source: Stanford Research Institute, Directory of Chemical Producers (1978).
-------
TABLE 3-20. U.S. PRODUCTION CAPACITY DATA FOR PERCHLOROETHYLENE
Annual production
capacity
Producer
Diamond Shamrock
Corporation
Dow Chemical, UiS.A.
E. I. du Pont de Nemours
and Company, Inc.
Ethyl Corporation
u>
do Occidental Petroleum
Corporation
PPG Industries, Inc.
Stauffer Chemical
Company
Vulcan Materials Company
Total
Location
Deer Park, TX
Freeport, TX
Pittsburg, CA
Plaquemine, LA
Corpus Christi, TX
Baton Rouge, LA
Taft, LA
Lake Charles , LA
Louisville, KY
Geismar, LA
Wichita, KS
MT
90,720
54,430
9,070
68,040
72,575
22,680
18,140
90,720
31,750
77,110
22,680
557,930
(x 10b Ib)
200
120
20
150
160
50
40
200
70
170
50
1,230
7» of
total
capacity
16.3
9.7
1.6
12.2
13.0
4.1
3.2
16.3
5.7
13.8
4.1
100.0
Raw
materials
Ethylene
dichloride
Various
Various
Various
Various
Ethylene
dichloride
Acetylene
Ethylene
dichloride
Various
Various
Various
Source: Stanford Research Institute, Directory of Chemical Producers (1978).
-------
Recycle
Ethylene—
Oichloride
Chlorine—-
Oxygen
Steam • •-.
H2O
u
Reactor
H2O
NH3 H2O
U
Neutralizer
1
a
O
i i
Recycle
•TCE
F
D
a
1
U.
H2O
t/1
J
y
n"
1
NH3 H2O
U
• PCE
Source: Lowenheim and Moran (1975).
Figure 3-1. Production schematic for trichloroethylene based on ethylene
dichloride.
Trichloroethylene and perchloroethylene are produced as co-products in
a single-stage oxychlorination process from ethylene dichloride and chlorine.
As market demands dictate, the product ratios can be varied from nearly 100%
trichloroethylene to 100% perchloroethylene by adjusting the proportions of
raw materials and process conditions (Lowenheim and Moran, 1975).
The principal reactions in this process are:
2C2H4C12 + 5C12 - ^ C2H2C14 + C2HC15 + 5HCl
2Cl4 + C2HC15
7HG1 + 1.7502
C2HC13
1.5C1
1.750
2HC1 + C2C1^
3.5H20 + 3.5C12 (Deacon)
3<5H2°
C2HC13
C2C14
3-36
-------
Based on a final production of 1 kg of perchloroethylene and 0.793 kg of tri-
chloroethylene, the quantities of raw materials are 1.195 kg of ethylene di-
chloride, 0.642 kg of chlorine, 0.388 kg of oxygen, and a small quantity of
oxychlorination catalyst (Lowenheim and Moran, 1975).
Ethylene dichloride, recycled chlorinated organics, chlorine, and oxygen
are charged to a fluid bed reactor which is maintained under pressure and at a
temperature of about 425°C. The reaction product, containing trichloroethylene,
perchloroethylene, and hydrogen chloride, is passed through a vent scrubber.
After vent scrubbing of the product gas stream with water, the weak hydro-
chloric acid and the condensed crude product are phase separated. Azeotropic
distillation is used to dry the crude; the overhead stream from this dehydra-
tion step is vented to the atmosphere. The dehydrated crude is fed to a perchlor-
trichlor still column in which the crude is split into two streams, one rich in
trichloroethylene and the other rich in perchloroethylene.
The crude trichloroethylene stream is fed into a product still in which
low boiling components, such as dichloroethylenes, are removed as an overhead
stream and recycled to the reactor. The purified product (99.9+ wt % purity)
is removed from the bottom of the still, neutralized with ammonia, washed, and
dried. The overall yield of trichloroethylene in this process is 85 to 90%.
By-products and wastes from this process are hydrogen chloride (recovered
as hydrochloric acid); chlorine (produced from hydrogen chloride by the Deacon
process using a copper chloride catalyst); and atmospheric (water vapor) emis-
sions from the crude product dehydrator unit (Lowenheim and Moran, 1975).
3.3.2.2 Production From Acetylene —
A typical process flow diagram for the chlorination of acetylene to tetra-
chloroethane followed by dehydrochlorination to trichloroethylene is shown in
Figure 3-2. The features presented give a composite picture of the usual opera-
tions (Gruber, 1976).
The principal reactions are:
SbCl
2C12
C2H2C14 > C1HC=CC12 + HCl
The acetylene and chlorine (each premixed with recycled tetrachlorpethane
and antimony trichloride catalyst) are fed into a chlorinator reactor (packed
tower)» The reaction product from this chlorination reaction is fed to a still
and separated into spent catalyst, tetrachloroethane, and vent gas. The spent
catalyst is sent to a recovery system (Gruber, 1976).
3-37
-------
Basis: 1.0 Kg Trichloroethylene
CJ
oo
Acetylene 0.21
Chlorine 1.14
Tetrochloro-
ethane 0.3
Antimony •
Trichloride
(Catalyst)
Spent Antimony
Trichloride
to Recovery
0
Vent on Reflux Condenser (Gas)
Ethane 0.001252
Methane 0.001252
Tetrachloroerhone 0.0004997
Tail Gas Absorber (Gas)
Hydrogen Chloride 0.00099
Tetrachloroethane 0.000499
Trichloroethylene 0.0003502
Tetrochloroethyfene 0.00099
Air
Air
Source: Adapted from Gruber (1976).
>• • ««
Tail Gas Absorber
•HCI 0.28
Condenser
Degasser
TCE
Column
Heavy Ends
Heavy Ends from TCE Columns (Liquid-Solid)
Max. Limits are:
Hexachlorobutadiene 0.23
Chlorobenzenes 0.02
Chloroethanes 0.01
Chlorobutadier.es 0.01
Tars and Residues 0.02
Land
Figure 3-2. Production schematic for trichloroethylene from acetylene.
-------
The tetrachloroethane is split into a dehydrochlorinator feed stream and
a recycle stream. Dehydrochlorination of tetrachloroethane is accomplished in
a packed tower filled with activated carbon held at 300°C. The reaction prod-
ucts, consisting of trichloroethylene and hydrogen chloride, are cooled and
separated. The gaseous phase hydrogen chloride is absorbed in water and sold
as a commercial grade of muriatic acid*
The trichloroethylene is passed through a degasser to a distillation col-
umn for purification. The heavy ends waste from the distillation column con-
tains various chlorinated compounds as shown in Figure 3-2 (Item 3). This waste
is usually sent to land disposal (Gruber, 1976).
The vent gas released to the atmosphere from the tetrachloroethane still
contains small quantities of ethane, methane, and tetrachloroethane as shown
in Figure 3-2 (Item 1).
Gas vented to the atmosphere from the hydrogen chloride recovery step
(Item 2) contains small amounts of trichloroethylene, tetrachloroethane, per-
chloroethylene, and hydrogen chloride.
In some plants, the conversion of tetrachloroethane is accomplished by
contact with milk-of-lime suspension in a packed tower. Trichloroethylene dis-
tills overhead and is then condensed and purified. The reaction using milk-of-
lime is:
2CHC12CHC12 + Ca(OH)2 > ClHG=CCl2 + CaCl2 + 2H20
If the conversion is accomplished by use of milk-of-lime, the additional by-
products are calcium chloride and water.
For all of the production plants, the principal product grades are tech-
nical (high purity) and extraction (no acidity) grade (Lowenheim'and Moran,
1975).
3.3.3 Methyl Chloroform Production Technology
In 1975, about 60% of the domestic production of this chemical was derived
from vinyl chloride, almost 30% was based on the use of vinylidene chloride as
raw material, and the remainder was produced by thermal chlorination of ethane.
3.3.3.1 Production From Vinyl Chloride--
A representative process diagram for production of methyl chloroform from
vinyl chloride and chlorine is presented in Figure 3-3. The principal reactions
in this process are:
3-39
-------
Basis: 1 Kg Methyl Chloroform
Vinyl
Chloride -
0.5
Hydrogen
Chloride -
Start Up
Co
•F-
O
Hydrochlorinator Vent
Hydrochlorinator
Reactor
HCI Recycle Stream
i not or I
or /"^\
Chlorinotor
Reactor
Chlorine 0.525-#«
Purification
Column
Dichloro-
ethane
Steam-*.
Steam
Strippe
Crude
Trichloro-
ethane
Steam Stripper
Gas Effluent
MC, 1.0 Kg
• Steam Stripper
Water Effluent
Hydrochlorinator Vent (Gas)
Dichloroethane 0.0085
Trichloroethane 0.009
Air
Source: Gruber (1976).
Steam Stripper Gas Effluent (Gas) Steam Stripper Water Effluent (Water)
Dichloroethane 0.0005
Trichloroethane 0.0005
Vinyl Chloride 0.0005
Air
Organic Chlorides - Traces
Hydrochloric Acid - Traces
Wafer
Figure 3-3. Flow diagram for production of methyl chloroform from vinyl chloride^
-------
CH9=CHC1 + HC1 n.0
*• 242
+ C12 -^ ^> CH3CC13 + HC1 (by-product, reused
in process)
Based on 1 kg of methyl chloroform, the quantities of raw material con-
sumed are 0.5 kg vinyl chloride, 0.525 kg chlorine, and a small quantity of
ferric chloride catalyst (Gruber, 1976).
Methyl chloroform is made in two steps: (a) hydrochlorination of vinyl
chloride to form 1,1-dichloroethane, and (b) thermal chlorination of the lat-
ter to produce the compound in yields greater than 95% (Lowenheim and Moran,
1975).
Vinyl chloride, recycled and make-up hydrogen chloride, recycled dichloro-
ethane, recycled trichloroethane, and ferric chloride catalyst are fed to a
tower-type reactor where a catalyzed hydrochlorination reaction between vinyl
chloride and hydrogen chloride at 35 to 40°C produces dichloroethane (Gruber,
1976).
The reaction products are sent to a purification column. The dichloro-
ethane fraction is separated as an overhead stream from the column and chlori-
nated (atmospheric pressure and about 400°C) with chlorine gas to produce
crude trichloroethane and by-product hydrogen chloride. The crude trichloro-
ethane, by-product hydrogen chloride, and excess dichloroethane are recycled
from the chlorinator reactor to the hydrochlorinator reactor (Lowenheim and
Moran, 1975).
The crude product, separated in the purification column as the high boil-
ing fraction, is sent to a stripper column where it is steam stripped and dis-
tilled to yield purified methyl chloroform. The product yield is over 95%
(Lowenheim and Moran, 1975).
Figure 3-3 shows the gas and liquid waste streams for this process; the
quantities of wastes are given in kilograms of waste constituents produced per
kilogram of product. The water effluent from the steam stripper contains traces
of organic chlorides. Currently (1976) no land-destined hazardous wastes are
discharged by this process (Gruber, 1976).
By-products and waste material are hydrogen chloride; waste gas from hy-
drochlorinator vent (Figure 3-3, Item 1) containing 0.0085 kg of dichloroethane
and 0.009 kg of trichloroethane for each kilogram of product; waste gas from
steam stripper (Figure 3-3, Item 2) containing 0.0005 kg each of dichloro-
ethane, trichloroethane, and vinyl chloride for each kilogram of product; and
waste water from steam stripper (Figure 3-3, Item 3) containing traces of or-
ganic chlorides and hydrochloric acid.
3-41
-------
3.3.3.2 Production From Vinylidene Chloride--
The basic reaction involved in this process is:
CH2=CC12
HC1
On the basis of 1 kg of product, the raw material requirements are 0.727 kg
vinylidene chloride, 0.274 kg hydrochloric acid, and a small quantity of ferric
chloride catalyst. A representative flow diagram for this process is shown in
Figure 3-4.
Vinylidene-^
Chloride
Ferric ^
Chloride
r
orinqtor
_c
u
8
£
t
— ^
n
Fractionator
MC
Recycle
o
u
o
Heavy
Ends
Waste
Source: Lowenheim and Moran (1975).
Figure 3-4.
Flow diagram for production of methyl chloroform from
vinylidene chloride by hydrochlorination.
The vinylidene chloride used as raw material is obtained by: (a) chlori-
nation of ethylene or 1,2-dichloroethane with chlorine to form 1,1,2-trichloro-
ethane and by-product hydrogen chloride; and (b) dehydrochlorination of the
1,1,2-trichloroethane to form vinylidene chloride. The reaction of vinylidene
chloride with the hydrogen chloride evolved in step (a) yields methyl chloro-
form (Lowenheim and Moran, 1975).
3-42
-------
Reaction of vinylidene chloride with the by-product hydrogen chloride is
ideally conducted in the liquid phase with ferric chloride as a catalyst. The
chemical reaction is conducted at 25 to 35°C under slightly superatmospheric
pressure. Crude product is continuously withdrawn from the hydrochlorination
step and purified by fraction distillation. The purified product is treated
to remove moisture and is combined with appropriate stabilizers to make the
material suitable for various commercial uses. The yield of product is over
98% (Lowenheim and Moran, 1975).
No by-products are formed in this process. A heavy ends waste stream is
discharged from the fractionator.
3.3.3.3 Production From Ethane—
In this process, methyl chloroform is produced by the continuous noncata-
lytic chlorination of ethane. Based on 1 kg of methyl chloroform, the raw ma-
terials are 0.386 kg ethane and 2.022 kg chlorine. Figure 3-5 presents a flow
diagram for this process.
By suitable modification of operating conditions, ethyl chloride, vinyl
chloride, vinylidene chloride, and 1,1-dichloroethane may also be produced in
this process. When methyl chloroform is the desired product, the recycling of
ethyl chloride and 1,1-dichloroethane is essential.
Chlorine, ethane, and a recycle stream, containing 1,1-dichloroethane and
ethyl chloride, are fed into a chlorination vessel. The reaction system is
thermally self-sustaining at a reaction temperature of about 345°C and a pres-
sure of 40 to 80 psig. A residence time of 5 to 30 sec is allowed for the gas-
eous mixture (Lowenheim and Moran, 1975).
The hot gases discharged from the chlorination vessel are sent to a quench
tower. The light ends (overhead stream) from the quench tower flow to a strip-
per, while the remaining material is fed to a heavy ends tower. Heavy ends are
purged and the lighter products are removed overhead, cooled to -20°C, and sent
to the stripper. The stripper overhead, which contains vinyl chloride and hydro-
gen chloride, is fed into a hydrochlorination reactor (a liquid reservoir of
1,1-dichloroethane and ferric chloride catalyst at a temperature of 35 to 65°C
and a pressure of 40 to 50 psig). In this reactor, the vinyl chloride reacts
in the liquid phase with hydrogen chloride to form 1,1-dichloroethane. From
the hydrochlorination reactor, 1,1-dichloroethane is fractionated in a series
of three columns (a light ends tower, a recovery tower, and a methyl chloro-
form tower). The product is withdrawn as overhead from the last column in a
total product yield of about 93% (includes product and hydrogen chloride based
on chlorine) (Lowenheim and Moran, 1975).
By-products are hydrogen chloride (1.11 kg/kg of product) and ethylene
(0.073 kg/kg of product). A heavy ends waste stream is discharged from the
process.
3-43
-------
Ethane—
Chlorine"
c
o
u
in
~O
0>
8.
to
Hydrogen
Chloride
Heavy
Ends
c
_o
II
E «
« S
•ft o
X V
UO Q£
at
TJ
(1)
I i-
•£ Q)
f I
X
a>
u
0)
2
o
u
- I
^ I
MC
j I
o o
00 I—
Source: Lowenheim and Moran (1975),
Figure 3-5» Flow diagram for production of methyl chloroform
from ethane by chlorination.
3-44
-------
3.3.4 Perchloroethylene Production Technology
In 1975 nearly all of the perchloroethylene output in the United States
was derived from the oxychlorination of ethylene dichloride (about 34% of out-
put), or by the simultaneous chlorination and pyrolysis of hydrocarbons (about
63% of output). Approximately 3% was based on the use of acetylene as a raw
material (Lowenheim and Moran, 1975).
3.3.4.1 Production From Ethylene Dichloride--
The typical process for manufacture of perchloroethylene and trichloro-
ethylene from ethylene dichloride was shown in Figure 3-1 and the process de-
scribed in Subsection 3.3.2.1.
3.3.4.2 Production by Ghlorination of Hydrocarbons--
Perchloroethylene is produced by the simultaneous chlorination and pyroly-
sis of hydrocarbons. Various hydrocarbons and chlorinated hydrocarbons, such
as methane, ethane, propane, or higher paraffins, may be used as raw materials.
The principal reactions are:
8C1
CC12=CC12
8HC1
2CC1,
CC12=CC12 + 2C12
Based on a single pass reaction process, 1 kg of perchloroethylene would re-
quire 0.2 kg propane and 2.5 kg chlorine. A by-product of 1.35 kg hydrogen
chloride would be produced and recovered from a gas scrubber as hydrochloric
acid. A typical process flowchart in which propane is used as raw material is
shown in Figure 3-6 (Lowenheim and Moran, 1975).
HCI (to absorption and recovery)
(to recovery)
Bottoms to Recycle
Source: Lowenheim and Moran (1975).
Figure 3-6. Flow diagram for production of perchloroethylene from propane.
3-45
-------
Chlorine, propane, and several recycle streams are mixed and fed into a
chlorination furnace which is operated at 550 to 700°C. Chlorination of the
hydrocarbon occurs readily, producing carbon tetrachloride and perchloro-
ethylene. However, perchloroethylene is formed largely by pyrolysis of the
carbon tetrachloride* Effluent gases from the furnace are quenched, and the
chlorinated hydrocarbons are separated from the quenching medium in a blowback
column* Hydrogen chloride gas is sent to an absorption and recovery system.
The chlorocarbon mixture is then fractionated in a distillation column; carbon
tetrachloride passes overhead and is recycled back to the chlorination furnace.
The crude perchloroethylene is purified by distillation and the still bottoms
recycled to the chlorination furnace* Overall yield of perchloroethylene is
more than 95% based on chlorine, after accounting for hydrochloric acid recov-
ered as a co-product (Lowenheim and Moran, 1975).
3.3.4.3 Production From Acetylene Via Trichloroethylene--
The production of trichloroethylene from acetylene was described in Sub-
section 3*3.2.2 For the manufacture of perchloroethylene, the trichloroethylene
is transferred to a chlorination tower and chlorine added in the presence of
a catalyst (e.g., ferric chloride), Chlorination is carried out at 70 to 80°C
to produce pentachloroethane, which is, in turn, treated with calcium hydroxide
(milk-of-lime) to produce perchloroethylene* The overall yield is about 83%
(Lowenheim and Moran, 1975)*
The principal reactions are:
CHC1=CC12 + C12 > CHC12-CC13
2CHC12CC13 + Ca(OH)2 > 2CC12=CC12 + CaCl2 + 2H20
Based on 1 kg of perchloroethylene, the raw materials for the overall reaction
from acetylene are 0.19 kg acetylene, 1.50 kg chlorine, 0.45 kg lime (hydrate),
and a small quantity of catalyst. The by-products are calcium chloride and
water. A typical process flow diagram is shown in Figure 3-7.
The calcium-bearing wastes contain trace amounts of chlorinated solvents
plus 0.2405 Ib calcium hydroxide and 0.3445 Ib of calcium chloride per pound
of perchloroethylene product. Heavy ends waste from still operations contain,
among other by-products, 0.23 Ib of hexachlorobutadiene and 0.02 Ib of chloro-
benzenes per pound of perchloroethylene product (Gruber, 1976).
3-46
-------
Purge Gas
Acetylene-
Chlorine—
Trichloroethylene
Manufacture
Trichloroethylene
i
Waste
Chlorine-
Pentachloroethane
§
|
U
PCE
Waste
Figure 3-7,
Waste
Source: Lowenheim and Moran (1975).
Flow diagram for production of perchloroethylene from acetylene.
3.3.5 Manufacturing Processes by Site
The discussion of the specific solvent manufacturing processes operated
at domestic plant sites includes information on process methods, plant capaci-
ties, production volumes, waste materials, and grades of products. No informa-
tion could be obtained regarding the capital valuation of any of the production
facilities.
3.3.5.1 PPG Industries, Inc.—
This company manufactures trichloroethylene, methyl chloroform, and per-
chloroethylene at the Lake Charles, Louisiana, facility. The facility has been
expanded several times (Knoop and Neikerk, 1972).
In 1977 the reported annual plant capacity for trichloroethylene was
126,980 MT (280 million pounds) (SRI, 1978). The trichloroethylene production
process is very similar to the manufacturing process based on ethylene dichlo-
ride.
3-47
-------
Methyl chloroform is produced at the Lake Charles plant by hydrochlori-
nation of vinylidene chloride. In 1976 the company reported their facility was
operated at the rated capacity of 79,379 MT (175 million pounds) per year (MRI
Questionnaire, 1976, Appendix B). The facility is scheduled to be expanded to
an annual production capacity of 136,080 MT (300 million pounds) in 1978
(Chemical Marketing Reporter, 1977).
For perchloroethylene, the reported annual plant capacity in 1976 was
75,750 MT (167 million pounds) and the plant operated at about 80% of capacity
(MRI Questionnaire, 1976). The capacity for 1977 is stated to be 200 million
pounds (SRI, 1978).
The estimated production quantities, market price, and market value for
trichloroethylene, methyl chloroform, and perchloroethylene are as follows:
Trichloroethylene production—
Year
1970
1971
1972
1973
1974
1975
1976
MT
34,350
12,200
73,000
92,600
79,550
60,900
69,690
106 Ib
75.7
26.9
160.9
204.2
175.4
134.3
153.6
Price
10.5
8.8
9.8
10.3
12.8
15.0
15.0
Market value
($)
7,949,000
2,367,000
15,768,000
21,033,000
22,451,000
20,145,000
23,040,000
Methyl chloroform production-
Year
1970
1971
1972
1973
1974
1975
1976
MT
38,200
51,250
55,550
69,100
74,550
51,800
79,405
106 Ib
84.3
113.0
122.4
152.3
164.3
114.2
175.0
Price
(t/lb)
11.3
-
11.8
14.5
18.5
19.3
19.0
Market value
($)
9,520,000
-
14,446,000
22,090,000
30,404,000
22,049,000
33,250,000
3-48
-------
Perchloroethylene production-
a/
Year
1970
1971
1972
1973
1974
1975
1976
MT
36,800
72,550
60,200
62,800
56,500
52,300
58,980
106 Ib
81.2
159.9
132.7
138.4
124.5
115.2
130.0
Price
(
-------
Stabilized or inhibited methyl chloroform carries the tradename of Tri-
Ethane®. This product is an all-purpose solvent for cold cleaning and vapor
degreasing purposes, use in resin application, as an adhesive solvent, and in
aerosols as a solvent and vapor pressure depressant. A low stabilized grade
is produced for use with special adhesives, in synthesis, and in the film pro-
cessing industry.
Three grades of perchloroethylene are offered: dry cleaning grade
Perchlor®, degreasing and general solvent grade Perchlor®, and a heavy duty
grade called Perchlor HD®.
3.3.5.2 Dow Chemical Company--
Dow Chemical Company produces trichloroethylene from ethylene at the
Freeport, Texas, facility. The annual production capacity in 1976 was reported
to be 68,040 MT (150 million pounds).
Methyl chloroform is produced at the Freeport facility using vinyl chlo-
ride as the raw material. Reported production capacity in 1976 was 204,119 MT
(450 million pounds). In early 1978, a new methyl chloroform production facil-
ity was scheduled to come "on-stream" in Plaquemine, Louisiana, with an annual
capacity of 136,080 MT (300 million pounds). This expansion would give Dow a
total production capacity for methyl chloroform of 340,200 MT (750 million
pounds) (Chemical Marketing Reporter, 1977). However, as of November 14, 1978,
the expanded plant had not come "on-streani" (Farber, 1978).
In 1976 Dow produced perchloroethylene at three facilities: Freeport,
Texas (capacity of 54,432 MT, or 120 million pounds), Pittsburg, California
(capacity of 9,072 MT, or 20 million pounds), and Plaquemine, Louisiana (ca-
pacity of 68,040 MT, or 150 million pounds).
Estimated production quantities, market price, and market value for each
of the three compounds are as follows:
a/
Trichloroethylene production"
Year
1970
1971
1972
1973
1974
MT
85,850
41,800
54,800
49,600
42,600
106 lb
189.3
92.1
120.8
109.3
93.9
Price
(4/lb)
10.5
8.8
9.8
10.3
12.8
Market value
($)
19,877,000
8,105,000
11,838,000
11,258,000
12,019,000
1975 32,650 72.0 15.0 10,800,000
1976 37,385 82.4 15.0 12,360,000
3-50
-------
Year
Methyl chloroform production-
a/
MT
106 Ib
Price
Market value
($)
1970
1971
1972
1973
1974
1975
1976
89,750
87,900
107,900
134,200
144,800
133,400
180,935
197.9
193.7
237.8
295.9
319.2
294.1
398.8
11.3
-
11.8
14.5
18.5
19.3
19.0
22,360,000
-
28,061,000
42,908,000
59,057,000
56,760,000
75,770,000
Perchloroethylene production-
a/
Year
1970
1971
1972
1973
1974
1975
1976
MT
89,350
72,500
92,200
91,000
81,600
75,600
68,690
106 Ib
196.9
159.8
203.3
200.7
179.9
166.7
151.4
Price
((t/lb)
10.25
10.25
10.25
10.25
11.00
16.00
15.00
Market value
($)
20,187,000
16,382,000
20,838,000
20,568,000
19,792,000
26,674,000
22,710,000
_a/ MRI estimates based on plant production capac-
ity and on national production and capacity.
No information could be obtained concerning specific waste products from
any production facility. The current method of disposal of unwanted by-products
from the production of all three compounds is by incineration (Farber, 1978).
Dow operates a waste incinerator at all of its perchloroethylene facilities
to treat waste material.
Dow produces five grades of trichloroethylene; these are:
Product Application
solvent Vapor degreasing
solvent Vapor degreasing
solvent
Vapor degreasing (precision applications), PVC chain length
modifier, adhesive formulating, extraction processes,
chemical intermediate, and carrier solvent
3-51
-------
EX-TRI® solvent Extraction processes
TRI-PAINT®GRADE Industrial paint thinning
Each product is formulated with a special inhibitor system to protect against
decomposition from oxidation or the catalytic effect of reactive materials.
Dow produces technical grade methyl chloroform and other products under
the tradenames of Chlorothene NU® and Ghlorothene VG®. All U.S. government
organizations may purchase Chlorothene NU under Federal Specification 0-T-
620c (GSA-F55). The material covered by this specification shall be of one
grade and of either type I (general cleaning and degreasing), II (typewriter
cleaner), or III (same as II but aerosol can). Chlorothene VG®meets the re-
quirements of MIL-T-81533A entitled 1.1,1-Trichloroethane, Inhibited Vapor
Degreasing Grade, plus Federal Specification 0-T-620c, entitled 1.1.1-Tri-
chloroethane, Technical, Inhibited. The latter covers cold cleaning applica-
tions only.
3.3.5.3 Ethyl Corporation--
The production facility for trichloroethylene and perchloroethylene is
located in Baton Rouge, Louisiana. The facility for methyl chloroform was also
located at this site until production ceased during the first quarter of 1976.
Trichloroethylene and perchloroethylene are produced using ethylene as the raw
material. Methyl chloroform was produced from vinyl chloride. In 1976 the re-
ported production capacity was 18,144 MT (40 million pounds) for trichloro-
ethylene and 22,675 MT (50 million pounds) for perchloroethylene (SRI, 1978;
MRI Questionnaire, 1976, Appendix B).
Estimated production quantities, market price, and market value for each
of the three compounds are as follows:
a/
Trichloroethylene production"
Year
1970
1971
1972
1973
1974
1975
1976
MT
17,200
8,400
18,200
16,600
14,250
8,750
9,845
106 Ib
37.9
18.5
40.1
36.6
31.4
19.3
21.7
Price
(t/lb)
10.5
8.8
9.8
10.3
12.8
15.0
15.0
Market value
($)
3,980,000
1,628,000
3,930,000
3,770,000
4,019,000
2,895,000
3,255,000
3-52
-------
Methyl chloroform production^
Year
1970
1971
1972
1973
1974
1975
MT
19,100
19,050
20,650
25,700
27,700
19,350
106 Ib
42.1
42.0
45.5
56.6
61.0
42.7
Perch loroethylene
Year
1970
1971
1972
1973
1974
1975
1976
MT
26,300
14,800
28,200
15,700
14,100
13,200
11,978
106 Ib
58.0
32.6
62.2
34.6
31.1
29.1
26.4
Price
(t/lb)
11.3
-
11.8
14.5
18.5
19.3
Market value
($)
4,756,000
-
5,367,000
8,206,000
11,295,000
8,235,000
production-
Price
((t/lb)
10.25
10.25
10.25
10.25
11.00
16.00
15.00
Market value
($)
5,942,000
3,344,000
6,374,000
3,545,000
3,425,000
4,663,000
3,960,000
MRI estimates based on plant production capac-
ity and on national production and capacity.
The still bottoms from the trichloroethylene and methyl chloroform (prior
to 1976) production process contain about 667» hexachlorobutadiene, 67» hexa-
chloroethane, 1% hexachlorobenzene, and other organic compounds (Mumma and
Lawless, 1975). These wastes are disposed by injection into a private, state-
permitted, deep (~ 9,000-ft) disposal well (Park, 1978).
The types of trichloroethylene manufactured include metal degreasing grade,
electronic grade, extraction grade, and reagent grade. The metal degreasing
grade meets MIL-T-27602A and Federal 0-T-634b (types I and II) specifications.
All other grades meet Federal 0-T-634b (type I) specifications.
Ethyl Corporation produces two grades of perchloroethylene: an industrial
grade and a dry cleaning grade. Both grades meet Federal specifications 0-T-
236b, including Amendment I.
3-53
-------
3.3.5.4 Diamond Shamrock Chemical Company--
Diamond Shamrock manufactures trichloroethylene and perchloroethylene at
its Deer Park, Texas, facility. In 1977 the annual production capacity was re-
ported to be 24,950 MT (55 million pounds) for trichloroethylene and 90,720 MT
(200 million pounds) for perchloroethylene (SRI, 1978).
Trichloroethylene is manufactured from ethylene. Perchloroethylene is pro-
duced by the method described in U.S. Patent No. 3,674,881. A simplified flow-
chart for this process is presented in Figure 3-8. The process, which is based
on the chlorination of ethylene dichloride, involves the preparation of tri-
chloroethylene and perchloroethylene in separate but similar production trains.
Operation of the trains is integrated with respect to the recycling of certain
organic streams for the purpose of improving product purity and simplifying
separation procedures.
The estimated production quantities, market price, and market value are
as follows:
Trichloroethylene production"
a/
Price Market value
Year
1970
1971
1972
1973
1974
1975
1976
MT
25,750
13,800
21,850
33,000
28,350
19,650
13,747
106 Ib
56.8
30.4
48.2
72.7
62.5
43.3
30.3
Perchloroethylene
fe/lb)
10.5
8.8
9.8
10.3
12.8
15.0
15.0
production—
($)
5,964,000
2,675,000
4,724,000
7,491,000
8,000,000
6,495,000
4,545,000
Price
Year
MT
10 Ib
Market value
($)
1970
1971
1972
1973
1974
1975
1976
52,550
44,400
37,650
50,200
42,200
43,000
47,595
115.9
97.9
83.0
110.7
99.7
94.9
104.9
10.25
10.25
10.25
10.25
11.00
16.00
15.00
11,876,000
10,033,000
8,504,000
11,351,000
10,962,000
11,980,000
15,735,000
MRI estimates based on plant production capac-
ity and on national production and capacity.
3-54
-------
i
Ul
Column
Chlorine
Ethylene
Dicliloride
Trichloroethylene
Out
lion
Distillation
Column
1 1
Dirfiliatlon
Column
Waste Out
Perch loroelliylene
Source: Adapted from U.S. Patent No. 3.674.881 (July 1972).
Figure 3-8• Flowchart of perchloroethylene production process used by Diamond
Shamrock Chemical Company.
-------
The trichloroethylene and perchloroethylene process wastes (heavy ends)
are recovered and used as a part of the raw materials for the vinyl chloride
monomer plant operated at the same site (Heble, 1978).
The trade name for the trichloroethylene product is Triclene®. Triclene®
is available in the following grades: Triclene D®, Triclene MD®, Triclene ME®,
Triclene Technical®, and Triclene Paint Grade®. Triclene D®meets MIL-T-27602A,
Federal 0-T-634b (types I and II), FDA 121.2520 (extracting adhesives), and FDA
121.1041 (extracting caffeine and spice oleoresins) specifications. Information
was not available on the other grades. Since trichloroethylene is no longer
employed for the extraction of caffeine and spice oleoresins, FDA 121.1041 grade
has probably been discontinued for sale in the United States.
The company produces three types of perchloroethylene product: a dry clean-
ing grade (Perclene®), a vapor degreasing grade (Perclene D®), and a Freon grade.
The Freon grade is used as a chemical intermediate in the manufacture of Fluoro-
carbons 113, 114, 115, and 116. Perclene®meets MIL-P-12050, Federal 0-T-236b,
and FDA 121.2583 (foamed polystyrene) specifications. Perclene D®meets Federal
0-T-236b specifications. The company has reported that their product is contami-
nated with less than 100 ppm of trichloroethylene. Perchloroethylene is not ex-
ported or imported by this company.
3.3.5.5 Occidental Petroleum Corporation (Hooker Chemical Company)—
The Hooker Chemicals and Plastics Corporation, a subsidiary of Occidental
Petroleum Corporation, had operated trichloroethylene production plants at
Taft, Louisiana, Tacoma, Washington, and Niagara Falls, New York. The facility
in Niagara Falls was closed in early 1972 and the Tacoma site in May 1973. Per-
chloroethylene was produced at Tacoma, Washington, and Taft, .Louisiana, but the
Tacoma plant was closed in July 1973. In January 1978, the facility for tri-
chloroethylene and perchloroethylene at Taft, Louisiana, was shut down (Hebert,
1978).
Prior to January 1978, trichloroethylene and perchloroethylene were pro-
duced at the Taft, Louisiana, facility using the chlorination of acetylene
process.
The estimated production quantities, market price, and market value of
each of the compounds are as follows:
3-56
-------
a/
Trichloroethylene productiort"
Year
1970
1971
1972
1973
1974
1975
1976
MT
55,950
27,300
25,550
13,350
11,450
10,900
12,477
106 Ib
180.2
60.2
56.3
29.4
25.2
24.0
27.5
Price
(t/lb)
10.5
8.8
9.8
10.3
12.8
15.0
15.0
Market value
($)
12,957,000
5,298,000
5,517,000
3,028,000
3,226,000
3,600,000
4,125,000
a/
Perchloroethylene production"
Year
1970
1971
1972
1973
1974
1975
1976
MT
23,700
13,300
16,900
15,700
14,100
10,500
9,346
106 Ib
52.2
29.4
37.3
34.6
31.1
23.0
20.6
Price
10.25
10.25
10.25
10.25
11.00
16.00
15.00
Market value
($)
5,347,000
3,012,000
3,823,000
3,545,000
3,425,000
3,687,000
3,090,000
_a/ MRI estimates based on plant production capac-
ity and on national production and capacity.
Prior to the plant closure at Taft, the waste by-products were incinerated
(Hebert, 1978).
The trichloroethylene product types included metal degreasing grade, elec-
tronic grade for cleaning applications where a low stabilizer content in the
product is required, missile grade for cleaning rocket and missile components,
an extraction grade, and an X-l grade. The missile grade met MIL-T-27602A and
Federal 0-T-634b (types I and II) specifications.
Perchloroethylene products consisted of a dry cleaning grade, a metal de-
greasing grade, and an industrial grade. The dry cleaning grade was a stabil-
ized solvent of high purity formulated specifically for this application. The
degreasing grade was used principally for vapor degreasing, cold cleaning, and
as an additive in cleaning compounds; and was also used for textile finishing,
oil extraction, and as a metal drying agent. The industrial grade was used for
metal cleaning and as an organic chemical intermediate.
3-57
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3.3.5.6 Vulcan Materials Company--
Vulcan manufactures methyl chloroform by the chlorination of ethane pro-
cess at Geismar, Louisiana (1977 capacity: 29,480 MT, or 65 million pounds),
and perchloroethylene by the chlorination of various hydrocarbons at Wichita,
Kansas (1977 capacity: 22,680 MT, or 50 million pounds), and Geismar (1977
capacity: 77,110 MT, or 170 million pounds) (SRI, 1978). Vulcan has recently
started construction of a new methyl chloroform plant (capacity: 63,500 MT,
or 140 million pounds) which is scheduled for completion about mid-1979 (Chem-
ical Week, 1978).
No detailed production information could be obtained on the current pro-
cesses. The company has reported carbon tetrachloride is a co-product of the
perchloroethylene plant and that the process is based on chlorination of vari-
ous hydrocarbons. The process also utilizes as feed material the by-products
and wastes from other processes on the same site, e.g., manufacture of methyl
chloroform and vinylidene chloride (MRI Questionnaire, 1976, Appendix B).
Estimated production quantities, market prices, and market values of methyl
chloroform and perchloroethylene are as follows:
Methyl chloroform production—
Year
1970
1971
1972
1973
1974
1975
1976
MT
19,100
11,700
15,900
19,800
21,300
18,280
26,088
106 Ib
42.1
25.8
35.0
43.5
47.0
40.3
57.5
Perchloroethylene
Year
1970
1971
1972
1973
1974
1975
1976
MT
42,000
56,200
71,500
62,800
56,400
52,600
52,266
106 Ib
92.7
124.0
157.6
138.4
124.4
115.9
115.2
Price
(t/lb)
11.3
-
11.8
14.5
18.5
19.3
19.0
Market value
($)
4,756,000
-
4,129,000
6,314,000
8,690,000
7,778,000
10,925,000
production^
Price
(t/ib)
10.25
10.25
10.25
10.25
11.00
16.00
15.00
Market value
($)
9,499,000
12,705,000
16,157,000
14,187,000
13,685,000
18,542,000
17,280,000
a./ MRI estimates based on plant production capac-
ity and on national production and capacity.
3-58
-------
Methyl chloroform does not occur in by-products from the production pro-
cess. All waste or undesirable by-product is used as feed for the perchloro-
ethylene plant. The tarry residue waste from the perchloroethylene plant is
impounded in a landfill at the Geismar site and incinerated in a specially de-
signed system at the Wichita facility (MRI Questionnaire, 1976).
Solvent 111® is the company's registered trademark name for stabilized
methyl chloroform. This product is a single grade solvent for vapor degreas-
ing, cold cleaning, and other miscellaneous uses. Specialty grades of methyl
chloroform tailored to individual customer requirements are also available.
Solvent 111® meets MIL-T-81533A and Federal 0-T-620c specifications.
Three types of perchloroethylene are produced by Vulcan: dry cleaning
grade, industrial grade, and vapor degreasing grade.
3.3.5.7 Stauffer Chemical Company—
Stauffer produces perchloroethylene at Louisville, Kentucky. In 1977 the
plant's annual production capacity was 31,752 MT (70 million pounds) (SRI,
1978). The process is based on the chlorination of low molecular weight hy-
drocarbons, such as ethane and propane.
The estimated production quantities, market price, and market value are
as follows:
Perchloroethylene production—
Year
1970
1971
1972
1973
1974
1975
1976
MT
36,800
20,700
26,350
22,000
19,800
18,400
16,650
106 Ib
81.2
45.7
58.1
48.4
43.6
40.7
36.7
Price
10.25
10.25
10.25
10.25
11.00
16.00
15.00
Market value
($)
8,318,000
4,681,000
5,953,000
4,963,000
4,791,000
6,506,000
5,505,000
a^l MRI estimates based on plant production capac-
ity and on national production and capacity.
The principal process wastes are called "hex" waste. This solid waste from
the production plant is gravity fed into drums. The drums are removed from the
plant area, loaded onto trucks, and taken to an EPA-approved secured chemical
landfill site approximately 24 km (15 miles) from the plant. Cooling water and
3-59
-------
surface runoff from the plant area are fed to a sump where the pH is adjusted
to between 6 and 9. The liquid is pumped to a concrete settling pond and grav-
ity fed through a pipeline into the Ohio River (MRI, 1976b; Blunk, 1978).
Stauffer produces a dry cleaning grade and an industrial grade of per-
chloroethylene. The dry cleaning grade has a purity of 99.98% minimum C2Cl^,
and the industrial grade has a composition of 99.97% minimum 02014. The com-
pany trademark for these products is "Perk®."
3.3.5.8 E. I. du Pont de Nemours and Company, Inc.--
This company has operated a production facility at Corpus Christi, Texas,
since about 1972 for the manufacture of perchloroethylene. All of the product
is used captively for the manufacture of fluorocarbon products (i.e., F-113,
F-114, F-115, and F-116). Current production capacity is listed at approxi-
mately 72,500 MT (160 million pounds) per year (SRI, 1978).
The estimated production quantities, market price, and market value are
as follows:
a/
Perchloroethylene production—
Price Market value
Year MT 106 Ib U/lb) ($)
4,016,000
1971
1972
1973
1974
17,800
None
None
45,200
39.2
None
None
99.6
10.25
10.25
10.25
11.00
10,954,000
1975 41,800 92.2 16.00 14,747,000
1976 37,975 83.7 15.00 12,555,000
_a/ MRI estimates based on plant production capac-
ity and on national production and capacity.
3.4 CONSUMPTION AND UTILIZATION
This subsection presents a discussion of the industrial and nonindustrial
consumption processes for trichloroethylene, methyl chloroform, and perchloro-
ethylene. End-use patterns for each of the three compounds were summarized ear-
lier in 3.2.2, 3.2.5, and 3.2.8. A more detailed discussion, particularly of
the solvent metal cleaning industry, is presented in this subsection.
3-60
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3.4.1 Solvent Metal Cleaning
There are two basic methods of metal cleaning which employ these chlori-
nated hydrocarbon solvents: cold cleaning and vapor degreasing. The specific
sources of solvent emission from each of these methods and techniques which
may be employed to reduce the emissions will be discussed in Section 9. This
discussion will focus on the quantity of solvent consumed and the major users
of these solvents.
3.4.1.1 Consumption of Degreasing Solvents--
Two reports have recently been issued which are directly concerned with
emissions of chlorinated hydrocarbon solvents and techniques for reducing these
emissions. The report by the Office of Air Quality Planning and Standards (EPA,
1977) and the draft final report by the Metrek Division of Mitre (Mitre, 1978)
give 1974 consumption figures for trichloroethylene, methyl chloroform, and
perchloroethylene as shown in Table 3-21.
TABLE 3-21. CONSUMPTION OF DEGREASING SOLVENTS IN 1974s
Method
Cold cleaning
Conveyorized cold
Subtotal
cleaning
23
_2
25
76
_6
82
13
-
13
Vapor degreasing 90 57 29
Conveyorized vapor degreasing 38 23 12
Subtotal 128 80 41
Total quantity 153 162 54
a/ 103 MT.
b/ Trichloroethylene.
_c/ Methyl chloroform.
_d/ Perchloroethylene.
3-61
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3.4.1.2 Dow Chemical Study--
A comprehensive survey of the users of trichloroethylene, methyl chloro-
form, and perchloroethylene in the metal cleaning industry was performed for
EPA by the Dow Chemical Company in 1976 (Dow Chemical Company, 1976). Because
of the relevance of their report to the current study, a summary of selected
portions on solvent users is included in this subsection.
The nationwide survey by Dow polled the eight Standard Industrial Classi-
fication (SIC) categories of manufacturers who were the largest users of sol-
vents for metal cleaning in 1974. The eight categories were:
SIC 25 Furniture and Fixtures
SIC 33 Primary Metal Industries
SIC 34 Fabricated Metal Products
SIC 35 Machinery Except Electrical
SIC 36 Electrical and Electronic Equipment
SIC 37 Transportation Equipment
SIC 38 Instruments and Related Products
SIC 39 Miscellaneous Manufacturing Industries
The areas of solvent use for metal cleaning not polled in this survey are:
(a) manufacturing firms outside the eight SIC codes--including paper, glass,
textiles and chemicals; (b) firms employing 19 or fewer people; and (c) main-
tenance and service operations, such as automobile maintenance, railroad re-
pair, and electric motor rebuilding.
The survey results were obtained from personal telephone interviews con-
ducted with plant personnel at each of 2,578 plant sites engaged in a manufac-
turing activity within one of the metalworking industries.
In 1974 there were 41,670 metalworking plants employing 20 or more work-
ers, with a total employment of about 10 million. The study excluded 1,892 re-
search and development (R&D) sites and headquarters locations, as well as
83,074 metalworking plants which employed fewer than 20 people.
The survey showed that a total of 20,320 plants (49% of the metalworking
industry) used solvents for metal cleaning activities. Of this total, 5,365
plants had vapor degreasing systems only; 11,028 plants had room temperature
cleaning (cold cleaning) systems only; and 3,927 plants had both types of
cleaning systems.
A large number of individual metal cleaning plants in the United States
use trichloroethylene, methyl chloroform, or perchloroethylene as cleaning sol-
vents. In 1974, for example, the survey showed there were a total of 8,843
plants which used one of these solvents; the total number of cold cleaning fa-
cilities using these solvents was 5,103 plants. Because there are so many do-
mestic cleaning facilities using these solvents, no identification has been
3-62
-------
made of all of these cleaning plants. [For these reasons, MRI did not attempt
to identify each metal cleaning facility and consumption process by site and
company. MRI did, however, identify some major users and has provided site-
specific information on use patterns and consumption quantities. These data
are discussed later in this section.]
A breakdown of survey data according to type of cleaning system in each
SIC group is shown in Table 3-22. Group 35 had 4,147 plants using cold clean-
ing; this value was by far the largest number for any of the groups. The ma-
jority of the plants which do vapor degreasing are in Groups 34, 35, and 36.
The survey also established that there is a direct relationship between
plant size in terms of employment and the type of solvent metal cleaning being
done. These data indicate that the larger the plant size, the greater the per-
centage of plants using vapor degreasing only, and the smaller the percentage
of cold cleaning only.
It was also determined that various regions of the country differ somewhat
in the types of solvent cleaning systems utilized (Table 3-23). The Far West
and the Northeast regions had the highest percentage of vapor degreasing plants
(28%), and the Southwest, the lowest percentage (16%). The states comprising
each of the regions are shown in Table 3-24.
The study determined that in 1974, 9,292 of the plants which conduct metal
cleaning activities operated vapor degreasing equipment. Also, it was found
that there were 18,090 vapor degreasers in the 9,292 plants, giving an average
of about two units per plant.
The survey also included a study of solvent vapor recovery and control
systems utilized in metal cleaning plants. Geographic distribution of vapor
recovery and control systems in 1974 is indicated in Table 3-25. Carbon adsorp-
tion was distributed among the Northeast, Midwest, and Far West regions. The
percentage utilization of refrigeration systems varied from a low of 4.8% in
the Southwest to a high of 19.3% in the Far West. The percentage of plants that
did not use either recovery or control systems ranged from a low of about 68%
in the Far West to a high of 87% in the Southwest.
Several routes, including burning, flushing, landfill, disposal service,
and reclaimer, are used for the disposal of solvents from metal cleaning opera-
tions (vapor degreasing and cold cleaning). The disposal methods and quantities
employed in 1974 are shown in Table 3-26. Most plants (39%) used disposal ser-
vice, but the largest quantity of solvents went to reclaimers. In 1974, 65% of
the solvent used was lost to emissions and not recovered (Dow Chemical Company,
1976).
3-63
-------
TABLE 3-22. SOLVENT CLEANING--ROOM TEMPERATURE AND VAPOR DEGREASING--BY SIC
Number of plants using solvent cleaning systems
SIC No. 25 33
Type of solvent Metal Primary
system used furniture metals
Vapor degreasing 95 348
systems only
Room temperature 209 825
(cold cleaning)
systems only
Both types of 95 246
systems
Total 399 1,417
Source: Dow Chemical Company (1976).
OJ
1
-P-
TABLE 3-23. SOLVENT CLEANING- -ROOM
Type of cleaning
system used Northeast % Southeast %
Vapor degreasing 1,910 28 442 24
systems only
Room temperature 3,511 50 1,178 62
(cold cleaning)
systems only
Both types of 1,549 22 258 14
systems
Total 6,970 100 1,878 100
34 35 36 37 38 39
Fabricated Nonelectric Electric Transportation Instruments Misc.
products machinery equipment equipment and clocks industry Total
1,282 1,086 1,367 376 575 236 5,365
2,826 4,147 1,191 962 605 263 11,028
696 955 1,058 362 410 105 3,927
4,804 6,188 3,616 1,702 1,590 604 20,320
TEMPERATURE AND VAPOR DEGREASING--BY GEOGRAPHIC REGION
Number and percentage of plants at "geographic location
Mid-West °U Southwest 7. North Central % Far West % Total T.
1,738 27 119 16 328 24 828 28 5,365 26
3,614 56 530 71 872 63 1,323 45 11,028 54
1,062 17 96 13 186 13 778 27 3,927 20
6,412 100 745 100 1,386 100 2,929 100 20,320 100
Source: Dow Chemical Company (1976).
-------
TABLE 3-24. GEOGRAPHICAL BREAKDOWN OF STATES BY REGION
Northeast
Southeast
Connecticut
Delaware
Maine
Maryland
Massachusetts
New Hampshire
New Jersey
New York
Pennsylvania
Rhode Island
Vermont
Alabama
Florida
Georgia
North Carolina
South Carolina
Tennessee
Virginia
Arkansas
Washington, D.C.
Puerto Rico
Mid-West
Far West
Illinois
Indiana
Kentucky
Michigan
Ohio
West Virginia
Wisconsin
Arizona
California
Hawaii
Idaho
Nevada
Oregon
Washington
Utah
Alaska
North Central
Southwest
Colorado
Iowa
Kansas
Minnesota
Missouri
Montana
Nebraska
North Dakota
South Dakota
Wyoming
Louisiana
Mississippi
Oklahoma
Texas
New Mexico
3-65
-------
TABLE 3-25. GEOGRAPHICAL DISTRIBUTION OF VAPOR RECOVERY AND CONTROL SYSTEMS IN 1974
Number and percent of plants using disposal routes in geographic areas-
Plant system
Carbon adsorption
Refrigeration
Vapor burning
Water barrier
Some other type
Plants that do
not use re-
covery or con-
trol systems
Total
Northeast 7. Southeast %
127 1.8
861 12.4 173 9.2
142 2.0 26 .1.4
19 0.3
612 8.8 73 3.9
5_t209 74.7 1,606 85.5
6,970 100 1,878 100
Midwest 7.
141 2.2
717 11.2
136 2.1
18 0.3
439 6.8
4,961 77.4
6,412 100
Southwest % North Central 7. Far West % Total %
37 1.3 305 1.5
36 4.8 124 8.9 566 19.3 2,477 12.2
26 3.6 - - 21 0.7 351 1.7
37 0.2
36 4.8 143 10.3 328 11.2 1,631 8.0
647 86.8 1,119 80.7 1,977 67.5 15,519 76.4
745 100 1,386 100 2,929 100 20,320 100
U5
I _a/ Some projections are not made because o£ an inadequate sample size
Source: Dow Chemical Conpany (1976).
-------
CO
i
TABLE 3-26. DISPOSAL METHOD AND QUANTITY OF ALL
SOLVENTS DISPOSED IN 1974
Quantity of solvent disposed
Disposal method
Burning
Flushing
Landfill
Disposal service
Reclaimer
Total
Number
of
plants
382
2,667
3,674
7,989
4,323
19,035
% of
total
plants
2
13
18
39
21
100
4/year
(x 103)
363
5,087
6,132
24,845
41,060
77,487
Gal/year
(x 103)
96
1,344
1,620
6,564
10,848
20,472
Average
4/year/
plant
950
1,908
1,669
3,111
9,497
Average
gal/year/
plant
251
504
441
822
2,509
Source: Dow Chemical Company (1976).
-------
The Southwest Region had the greatest percentage of plants using disposal
routes in 1974. Reclaiming was conducted in the largest percentage of plants
in the Far West and in the lowest percentage in the Southeast. The distribution
of disposal service usage ranged from a low of 2470 in the Southeast to a high
of 54% in the Southwest.
3.4.1.3 Specific Site Data--
During this study, telephone and letter inquiries were made to selected
companies, who are consumers of trichloroethylene or methyl chloroform in metal
cleaning operations. These inquiries requested site-specific information con-
cerning type and quantity of solvents used, the use processes, and pollution
control equipment and procedures. Data and information collected by this sur-
vey and summarized in Table 3-27 are for 1976.
The Western Electric Company plant at Omaha, Nebraska, consumed about
212,000 liters (56,000 gal.) of methyl chloroform for both cold cleaning and
vapor degreasing operations associated with cleaning communication equipment.
No trichloroethylene was used at this plant.
In Skokie, Illinois, the Teletype Corporation consumed about 75,700 li-
ters (20,000 gal.) per year of methyl chloroform for vapor degreasing of com-
munication equipment. About 5 to 6 years ago, the company switched from tri-
chloroethylene to methyl chloroform.
The Eaton Company operates a plant in Cleveland, Ohio, which consumed
about 53,000 liters (14,000 gal.) of methyl chloroform annually for cleaning
fasteners by vapor degreasing. A waste recovery system reclaims about 20% of
the solvent.
Site specific information was not obtained for the plant operations of
the Ford Motor Company. However, the company has reported that a "typical
plant" consumes 51,100 liters (13,500 gal.) of trichloroethylene and 37,850
liters (10,000 gal.) of methyl chloroform annually in metal cleaning opera-
tions. Both solvents are used in cold cleaning and in vapor degreasing opera-
tions. Cold cleaning is used largely for maintenance purposes and vapor de-
greasing for cleaning vehicle components. Typical pollution controls include
a slotted hood over vapor degreaser tanks with an exhaust system and curbed
floor areas to contain spills. The company has about 25 plants in the United
States which use one or both of those solvents for metal cleaning operations.
The National Cash Register Company operates a metal cleaning plant in
Dayton, Ohio; in 1976 this plant consumed about 10,400 liters (2,750 gal.) of
methyl chloroform annually largely for vapor degreasing of circuit boards and
similar work. Small amounts of methyl chloroform are employed with Stoddard
solvent in cold cleaning applications. Another plant operated by the same com-
pany in Cambridge, Ohio, consumed about 12,500 liters (3,300 gal.) of methyl
chloroform per year for vapor degreasing work.
3-68
-------
TABLE 3-27. USAGE OF SOLVENTS IN METAL CLEANING PLANTS
vO
Company plant site
General Electric Company
Louisville, KY
General Electric Company
Schenectady, NY
General Motors
Saginaw Steering Gear Company
Saginaw, MI
Western Electric Company
Omaha , NE
Western Electric Company
Lee's Summit, MO
Teletype Corporation
Skokle, 1L
Eaton Company
Cleveland, Oil
Ford Motor Company
"a typical plant"
National Cash Register Company
Dayton, Oil
National Cash Register Company
Cambridge, OH
Pratt and Whitney
WV
Hewlett-Packard Company
Colorado plant
Quantities of
solvents used
per year, t (gal. )
TCE5/ MCb/
NA NA
3,028 1,249
(800) (330)
NA NA
none 211,960
(56,000)
NA NA
none 75 , 700
(20,000)
none 52 ,990
(14,000)
51,100 37,850
(13,500) (10,000)
none 10,410
(2.750)
none 12 ,490
(3,300)
11,450 none
(3,025)
NA very
little
Cleaning process
Vapor Cold
decreasing cleaning
MC small
amount
J*
MG or
TCE
y y
MC or
TCE
/
/
both both
solvents solvents ,
maintenance
V small
amounts;
Stoddard
solvent
v/
/
both
solvents
Remarks
Switched from TCE to MC 5 years ago
Use degreasers 3 hr/week
Closed systems with air vents
Components for communications equipment
Electronic products
Communication equipment. Switched from TCE to MC
5-6 years ago
Cleaning fasteners—company has nine other plants
some of which use TCE. 20X of MC reclaimed in
waste recovery system
Company has about 25 plants using MC and/or TCE.
Cleaning vehicle components. Pollution con-
trols: slotted hood over vapor tank with ex-
haust; curbed area
Circuit boards, etc. --some other plants use 25
drums /day
Company has large plant at East Hartford, CT,
using solvents, also a smaller plant in PL
Circuits, aluminum chassis, etc.
a/ Trichloroethylene.
b/ Methyl chloroform.
c/ I/denotes that the process was employed but no solvent specified.
NA = Not available.
Source: Data obtained from plant representatives.
-------
The Saginaw Steering Gear Company of General Motors, located in Saginaw,
Michigan, uses methyl chloroform or trichloroethylene for vapor degreasing
work. No consumption data on solvents were supplied by the company. The com-
pany has reported that the degreasers are operated as closed systems with air
vents.
At the Schenectady, New York, plant of General Electric Company, 3,030
liters (800 gal.) of trichloroethylene and 1,250 liters (300 gal.) of methyl
chloroform are consumed annually in vapor degreasing operations. At the
Louisville, Kentucky facility, General Electric uses methyl chloroform largely
for vapor degreasing work; the plant switched from trichloroethylene to methyl
chloroform in about 1971. Data on the quantity of solvent consumed were not
supplied by the company.
The Hewlett-Packard Company uses trichloroethylene for vapor degreasing
of circuits and aluminum chassis at its Colorado plant. No data were obtained
concerning solvent quantities consumed each year.
Data were supplied by the Defense General Supply Center, Richmond,
Virginia, and the General Services Administration, Fort Worth, Texas, concern-
ing governmental purchase and use of trichloroethylene, methyl chloroform, and
perchloroethylene in 1976. These data are presented in Table 3-28.
In 1976, the total demand for trichloroethylene was about 2,400 MT (5.3
million pounds), of which nearly 1,996 MT (4.4 million pounds) were Federal
specification O-T-634 (Stock No. 6810-00-184-4800) for use by the Navy and
Air Force for vapor degreasing, general solvent purposes, and dry cleaning.
The Air Force used about 180 MT (397,000 Ib) of Federal specification MIL-T-
27602 (Stock No. 6810-00-812-9181) for cleaning of propellant oxygen handling
systems.
The 1976 demand for methyl chloroform, including General Services Admin-
istration items, was approximately 3,880 MT (8.5 million pounds). Of this total
quantity, about 1,538 MT (3.4 million pounds) were used by the Army and about
2,268 MT (5 million pounds) by the Navy. Various civilian agencies supplied by
the General Services Administration used about 27.7 MT (61,000 Ib) during 1976.
The Navy and the Air Force used about 49.5 MT (109,000 Ib) of perchloro-
ethylene (Federal specification O-T-236) for vapor degreasing and dry cleaning
applications in 1976. Civilian agencies used only about 1.53 MT (3,380 Ib) dur-
ing the same year.
3-70
-------
TABLE 3-28. U.S. GOVERNMENT PURCHASES AND MAJOR USES OF TRICHLOROETHYLENE,
METHYL CHLOROFORM, AND PERCHLOROETHYLENE IN 1976
Yearly
National stock No.
Trichloroethylene
Mil. SPEC MIL-T-
27602
6810-00-812-9181
FED SPEC O-T-634
6810-00-184-4794
6810-00-184-4800
6810-00-223-2731
6810-00-678-4418
6810-00-754-2813
6810-00-924-7107
Package
55-gal
5-gal.
55-gal
55-gal
1-gal.
1-pt.
1-gal.
. dr.
en.
. dr.
. dr.
en.
en.
en.
Total
Methyl chloroform
MIL SPEC MIL-T-
81533
6810-00-476-5612
6810-00-476-5613
FED SPEC O-T-620
6810-00-292-9625
6810-00-664-0388
6810-00-930-6311
6810-00-551-1487
6810-00-664-0387
5-gal.
55-gal
1 qt
5-gal.
5-gal.
55-gai
1-gal.
en.
. dr.
en.
en.
. dr.
en.
Total
Perchloroethylene
FED SPEC O-T-236
6810-00-819-1128
6810-00-270-9982
5-gal.
55-gal
en.
. dr.
Total
MT
179.
95.
1,995.
105.
14.
1.
5.
2,396.
87.
1.538.
12.
173.
2,041.
27.
0.
3,881.
49.
1.
51.
88
54
71
31
27
04
03
78
24
98
78
14
76
08
68
66
61
53
14
demand
U)
396
210
4,399
232
31
2
U
5,283
192
3,392
28
381
4,501
59
1
8,557
109
3
112
,560
,630
,750
,170
,460
,290
.080
,940
,340
,840
,180
,700
,260
,690
.510
,520
,360
.380
,740
Malor user End-use and comments
!Used for cleaning propel lant oxygen
handling systems (a grade of low-
residue TCE)
Navy
Navy, AF
Army, AF
AF
AF, Navy, Army
AF, Navy, Army
Specification covers two types of tech-
nical grade TCE. One type is intended
for use In dry cleaning and for gen-
eral solvent purposes. Other type Is
Intended for vapor degreasing of
metals
\
Navy
Army
Intended for vapor degreasing use where
air pollution regulations preclude
the use of other materials
Navy, AF / Intended primarily for degreasing of
Navy < electrical equipment and typewriters
Navy I
Various civilian
Procured and managed by General Services
agencies Administration
Used In dry cleaning and vapor degreas-
Navy, AF
ing
Various civilian Procured and managed by General Services
agencies
Administration
Sources: Thomas (1977); Gelsler (1977).
-------
3.4.2 Textile Industries
3.4.2.1 The Dry Cleaning Industry—
Perchloroethylene is used by the textile industry for dry cleaning and
for processing and finishing. It is particularly useful as a dry cleaning
agent, since it is an excellent cleaner of all fabrics, is easily recovered
for reuse, and is nonflammable.
The dry cleaning industry is generally considered as that part of the
laundry and cleaning services industry concerned with the cleaning of wearing
apparel, rented uniforms, and specialty items such as draperies, furs, and
rugs. Dry cleaning is distinguished from laundry services by the use of or-
ganic solvents to remove grease, oils, and insoluble soils from fabrics.
For purposes of classification, the dry cleaning industry can be segre-
gated into three major categories based on the type of services offered. These
are: (a) coin-operated facilities, (b) commercial dry cleaners, and (c) in-
dustrial dry cleaners. Coin-operated units are generally associated with
Laundromat services and permit "self-service" dry-cleaning on a per load basis.
They may operate either on an independent or a franchise basis. About 36,000
kg of clothes per year are processed by a typical installation of coin-operated
machines (TRW, 1976).
In 1972, coin-operated installations accounted for approximately 37% of
the total number of dry cleaning establishments in the United States and em-
ployed about 16% of the industry work force (see Table 3-29).
TABLE 3-29. U.S. DRY CLEANING INDUSTRY - 1972
Industry Establishments Paid employees Gross receipts
classification Number Percent Number Percent ($1.000) Percent
Coin-operated 17,550 37.3 46,110 16.4 673,361 20.9
(SIC 7215)
Commercial 28,422 60.5 186,701 66.3 1,759,486 54.7
(SIC 7216)
Industrial 1,020 2.2 48.859 17.3 782,228 24.3
(SIC 7218)
Total 46,992 - 281,670 - 3,215,075
Source: Bureau of Census (1972).
3-72
-------
Commercial plants offer cleaning and pressing services on a per garment
basis and include specialty cleaning of leather, suede, furs, and other fine
goods. These facilities include small neighborhood dry cleaning shops, fran-
chise operations, and specialty cleaners. Overall, these establishments each
generally process about 45,500 kg of clothes per plant per year. They comprised
about 61% of the total number of dry cleaning plants in 1972 and employed about
66% of the workers in the industry.
Industrial cleaners are establishments that supply-on a large scale--
rental services for uniforms or similar items to business, industrial, or insti-
tutional customers. These industrial cleaners process from 450,000 to 700,000
kg of clothes per plant per year. By number of plants, this category represents
the smallest fraction of the industry (2.2%).
Two classes of organic solvents are used most frequently in the dry clean-
ing industries. One solvent class includes chlorinated hydrocarbon solvents
(synthetic solvents) consisting almost exclusively of perchloroethylene and
small amounts of trichlorotrifluoroethane (F-113). The other class includes
petroleum solvents, such as Stoddard solvent or 140-F solvent. The two basic
designs of domestic dry cleaning equipment conform to the process requirements
for each of these types of solvents. Primary consideration is given to the rel-
ative flammabilities of petroleum and synthetic solvents, so that explosion-
proof equipment is required for petroleum solvent operations.
According to one source, the quantities of solvents consumed in domestic
dry cleaning operations during 1975 were perchloroethylene, 345 million pounds;
fluorocarbon solvent (F-113), 2 million pounds; and petroleum solvents, 150
million pounds (International Fabricare Institute, 1977).
The basic process of dry-cleaning with perchloroethylene consists of three
distinct operations. In the first step, "washing," the fabric is cleaned by
agitation (usually in a rotating cylinder) in a solvent bath and then rinsed
with clean solvent. Next, excess solvent is removed by centrifuging in the
"extraction" step. The fabric is then tumbled while warm air is passed through
it to completely vaporize and remove the remaining solvent; this third step is
"reclaiming."
Establishments using perchloroethylene utilize machines which combine the
washing and extracting stages with a separate unit for reclaiming the solvent
(Danielson, 1973)» Actual transfer of garments may be accomplished automatically
or manually by the machine operator. The most modern equipment, which includes
all coin-operated units, combines all three cleaning phases in one machine (dry-
to-dry machine) and requires no fabric handling between phases.
3-73
-------
The dry-to-dry machine consists of a horizontal rotating drum which is
mounted with one door in the vapor tight housing. This drum rotates slowly
during the wash cycle. When washing is completed, the solvent is drained to
a base tank, and the drum rotates at very high speed to extract more solvent,
which is also returned to the tank. Then the drum again rotates slowly while
heated air is blown through the fabrics. This air is recycled to the tumbler
through a condenser to recover the evaporated solvent. This machine is used
only with synthetic solvent (Danielson, 1973).
3.4.2.2 Consumption of Perchloroethylene by State—
Information was acquired from the International Fabricare Institute (IFI,
1977), Silver Springs, Maryland, concerning perchloroethylene consumption for
dry cleaning applications in 1975. These data show a total consumption of
157,385 MT (347 million pounds). Of this total, 13,220 MT (29.1 million pounds,
8.4%) were used in industrial operations; 21,404 MT (47.2 million pounds, 13.6%)
were used in coin-operated unitsj and 122,760 MT (270.6 million pounds, 78.0%)
were used in commercial applications. The IFI data on perchloroethylene consump-
tion by state for 1975 are shown in Table 3-30.
The data listed in the table were organized to permit an estimate of the
distribution of perchloroethylene consumption by domestic dry cleaning opera-
tions during 1975. The consumption values for the states in each federal region
were added to obtain a total consumption value for that region. The federal
Region V had the largest share (22.3% of total) of the consumption. Region II
accounted for 18.1% of total, while Regions IX (13.1%) and III (12.9%) ranked
third and fourth, respectively, in quantity of consumption. Region IV contri-
buted 12.6% of total consumption. The aggregate of these five regions repre-
sented 79.1% of the total consumption. Region VIII had the lowest share (1.9%)
of the total.
3.4.3 Miscellaneous Uses
3.4.3.1 Trichloroethylene—
These applications are chiefly related to the value of trichloroethylene
as a solvent. For 1976, exports and miscellaneous uses comprised 13% of the
total market for trichloroethylene (see Section 3.2.2). This percentage cor-
responds to 18,598 MT (41 million pounds); however, it was previously shown
(Section 3.2.3) that exports for 1976 were 35.5 million pounds so that the to-
tal quantity available for all miscellaneous uses is only approximately 2,500
MT (5.5 million pounds).
In the past, trichloroethylene has found significant markets in extraction
of caffeine to prepare decaffeinated coffee and in the processing of hop ex-
tracts. Also, it has been used in the processing of fish meal, meat meal, alka-
loids, oil-containing seeds (e.g., soy beans), spice oleoresins and color addi-
tives (e.g., annato extract, paprika oleoresins and cumeric oleoresins). At
3-74
-------
TABLE 3-30. CONSUMPTION OF PERCHLOROETHYLENE IN
DRY CLEANING FOR 1975
Federal region
I
II
III
IV
V
State
Maine
Massachusetts
Rhode Island
Connecticut
New Hampshire
Vermont
Total
New York
New Jersey
Total
Pennsylvania
Delaware
Mary land
West Virginia
Virginia
District of Columbia
Total
Kentucky
Tennessee
North Carolina
South Carolina
Mississippi
Alabama
Georgia
Florida
Total
Ohio
Indiana
Illinois
Michigan
Wisconsin
Minnesota
Total
(continued)
MI
440
6,237
724
4,069
440
142
12,052
20,594
7 , 949
28,543
8,231
393
3,802
880
6,001
1.022
20,329
2,639
3,094
3,395
1,335
471
1,712
2,906
3.786
19,838
10,273
3,770
8,184
7,854
2,388
2.670
35,139
Million Ib
0.969
13.749
1.597
8.970
0.969
0.312
26.566
45.402
17.524
62.926
18.147
0.866
8.381
1.940
13 . 230
2.252
44.816
5.818
6.822
8.588
2.944
1.039
3.775
6.407
8.346
43.739
22.649
8.312
18.043
17.316
5.264
5.387
77.471
3-75
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TABLE 3-30. (continued)
Federal region
VI
VII
VIII
IX
X
State
New Mexico
Texas
Oklahoma
Arkansas
Louisiana
Kansas
Missouri
Nebraska
Iowa
Colorado
Utah
Wyoming
Montana
North Dakota
South Dakota
California
Nevada
Arizona
Hawaii
Washington
Oregon
Idaho
Alaska
MI
377
5,059
1,005
593
1.508
Total 8,542
1,037
2,828
1,005
1.257
Total 6,127
1,728
409
157
267
220
204
Total 2,985
18,709
566
1,194
220
Total 20,689
1,979
958
189
15
Total 3,141
Million Ib
0.831
11.152
2.216
1.308
3.325
18.832
2.286
6.234
2.216
2.771
13.507
3.810
0.901
0.346
0.589
0.485
0.450
6.581
41 . 246
1.247
2.632
0.485
45.610
4.364
2.112
0.416
0.034
6.926
Source: International Fabricare Institute (1977).
3-76
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present, however, trichloroethylene is not used in the United States for de-
caffeinating coffee or in the processing of modified hop extracts (FDA, 1977a);
this is the result of voluntary action by the involved companies who have
changed to methylene chloride in expectation of an eventual ban by the Food
and Drug Administration (FDA) on trichloroethylene for processing food.
Trichloroethylene is utilized as a chemical raw material to produce
1,1,2,2-tetrachloroethyl sulfenyl chloride. The latter compound is an inter-
mediate used in production of Difolatan® fungicide (a product of Chevron Chem-
ical Company).
It is also used as a chain terminator for polyvinyl chloride production,
as a solvent for silicones, and as an intermediate in the production of chloro-
fluorocarbons (Franklin Institute, 1975).
In the textile industry, trichloroethylene is used as a carrier solvent
for spotting fluids. In a "closed-loop process," chemicals are dispersed, dis-
solved, or emulsified in the solvent and then applied to fabric by pad or spray
application. During drying of the fabric in a recovery system, the solvent is
recovered and recycled for use in subsequent processing (Lowenheim and Moran,
1975). It is also used in scouring and cleaning of raw wool, in desizing of
synthetic fibers, and to dissolve polycarbonate basting threads.
Minor amounts of trichloroethylene are used as a solvent, solvent carrier
or base for adhesives and lubricants, as well as for combination vapor
degreasing-phosphatizing processes and dip painting processes. It is also used
as a low temperature heat transfer fluid (Lowenheim and Moran, 1975).
Trichloroethylene has been used to a very limited extent as an anesthetic
and analgesic. It has been estimated that a maximum of 60,000 hospital patients
per year are exposed; a small number of dental patients are also exposed each
year. For a more detailed discussion, see Section 5.
3.4.3.2 Methyl Chloroform--
According to information in a trade publication, aerosol and adhesive
uses each comprised 77o of the 1976 consumption of methyl chloroform. This cor-
responds to 19,527 MT (43 million pounds) in each of these use areas. All other
uses comprised 6% of the 1976 total figure or 16,737 MT (36.9 million pounds)
(Chemical Marketing Reporter, 1977).
Methyl chloroform is used in aerosol products where it serves as a vapor-
pressure depressant and also as a primary solvent and carrier for several of
the active materials contained in the aerosols. The domestic aerosol products
include hair sprays, cosmetics, and medicated vapors. The properties which
make it a useful aerosol ingredient include its good evaporation rate, lack
of flash and fire points, and moderate vapor pressure.
3-77
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In July 1973, the FDA recalled medicated vaporizers containing methyl
chloroform, and an order for manufacturers to register drugs containing this
compound has been issued. Current information obtained from the FDA indicates
that no domestic drug manufacturers are using methyl chloroform in any of their
products (FDA, 1977b).
Methyl chloroform is used by formulators of adhesives as a resin solvent
for factory-applied adhesives and also as an on-the-job adhesive activator.
In this application, it has replaced flammable toxic solvents.
In another application, it is used as a lubricant carrier to facilitate
the injection of graphite, grease, and many viscous or dry lubricants into
difficult-to-reach places. Following the injection, the solvent evaporates,
leaving a film of lubricant.
In some refineries, small quantities are used in the preparation of cata-
lysts for reforming and hydroprocessing equipment.
Methyl chloroform is being used in motion picture film cleaning and as
the developer in a dry film process for printed circuit board development. It
is utilized by the textile industry for processing and finishing operations
as a spot remover for bulk fabrics during final inspection. It also finds use
in the formulation of drain cleaner for household applications, as a solvent
for formulation of shoe polishes, spot cleaners, insecticides, printing inks,
stain repellents for upholstery fabrics and clothing, and for wig cleaning.
3.4.3.3 Perchloroethylene--
As stated previously in Section 3.2.8, use of perchloroethylene as a chem-
ical intermediate comprised 11% of the 1975 volume and other miscellaneous uses
were 3% of the total quantity.
Use of perchloroethylene as a chemical intermediate in the manufacture
of chlorofluorocarbons F-113, F-114, F-115, and F-116 consumed approximately
33,884 MT (74.7 million pounds) in 1975.
Other miscellaneous uses of perchloroethylene accounted for about 9,241
MT (20.4 million pounds) in 1975. Small quantities are used as a solvent for
silicones and also in home laundry pretreatment products. In this latter ap-
plication, perchloroethylene and a petroleum distillate are packaged in an
aerosol container and used for dissolving greases. The dissolved greases are
carried away by the laundry detergent. These aerosol products are intended for
use on washable garments containing resins which tend to retain oils and
greases.
3-78
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3.5 FUTURE PROJECTIONS
Ten-year projections for manufacturing and use processes and market levels
for trichloroethylene, methyl chloroform, and perchloroethylene are extremely
difficult because of the controversy surrounding these three compounds. Due to
the interrelationship between the compounds, a negative effect on one may pro-
duce a positive effect on another. With respect to methyl chloroform, one pub-
lication prefaced their projection by stating "long term forecasting is out
of the question" (Chemical Marketing Reporter, 1977). The data and forecasts
presented in the following paragraphs are, in reality, best estimates based on
industrial and other sources of what may occur in the future. Sources of in-
formation for this discussion are industrial contacts: Chmielnicki, 1978;
Gagnon, 1977; Berthold, 1977; and Hurley, 1977; and Chemical Economics Handbook.
Stanford Research Institute: Trichloroethylene (Nov. 1975); 1,1,1-Trichloro-
ethylene (Oct. 1975); and Perchloroethylene (Nov. 1975); and the Chemical Mar-
keting Reporter (January 1977 and June 1978).
3.5.1 Trichloroethylene
The domestic consumption of trichloroethylene declined from 1970 to 1977
to a level of 132,768 MT (292.5 million pounds). The rapid decline was caused
by a combination of factors including reduced economic growth, increased use
efficiencies on the part of consumers, the substitution of other solvents due
to air emission regulations, and a general reluctance by users to commit to
trichloroethylene because of the risk of future restrictive regulations on its
use.
The stabilized demand in 1976 was due to the increased economic activity
counterbalanced by continued conversions to other solvents because of air pol-
lution regulations.
Future demand for trichloroethylene will be directly affected by government
regulations for air pollution control and by Occupational Safety and Health
Administration (OSHA) standards for worker exposure. Consumption is expected
to decline from the 1977 level at a rate of 5.5% compounded annually to a value
of about 100,000 MT (220.5 million pounds) by 1982 (Chemical Marketing Reporter,
1978). For the period of 1982 to 1985, the decline is estimated to be about 3%
compounded annually to a level of 91,360 MT (201.4 million pounds) by 1985.
Consumption is expected to level off from 1985 to 1988 and to be at a level of
about 90,000 MT (198.5 million pounds) by 1988.
3.5.1.1 Metal Cleaning Applications--
Historically, over 90% of the trichloroethylene consumption has been in
cleaning metal parts prior to their assembly or in preparation for painting,
rustproofing, electroplating, or galvanizing. It is also used to a limited ex-
tent as a cold cleaner and in specialty cleaners. Cold cleaning and chemically
3-79
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formulated cleaners represent about 5 to 10% of the total metal cleaning uses.
Thus, the future of trichloroethylene depends upon its use in vapor degreasing
operations*
As a result of Rule 66, the Clean Air Act, and OSHA limits in the work-
place, a search for other substitute products was initiated, and methyl chloro-
form, which had been extensively used for cold cleaning of metal parts, was
found to be an acceptable substitute in vapor degreasing operations. Perchloro-
ethylene can also be effectively used in vapor degreasing, but its higher cost
and higher boiling point, along with the need for high pressure steam, has lim-
ited its use to specialized applications.
These factors have all contributed to a decline in trichloroethylene con-
sumption in vapor degreasing from 235,870 MT (520 million pounds) in 1966 to
about 114,000 MT (251.4 million pounds) in 1977.
Stricter environmental regulations are expected to cause trichloroethylene
use in vapor degreasing to further decline, at a rate of about 5.5%/year to a
level of 86,000 MT (189 million pounds) by 1982, and then decline at 3%/year
to 79,000 MT (174 million pounds) by 1985. Consumption is expected to level off
during the period 1985 to 1988. It is estimated that 90% of the replacement of
trichloroethylene will be methyl chloroform and 10% will be perchloroethylene.
The demand for vapor degreasing solvents has grown at a much slower rate
in recent years. Increasing energy costs and pollution regulations have induced
higher operating efficiencies in many vapor degreasing facilities through re-
covery systems and reduced vapor emissions. Improvements can be expected to
continue as more facilities install the necessary equipment to meet emission
regulations.
An estimated 5,534 MT (12.2 million pounds) of trichloroethylene were used
for cold cleaning metal parts in 1975. This use has been steadily declining for
many of the same reasons as the use in vapor degreasing, and will continue to
decline as trichloroethylene is replaced by methyl chloroform.
3.5.1.2 Other Uses—
Approximately 6,850 MT (15.1 million pounds) of trichloroethylene were
consumed in 1975 for miscellaneous uses. These uses included chemical raw ma-
terials, primarily for the production of Difolatan® (a fungicide) and as a
chain terminator for controlling the polymerization of polyvinyl chloride. A
small amount was used in the textile industry for dissolving polycarbonate
basting threads.
Many uses for trichloroethylene have been discontinued. Several million
pounds per year had been used to decaffeinate coffee, but this is now being
done by other solvents (e.g., methylene chloride).
3-80
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Demand for trichloroethylene in other uses should remain at the present
level for the next decade. Its growth will occur as a chemical intermediate
as the demand for Difolatan® increases, but this will be offset by the replace-
ment of trichloroethylene as a chain terminator. About four or five producers
are presently using trichloroethylene for this purpose, but they are modifying
their equipment to eliminate its use*
No new uses or growth in other areas are anticipated because of the poten-
tial environmental and health restrictions.
3.5.1.3 Imports and Exports--
Approximately 15,420 MT (34 million pounds) of trichloroethylene were ex-
ported in 1975, a decline from 19,505 MT (43 million pounds) in 1974. Most of
the exports were to European countries, Japan, Canada, and Mexico. It is likely
that exports will continue at a rate of 13,600 to 22,680 MT (30 to 50 million
pounds) per year. With substantial capacity available in the United States,
export markets are expected to be attractive to producers. Possible markets
could occur in the Mideast as the economies of these nations expand and they
develop a need for metal degreasing solvents.
Imports in 1976 were 7,056 MT (15.6 million pounds) and have varied sig-
nificantly from a peak of 53,978 MT (119 million pounds) in 1966 to a low of
590 MT (1.3 million pounds) in 1974. The increased cost of chlorine and higher
hydrocarbon costs to foreign producers coupled with the increasing over-capacity
of domestic producers will likely keep imports between 2,268 to 9,072 MT (5 to
20 million pounds) per year during the period 1975 to 1985. If one or more of
the existing producers should close their plants during this period, imports
could temporarily increase until domestic capacity again exceeds demand.
3.5.1.4 Production Capacity--
There were four producers in 1978 with a total capacity estimated at
238,095 MT (525 million pounds). As demand continues to decline, some of the
existing producers could withdraw from the market. One producer (Occidental
Petroleum) has reported a permanent shutdown of trichloroethylene production
operations effective in January 1978. It should be noted that Diamond Shamrock
and Ethyl Corporation manufacture both perchloroethylene and trichloroethylene
in the same facilities and can maximize perchloroethylene production. PPG also
has the flexibility in their plant to manufacture trichloroethylene, perchloro-
ethylene, and methyl chloroform. It is possible that these producers will con-
tinue production until their facilities become uneconomical to operate.
No new facilities, producers, or technology are anticipated in the United
States in the next decade.
3-81
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3.5.2 Methyl Chloroform
Production in 1977 was 287,945 MT (634.8 million pounds). In 1976 and
1977, production represented 91.5 and 92.0% of capacity, respectively. Using
the estimated production figures for 1978 (282,547 MT), production is 90.3%
of capacity. Actual or planned plant capacity expansions will increase methyl
chloroform production capacities from 690 million pounds in 1978 to 1,235 mil-
lion pounds by approximately the end of 1979 (see Section 3.5.2.5). Thus, a
potential exists for very large increases in the annual production quantities
of methyl chloroform. If one assumes a straight line approach, a compounded
annual growth rate of approximately 770 will show production quantities equal
to capacity in 1988. However, growth very seldom, if ever, occurs in this man-
ner. The future growth of methyl chloroform will be governed by future air
quality regulations and the future of trichloroethylene, both within the United
States and world-wide. With the very large production capacities available, it
would be difficult to attempt to further predict production quantities.
3.5.2.1 Vapor Degreasing--
Nearly all of the methyl chloroform growth has occurred since 1966 when
restrictions were placed on trichloroethylene. The subsequent decline in the
use of trichloroethylene was a result of replacement by methyl chloroform.
Thus, methyl chloroform has achieved most of its growth from substitution
rather than general market growth.
Future demand in vapor degreasing is projected to be directly related to
the future of trichloroethylene and future regulations. Continued emphasis is
expected to be placed on the substitution of methyl chloroform for trichloro-
ethylene, based on current air quality laws and OSHA standards for worker ex-
posure. Overall growth for chlorinated solvents in metal vapor degreasing can-
not be realistically estimated because of the large production capacity.
3.5.2.2 Cold Cleaning-
Consumption in cold cleaning applications is projected to be about 109,000
MT (240 million pounds) by 1980. Growth rates of 3%/year to 1985 and 1%/year
to 1988 are expected. Because there are myriads of small users, these data are
difficult to develop. The growth rate will be affected mostly by the growth of
the metalworking industries*
3.5.2.3 Miscellaneous Uses--
There are several miscellaneous uses for methyl chloroform. These include
formulated cleaners, aerosol propellants, textile spotting fluids and adhe-
sives; carburetor cleaners, business machine cleaning fluids, and as solvent
for adhesives. Demand as a vapor pressure depressant and flame retardant in
aerosols continues to decline, and its use in some drain cleaners was discon-
tinued because of possible health effects.
3-82
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The growth rate is projected at 5%/year from 1980 to 1988. Because there
are so many diverse uses, declines in several areas will probably be offset by
growth in others.
Future markets that could achieve above normal growth rates include tex-
tile processing and finishing and adhesive solvents. As the textile industry
increases their attempts to reduce water pollution, methyl chloroform could be
used to replace aqueous systems in the finishing operations.
The Consumer Product Safety Commission recognizes the hazardous nature
of hydrocarbon adhesive solvents. If legislation should be enacted limiting
the use of hydrocarbons, methyl chloroform would be a suitable replacement,
resulting in a new market of several million pounds per year.
3.5.2.4 Exports and Imports--
The amount of methyl chloroform that is imported and exported is not re-
ported in published literature. It is believed that imports into this country
are minimal because of the ability of the domestic suppliers to fill the mar-
ket needs. Exports are about 5 to 10% of the annual production, ranging from
15,876 to 31,752 MT (35 to 70 million pounds) per year. It is expected that
future export demand will be less than 5% of production as recent expansions
of several foreign plants begin to compete for world markets.
3.5.2.5 Production Capacity-
There were three producers of methyl chloroform in 1977. Production ca-
pacity in 1977 was 312,982 MT (690 million pounds) per year; capacity is ex-
pected to increase to 569,260 MT (1,255 million pounds) annually by the end
of 1979 when PPG Industries completes its current plant expansion, Dow adds
136,050 MT (300 million pounds) of capacity, and Vulcan increases capacity to
92,980 MT (205 million pounds). This capacity should be adequate to meet de-
mand until the later 1980's unless significant new uses develop.
It is unlikely that any new producers will enter the market in the next
decade. The ability of the above producers to manufacture other co-products
and the economics of large plants will probably limit any capacity growth to
the above producers. If additional competition does arise, it will probably
come from existing chlorinated solvent producers who manufacture chlorine and
have an available source of hydrocarbon supply. Increasing costs of shipping
chlorine and its hazards will make a chlorine source a highly desirable factor
in the future for any solvent producer.
Dow Chemical has been reported to use methyl chloroform to produce vinyli-
dene chloride at its Freeport, Texas, plant. Dow has the option of using either
methyl chloroform or 1,1,2-trichloroethane, depending upon the economics of
the materials available at the producing facility.
3-83
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3.5.3 Perchloroethylene
U.S. consumption grew at an annual rate of 3% from 1969 to 1974, but de-
clined from 1975 to 1977. However, production for 1978 is expected to increase
to about 310,000 MT. The future growth rate is anticipated to be 3 to 4%/year.
The major use of perchloroethylene is 'as a dry cleaning solvent in the textile
industry, but its use in the metal cleaning industry will probably increase at
a more rapid rate. Perchloroethylene will pick up some of the decrease in de-
mand for trichloroethylene as a vapor degreaser, as discussed in Section 3.5.1.
3.5.3.1 Textile Industry--
The textile industry currently uses about two-thirds of the perchloro-
ethylene currently produced. About 70% of the domestic dry cleaning establish-
ments use perchloroethylene; about 30% use petroleum solvents or fluorocarbon
solvent (F-113). Although the trend to wash and wear clothing has decreased
the demand for dry cleaning, growth in the coin-operated dry cleaning industry
has increased demand because these facilities use more perchloroethylene per
pound of clothing than do professional dry cleaning shops. The use of perchloro-
ethylene in the textile industry decreased in 1975, but it is anticipated that
a 4% growth rate will resume about 1980. Part of the increase will be due to a
probable increase in industrial dry cleaning. Perchloroethylene is used to man-
ufacture trichlorotrifluoroethane (Fluorocarbon 113), which is also used as a
dry cleaning agent. Fluorocarbon 113 has advantages for certain types of dry
cleaning such as furs and leather, but its high cost may limit its growth.
3.5.3.2 Metal Cleaning--
About 807» of the total amount of perchloroethylene used in the metal in-
dustry is for vapor degreasing, and the remainder is for cold cleaning.
The advantage of perchloroethylene over methyl chloroform is that water
contamination is not as serious a problem. Also, because perchloroethylene has
a high boiling point, the vapors are in contact with the metal longer to give
more effective cleaning. High melting waxes, which may be missed by low boiling
solvents, are removed by perchloroethylene. The major disadvantages of per-
chloroethylene are the higher energy requirements, and the necessity for using
high pressure steam if the liquid is steam heated.
The growth rate for consumption of perchloroethylene by the metal clean-
ing industry is expected to be about 10 to 12% during the next decade.
3.5.3.3 Intermediate Chemical--
Approximately 10 to 12% of the perchloroethylene is used as an intermedi-
ate in the production of four fluorocarbons: F-113, F-114, F-115, and F-116.
These fluorocarbons are used as solvents, refrigerants, aerosols, and for dry
cleaning of certain items.
3-84
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3.5.3.4 Miscellaneous Uses--
Perchloroethylene is used as a solvent for silicones and is finding use
as a home laundry treatment product. For the latter use, perchloroethylene in
combination with a petroleum distillate is packaged in an aerosol container
and used for dissolving greases, which are then carried away by the detergent.
Only about 1 to 27, of perchloroethylene is currently used for this purpose,
and the potential market is difficult to estimate.
3.5.3.5 Exports and Imports--
Imports did not show a definite trend in either direction from 1965 to
1975. Imports ranged from 10,433 to 30,845 MT (23 to 68 million pounds). Ex-
port quantities ranged from 12,700 to 48,988 MT (28 to 108 million pounds)
since 1972, and like imports, exports have shown no definite trend. Trade fig-
ures may vary considerably from one year to the next, due to new foreign manu-
facturing plants. Exports decreased considerably from 1972 to 1974 due to the
startup of a new Dow plant in West Germany. Europe and Canada are the primary
trading partners of the United States. A thorough study of market conditions
in Europe has not been made, so future trading trends are not projected.
3.5.3.6 Production Capacity—
In 1978, there were seven producers of perchloroethylene with a total
production capacity of 539,683 MT (1,190 million pounds). It is expected there
will probably be expansion of the present production plants to meet increased
demand during the next decade. No new producers are anticipated in the United
States during the next decade.
3.6 OVERALL MATERIALS BALANCE
A discussion of various sources of solvent emissions is presented in the
following subsections. These sources include natural sources, manufacturing,
importers, consumption (users), distributors, exporters, final disposal, and
environmental loss.
3.6.1 Natural Sources
Evidence is that all trichloroethylene, methyl chloroform, and perchloro-
ethylene that appear in the environment are anthropogenic in origin. No natu-
rally occurring sources are known to exist (Singh, 1977; Gay et al., 1976)j a
survey of the technical information did not identify any natural sources.
3.6.2 Manufacturing
The following paragraphs discuss the material balances for the manufac-
ture of each of the three compounds.
3-85
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3.6.2.1 Trichloroethylene Production—
In 1976, 90% of the U.S. production of trichloroethylene, or 128,800 MT
(284 million pounds), with a market value of about $42.6 million, was by the
ethylene dichloride process. The remaining 10%, or 14,311 MT (31.5 million
pounds), with a value of $4.7 million, was manufactured by a process involving
chlorination of acetylene followed by dehydrochlorination of the 1,1,2,2-tetra-
chloroethane intermediate. The material balance and data for 1976 for these
two processes are as follows.
Production from ethylene dichloride
Raw materials
Ethylene dichloride
Chlorine
Oxygen
Catalyst (loss)
By-product
Hydrogen chloride
Ib/lb TCE
0.860
0.307
0.208
Small
Estimated
MT x 10J
110.8
39.6
26.8
Small
quantity
10b Ib
244.2
87.2
59.1
Small
Approximate
value ($)
19,536,000
5,670,000
1,186,300
1.187
152.9
337
18,535,000
The Deacon process can be used to convert the by-product HCl to chlorine
which is recycled to the process.
Wastes--Wastes consist of water vapor emissions to the atmosphere from
the crude product dehydrator unit.
Acetylene-based process
Raw materials
Acetylene
Chlorine
Catalyst (loss)
By-product
Hydrogen chloride
Ib/lb TCE
0.21
1.14
Small
0.28
Estimated quantity
MT x 10310b Ib
3.0
16.3
Small
4.0
6.62
35.91
Small
8.82
Approximate
value ($)
993,000
2,334,000
485,000
3-86
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Waste tail gas from HCl recovery unlt--In the acetylene-based process,
the waste tail gas vented to the atmosphere from the HCl recovery unit con-
tains the following quantities of components:
Waste
component
Trichloroethylene
Perchloroethylene
Tetrachloroethane
Hydrogen chloride
Estimated quantity Approximate
lb/1.000 Ib TCE MT tb value ($)
0.35
0.99
0.50
0.99
5.00
14.15
7.14
14.15
11,025
31,185
15,750
31,185
1,654
4,678
2,265
1,715
Heavy ends waste from distillation--For the same process, the heavy ends
waste (liquid-solid) sent to land disposal from the trichloroethylene columns
contains the following maximum amounts of components:
Waste
component Ib/lb TCE
Hexachlorobutadiene 0.23
Chlorobenzenes 0.02
Chloroethanes 0.01
Chlorobutadienes 0.01
Tars and residues 0.02
Estimated quantity
MT 103 Ib
3,287
286
143
143
286
7,245
630
315
315
630
Approximate
value ($)
2,535,500
157,500
NA
NA
NA
Waste gas^ from still condenser--In the same process, the waste gas vented
to the atmosphere from the reflux condenser on the crude trichloroethylene i
still contains the following components:
Waste
component
Ethane
Methane
Tetrachloroethane
Estimated quantity Approximate
lb/1.000 Ib TCE ~"MT103 Ib value ($)
1.252
1.252
0.500
17.9
17.9
7.2
39.4
39.4
15.8
NA
430
2,270
3.6.2.2 Methyl Chloroform Production—
In 1976, 60% of the production of methyl chloroform, or 171,824 MT (378.8
million pounds), was derived from vinyl chloride; 30%, or 85,912 MT (189.4 mil-
lion pounds), was based on vinylidene chloride as raw material; and 10%, or
3-87
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28,622 MT (63.1 million pounds), was produced by chlorination of ethane. The
total market value for all of the domestically produced methyl chloroform in
1976 was about $120,000,000.
Production from vinyl chloride
Raw materials Ib/lb MC
Vinyl chloride 0.5
Chlorine 0.525
Ferric chloride Small
(catalyst)
By-products
Vent gas components
from hydrochlori-
nation reactor (to
atmosphere)
Dichloroethane 0.0035
Trichloroethane 0.009
Steam stripper gas
components (vent to
atmosphere)
Dichloroethane 0.0005
Trichloroethane 0.0005
Vinyl chloride 0.0005
Steam stripper
water effluent
Estimated quantity
MT x 103103 Ib
85.9
90.2
Small
602
1,547
86
86
86
Approximate
value ($)
189,400 18,940,000
198,870 12,927,000
Small
1,326
3,409
106,100
657,700
189
189
189
15,120
36,500
18,900
Organic chloride
Hydrochloric acid
Traces
Traces
Vinylidene chloride-based process
Raw materials Ib/lb MC
Vinylidene chloride 0.727
Hydrochloric acid 0.274
Ferric chloride Small
(catalyst)
Estimated quantity Approximate
MT x 103103 Ib value ($)
62.46
23.54
Small
137,694 30,960,000
51,896 3,303,000
Small
3-88
-------
By-products--No by-products are formed in the basic process.
Waste streams--A heavy ends waste stream containing < 0.1% methyl chloro-
form is discharged from the fractionator. An aqueous effluent waste stream con-
tains < 0.1% methyl chloroform.
Chlorination of ethane
Estimated quantity Approximate
Raw materials Ib/lb MC MT x 103103 Ib value ($)
Ethane 0.386 11.05 24,357
Chlorine 2.022 57.87 127,588 8,298,000
By-products
Hydrogen chloride 1.11 31.77 70,041 3,852,000
Ethylene 0.073 2.09 4,606 515,900
Waste stream--A heavy ends waste stream is used as feed to a perchloro-
ethylene plant. Waste from the perchloroethylene plant consists of hexachloro-
benzene, hexachlorobutadiene, and hexachloroethane.
3.6.2.3 Perchloroethylene Production--
During 1976, domestic production of perchloroethylene amounted to 668.9
million pounds. About 63% of the output of 190,966 MT (421 million pounds with
a value of $63,150,000) was produced by chlorination and pyrolysis of various
hydrocarbons (e.g., propane). Approximately 34% of the total production, or
102,967 MT (227 million pounds with a value of $34,050,000), was based on the
ethylene dichloride process. The remaining 3% of production, or 9,480 MT (20.9
million pounds with a value of $3,135,000), was based on the use of acetylene
as raw material. A material balance for 1976 representative of each of these
processes follows:
Production from propane
Estimated quantity Approximate
Raw materials Ib/lb PCE MT x 103 1Q3 Ib value ($)
Propane 0.20 38.19 84,200 6,147,000
Chlorine 2.50 477.41 1,052,500 68,412,500
By-product
Hydrogen chloride 225.40 496,918 27,330,000
3-89
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Production from ethylene dichloride
Raw materials Ib/lb PCE
Ethylene dichloride 0.681
Chlorine 0.611
Oxygen 0.193
Catalyst (loss) Small
By-product
Hydrogen chloride 0.11
Production from acetylene
Raw materials Ib/lb PCE
Acetylene 0.19
Chlorine 1.50
Lime 0.45
Catalyst (loss) Small
By-product
Hydrogen chloride 0.118
Waste tail gas and
Surge gas
TCE in waste gas 0.32
TCE in purge gas 2.80
Perchloroethylene 0.90
Calcium- bearing wastes
Calcium hydroxide 0.24
Calcium chloride 0.34
Heavy ends waste from
still
Hexachloro butadiene 0.23
Chlorobenzene 0.02
Estimated quantity Approximate
MT x 103 103 ib value ($)
70.12 154,587 12,367,000
62.91 138,697 9,015,000
19.87 43,811 879,200
Small Small
11.33 24,970 1,373,000
Estimated quantity Approximate
MT 103 Ib value ($)
1,801 3,971 595,700
14,220 31,350 2,038,000
4,266 9,405 136,000
Small Small
1,119 2,466 135,600
3 6 900
24 53 7,950
9 19 3,610
2,275 5,016 70,000
3,223 7,106 213,500
2,180 4,807 1,682,500
190 418 105,000
3-90
-------
3.6.3 Importation
During 1976, the total imports of trichloroethylene were 7,056 MT (15.6
million pounds) and imports of perchloroethylene during the same year were
28,277 MT (62.2 million pounds). The imports of methyl chloroform were neg-
ligible. Estimated total value of the imports of trichloroethylene is $2.2
million and for perchloroethylene, $6.8 million. Losses of any of the three
compounds during domestic transport and storage at the consumer or distribu-
tor site are considered to be negligible.
3.6.4 Consumption
The U.S. consumption of trichloroethylene in 1976 was 124,497 MT (274.5
million pounds) to metal cleaning, 16,124 MT (35.5 million pounds) to exports,
and 2,495 MT (5.5 million pounds) to miscellaneous uses (see Table 3-8). The
estimated 1976 market value for the total solvent consumed in each category
is: metal cleaning, $41.2 million; exports, $5.8 million; and miscellaneous
uses, $0.8 million. The total value of trichloroethylene for all uses in 1976
was $47.3 million.
During 1976, the usage of methyl chloroform was 214,780 MT (473.5 million
pounds) to metal cleaning, 14,334 MT (31.6 million pounds) to exports, 37,241
MT (82.1 million pounds) to production of vinylidene chloride, and 20,049 MT
(44.2 million pounds) to miscellaneous uses (see Table 3-12). The estimated
market value in 1976 for the total solvent used in each category is: metal
cleaning, $90.0 million; exports, $6.0 million; production of vinylidene chlo-
ride, $15.6 million; and miscellaneous uses, $8.4 million. The total value of
methyl chloroform for all uses in 1976 was $120 million.
The consumption of perchloroethylene in 1976 was 191,147 MT (421.4 million
pounds) to the textile industry (146,377 MT to dry-cleaning and 44,770 MT to
textile scouring), 33,249 MT (73.3 million pounds) to vapor degreasing, 15,286
MT (33.7 million pounds) to cold cleaning, 32,432 MT (71.5 million pounds) to
use as a chemical intermediate, 9,117 MT (20.1 million pounds) for miscellane-
ous uses, and 22,181 MT (48.9 million pounds) to exports (Table 3-15). The es-
timated market value in 1976 for the total solvent used in each category is:
dry-cleaning, $48.4 million; textile scouring, $14.8 million; vapor degreasing,
$11.0 million; cold cleaning, $5.1 million; chemical intermediate, $10.7 mil-
lion; miscellaneous uses, $3.0 million; and exports, $7.3 million. The total
value of perchloroethylene for all uses in 1976 was $100.3 million.
3.6.5 Distributors
No specific data were obtained on possible losses of solvent from han-
dling and storage by distributors. However, published reports (A. D. Little,
1975; Fuller, 1976a; 1976b) indicate that these losses are negligible.
3-91
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'3.6.6 Exportation
The total exports of trichloroethylene in 1976 amounted to 16,124 MX
(35.5 million pounds) with an estimated market value of $5.3 million (Table
3-10). During the same year, the exports of methyl chloroform were estimated
at 14,000 MT (30.9 million pounds) with an estimated market value of $5.9 mil-
lion (Table 3-13). The exports of perchloroethylene amounted to 22,181 MT (48.9
million pounds) and had an estimated market value of $7.3 million (Table 3-17).
3.6.7 Final Disposal and Environmental Loss
This subsection discusses final disposal for the solvents of interest,
the material balances for production and consumption, and the estimated envi-
ronmental losses for each solvent.
3.6.7.1 Trichloroethylene--
An input-output summary for trichloroethylene showing emissions to the
environment is presented in Figure 3-9. The total U.S. production in 1976
amounted to 143,111 MT (315.5 million pounds). The estimated total emission
losses to the atmosphere during production, transportation, and storage are
2,147 MT (4.73 million pounds) or 1.5% of annual production; this estimate is
based on data presented in the technical literature (A. D. Little, 1975j Fuller,
1976a). The total U.S. consumption of 131,896 MT (290.7 million pounds) for
the same year was computed by adding the domestic production value to the im-
ports and subtracting exports and emission losses in production, transporta-
tion, and storage. Losses to the environment during importation and exporta-
tion operations are considered to be negligible.
The amount of trichloroethylene consumed for metal cleaning work in 1976
was calculated to be 128,928 MT (284 million pounds). A report by EPA (1979,
p. 2-5) states that in 1974 the distribution in metal cleaning applications
was 83% to vapor degreasing and 17% to cold cleaning. In this study, it was
assumed that the same distribution applied for 1976, and on this basis the
quantity of trichloroethylene used for vapor degreasing was 107,010 MT (235.9
million pounds), and the amount used in cold cleaning was 21,918 MT (48.3 mil-
lion pounds). The atmospheric emissions from vapor degreasing and cold clean-
ing operations are estimated, on the basis of data supplied by an equipment
manufacturer (Schlossberg, 1976), to be the same as the quantities of solvent
used in the cleaning operations. Emissions from miscellaneous uses are 507«
of the quantity used (A. D. Little, 1975).
An assessment was made of the geographic distribution of the metal clean-
ing usage and the atmospheric emissions of trichloroethylene in 1976. Dow Chem-
ical Company (1976) reported data applicable to 1974 for the domestic metal
cleaning industries which use each of the three solvents; these data were used
as a point of departure for these assessments.
3-92
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I
v£>
UJ
IMPORTS
7,056
EXPORTS
16,124
TOTAL U.S.
PRODUCTION
143,111
i
TOTAL U.S.
CONSUMPTION
131,896
EMISSION LOSSES
IN PRODUCTION,
TRANSPORTATION
AND STORAGE
2,147
All Quantities in Metric Tons
Source: MRI - Based on Data Cited EarlieMn
Section 3 and Industrial Estimates
128,928
VAPOR
DECREASING
2,968
ATMOSPHERIC
EMISSIONS
-^.107,010
COLD
CLEANING
MISC.
USES
21,918
1,484
Figure 3-9. Input/output summary for trichloroethylene for 1976.
-------
For purposes of this study, it was assumed that the 1974 Dow data also
apply to 1976, that the distribution of solvent usage was directly propor-
tional to the distribution of each cleaning method, and that all solvent used
was eventually emitted to the atmosphere (either as a direct atmospheric emis-
sion or from waste liquids or solids). The geographic distribution of solvent
usage and emissions was then estimated as follows (see also Figure 3-10):
Geographic
district
Northeast
Southeast
Midwest
North Central
Southwest
Far West
Percent of
total cold
cleaning
units
33.8
9.6
31.3
7.1
4.2
14.0
Quantity
(MT)
7,408
2,104
6,860
1,556
921
3,069
Percent of
total vapor
degreaser
units
35.1
6.7
28.1
4.8
2.1
23.2
Quantity
(MT)
37,561
7,170
30,070
5,136
2,247
24,826
Total
quantity
(MT)
44,969
9,274
36,930
6,692
3,168
27,895
Total quantity (MT) 21,918
107,010 128,928
3.6.7.2 Methyl Chloroform—
An input-output summary for methyl chloroform showing estimated emissions
to the environment Is given in Figure 3-11. Total domestic production in 1976
was 286,358 MT (631.3 million pounds). The estimated total emission losses dur-
ing production, transportation, and storage of methyl chloroform are 4,296 MT
(9.47 million pounds, equivalent to 1.5% of total production). Consumption for
the same year amounted to 267,728 MT (590.1 million pounds) based on domestic
production plus imports minus exports and emission losses in production, trans-
portation, and storage. Losses to the environment during importation and expor-
tation activities are considered to be negligible.
The total quantity of methyl chloroform consumed in metal cleaning in 1976
was determined to be 214,182 MT (472 million pounds) as shown in Figure 3-11.
This quantity represents 80.0% of the total U.S. consumption for that year.
Based on information in reports (EPA, 1977; 1979) and from industrial sources,
the distribution of use categories in metal cleaning during 1976 was estimated
by MRI to be 59% or 126,367 MT (278 million pounds) to vapor degreasing and
41% or 87,815 MT (194 million pounds) to cold cleaning. The atmospheric emis-
sions from degreasing and cold cleaning are considered to be the same as the
quantities of solvent used in the metal cleaning operations (Schlossberg, 1976;
A. D. Little, 1975).
3-94
-------
Ol
NORTH CENTRAL
NORTHEAST
CC: l,556MTi
VD:5,136MT:
FAR WEST
CC:3,069 MT
VD:24,826MT
CC:6,860MT
VD:30,070MT
SOUTHEAST
CC:2,104MT
VD: 7,170 MT
SOUTHWEST
CC: 921 MT
VD:2,247MT
a/
CC = Cold Cleaning
y
VD = Vapor Degreasing
Source: Midwest Research Institute;
Dow Chemical Company ( 1976)
Figure 3-10. Distribution of trichloroethylene emissions from metal cleaning in 1976.
y
CC : 7,408 MT
VD-/:37,561 MT
-------
TOTAL U.S.
PRODUCTION
286,:
T
IMPORTS, EXPORTS
NEGLIGIBLE 14,334
TOTAL U.S.
CONSUMPTION
267,728
IN PRODUCTION,
TRANSPORTATION
4,296
All Quantities in Metric Tons
Source: MRI - Based on Data Cited Earlier in
Section 3 and Industrial Estimates
214,182
VAPOR
DECREASING
ATMOSPHERIC
EMISSIONS
COLD
CLEANING
18,741
18,741
16,064
. USES
87,815
18,741
18,741
8,032
Figure 3-11. Input/output summary for methyl chloroform for 1976.
-------
A study was also made of the geographic distribution of the metal cleaning
usage and emissions of methyl chloroform during 1976. The assumptions applied
were the same as those for the trichloroethylene assessment. On this basis,
the geographic distribution of methyl chloroform consumption and emissions
were estimated as follows (see also Figure 3-12).
Geographic
district
Northeast
Southeast
Midwest
North Central
Southwest
Far West
Percent of
total cold
cleaning
units
33.8
9.6
31.3
7.1
4.2
14.0
Quantity
(MT)
29,681
8,430
27,487
6,235
3,688
12,294
Percent of
total vapor
degreaser
units
35.1
6.7
28.1
4.8
2.1
23.2
Quantity
(MT)
44,354
8,467
35,509
6,066
2,654
29,317
Total
quantity
(MT)
74,035
16,897
62,996
12,301
6,342
41,611
Total quantity (MT) 87,815
126,367 214,182
3.6.7.3 Perchloroethylene--
The 1976 input-output summary for perchloroethylene showing estimated
emissions to the atmosphere is presented in Figure 3-13. In 1976 the total
domestic production amounted to 303,413 MT (668.9 million pounds). The total
emission losses occurring during production, transportation, and storage are
estimated to be 4,551 MT (10,0 million pounds). Total domestic consumption for
1976 was 304,908 MT (672.0 million pounds). Losses during importation and ex-
portation are negligible.
Atmospheric emissions from dry-cleaning and textile scouring are the same
as the input quantities (A. D. Little, 1975). Total atmospheric emissions from
these two sources are estimated to be 206,728 MT (455.6 million pounds). The
dry cleaning emission distribution is shown in Figure 3-14; the data are based
on International Fabricare Institute (1977) data on consumption of perchloro-
ethylene in dry cleaning operations for 1975 (see Table 3-30). Since the 1975
and 1976 U.S. production quantities are very similar, it was assumed that the
percent contribution from each region would be the same for 1976.
For metal cleaning operations, the estimated atmospheric emissions are
39,857 MT (87.8 million pounds) from vapor degreasing and 12,587 MT (27.7 mil-
lion pounds) from cold cleaning.
3-97
-------
Ijj
00
s 29,681 MT
VD-^S44,354MT
NORTH CENTRAL
NORTHEAST
CC: 6,235 MT
VD: 6,066 MT
FAR WEST
CC: 12,294 MT
VD:29,317MT
CC: 27,487 MT
VD:35,509MT
SOUTHEAST
CC: 8,430 MT
VD: 8,467 MT
SOUTHWEST
CC:3,688MT
VD:2,654MT
CC = Cold Cleaning
VD = Vapor Degreasing
Source: Midwest Research Institute;
Dow Chemical Company (1976)
Figure 3-12. Distribution of total methyl chloroform emissions from metal cleaning in 1976,
-------
CJ
vO
IMPORTS
28,227
EXPORTS
22,181
TOTAL U.S.
PRODUCTION
303,413
TOTAL U.S.
CONSUMPTION
304,908
EMISSION LOSSES
IN PRODUCTION,
TRANSPORTATION
AND STORAGE
4,551
All Quantities in Metric Tons
Source: MRI - Based on Data Cited Earlier in
Section 3 and Industrial Estimates
206,728
52,444
DRY
CLEANING
SOLVENT
TEXTILE
SCOURING
VAPOR
DECREASING
35,979
9,757
COLD
CLEANING
CHEMICAL
INTERMEDIATE
MISC.
USES
ATMOSPHERIC
EMISSIONS
-^ 158,312
48,416
39,857
12,587
543
4,879
Figure 3-13. Input/output summary for perchloroethylene for 1976.
-------
O
O
All Quantities in Metric Tons
Source: MRI - Based on Data from U.S.
International Trade Commission and
International Fabricare Institute
Figure 3-14. Distribution of perchloroethylene emissions from dry cleaning operations in 1976.
-------
The losses of perchloroethylene in its use as a chemical intermediate are
estimated to be 543 MT (1.2 million pounds). Atmospheric losses from miscellane-
ous uses are assumed to be one-half of the input quantity.
3.7 SUMMARY OF CHEMICAL LOSSES
This section summarizes the estimated total amount of trichloroethylene,
methyl chloroform, and perchloroethylene released to the environment from all
sources of emission. The technical literature indicates that essentially all
of the environmental emissions are discharged into the atmosphere, and that
the overall solvent discharges which remain in waterways or soil are negli-
gible (A. D. Little, 1975; Dow Chemical Company, 1976). Localized situations
can occur in which levels in waterways, water wells, or soils would present
a serious problem.
3.7.1 Atmospheric Emissions
The primary source of introduction of both trichloroethylene and methyl
chloroform into the environment is through atmospheric emissions resulting
from their ultimate use in metal cleaning. For perchloroethylene, the major
emission source is the textile industry.
3.7.1.1 Trichloroethylene—
A summary of trichloroethylene emissions in 1976 from manufacturing
plants, processing plants, and miscellaneous users was shown in Figure 3-9
(see 3.6.7.1). Total losses were 132,559 MT (292 million pounds). Degreasing
arid cleaning of metals accounted for 97.3% of the total emissions; 837o at-
tributable to vapor degreasing and 17% due to cold cleaning emissions. Losses
to the atmosphere from miscellaneous uses represented 1.1%, of the total loss,
and the category of production, transportation, and storage of trichloro-
ethylene generated only 1.6% of the total emissions.
3.7.1.2 Methyl Chloroform—
The estimated methyl chloroform emissions in 1976 were summarized in
Figure 3-11 (see 3.6.7.2). The total emissions were 263,992 MT (582 million
pounds). The largest emission source was estimated to be vapor degreasing of
metals; this usage resulted in 47.9% of the total emissions. The next largest
single emissions source was cold cleaning of metals which accounted for 33.3%
of the emissions. Total metal cleaning operations generated 81.1% of all methyl
chloroform emissions. The emissions represented by adhesives, aerosols, mis-
cellaneous uses, and the category of production, transportation, and storage
were 7.1, 7.1, 3.0, and 1.6%, respectively.
3-101
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3.7.1.3 Perchloroethylene--
The estimated breakdown of perchloroethylene emissions in 1976 were pre-
sented in Figure 3-13 (see 3.6.7.3). The total emissions were 269,145 MT (593
million pounds). Dry cleaning applications in the textile industry accounted
for 58.8% of the total emissions, while textile scouring applications repre-
sented an additional 18.0% of the emissions. The next largest source of emis-
sions was solvent metal cleaning operations; the losses from vapor degreasing
and cold cleaning were 14.8 and 4.7%, respectively, of the total emissions.
The miscellaneous uses category and the category of production transportation
and storage accounted for 1.8 and 1.77o, respectively, of the total emissions.
The environmental losses from uses as a chemical intermediate were estimated
to be about 0.2% of the total emissions.
3.7.2 Solid Waste Disposition
Possible sources of chemical losses resulting from any solid waste dis-
posal that may contain trichloroethylene, methyl chloroform, or perchloro-
ethylene were investigated in this study.
Some domestic production plants incinerate their liquid and gaseous
wastes at a high temperature (~ 1400°c). The effluent gases from the incinera-
tion units are commonly scrubbed with water (for HCl recovery) and/or an alka-
line aqueous solution (for chlorine destruction). Under this incineration
treatment, any solvents contained in the waste streams would be completely
decomposed and converted to other compounds. Therefore, the probability of
significant losses of solvents to the environment from this waste treatment
is considered to be negligible.
Deep-well disposal of "hex wastes" from trichloroethylene production was
reported for the Ethyl Corporation plant at Baton Rouge, Louisiana, in 1978
(Park, 1978). No other plants have used deep wells for disposal of wastes from
solvent manufacture. The "hex wastes" are the bottom residue (semisolid tars)
from a distillation process; because of the high volatility of the solvents
of interest, it is probable that very little, if any, of these chemicals con-
tained in the process streams remain in the waste residues.
On the basis of an analysis of the end-uses and physical properties of
these three compounds, it is evident that the only probable sources of solid
waste disposal would occur as a contaminant in the disposal of spent catalysts
and any semisolid tars resulting from solvent manufacturing processes. Small
quantities of catalyst are utilized in a number of production processes for
the chemicals of interest.
3-102
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Kirk-Othmer. 1964. Encyclopedia of chemical technology. Second edition.
Interscience Publishers, New York, New York. Vol. 5, p. 183.
Knoop, J. F., and G. R. Neikirk. 1972. Oxychlorinate for per/tri. Hydro-
carbon Process. 51(11):109.
Lowenheim, F. A., and M. K. Moran. 1975. Industrial chemicals. Wiley
Interscience, Inc., New York, New York.
Merck Index. 1976. Ninth edition. Merck and Company, Inc., Rahway, New
Jersey.
Mumma, C. E., and E. Lawless. 1975. Survey of industrial processing data -
Task I - hexachlorobenzene and hexachlorobutadiene pollution from chloro-
carbon processes. EPA-560/3-75-003. Office of Toxic Substances, Environ-
mental Protection Agency, Washington, D.C.
Noweir, M. H., E. A. Pfitzer, and T. F. Hatch. 1972. Decomposition of
chlorinated hydrocarbons: a review. Am. Ind. Hyg. Assoc. J. 33:454.
Park, D. E. 1978. Research and Development Department, Ethyl Corporation,
Baton Route, Louisiana. Personal communication.
Schlossberg, L. 1976. Detrex Chemical Industries, Inc., Detroit, Michigan.
Personal communication.
Singh, H. B. 1977. Preliminary estimation of average tropospheric HO con-
centrations in the northern and southern hemispheres. Geophysical Res.
Letters. 4(10):453.
Stanford Research Institute (SRI). 1978. Directory of chemical producers.
Menlo Park, California.
Thomas, F. R. 1977. Defense General Supply Center, Richmond, Virginia.
Personal communication.
3-106
-------
TRW» Inc. 1976* Study to support new source performance standards for the
dry cleaning industry. EPA Contract No. 68-02-1412, Task Order No. 4.
Environmental Protection Agency, Research Triangle Park, North Carolina.
U.S. International Trade Commission. 1972-1977. Synthetic organic chemicals:
U.S. production and sales. Washington, D.C,
Waters, E. M., H. B. Gerstner, and J. E. Huff. 1976. Trichloroethylene - I.
An impact overview. Oak Ridge National Laboratory, Report No. OSNL/TIRC-
76/2, Contract No. W7405-eng-26.
3-107
-------
CONTENTS
Page
4. Alternatives ' 4-3
4.1 Manufacturing Alternatives .... 4-3
4.1.1 Alternative chemicals for existing
processes 4-3
4.1.1.1 Trichloroethylene from ethylene
dichloride 4-3
4.1.1.2 Trichloroethylene from acetylene . . 4-4
4.1.1.3 Methyl chloroform from vinyl
chloride 4-4
4.1.1.4 Methyl chloroform from vinylidene
chloride 4-5
4.1.1.5 Methyl chloroform from ethane .... 4-5
4.1.1.6 Perchloroethylene from the chlorina-
tion of hydrocarbons . 4-5
4.1.1.7 Perchloroethylene from ethylene di-
chloride 4-6
4.1.1.8 Perchloroethylene from acetylene . . 4-6
4.1.2 Alternative production processes . 4-6
4.1.2.1 Trichloroethylene production .... 4-7
4.1.2.2 Methyl chloroform production .... 4-7
4.1.2.3 Perchloroethylene production „ . . . 4-8
4.2 Use Alternatives 4-9
4.2.1 Cold cleaning 4-9
4.2.1.1 Hydrocarbons . 4-11
4.2.1.2 Ketones 4-14
4.2.1.3 Alcohols 4-14
4.2.1.4 Chlorinated solvents 4-15
4-1
-------
CONTENTS (continued)
4.2.2 Vapor degreasing 4-16
4.2.2.1 Alcohols 4-16
4.2.2.2 Hydrocarbons 4-17
4.2.2.3 Ketones 4-17
4.2.2.4 Fluorocarbon 113 4-17
4.2.2.5 Methylene chloride 4-19
4.2.3 Use of alkaline cleaning solutions 4-21
4.2.4 Interchangeability 4-24
4.2.4.1 Methyl chloroform .... 4-24
4.2.4.2 Perchloroethylene 4-26
4.2.5 Alternative solvents for dry cleaning ... 4-27
4.2.5.1 Aliphatic hydrocarbons 4-28
4.2.5.2 Chlorinated solvents 4-30
4.2.5.3 Chlorofluorocarbons 4-30
References 4-31
4-2
-------
SECTION 4
ALTERNATIVES
This section presents a discussion of alternatives to the manufacture and
use of trichloroethylene, methyl chloroform, and perchloroethylene. Alterna-
tives to be considered are divided primarily into two groups: manufacturing
alternatives and use alternatives. Within the manufacturing sector, alterna-
tive starting materials in existing chemical processes and totally different
production processes are discussed. In the use sector, alternative chemicals,
the interchangeability of the three subject compounds, and alternative dry
cleaning solvents are discussed. .,
4.1 MANUFACTURING ALTERNATIVES
In this subsection, an evaluation is made of the feasibility of using
alternative starting materials in existing production processes and of alter-
native processes that could be used as replacements for existing processes.
4.1.1 Alternative Chemicals for Existing Processes
Preliminary assessments were made of the feasibility of using alterna-
tive chemicals as a replacement for starting materials in existing production
processes. These evaluations considered required design changes, new by-
products, wastes, and economic aspects.
4.1.1.1 Trichloroethylene From Ethylene Bichloride--
In 1975, 90% of the U.S. production of trichloroethylene was based on this
method. The method involves the oxychlorination of ethylene dichloride to form
symmetrical tetrachloroethane, followed by dehydrochlorination to yield tri-
chloroethylene. (The process was described in Section 3.3.2.1.) Perchloro-
ethylene is a by-product in this method.
Acetylene could be substituted for ethylene dichloride. In this case, the
chlorination reactor and the reaction product separation equipment would have
to be completely redesigned to operate under a different set of conditions.
The balance of the existing equipment could be used without modifications.
Instead of producing perchloroethylene as a by-product, the revised process
4-3
-------
would yield hydrogen chloride as a by-product (if a pyrolysis step were used
for dehydrochlorination) or calcium chloride (if an alkaline hydrolysis were
utilized)* It would not be economically feasible to substitute acetylene for
ethylene dichloride because acetylene is more expensive and currently is in
short supply in the United States*
4*1*1*2 Trichloroethylene From Acetylene—
During 1975, only 10% of the U*S* production was based on this method*
The process consists essentially of chlorinating acetylene in the presence
of a catalyst to form an intermediate tetrachloroethane followed by dehydro-
chlorination of the latter compound to produce trichloroethylene (see Section
,t 3.3.2.2).
Ethylene dichloride could be used as a replacement for acetylene in this
process. This substitution would require a complete redesign of the equipment
system for the first step of the process. The remainder of the process equip-
ment would not require any major modifications* In the existing process, the
by-products are hydrogen chloride, calcium chloride, and water if alkaline
hydrolysis is used for dehydrochlorination jaf tetrachloroethane* For the al-
ternate method, the by-product would be hydrogeji chloride and water, in addi-
tion to the same by-products from the final step (alkaline hydrolysis)* Because
of the costs Involved for equipment modification, it probably would not be eco-
nomically feasible to substitute ethylene dichloride for acetylene in this
. process*
4.1.1.3 Methyl Chloroform From Vinyl Chloride—
In 1975, approximately 60% of the U*S* production was from vinyl chloride*
In this process, vinyl chloride is hydrochlorinated to form 1,1-dichloroethane;
the latter compound is chlorinated to produce methyl chloroform (see 3.3.3.1).
Acetylene could be substituted for vinyl chloride as a raw material* Acet-
ylene can be reacted with hydrogen chloride at ordinary temperatures in the
presence of a catalyst (mercuric-ferric chloride) to give 1,1-dichloroethane
(Kirk-Othmer, 1964, p. 155)* No significant changes in process design would
be required. The required raw materials would change from vinyl chloride and
chlorine in the existing process, to acetylene, hydrogen chloride, and chlorine
for the alternate* Hydrogen chloride is the only by-product for the existing
process. For the alternate process, hydrogen chloride would also be the by-
product* However, since acetylene is in relatively short supply and is higher
priced than vinyl chloride, it appears that such a substitution of raw mate-
rial would not be economically feasible*
Another alternative process would involve the use of ethyl chloride as
a raw material for production of 1,1-dichloroethane according to the reaction:
C2H5C1 + C12 - * C2H4C12 + HCl
4-4
-------
This reaction could be substituted for the existing process step which hydro-
chlorinates vinyl chloride* The balance of the process would be identical*
4*1*1*4 Methyl Chloroform From Vinylidene Chloride—
Approximately 30% of the total 1975 production of methyl chloroform em-
ployed this method (see 3*3*3*2)* No chemicals were Identified which could be
directly substituted as a raw material for vinylidene chloride*
4.1.1.5 Methyl Chloroform From Ethane-
Only 10% of the 1975 production was by this method. This process consists
of the continuous noncatalytic chlorination of ethane (see 3.3.3.3).
1,1-Dichloroethane could be used as a raw material in this process as a
replacement for the ethane* The 1,1-dichloroethane could be chlorinated to
form methyl chloroform and by-product HCl according to the reaction (Kirk-
Othmer, 1964, p. 155):
400°C
C12 > CH3CC13 + HCl
This replacement would require significant modifications of process equipment
and processing conditions* In the existing process, the raw materials are
ethane and chlorine, and the by-products are hydrogen chloride and ethylene*
For the alternate case, the raw materials would be 1,1-dichloroethane and chlo-
rine and the by-product would be hydrogen chloride* This substitution would
probably not be economically feasible considering the probable costs for rede-
sign of process equipment*
4*1*1*6 Perchloroethylene From the Chlorination of Hydrocarbons—
In 1975, about 63% of the United States output was by the simultaneous
chlorination and pyrolysis of hydrocarbons (see 3*3*4*2)*
Perchloroethylene can be produced by reacting chlorine with a hydrocarbon
such as methane, ethane, propane, or higher paraffins* The choice of alternate
raw materials is normally determined by price and availability. No significant
process equipment changes are required for a change in these raw materials,
but operating procedures are modified. Carbon tetrachloride is formed as a by-
product, and HCl is formed. The carbon tetrachloride is normally recycled to
the chlorination furnace* Typical reactions are:
CC12=CC12 + CC14 + 12 HCl
2C2Hfi
CC12=CC12 + CC14 + 8 HCl
4-5
-------
Perchloroethylene can be manufactured as a means of disposal of "junk"
chlorinated hydrocarbons of one to three chlorine atoms* These compounds are
treated with excess chlorine in a reactor at 700°C to yield carbon tetrachlo-
ride (GCl^) and perchloroethylene* Either of these co-products can be recycled
to extinction in the process so that the supply can be controlled in relation
to market demands (Shreve, 1967). The recycling reaction is: 20014 ^""* C2Cl4 +
2C12* No important design changes are required in the existing process system*
Each of these processes would be economically feasible, provided the raw
materials were competitively priced*
4*1*1*7 Perchloroethylene From Ethylene Bichloride--
Approximately 34% of the total 1975 output of perchloroethylene was by
the oxychlorination of ethylene dichloride (see 3*3*4*1)* As noted in the dis-
cussion of trichloroethylene production, acetylene could be substituted for
ethylene dichloride as a raw material* Any attempt to substitute other chemi-
cals for ethylene dichloride would probably require major revisions of the en-
tire process equipment, particularly the reactor and product separation and
purification equipment* Such a substitution would probably not be economically
feasible*
4*1*1*8 Perchloroethylene From Acetylene-
Only 3% of the 1975 production was provided by the chlorination of acet-
ylene process* In this process, acetylene is chlorinated to form tetrachloro-
ethane which is dehydrochlorinated to trichloroethylene* Chlorination of tri-
chloroethylene (to pentachloroethane), followed by dehydrochlorination, yields
perchloroethylene (see 3.3.4.3).
Ethylene dichloride could probably be substituted for acetylene in this
process* In this case, the reactor would need to be redesigned to permit ef-
ficient operation in the chlorination step, and major changes would also be
required in the product separation and purification equipment* These changes
would probably require a large capital expenditure* In the existing process,
the raw materials are acetylene, chlorine, and lime hydrate; the by-products
are water and calcium chloride* For the alternate case, the raw materials would
be ethylene dichloride, chlorine, and oxygen; the by-products would be tri-
chloroethylene, hydrogen chloride, and water* Use of ethylene dichloride as
a substitute raw material for acetylene in this process would probably not be
economically feasible*
4*1*2 Alternative Production Processes
A second approach to alternative production processes would be to con-
sider completely new or different methods for manufacture of the solvents of
interest* In this subsection, an evaluation is made of the feasibility of pro-
ducing each of the solvents by alternative processes* This study considers
4-6
-------
the new materials and by-products which would be involved and provides a pre-
liminary assessment of economic feasibility*
4.1,2.1 Trichloroethylene Production—
An alternate production method comprises the chlorinatlon of ethylene to
1,2-dichloroethane and subjection of the latter compound to a complex series
of dehydrochlorinations and chlorinations leading to the final product* Several
intermediate compounds are formed* Simplified equations for these reactions
are:
GH2=CH2 + G12 > CH2G1CH2C1 (1)
GH2C1CH2G1 + 2C12 35°"45° °> CHC1=GC12 + 3HCl (2)
Reaction (1) can be conducted in either the liquid or gaseous phase (Kirk-
Othmer, 1964, p* 189-190), In a representative production procedure, chlorine
saturated with ethylene dibromide vapor and heated to 45 °G is reacted with a
stream of ethylene* The gas from the chlorination reactor is passed to a con-
denser to remove the ethylene dibromide* The second reaction is carried out at
350 to 450°G; this reaction can be conducted in a fluidized bed*
An existing plant producing trichloroethylene from acetylene could be modi-
fied to accommodate the alternative process system* The existing chlorination
reactor could probably be utilized with only minor modifications including in-
stallation of a condenser* A new fluid-bed type of chlorination reactor would
have to be installed* The existing dehydrochlorination reactor and the trichloro-
ethylene purification columns could probably be used with few alterations*
In the existing process, the raw materials are acetylene and chlorine,
and the by-product is hydrogen chloride* For the alternate production method,
the raw materials would be ethylene and chlorine, and hydrogen chloride would
be the only by-product •
4*1*2*2 Methyl Chloroform Production-
One alternate production process would involve producing methyl chloro-
form from ethylene and chlorine (Vogt, I960)* This method is carried out by a
unique sequence of steps including: (a) chlorinating ethylene with elemental
chlorine in the presence of a metal chloride catalyst (e«g*, ferric chloride)
to form 1,1,2-trichloroethane and hydrogen chloride; (b) dehydrochlorinating
the 1,1,2-trichloroe thane in an aqueous liquid alkaline medium at 10 to 85°C
to form vinylidene chloride; and (c) reacting the vinylidene chloride in the
presence of a catalyst at 10 to 80°C with the hydrogen chloride evolved in
step (a) to produce methyl chloroform* These reactions may be expressed as:
4-7
-------
2C12 + C2H^ >' HGl + C2H3C13 (1,1,2-trichloroethane) (1)
2C2H3C13 + 2NaOH - * 2NaCl + 2H20 + 2G2H2C12 (vinylidene chloride) (2)
C2H2C12 + HCl cata yst> GH3CC13 (methyl chloroform) (3)
This alternative process could be incorporated within an existing plant
which utilizes a hydrochlorination process with vinylidene chloride to produce
methyl chloroform. In this process, the appropriate equipment systems from re-
actions (1) and (2) could be added to the existing plant facility and integrated
with the existing (reaction 3) process system. The existing process equipment
and procedures would not need to be modified significantly.
The cast of materials for the revised process would differ significantly
from the existing process, which uses vinylidene chloride and hydrogen chloride
as raw materials. The alternate process raw materials would be ethylene, chlo-
rine, and sodium hydroxide.
The existing vinylidene process has no by-products, but produces heavy
ends wastes from a process fractionator. The alternative process produces hy-
drogen chloride, sodium chloride, and water as by-products. Practically all
of the by-product hydrogen chloride is reused in the process for the hydro-
chlorination reaction with vinylidene chloride. The alternate process would
produce heavy ends waste from a trichloroethane purification column.
Data are not available on the capital expenditures involved in install-
ing a suitable process plant for conducting reactions (1) and (2) and incor-
porating this system with an existing plant using the vinylidene chloride
process.
The alternate process would pose more problems in respect to waste man-
agement. An additional waste for the alternate process would be the sodium
chloride formed in the dehydrochlorination step.
4.1.2.3 Perch loroethylene Production--
One alternate production process would involve preparation of symmetri-
cal tetrachloroethane by chlorination of acetylene, followed by oxidation of
the tetrachloroethane to produce perchloroethylene and water. The chemical
reactions are:
G2H2 + 2G12 — ) CHG12GHG12 (tetrachloroethane) (1)
-
2GHC12CHC12 + 02 — - - - *> 2CC12=<3G12 + 2H20 (2)
4-8
-------
Reaction (1) is utilized commercially in the acetylene process for produc-
tion of perchloroethylene (via trichloroethylene); this process was described
in detail earlier in Section 3.3.4.3.
The second reaction is a departure from the regular acetylene process;
patents describe this oxidation process (Feathers and Rogerson, 1959; Vancamp
and Muren, 1959; Ellsworth and Vancamp, 1960). In this process, oxygen and
tetrachloroethane react at a temperature from 300 to 500°C in the presence
of a cupric and zinc chloride catalyst.
Existing facilities for the acetylene-based perchloroethylene process
could be converted satisfactorily to this process. The process equipment for
the conversion of acetylene to perchloroethylene would be kept intact and used
without change in equipment or procedure. The alkaline hydrolysis equipment,
which would not be needed for the revised process, could be placed in storage
or removed and sold as used equipment. The existing chlorination tower for con-
version of trichloroethylene to pentachloroethane could probably be modified
for higher temperature operation and used with a contact catalyst in order to
carry out reaction (2). The existing perchloroethylene still could probably
be used with only slight modification to purify the crude perchloroethylene
and produce the finished product.
4.2 USE ALTERNATIVES
The discussion of use alternatives for chlorinated solvents is divided
into five segments. In sequence, the topics to be discussed in this subsection
ares alternative chemicals in cold cleaning, alternative chemicals for vapor
degreasing, use of alkaline cleaning solutions, the interchangeability of the
three subject compounds, and alternative chemicals in dry cleaning.
4.2.1 Cold Cleaning
Halogenated degreasers account for approximately 3470 of all degreasers
used in the cold cleaning process (EPA, 1977). Of this 34%, methyl chloroform
comprises 5470, trichloroethylene 16%, and perchloroethylene 8%. Other haloge-
nated compounds comprise the remaining 22%. Aliphatic hydrocarbons are used
in about 49% of cold cleaning applications (EPA, 1977). Gold cleaners are of
two types—maintenance or manufacturing. Maintenance cleaners mainly use pe-
troleum solvents; manufacturing cleaners, because of the higher quality of
cleaning needed, use a wide variety of solvents (EPA, 1977). Table 4-1 lists
potential alternative chemicals and the properties which affect each chemical's
suitability as a solvent. Trichloroethylene, methyl chloroform, and perchloro-
ethylene are included for comparison.
4-9
-------
TABLE 4-1. METAL CLEANING SOLVENTS
-P-
Type of solvent/solvent
Alcohols
Ethanol (95%)
Isopropanol
Methanol
Aliphatic hydrocarbons
Heptane
Kerosene
Stoddard
Mineral Spirits 66
Aromatic hydrocarbons
Benzene£'
SC 150
Toluene
Turpentine
XyUne
Ke tones
Acetone
Methyl ethyl kctone
Fluortnated solvents
Trichlorotrifluoro-
ethane (FC-113)
Chlorinated solvents
Carbon tetrachloride
Methylene chloride
Pcrchloroethylene
1 1 1 , 1-Trich lorocthane
Ttichloroethylene
Solvency
for metal
working
soils
Poor
Poor
Poor
Good
Good
Good
Good
Good
Good
Good
Good
Good
Good
Good
Good
Excellent
Excellent
Excellent
Excellent
Excellent
TWA (ppm)
•1,000
400
200
400 '
-
100
-
10
-
100
100
100
1,000
200
1,000
10
200
100
350
100
Flash
point
(°F)
60
55
58
< 20
149
105
107
10
151
45
91
81
< 0
28
None
None
None
None
None
None
Evaporation
rateJ!'
24.7
19
45
26
0.6.1
2.2
1.5
132
0.48
17
2.9
4.7
122
45
439
111
363
16
103
62.4
Water
solubility
(7. wt)
™
„,
•-
< O.I
< 0.1
< 0.1
< 0.1
< 0.1
< 0.1
< 0.1
< 0.1
< O.I
^
21
< 0.1
< 0.1
0.2
< 0.1
< 0.1
< 0.1
K-uuri- Aniline
but-.iiiol point
values (°F)
-
_
-
38 1 28
29.2 152
36 134, 145
37.1 134.5
110 -44
91.8 -26
105 -57
64.5 62
99.:, -56
-
-
-
-
-
-
-
Boi ling
point
(range)
(°F)
165-176
179-181
147-149
201-207
354-525
1U3-380
318-382
176-1.77
370-410
230-232
314-327
281-284
132-134
174-176
117
170-172
104-105
250-254
165-194
188-190
Spr.ci fie
gravity
-
0.820
0.794
0.7305
0.8128
0.7669
0.78.39
0.883
0.8922
0.8702
0.867
0.8708
at 68°F
0.792
0.806
-
1.589
1.320
1.619
1.319
1.453
U>/gal.
6.76
6.55
6.60
5.79
6.74
6.38
6.40
7.36
7.42
7.26
7.17
7.23
6.59
6.71
13.16
13.22
10.98
13.47
10.97
12.14
Price/pal .
($>!"
1.12
0.99
0.47
.-
0.48
0.66
0.62
0.62
0.80-11.35
1.06
0. hit
2.40
0.63
1.18
1.41
-
7.84
!.7(l.
2.69
1.89
2.78
2.73
a^l Determined by weight loss of 50 ml in a 125-ml be.iker on an analytic.it balance (Dow Chemical Company method).
b/ Chemical Marketing Reporter (1978).
_c/ Not recommended or sold for metal cleaning.
Source: Environmental Protection Agency (1977) ,ind Midwest Research Institute.
-------
4.2.1.1 Hydrocarbons-
Aliphatic hydrocarbon solvents which are potential alternatives include
ii-heptane, mineral spirits, Stoddard solvent, and kerosene. Kerosene is a pale
yellow or clear, mobile liquid composed of aliphatic hydrocarbons (9 or 10 to
16 carbons per molecule) with benzene and naphthalene derivatives. Kerosene
distills between 175 and 325°C (NIOSH, 1977).
Stoddard solvent is a mixture of hydrocarbons (Cg to Cii) with a boiling
range between 160 and 210°C. Thirty to fifty percent of the mixture is straight
and branched chain paraffins, 30 to 40% naphthenes, and 10 to 20% aromatic hy-
drocarbons (NIOSH, 1977).
Mineral or white spirits are a mixture of hydrocarbons containing 30 to
65% paraffins, 15 to 55% naphthenes, and 10 to 30% aromatic hydrocarbons. The
boiling range is 150 to 200°G (NIOSH, 1977).
Generally, none of the aliphatic alternatives have as good solvating
power as trichloroethylene, perchloroethylene, or methyl chloroform. Except
for heptane, all have a relatively high flash point, and all, when compared
to chlorinated solvents, have low evaporation rates. The water solubility of
the aliphatics is less than 0.1 wt % (see Table 4-1). The cost per gallon of
the aliphatics is about one-fifth that of the chlorinated solvents. Because
of their low solvating power and slow evaporation rate, aliphatic hydrocarbons
cannot be considered as feasible alternatives for many manufacturing cold
cleaner operations.
A very brief synopsis of the major health effects of hydrocarbon solvents
is presented in the following paragraphs.
Kerosene has been shown to cause dermatitis (NIOSH, 1977). The odor
threshold for deodorized kerosene was determined to be approximately 0.09 ppm,
and 15-min exposures to a concentration of 20 ppm were tolerated without sen-
sory irritation (Carpenter et al., 1976). Kerosene is a mixture and may contain
various cyclic and branched compounds which have important toxicological prop-
erties of much greater significance than those of the quantitatively predomi-
nant aliphatics (Hamilton and Hardy, 1974).
Hexane has been reported to cause disruption of the horny layer of the
skin in humans upon dermal exposure. Several studies have linked hexane (and
possibly other alkanes) to the development of polyneuropathy (NIOSH, 1977).
Astrand et al. (1975) exposed men to white spirits (mineral spirits) at
concentrations of 2,500 or 5,000 mg/m^ for an unspecified time. Nausea and
vertigo were obvious effects at both concentrations. Exposure of human sub-
jects to 4,000 mg/m^ of white spirits for 50 min resulted in prolonged reac-
tion times and possibly impaired short-term memory (Gamberale, 1975).
4-11
-------
Nausea and follicular dermatitis resulted after 2 weeks of exposure to
liquid Stoddard solvent* The worker eventually developed obstructive and sub-
acute yellow liver atrophy (NIOSH, 1977). Aplastic anemia has been observed
after dermal exposure to liquid Stoddard solvent (NIOSH, 1977). The composi-
tion of the solvent was not known, so that the presence of myelotoxic com-
pounds, such as benzene, cannot be ruled out* For a 15-min exposure period,
the odor threshold for Stoddard solvent was determined to be 0,09 to 0,9 ppm,
and the sensory threshold between 150 and 470 ppnu At 470 ppm, transient eye
irritation and slight dizziness was reported (Carpenter et al., 1975)* Expo-
sure at concentrations in excess of 400 ppm for 3 to 5 min caused irritation
of the eyes, nose, and throat (NIOSH, 1977).
Aromatic hydrocarbons have good solvating properties and are used in ap-
proximately 10% of the cold cleaning operations. Of this 10% total, benzene
accounts for 15%, toluene 30%, xylene 26%, cyclohexane 2%, and heavy aromatics
26% (EPA, 1977).
Although possessing high solvating power, benzene has been recognized as
a toxic chemical since 1900, and the courts are in the process of determining
what should be the Occupational Safety and Health Administration (OSHA) expo-
sure standard for benzene (OSHA letter, 1978). Benzene vapor or liquid may
cause skin, eyes, and upper respiratory tract irritation. If aspirated into
the lungs, the liquid may cause pulmonary edema and hemorrhage. Upon acute ex-
posure, benzene is a central nervous system (CNS) depressant. Symptoms include
headache, dizziness, nausea, convulsions, and coma. Death may result from a
large acute exposure (NIOSH, 1977). Benzene is a myelotoxic and leukogenic
agent, and chronic exposure is well documented to cause blood changes (NIOSH,
1977).
Its application to cold cleaner degreasing operations would not be ad-
vised.
Toluene is used widely as a solvent, most commonly for dissolving syn-
thetic resins, although its rapid evaporation rate (relative to other aromatic
hydrocarbons) makes it desirable in applications where quick dry is an essen-
tial quality (Missouri Solvents and Chemicals Company, 1972). Application of
toluene to cold cleaner degreasing operations (the majority being open systems)
would be feasible, although flammability would pose a serious problem (flash
point, 45°F) and solvent loss due to evaporation could result in potentially
high employee exposure.
Toluene has been reported to cause irritation of the eyes, respiratory
tract, and skin. Prolonged and/or repeated contact with the skin may result
in dry, fissured dermatitis (NIOSH, 1977). Acute exposure results in depres-
sion of the CNS with symptoms including headache, dizziness, fatigue, muscular
weakness, drowsiness, staggering gait, skin paresthesias, collapse, and coma
(Hamilton and Hardy, 1974).
4-12
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Xylene is not quite as good a solvent, is more toxic, and does not evap-
orate as quickly as toluene. The flash point is higher; and in cases where fast
drying is not necessary and flammability is a problem, xylene could be a poten-
tial alternative.
Xylene vapor can cause eye, nose, and throat irritation; prolonged or re-
peated skin exposure may lead to dermatitis (NIOSH, 1977; Hamilton and Hardy,
1974)* Liquid xylene is also irritating to the eyes and mucous membranes. As-
piration of a few milliliters may cause chemical pneumonitis, pulmonary edema,
and hemorrhage. Acute systemic exposure may cause GNS depression. At high con-
centrations, the vapor may cause dizziness, staggering, drowsiness, unconsci-
ousness, pulmonary edema, anorexia, nausea, vomiting, and abdominal pain (NIOSH,
1977).
SC 150 is basically a complex mixture of aromatic hydrocarbons and may be
viewed as a high boiling xylene (xylene structure with an additional alkyl group
such ethyl) (Missouri Solvents and Chemicals Company, 1962). Low toxicity,
a hiv lash point, and good solvating properties make SC 150 useful as a paint
or enamel reducer in dip tanks. Additionally, it has a high boiling range. The
slow evaporation rate could limit its applicability in situations where rapid
drying is essential. No health effect information was available for SC 150.
Turpentine does not have as strong solvating properties as the aromatics,
but is used as a solvent for varnishes and a thinner for paints. The toxicity
is equivalent to that of xylene, but the flash point is higher and the evapo-
ration rate slower. These properties would be desirable unless rapid drying
was essential.
Exposure to turpentine occurs via inhalation of the vapor and/or percu-
taneous absorption of the liquid. High vapor concentrations are irritating to
the eyes, nose, and bronchi; aspiration of the liquid has been reported to
cause lung irritation resulting in pulmonary edema and hemorrhage (NIOSH, 1977).
The liquid may produce contact dermatitis, and if splashed in the eyes, may
cause corneal burns.
Acute systemic exposure to turpentine may result in CNS depression, char-
acterized by headache, anorexia (loss of appetite), anxiety, excitement, mental
confusion, and tinnitus (sensation of noise that is subjective). Chronic nephri-
tis (kidney damage) with albuminuria (albumin in the urine) and hematuria (blood
in the urine), and a predisposition to pneumonia have resulted from repeated
exposures to high concentrations (NIOSH, 1977).
The aromatic hydrocarbons are used in specific cold cleaning degreaser op-
erations and have stronger solvating properties than the aliphatics (Missouri
Solvents and Chemical Company, 1962). Evaporation rates are somewhat more rapid
for aromatics. The price per gallon of the aromatics is somewhat more than ali-
phatics (however, the increased efficiency of the solvent could help equalize
4-13
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costs). The aromatics have lower flash points (indicating a flammability haz-
ard), which could limit their use in cold cleaner degreasing operations.
4.2.1.2 Ketones—
Acetone and methyl ethyl ketone have good solvating properties and are
used in approximately 3.6% of all cold cleaning degreaser operations (EPA,
1977). Acetone has very low toxicity (1,000 ppm), a rapid evaporation rate,
and is miscible with water. It also has a very low flash point (< -18°G).
Methyl ethyl ketone (MEK) is somewhat more toxic and evaporates more slowly
than acetone (see Table 4-1). MEK has a flash point of -2°C. It is less solu-
ble in water than acetone (see Table 4-1).
Acetone and MEK produce dermatitis after repeated exposure and high vapor
concentrations are irritants of the conjunctiva and mucous membranes of the
nose and throat. High concentrations (undefined level by NIOSH) may produce
narcosis (NIOSH, 1977).
4.2.1.3 Alcohols—
Ethanol, isopropyl alcohol, and methanol are generally poor solvents. In
situations where the solute would be shellac, manila gum, natural kauri, phenol-
formaldehyde, or urea-formaldehyde, alcohols would be good solvents. However,
due to their poor solvating properties in general, and the fact that they read-
ily absorb water, alcohols would make poor alternatives to perchloroethylene,
trichloroethylene, or methyl chloroform.
Exposure inhalation of methanol as a vapor would have to be well in ex-
cess of the 200-ppm TLV to cause illness or significant discomfort (Hamilton
and Hardy, 1974). Below 2,000 ppm, methanol is virtually nonirritating to the
eyes or upper respiratory tract (NIOSH, 1977).
Liquid methanol can produce mild dermatitis (NIOSH, 1977). Symptoms ap-
pear between 1 and 3 hr after exposure with a common latency period of 12 to
18 hr. Symptoms of methanol intoxication include: headache, weakness, ver-
tigo, visual disturbances, and coma (NIOSH, 1976c). Metabolites of methanol
are thought to be responsible for the above symptoms. Methanol intoxication
occurs most often after oral ingestion and is very rarely observed after in-
halation (NIOSH, 1977). Treatment for methanol intoxication consists of in-
hibiting the metabolism of the methanol by introducing ethyl alcohol into the
system. Ethanol competes with methanol for active sites on the enzyme alcohol
dehydrogenase, and the enzyme has greater affinity for ethanol than methanol.
The ethanol is preferentially oxidized and diminishes the production of meth-
anol metabolites (Hamilton and Hardy, 1974).
4-14
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From a human health standpoint, industrial exposures to ethanol vapors
are of no practical importance (Hamilton and Hardy, 1974). A workman exposed
to 1,000 ppm ethanol would have to breathe at a rate of 65 liters/min in order
to absorb enough ethanol to incur systemic effects. This is unlikely since the
ventilatory rate while performing hard work is 30 liters/min. Exposure to 5,000
to 10,000 ppm may result in mild transient coughing and/or irritation of the
eyes and upper airways. Exposure to concentrations of 20,000 ppm or greater
are intolerable (Hamilton and Hardy, 1974); prolonged inhalation at high con-
centrations may produce headache, drowsiness, tremors and fatigue (NIOSH, 1977),
Ethyl alcohol can act as an synergist, increasing the toxicity of other ab-
sorbed, ingested, or inhaled chemical agents (NIOSH, 1977).
Ingestion of isopropyl alcohol can result in severe CNS depression and
ultimate respiratory failure. Reports of contact dermatitis resulting from ex-
posure to isopropyl alcohol have been made, and it can be regarded as a mild
irritant to the conjunctiva and mucous membranes of the upper respiratory tract
and the eye (NIOSH, 1977). No recorded cases of industrial poisoning by pure
isopropyl alcohol (by any route of entry) were found in the literature (NIOSH,
1976b).
4.2.1.4 Chlorinated Solvents--
Other alternatives for trichloroethylene, perchlorethylene, and methyl
chloroform as cold cleaning degreasers are carbon tetrachloride, methylene
chloride, and trichlorotrifluoroethane (F-113). Halogenated hydrocarbons ac-
count for 34% of all cold cleaning solvents used. Of the 34% total, methylene
chloride accounts for 15% (5.1% when considering all classes) and F-113 ac-
counts for 6% (or 2.2% of total when considering all classes). Methylene chlo-
ride has high solvency powers, low toxicity (500 ppm), no flash point, rapid
drying time, low water solubility, and a cost somewhat lower than trichloro-
ethylene or perchloroethylene. Methylene chloride is suspected of playing a
role in the ozone depletion, and it has been recommended that it be removed
from the list of exempt solvents (Federal Register, 1977).
Methylene chloride was reported to impair CNS function at exposures of
300 to 800 ppm. When compared with controls, those exposed had decreased crit-
ical flicker frequency (OFF) (OFF is a measure of the frequency of flickering
light at which perception of the flickering changes to nonperception or vice
versa), auditory vigilance, and decreased performance in psychomotor tasks.
Exposure at 50 and 100 ppm increased blood carboxyhemoglobin and carbon mon-
oxide (CO) in exhaled air (NIOSH, 1976a).
In experiments where exposure was 100 and 200 ppm, absorption of the in-
haled methylene chloride was between 50 and 66% (DiVincenzo et al., 1972).
Methylene chloride in the presence of flames forms phosgene gas as a combus-
tion product, and cases resembling phosgene poisoning have occurred (NIOSH,
1976). Methylene chloride is also an irritant, affecting the eyes, respira-
tory tract, and conjunctiva.
4-15
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Exposure at 1,000 ppm for 2 hr resulted in carboxyhemoglobin saturation
levels in excess of those permitted in the work place from exposure to GO alone.
The GNS effects of GO and methylene chloride are at least additive (Hamilton
and Hardy, 1974).
Carbon tetrachloride has strong solvency properties, no flash point, rela-
tively rapid evaporation rate, and low water solubility. Because of the toxicity
of the substance, use in cold cleaner degreasing would not be advised.
Repeated contact with carbon tetrachloride may lead to dry, fissured derma-
titis. Transient eye irritation may occur upon ocular exposure. Excessive expo-
sure may result in GNS depression characterized by nausea, dizziness, headache,
and weakness. Abdominal pain, nausea, vomiting, and diarrhea may be experienced
after CNS symptons have subsided (NIOSH, 1977). Hepatic and renal damage may
develop following acute exposure. Systemic effects are increased when carbon
tetrachloride exposure occurs in conjunction with ingestion of alcohol (NIOSH,
1977; Hamilton and Hardy, 1974). Hepatocellular carcinoma has been reported in
humans following acute carbon tetrachloride exposure, and this compound is a
potent hepatocarcinogen in animals (Hamilton and Hardy, 1974).
F-113 is a strong solvent, has low toxicity, no flash point, rapid evap-
oration rate, and low water solubility. This solvent has been implicated as
possibly playing a role in the ozone depletion hypothesis.
F-113 may produce mild irritation of the upper respiratory tract and has
occasionally been reported to cause dermatitis (NIOSH, 1977). Exposure to very
high concentrations may cause mild CNS depression. The main hazard posed by
this compound is from asphyxia (NIOSH, 1977).
4.2.2 Vapor Degreasing
Halogenated solvents are used, almost exclusively, in vapor degreasing
operations, not only because of their powerful solvency property, but also be-
cause they are essentially nonflammable and their vapors are much heavier than
air (EPA, 1977).
4.2.2.1 Alcohols--
Alcohols cannot be considered as feasible alternative solvents for vapor
degreasing operations for several reasons. They are weak solvents with low
flash points (13 to 16°C), intermediate evaporation rates, and high solubility
in water. In combination with F-113 (as azeotropes or blends), alcohols are
used in highly specialized, low volume vapor degreasing operations (MRI, 1976).
These azeotropes and blends, because of their high purity and low boiling point,
are used to clean and degrease components used in the electrical and electronic
industry. Solvent loss control technologies (freeboard chilling or carbon ab-
sorption) remove the stabilizers used in these blends, requiring replacement
before reuse.
4-16
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4.2.2,2 Hydrocarbons-
Aliphatic hydrocarbons such as hexane or heptane are not suitable for use
in vapor degreasing operations because of the flammability and explosion haz-
ard. Kerosene has an acceptable flash point and low water solubility, but the
slow evaporation rate and high boiling point offset these positive aspects.
Stoddard solvent has a relatively low flash point which presents flammabil-
ity problems. It has a slow evaporation rate which would somewhat reduce this
risk. The boiling point is high, which would substantially increase the energy
demands for a vapor degreasing operation.
Hydrocarbons, such as benzene, toluene, turpentine, and xylene, all have
low flash points and explosive limits which would necessitate extreme caution
if used in vapor degreasing operations. Vapor control and recovery equipment
would have to be utilized. Flammable solvents such as these are not considered
to be acceptable alternatives.
The aromatic hydrocarbon solvent SG 150 has a flash point of 66°G, and a
slow evaporation rate of 0.45. The boiling range is high, which would substan-
tially increase the energy demand of the system. High energy demands plus long
drying times would make this alternative provisional, at best.
4.2.2.3 Ketones—
Ketones, such as acetone or methyl ethyl ketone, are highly flammable,
have rapid evaporation rates, and are miscible in water. These are not accep-
table alternatives for the chlorinated solvents under study.
4.2.2.4 Fluorocarbon 113—
The fluorinated solvent (F-113) has no flash point, a rapid evaporation
rate, low boiling point, and is a good solvent for certain types of soils. The
solvent is not as strong a solvent as trichloroethylene and is at least twice
as expensive.
A listing of the advantages and disadvantages of F-113 in vapor degreas-
ing is given in Table 4-2.
F-113 attacks only the soil on plastic work parts and therefore is useful
in cleaning electromechanical parts. Stabilizers are not required to prevent
solvent decomposition.
Since it can be prepared with very high purity, has low toxicity, and
possesses excellent material compatibility, F-113 is utilized for whiteroom
metal cleaning applications. The major specific uses for F-113 are for flux
removal and for general cleaning of printed circuit boards in the electronics
industry. F-113 has a low boiling point, and good solvent recovery systems
are available for its applications in metal cleaning.
4-17
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TABLE 4-2. EVALUATION OF FLUOROSOLVENT F-113 AS SUBSTITUTE FOR
TRICHLOROETHYLENE IN METAL CLEANING
Advantages
Broad range of desirable cleaning properties
Attacks only soil - thus, useful in cleaning electromechanical parts
Inhibitors not required to prevent decomposition
High purity makes possible ultraclean work
Extremely low toxicity levels
Low boiling point (like methylene chloride)
Good recovery methods
Disadvantages
Requires a low condensing temperature for coolant system
Extremely high relative cost
Potential role in stratospheric ozone depletion hypothesis
Relatively mild solvent
Source: Midwest Research Institute (1976).
4-18
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Among the disadvantages are the requirement in vapor degreasing for a low
condensing temperature system and the relatively high cost ($8.30/gal. for F-
113 versus $2,55 for trichloroethylene). F-113 is a relatively mild solvent
compared to the subject compounds; and, therefore, it is not satisfactory for
many vapor degreasing applications. Future uses of F-113 are not certain at
the present time because of its potential role in the ozone depletion hypothe-
sis. Federal hearings concerning the future use of this material are scheduled
to begin in early 1979.
4.2.2.5 Methylene Chloride—
The major advantages and disadvantages of methylene chloride as compared
to trichloroethylene in vapor degreasing are listed in Table 4-3.
This solvent may be the choice for removal of a difficult soil or polymer
residue because of its high solvency power (Archer, 1974). The low temperature
of its vapor blanket makes it useful for degreasing temperature-sensitive parts.
Because of its low boiling point, parts coming from the degreaser are cooler,
the radiation heat loss is low, and the parts can be handled by workers immedi-
ately after degreasing (Anonymous, 1972). Another advantage is its high solvency
power (Anonymous, 1973).
The ether-like odor of methylene chloride is detectable only as the atmos-
pheric concentration approaches 200 ppm; the odor of trichloroethylene is de-
tectable at about 50 ppm.
The time weighted average (TWA) recommended for methylene chloride is 75
ppm for a 10-hr workday, 40-hr workweek with a peak concentration of 500 ppm
as determined by any 15-min sampling period (NIOSH, 1976a).
Use of methylene chloride as a solvent in vapor degreasing permits faster
start-up and less frequent and faster equipment cleanout. Degreasers using this
solvent can be cleaned simply by the use of a water hose, whereas with other
solvents a crusty buildup, especially on heating coils, sometimes has to be
removed by chipping (Anonymous, 1972).
Disadvantages of methylene chloride include a low vapor density as com-
pared to trichloroethylene, 2.93 versus 4.5 (Archer, 1974). Lighter vapors dif-
fuse more readily in the air blanket, thereby increasing the solvent losses.
Because of its high latent heat requirement, methylene chloride requires 40%
more heat to vaporize than trichloroethylene, even though its boiling point
is lower (Anonymous, 1973). Also, more water and colder water is required to
condense methylene chloride vapor.
4-19
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TABLE 4-3. EVALUATION OF METHYLENE CHLORIDE AS AN
ALTERNATIVE SOLVENT
Advantages
EPA has proposed a policy to the States which deletes methylene chloride and
perchloroethylene as exempt solvents (Federal Register, Vol. 42, No. 131,
p. 35314, July 8, 1977)
High solvency power - for difficult soils
Low vapor temperature - for temperature sensitive parts
Low steam pressure (1 psi)
High TLV
Faster degreaser start-up, less frequent and faster cleanout
Normally odor-free (threshold, 200 ppm)
Low heat requirement (3.7 Btu/lb steel versus 13.7 for trichloroethylene)
Lower cost ($2.69/gal. versus $2.73/gal. for trichloroethylene)
Pi sadvant age s
Low vapor density (2.93 versus 4.5 for trichloroethylene) - greater diffusion
tendency
High latent heat (40% more)
More and cooler water required for cooling
Converting trichloroethylene degreaser requires extensive modifications
Low condensate volume (0,25 gal/100 Ib steel versus 1*1 for trichloroethylene)
Health effects - biotransformation to carbon monoxide
Possible mutagen
Source: Midwest Research Institute.
4-20
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Conversion of a trichloroethylene vapor degreaser to an operation using
methylene chloride usually requires extensive modifications to the machine's
cooling capacity (Archer, 1974). Most small degreasers designed for operation
with methylene chloride require a refrigerated cooling coil assembly in addi-
tion to the normal water-cooled condensing surface.
Methylene chloride may be the solvent of choice for removal of certain
difficult soils, but generally the disadvantages outweigh the advantages of
substituting methylene chloride for trichloroethylene.
4.2»3 Use of Alkaline Cleaning Solutions
Another alternative is the partial or complete substitution of alkaline
cleaning systems to perform the same functions as the subject chlorinated sol-
vents.
One obvious means for reducing atmospheric emissions of solvent from metal
cleaning is to use aqueous cleaning agents (e.g., alkaline washing, which is
the most common aqueous cleaning method).
The liquid and solid alkaline washing compounds currently available con-
tain various amounts of caustic, sodium or potassium carbonates, phosphates,
silicates and borates, soaps, and synthetic surfactants. These alkaline wash
compounds are normally used at concentrations of approximately 4 to 15 g/liter
for spray application, although concentrations as high as about 90 g/liter are
reported for nonagitated soak tanks (Dow Chemical Company, 1976).
The cleaning agents in these formulations emulsify water-insoluble soils
at solution temperatures of approximately 70 to 90°C. However, compounds suit-
able for use from room temperature to 55°C have been offered as a means of re-
ducing the large energy requirements of this cleaning method. Thorough rinsing
is required to remove the residues of the soil emulsions formed in the cleaning
baths. The final step in the operation is drying the parts. Wherever alkaline
washing is used prior to wet processing (e.g., plating or phosphatizing), dry-
ing of parts is not required. The alkaline washing operations are carried out
in a variety of equipment such as soak tanks, rotary drum washers, mesh belt
washers, and monorail washers (Dow Chemical Company, 1976).
Table 4-4 shows the major advantages and disadvantages of alkaline clean-
ing solutions as a replacement for solvent metal cleaning.
Alkaline washing solution has a low cost of only a few cents per gallon.
This low unit cost economically offsets the increase in leakage losses, spills,
and solution "drag-out" compared to some other cleaning methods. Cost compari-
sons described in the technical literature have concluded, however, that vapor
degreasing is either competitive with or less expensive than alkaline washing
(Dow Chemical Company, 1976).
4-21
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TABLE 4-4. EVALUATION OF ALKALINE GLEANING SOLUTIONS AS REPLACEMENT
FOR SOLVENT METAL CLEANING
Advantages
Low cost per gallon
Useful as prewet process
High pressure sprays can be used
Physical action removal special soils
Prevention of air pollution by solvent emissions
Pi sadvantages
Water pollution) low quality cleaning) high energy demand
Long start-up time, corrosion, staining nonferrous metals
Electrically conductive residues
Equipment requires more floor space than solvent cleaning
Source: Dow Chemical Company (1976).
A substantial energy demand is avoided by not drying the parts. In addi-
tion, alkaline washing creates a hydrophilic metal surface which benefits sub-
sequent wet processing operations*
The decreased need for confinement in alkaline washing allows the use of
higher spray pressures* Removal of insoluble particles or metal chips can be
improved if the sprays are specifically designed to provide physical cleaning
by spray action* Alkaline washing can effectively remove soaps, some buffing
compounds, and solid dry lubricants* The special cleaning action may result
from the higher pressures used in the sprays or from chemical reaction with
the soils. These special soils cannot be handled as efficiently in vapor de-
greasing*
No solvent vapor emissions occur in normal alkaline washing operations.
This would not be true if a volatile solvent were used to rinse the work part
following the alkaline wash treatment.
4-22
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Alkaline washing has a number of disadvantages compared to solvent metal
cleaning* The washing process tends to dilute and discharge all of the soils
removed from parts* In contrast, solvent metal cleaning concentrates the re-
moved soils and no water pollution occurs (Dow Chemical Company, 1976)* Alka-
line washing results in a lower quality of cleaning than in the case of vapor
degreasing. This disadvantage has been demonstrated by the Increased rejection
rates of vacuum-welded or induction-fused parts that were cleaned by alkaline
washing instead of by vapor degreasing (Dow Chemical Company, 1976).
Alkaline washing has a much higher energy demand than solvent vapor de-
greasing* Large quantities of heated water vapor are exhausted from alkaline
washing systems. A long start-up time is required for the wash solution. To
avoid loss of production or poor cleaning while the temperature is brought up
to the desired level, the washing equipment may be heated during nonoperated
periods or the heating may begin before the operating shift (Dow Chemical Com-
pany, 1976).
Residual water left on ferrous parts can cause rust formation* Also, non-
ferrous metals may be subject to corrosion or staining, if the washing chemi-
cal is not carefully selected or if the chemical concentration is not properly
controlled.
Any entrapped water or residue of detergent remaining on the work part
following the cleaning treatment will have high electrical conductivity. There-
fore, alkaline washing is seldom used where electrical insulating properties
of the parts are important*
Table 4-5 shows the application areas in metal cleaning where either the
solvent cleaning or the alkaline washing process currently dominates*
TABLE 4-5. CATEGORIES OF METAL CLEANING BY PROCESS
Solvent cleaning Alkaline washing
Nonferrous metals Ferrous metals
Small parts Large work pieces
High precision parts Low tolerance parts
High cleaning requirements Lower cleaning standards
Electric and electronic Preplating, phosphatizing
parts and assemblies or other wet processes
Source: Dow Chemical Company (1976).
4-23
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Although there are exceptions to the generalizations given in Table 4-5,
the areas of application are sufficiently distinct that there is little compe-
tition between the two cleaning processes* Therefore, few solvent metal clean-
ing operations could be converted satisfactorily to alkaline washing in order
to control emissions to the atmosphere* In some instances, the disadvantages
of substituting alkaline washing for solvent metal cleaning far outweigh the
advantages*
4*2*4 Interchangeability
In this subsection, a brief discussion will be presented on the interchange-
ability of methyl chloroform and perchloroethylene with trichloroethylene (i*e*,
trichloroethylene will be the base solvent and all comparisons will be made to
it)» Within the past 2 years, considerable conversion from trichloroethylene to
methyl chloroform has already transpired because methyl chloroform is not re-
stricted by air quality regulations*
4*2*4*1 Methyl Chloroform--
Table 4-6 describes the advantages and disadvantages of methyl chloroform
compared to trichloroethylene in vapor degreasing operations*
Methyl chloroform meets all of the present air pollution requirements.
A major advantage is its increased safety margin: a TLV of 350 ppm compared
to 100 ppm for trichloroethylene* It is reported that extensive use data show
that exposure limits in degreasing operations are less likely to be exceeded
when methyl chloroform is substituted for trichloroethylene (Archer, 1974)*
Methyl chloroform is well adapted to cold cleaning operations* Thus, by
specifying a degreasing grade, users get a solvent suitable for use in both
vapor degreasing and cold cleaning applications* In addition, dirty cold clean-
ing solvent can be reclaimed in a vapor degreaser system, thus avoiding the
need for a separate solvent recovery system (Archer, 1974)*
Degreasers can usually be converted to operation with methyl chloroform
without major equipment changes. In this event, the same cooling system can
be used, but the steam pressure used to vaporize the solvent must be reduced*
In comparison with trichloroethylene, methyl chloroform is slow to attack
elastics and plastics in the work materials*
Several disadvantages must be considered* Methyl chloroform vapors cannot
be recovered effectively with carbon adsorption systems* Whenever the stabiliz-
ers become depleted, the solvent hydrolyzes to form acids which create serious
corrosion problems* In the conventional separator used with vapor degreasers,
it is difficult to separate water from methyl chloroform.
4-24
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TABLE 4-6. EVALUATION OF METHYL CHLOROFORM AS SUBSTITUTE FOR TRICHLOROETHYLENE
Advantages
Meets current tropospheric pollution regulations
Relatively high TLV (350 ppm) - expanded safety margin
Vapor degreasing grades suitable for cold cleaning
Low boiling point (74 to 76°C)j low steam pressures (3 to 6 psi)
Trichloroethylene degreasers converted without changing cooling system
Low heat requirement (10.9 Btu/lb steel versus 13»7 for trichloroethylene)
Slow to attack elastomers and plastics
Pi sadvant ages
Degreaser vapors cannot be recovered effectively with carbon adsorption
systems
Hydrolyzes in water to form acids when stabilizers are depleted
Water difficult to eliminate in conventional separator
Sensitive to Al, Mg, Zn
Higher price ($2.78/gal. versus $2.73/gal.) (December 1978)
Potential role in stratospheric ozone depletion
Possible mutagen
Source: Midwest Research Institute.
4-25
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In most degreasing applications, the advantages of methyl chloroform far
outweigh its disadvantages. In many cases, suitably inhibited methyl chloroform
is the most logical substitute as witnessed by the fact that the majority of
the conversions from trichloroethylene have been to methyl chloroform.
4.2.4.2 Perchloroethylene—
The advantages and disadvantages of perchloroethylene relative to tri-
chloroethylene in vapor degreasing are described in Table 4-7.
TABLE 4-7. PERCHLOEDETHYLENE AS A SUBSTITUTE FOR TRICHLOROETHYLENE
Advantages
Preferred for degreasing operations which also require drying of water-wet
parts
Removes high-melting waxes
Preferred for cleaning parts with large areas due to high solvent condensate
volume (1.7 gal/100 Ib steel versus 1.1 for trichloroethylene)
Low susceptibility to hydrolysis and to reaction with aluminum
Lower price ($1.89/gal. versus $2.73 for trichloroethylene in 1978)
Disadvantages
High heat requirement - b.p., 121°C versus 87, increased steam pressure
(45 to 60 psi versus 10 to 15 psi for trichloroethylene) may require
licensed boiler operator, 20.6 Btu/lb steel versus 13.7. National need
for reduced energy use
High operating temperature damages plastics
Perchloroethylene is the preferred solvent when a vapor degreasing opera-
tion is used to dry water-wet parts. The azeotrope between the solvent and wa-
ter contains nearly 16% water. The high boiling point also helps to flash off
the water, reduce staining of the work, and shorten degreaser dwell time. In
addition, perchloroethylene may be needed to remove high melting wax residues
during certain cleaning processes (Archer, 1974).
4-26
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In vapor degreasing, solvent vapor condenses on the work parts until the
temperature of the latter reaches that of the hot solvent vapors. The higher
temperature vapor zone of perchloroethylene means that more liquid solvent con-
densate will form. Thus, perchloroethylene is often preferred for cleaning thin-
gauge, low-mass metal parts with large surface areas (Archer, 1974).
Other advantages of perchloroethylene are its stability, low hydrolysis
rate, and low decomposition rate (Anonymous, 1973). Water elimination can be
readily effected using a simple separator. Since perchloroethylene has a high
vapor density, vapor losses to the environment are relatively low. A carbon
adsorber system can be used satisfactorily to recover the solvent from vapor
emissions; perchloroethylene has a long history of satisfactory performance
in combination with carbon adsorbers in the dry cleaning industry.
The disadvantages of perchloroethylene in degreasers include its greater
energy requirement (boiling point of 121°C), its requirement of high pressure
steam heating (50 to 60 psi to boil the solvent and establish a stable vapor
blanket), and the fact that some parts to be cleaned cannot tolerate its high
operating temperature (Anonymous, 1973). In many states, the steam requirement
means that a licensed engineer must be on the premises to regulate the high
pressure boiler (Archer, 1974). In comparison with trichloroethylene, more
heat is required for operation with perchloroethylene since more heat per
pound of work processed is required (Anonymous, 1973). Also, insulation may
be needed to reduce heat loss and provide for operator comfort and safety.
Solvent consumption will normally be higher compared to trichloroethylene be-
cause of the higher temperature vapor blanket.
For degreaser applications that require a drying operation, perchloro-
ethylene may be the solvent of choice. For all other applications, the higher
energy requirements are a major drawback, making it unattractive as a substi-
tute for trichloroethylene.
4.2.5 Alternative Solvents for Dry Cleaning
There are three basic types of dry cleaning equipment systems: transfer
type, dry-to-dry type, and coin-operated. A detailed discussion of dry clean-
ing equipment and solvent mileage can be found in a published report (TRW,
1976).
To qualify as a dry cleaning solvent, a substance must possess certain
physical and chemical characteristics. The National Institute of Dry-Cleaning
has set seven general criteria for a dry cleaning agent (MRI, 1976). These cri-
teria are as follows:
1. The dry cleaning agent must be safe to use on all common textile fab-
rics and dyes.
2. It must be a good solvent for fats and oils.
4-27
-------
3. The candidate must be free of objectionable odors.
4. It must be chemically stable under all use conditions.
5. The dry cleaning solvent should be noncorrosive towards ordinary met-
als used in machine, pipe and pump construction; it must also not swell or dis-
solve a wide range of plastics.
6. The candidate should be sufficiently volatile to permit economical
reclamation by distillation and to permit rapid, economical, and safe drying
conditions.
7. The solvent must also be compatible with a wide range of detergents
so as to enhance its cleaning ability.
In conjunction with the above criteria, the solvent must be low in toxic-
ity to minimize any hazard to the worker during processing and to the customer
should residual solvent be left in the clothing. The solvent should have a flash
point above 38°G or should be nonflammable. The dry cleaning agent should not
bleed dyes or weaken, dissolve, or shrink textile fibers.
As shown in Table 4-8, perchloroethylene is the solvent of choice in ap-
proximately 72% of the domestic dry cleaning operations with an estimated 400
million pounds being used in 1975.
4.2.5.1 Aliphatic Hydrocarbons--
The two major petroleum distillates still used extensively in domestic
dry cleaning are Stoddard solvent and 140-F. Stoddard solvent is a water-white,
basically odor free petroleum distillate with a flash point of 41°G, 140-F is
a petroleum distillate solvent, so named because its flash point is 59°G
(140°F). 140-F is somewhat more expensive than Stoddard solvent and is slower
drying. A summary of the physical properties of these distillates can be found
in Table 4-1.
These solvents are used strictly in transfer type operations. Because of
the high emissions and potential fire hazard associated with the use of hydro-
carbon solvents, operations utilizing these solvents tend to be located away
from residential areas and shopping centers. Due to the highly flammable na-
ture of these solvents, many dry cleaning establishments are restricted (by
fire codes) from using petroleum distillates as solvents. Thus, these solvents
are not practical alternatives to perchloroethylene. Alcohols, aromatic hydro-
carbons, and ketones cannot be considered as feasible alternatives for the same
reasons.
4-28
-------
TABLE 4-8. COMMONLY USED DRY CLEANING SOLVENT;
.a-d/
A r ana tic
% Domestic Flash Boiling Dry end Density content Heat of
dry-cleaning point point point Sp«ri fie lb/gal* ( vol ume, Vaporization
Solvent market^ (°G/°F) (nC/°F) (°C/°F) gravity (25°G) %) Corrosiveness (Btu/lb)
Perchlorocthylene 72 None 121/250 123/254 1.623 13.47 0 Slight on metal 90
Stoddard solvent
140-F
Fluorochlorocarbons
F-1131'
F-il
Trichloroethylene
' Methylene chloride
vO
41/105 152/305 177/350 0.766 6.38 11.6 None 500
26
59/138 181/358 202/396 0.789 6.57 12.1 None 500
None 48/113 NAfi/ 1.574 13.16 0 None 63
None 24/75 NA 1.494 12.34 0 None 78.31
2
32.90 87/189 NA 1.462 12.16 0 None NA
(20°C)
None 40/104 NA 1.320 10.98 0 NA 142
Methyl chloroform None 75/165 NA 1.385 10.97 0 NA NA
Toxiclty
TLV
(pom)
100
200
200
1,000
1,000
100
250
500
Odor Color
Ether-like Water white
Sweet Water white
Mild Water white
Like CC14 Water white
Slight Water white
Chloroform- Water white
like
Ether-like Water white
Chloroform- Water white
like
Vapor
density
(air =
1.00)
5.5
1.0
1.0
6.3
5.0
NA
NA
NA
al Arthur D. Little (1976).
y E. I. du Pont de Nemours and Company.
ci Physical properties of Common Organic Solvents (1976).
Al The Condensed Chemical Dictionary (1971).
_£/ MRI estimates.
if Valclene® (E. 1. du Pont de Nemours and Company trade name) = F-113 -t- 0.1% cationic detergent.
£/ Not available or not known.
-------
4.2.5.2 Chlorinated Solvents—
Methylene chloride, trichloroethylene, and methyl chloroform are not used
in significant quantities in the United States because of incompatibility with
many synthetic fibers (e.g., trichloroethylene tends to bleed dyes from acetate
fabrics) (TRW, 1976).
The toxicity of carbon tetrachloride rules out the possibility of using
it as an alternative for perchloroethylene.
4.2*5.3 Ghlorofluorocarbons—
F-113 is used domestically as a dry cleaning solvent. E. I. du Pont de
Nemours and Company offers a F-113 detergent combination, Valclene®. This com-
pound is expensive ($10.50/gal.) in comparison to the petroleum distillate and
chlorinated hydrocarbon solvents and is used primarily for specialty cleaning,
i.e., furs and leather (TRW, 1976). The solvent is used in dry-to-dry (often
called Valclene®) machines. Valclene® is used in 1% of the commercial busi-
nesses and about 1% of coin-operated systems (Fisher, 1978). To prevent sol-
vent loss, the machines in which this solvent is used must b.e constructed much
"tighter" than machines using perchloroethylene. There are a limited number of
both machines and manufacturers of machines suitable for using Valclene®. The
use of this solvent will increase, but not to a great extent.
According to MRI information, F-ll (CC^F) is beginning to see limited
use in dry cleaning systems in the United States (Fisher, 1978). No data are
presently available to estimate quantities used.
4-30
-------
REFERENCES
Anonymous. 1972. Methylene chloride for vapor degreasing. Industrial Finish-
ing, pp. 39-42. August 1972.
Anonymous. 1973. Vapor degreasing. Industrial Finishing, pp. 19-23. October
1973.
Archer, W. L. 1974. Selecting alternative chlorinated solvents. Metal Progress.
pp. 133-146. October 1974.
Arthur D. Little, Inc. 1975. Preliminary economic impact of possible regulatory
action to control atmospheric emissions of selected halocarbons. EPA Contract
No. 68-02-1439, Task 8, Publication No. EPA-450/3-75-073. NTIS No. PB-247-115.
Astrand, I., A. Kelbam, and P. Ovruml. 1975. Exposure to white spirit - I. Con-
centration in alveolar air and blood during rest and exercise* Scand. J« Work
Environ. Health, 1:15-30.
Carpenter, C. P., E. R. Kinkead, D. L. Geary, Jr., L. J. Sullivan, and J. M.
King. 1975. Petroleum hydrocarbon toxicity studies—VIII. Animal and human
response to vapors of 140 flash aliphatic solvent. Toxicol. Appl. Pharmacol.,
34:413-429.
Carpenter, C. P., D. L. Geary, Jr., R. C. Myers, D. J. Nachreiner, L. J.
Sullivan, and J. M. King. 1976. Petroleum hydrocarbon toxicity studies--XI.
Animal and human response to vapors of deodorized kerosene. Toxicol. Appl.
Pharmacol., 36:443-456.
Chemical Marketing Reporter. 1978. Volume 214, No. 25, Schnell Publishing Com-
pany, New York. December 18. pp. 38-49.
Condensed Chemical Dictionary. Van Nostrand Reinhold Company. 8th ed., G. G.
Hawley, ed.
DiVincenzo, G. D., F. J. Yanno, and B. D. Astill. 1972. Human and canine expo-
sures to methylene chloride vapor. Am. Ind. Hyg. Assoc. J., 33:125-135.
Dow Chemical Company. 1976. Study to support new source performance standards
for solvent metal cleaning operations. Final report prepared for the U.S.
Environmental Protection Agency, Contract No. 68-02-1329, Task 9. June 30,
1976.
E. I. du Pont de Nemours and Company. Technical bulletins 5-16, FS-1, FST-1,
and FST-5A, Wilmington, Delaware.
4-31
-------
Ellsworth, A. C., and R. M. Vancamp. 1960. Perchloroethylene production. U.S.
Patent No. 2,951,103. August 30, 1960.
Environmental Protection Agency. 1977. Control of volatile organic emissions
from solvent metal cleaning. U.S. Environmental Protection Agency, Report
No. 450/2-77-022. Research Triangle Park, North Carolina, November 1977.
Feathers, R. E., and R. H. Rogerson. 1959. Perchloroethylene. Brit. Patent No.
811,833. (See also U.S. Patent No. 2,914,575.) April 15, 1959. Chem. Abst.
53:19875f.
Federal Register. 1977. Vol. 42, No. 131, p. 35314. July 8, 1977.
Fisher, B. International Fabricare Institute. Personal communication, Silver
Spring, Maryland. September 1978.
Gamberale, F., G. Annwall, and M. Hultengen. 1975. Exposure to white spirit -
II. Psychological functions. Scand. J. Work Environ. Health, 1:31-39.
Hamilton, A., and H. L. Hardy. 1974. Industrial Toxicology. Third ed. Publish-
ing Sciences Group, Inc. pp. 575.
Kirk-Othmer Encyclopedia of Chemical Technology. 1964. Volume 5. Second ed.
A. Standen, Exec. Editor, Interscience Publishers, New York.
Missouri Solvents and Chemicals Company. 1962. Organic solvents. Missouri Sol-
vents and Chemicals Company. Chicago, Illinois.
MRI. 1976. Chemical technology and economics in environmental perspectives.
Task 1. Technical alternatives to selected chlorofluorocarbon uses. Report
prepared for U.S. Environmental Protection Agency, Publication No. EPA-
560/1-76-002. Washington, D.C.
NIOSH. 1976a. Criteria for a recommended standard ... occupational exposure
to methylene chloride. U.S. Department of Health, Education, and Welfare.
HEW Publication No. (NIOSH) 76-138. March 1976.
NIOSH. 1976b. Criteria for a recommended standard ... occupational exposure
to isopropyl alcohol. U.S. Department of Health, Education, and)Welfare.
HEW Publication No. (NIOSH) 76-42. March 1976.
NIOSH. 1976c. Criteria for a recommended standard ... occupational exposure
to methyl alcohol. U.S. Department of Health, Education, and Welfare. HEW
Publication No. (NIOSH) 76-148. March 1976.
NIOSH. 1977. Occupational diseases. A guide to their recognition. U.S. Depart-
ment of Health, Education, and Welfare. HEW Publication No. (NIOSH) 77-18.
p. 608. June 1977.
4-32
-------
Occupational Safety and Health Letter. 1978. Vol. 8, No. 19. October 8, 1978.
Published by Gershon W. Fishbein, 1907 National Press Building, Washington,
B.C.
Physical Properties of Common Organic Solvents. 1976. Wisconsin Solvents and
Chemicals Corporation, New Berlin, Wisconsin.
Shreve, R. N. 1967. Chemical process industries. Third ed. McGraw-Hill, New
York. p. 794.
TRW, Inc. 1976. Study to support new source performance standards for the dry
cleaning industry. Final report prepared for the U.S. Environmental Protec-
tion Agency, Contract No. 68-02-1412, Task 4, May 7, 1976.
Vancamp, R. M., and A. P. Muren, Jr. 1959. Perchloroethylene manufacture and
catalyst therefor. U.S. Patent No. 2,914,576. November 24, 1959. Chem. Abst.
54:5462e (1960).
Vogt, H. J. 1960. Production of methyl chloroform. U.S. Patent No. 3,065,280.
Filed September 19, 1960.
4-33
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CONTENTS
Page
5. Health Impacts 5-7
5.1 Trichloroethylene 5-7
5.1.1 Uptake, absorption, transport,
distribution 5-7
5.1.1.1 Uptake (routes of entry) 5-7
5.1.1.1.1 Inhalation 5-8
5.1.1.1.2 Oral 5-8
5.1.1.1.3 Dermal 5-8
5.1.1.2 Absorption 5-8
5.1.1.3 Transport 5-9
5.1.1.4 Distribution 5-11
5.1.2 Metabolism and excretion 5-13
5.1.2.1 Metabolism 5-13
5.1.2.2 Excretion 5-19
5.1.2.2.1 Biological half-life . . . 5-19
5.1.2.2.2 Effects of drugs 5-22
5.1.2.2.3 Routes and rates of
elimination 5-23
5.1.3 Biochemical effects 5-31
5.1.3.1 Organ/cell effects 5-31
5.1.3.2 Effects on enzyme systems .... 5-31
5.1.3.3 Histologic and pathologic
effects 5-33
5-1
-------
CONTENTS (continued)
Page
5.1.4 Toxicology data 5-34
5.1.4.1 Target organs 5-34
5.1.4.1.1 Central nervous system . . 5-34
5.1.4.1.2 Liver 5-36
5.1.4.1.3 Kidney 5-38
5.1.4.1.4 Lungs 5-39
5.1.4.1.5 Heart 5-40
5.1.4.2 Dose-response 5-42
5.1.4.2.1 Acute effects 5-42
5.1.4.2.1.1 Man 5-42
5.1.4.2.1.2 Mice 5-47
5.1.4.2.1.3 Rats. 5-48
5.1.4.2.1.4 Dogs 5-49
5.1.4.2.1.5 Rabbits 5-50
5.1.4.2.1.6 Other species . . . 5-50
5.1.4.2.2 Subacute effects 5-51
5.1.4.2.2.1 Man 5-51
5.1.4.2.2.2 Mice 5-51
5.1.4.2.2.3 Rats 5-51
5.1.4.2.2.4 Guinea pigs .... 5-52
5.1.4.2.2.5 Cats 5-53
5.1.4.2.2.6 Dogs 5-53
5.1.4.2.2.7 Rabbits ...... 5-53
5.1.4.2.2.8 Monkeys 5-54
5.1.4.2.3 Chronic effects 5-54
5.1.4.2.3.1 Man 5-54
5.1.4.2.3.2 Rats 5-54
5.1.4.2.3.3 Rabbits 5-55
5.1.4.2.3.4 Guinea pigs .... 5-55
5-2
-------
CONTENTS (continued)
Page
5.1.4.3 Sensitization 5-55
5.1.4.4 Teratogenic effects 5-56
5.1.4.5 Mutagenic effects 5-57
5.1.4.6 Carcinogenic effects 5-60
5.1.4.7 Factors affecting toxicity. . . . 5-63
5.1.4.7.1 Synergistic effects with
other chemical 5-63
5.1.4.7.2 Stabilizer toxicity. . . . 5-64
5.1.5 Human epidemiology 5-65
5.1.5.1 Occupational exposure 5-65
5.1.5.2 Medical surveillance 5-66
5.1.5.3 Epidemiology/other human exposure
studies . 5-67
5.1.5.4 Accidental ingestion and addic-
tion and abuse 5-69
5.1.5.4.1 Accidental ingestion . . . 5-69
5.1.5.4.2 Misuse/abuse 5-70
5.1.6 Anesthetic and analgesic use 5-71
References 5-73
5.2 Methyl Chloroform (1,1,1-trichloroethane) . . . 5-102
5.2.1 Uptake and absorption 5-102
5.2.2 Transportation and distribution 5-104
5.2.3 Metabolic effects -,. 5-106
5.2.3.1 Biotransformation 5-106
5.2.3.2 Detoxification and activation . . 5-108
5.2.4 Excretion 5-108
5.2.5 Biochemical studies 5-110
5.2.5.1 Organ/cell effects 5-110
5.2.5.2 Effects on enzyme systems .... 5-113
5-3
-------
CONTENTS (continued)
5.2.6 Toxicologic data 5-115
5.2.6.1 Target organs 5-115
5.2.6.1.1 Brain, CNS effects .... 5-116
5.2.6.1.2 Cardiovascular toxicity. . 5-118
5.2.6.1.3 Liver and kidney effects . 5-121
5.2.6.1.4 Lung-respiratory tract
effects 5-124
5.2.6.2 Dose-response data 5-125
5.2.6.2.1 Acute toxicity 5-125
5.2.6.2.1.1 Human (inhalation). 5-125
5.2.6.2.1.2 Human (oral). . . . 5-130
5.2.6.2.1.3 Animal data .... 5-130
5.2.6.2.2 Subacute toxicity 5-131
5.2.6.2.2.1 Humans 5-131
5.2.6.2.2.2 Animals 5-132
5.2.6.3 Sensitization 5-136
5.2.6.3.1 Delayed effects 5-136
5.2.6.3.2 Allergic effects 5-147
5.2.6.4 Teratogenic effects 5-147
5.2.6.5 Mutagenic effects 5-148
5.2.6.6 Carcinogenic effects 5-149
5.2.6.7 Factors affecting toxicity. . . . 5-151
5.2.6.7.1 Cardiac hypersensitivity . 5-151
5.2.6.7.2 Misuse/abuse 5-154
5.2.6.7.3 Stabilizers/inhibitors . . 5-155
5-4
-------
CONTENTS (continued)
5.2.7 Human epidemiology 5-157
5.2.7.1 Occupational exposure 5-157
5.2.7.2 Detection of exposure 5-158
5.2.7.3 Epidemiological and other con-
trolled studies 5-159
References 5-164
5.3 Perchloroethylene (tetrachloroethylene) .... 5-176
5.3.1 Absorption, transport, distribution. . . 5-176
5.3.2 Metabolism and excretion 5-177
5.3.2.1 Biological half-life 5-177
5.3.2.2 Routes and rates of elimination . 5-179
5.3.3 Biochemical interactions 5-186
5.3.4 Toxicological data 5-188
5.3.4.1 Target organs 5-188
5.3.4.1.1 Central nervous system
(CNS) 5-189
5.3.4.1.2 Liver 5-193
5.3.4.1.3 Kidney 5-195
5.3.4.1.4 Adrenals 5-196
5.3.4.2 Dose-response data 5-196
5.3.4.2.1 Acute/subacute toxicity
in animals 5-196
5.3.4.2.2 Acute/subacute toxicity
in humans 5-202
5.3.4.2.3 Chronic toxicity 5-205
5.3.4.3 Sensitization on chronic use. . . 5-210
5-5
-------
CONTENTS (concluded)
Page
5.3.4.3.1 Tolerance, resistance, and
dependence 5-210
5.3.4.3.2 Allergic effects 5-210
5.3.4.4 Teratology 5-211
5.3.4.5 Mutagenicity 5-213
5.3.4.6 Carcinogenic effects 5-214
5.3.4.7 Factors affecting toxicity. . . . 5-220
5.3.4.7.1 Cardiac sensitization. . . 5-220
5.3.4.7.2 Synergistic effects. . . . 5-221
5.3.4.7.3 Stabilizer toxicity. . . . 5-224
5.3.4.7.4 Medical surveillance;
signs of overexposure. . 5-225
5.3.5 Human epidemiology 5-226
5.3.5.1 Occupational exposure 5-226
5.3.5.2 Other human exposure studies. . . 5-228
References. ...... 5-231
5-6
-------
SECTION 5
HEALTH IMPACTS
In this section, an assessment of the health impacts of trichloroethylene
(TCE), methyl chloroform (MC), and perchloroethylene (tetrachloroethylene,
PCE) is presented. This review is the result of an extensive search of the pub-
lished and unpublished literature on each of these compounds. The data reviewed
include absorption, excretion, transport, metabolism, effects on target organs,
toxicity, sensitization, carcinogenicity, mutagenicity, and many others. Very
few epidemiological studies have been conducted. Assessments are made of the
existing data to present a review of the current state of knowledge. Case his-
tories of reported exposures are reviewed. The order of presentation in this
section is: trichloroethylene, methyl chloroform, and perchloroethylene.
5.1 TRICHLOROETHYLENE
The National Institute for Occupational Safety and Health (NIOSH) con-
ducted a survey in 1975 which estimated that 300,000 workers are exposed daily
to this compound (Medical World News, 1975). One important fact must be noted
before beginning this review; most of the studies reviewed fail to mention the
grade or purity of trichloroethylene used. The solvent used in industry before
the mid-1960's contained impurities, such as 1,1,2,2-tetrachloroethane, and
stabilizers (~ 3%). Some of the impurities, such as tetrachloroethane, and
some of the stabilizers, such as epichlorohydrin, are more toxic to animals
and humans than is the parent compound, trichloroethylene. Therefore, some of
the toxic signs and symptoms previously attributed to trichloroethylene might
have been caused by these impurities. A more pure product was obtained in the
early 1960's, because a change was made in the manufacturing process. More em-
phasis, therefore, should be placed on laboratory studies conducted after the
early 1960's, unless prior investigators specified that a pure grade of tri-
chloroethylene had been used in their experiments.
5.1.1 Uptake, Absorption, Transport, Distribution
5.1.1.1 Uptake (Routes of Entry)--
Trichloroethylene may enter the human body by three routes: inhalation,
oral ingestion, and dermal absorption. This chlorinated hydrocarbon is rap-
idly absorbed through the lungs and gastrointestinal tract.
5-7
-------
5.1.1.1.1 Inhalation—The major route of entry is by vapor inhalation.
Soucek and Vlachova (1960) showed that an average of 64% (range: 58 to 70%)
of inhaled trichloroethylene was retained in the body. Other studies of tri-
chloroethylene retention generally agree with this average. Teisinger (1961)
reported an average of 56%; Soucek et al. (1952) recorded a range between 51
to 64% with an average of 58%, and Urban and Muller (1974) recorded an average
of 60%. Retention from industrial exposures was calculated by Grandjean et al.
(1955) to be 70%. i
5.1.1.1.2 Oral—Oral ingestion of trichloroethylene is not very common.
This method of uptake occurs either through accidental ingestion or misuse
(suicide and abuse). However, when trichloroethylene is absorbed through the
gastrointestinal tract, poisoning can occur (Kleinfeld and Tabershaw, 1954;
Stentiford and Logan, 1956; Longley and Jones, 1963; Meyer, 1966; Gibitz and
Ploechl, 1973).
5.1.1.1.3 Dermal—Stewart and Dodd (1964) demonstrated that the alveolar
breath concentration from skin exposure to trichloroethylene was only 0.5 ppm
after the subjects had immersed their hands in a beaker containing the compound
for 30 min. Using alveolar breath levels as a measure of absorption and appar-
ently assuming no body retention, the authors stated that unless trichloro-
ethylene was trapped against the skin, it was not absorbed in any significant
quantities. Schwander (1936) demonstrated that trichloroethylene penetrated
the skin of rabbits and was detected in the expired air. However, one report
by McBirdney (1954) stated that paralysis of the thumb and forefinger was ob-
served in an individual who intermittently soaked his hand in liquid trichloro-
ethylene. Frant and Westendorp (1950) showed that when a volunteer's hands had
been dipped into the solvent for 10 min, absorption through the skin was of
minor Importance, and that 3 days later the trichloroethylene content in the
urine was found to be only 1.5 mg/liter. The subject wore a gas mask during
the experiment in order to insure that the only mode of entry of trichloro-
ethylene was through the skin.
A series of chlorinated solvents, including trichloroethylene, were used
for in vivo cutaneous absorption studies through mouse skin (Tsuruta, 1975).
The results of the study showed that mouse skin was not a good model to ap-
proximate human skin characteristics.
5.1.1.2 Absorption—
Once trichloroethylene enters the body, it is readily absorbed into the
bloodstream. Powell (1947) conducted equilibration experiments with
trichloroethylene-air mixtures; from the results the author suggested that
red cell hemoglobin may absorb large amounts of trichloroethylene. Absorption
of trichloroethylene by artificial plasmas, representing only the aqueous and
fatty contents, indicated that absorption is probably dependent on the protein
content, and is certainly dependent on the fat content within an organism.
5-8
-------
Distribution coefficients of solubility for trichloroethylene-air mix-
tures were reported by Powell (1947). These partition coefficients are re-
ported as follows:
Water/air Blood/air Plasma/air
3 at 20°C 18 to 22 at 20°C 16 to 20 at 20°C
1.6 at 37°C 8 to 10 at 37°C
Other studies also agree with these results. McConnell et al. (1975) reported
that the water/air coefficient from their research was 2.74. Kylin et al.
(1967) found a blood/air coefficient of 9.7 at 37°C, which agrees with Powell.
Other distribution coefficients have been reported in the literature. Morgan
et al. (1972) recorded that a blood/gas (tirichloroethylene vapor) partition
coefficient was 15 at 25°C (using °Cl techniques). A fat/gas coefficient of
960 at 37°C was reported by Mapleson (1963).
Metabolites of trichloroethylene are also absorbed. Since plasma contained
an average of 4.8 times more metabolite (trichloroacetic acid) than red blood
cells and the metabolite could only be removed from the erythrocytes by elu-
tion, Bartonicek (1962) concluded that red cells selectively absorb trichloro-
acetic acid. A similar study by Fabre and Truhaut (1952) on rats was more spe-
cific: the red cell membrane absorbed the solvent metabolite. However, in
rabbits, trichloroacetic acid had a tendency to bind with the serum albumin.
Trichloroethanol, another metabolite, is also absorbed by the blood.
5.1.1.3 Transport—
Trichloroethylene and its metabolites are transported by the blood, but
the mechanism is still unknown. Powell (1947) suggested that this solvent is
absorbed and transported by the hemoglobin in the erythrocytes. However, Fabre
and Truhaut (1952) believe that lipids in the membrane of red blood cells fa-
cilitate transport of trichloroethylene. Of all the metabolites, trichloro-
acetic acid is found in the blood in the highest concentrations, and remains
for a longer time period than either unchanged trichloroethylene or another
trichloroethylene metabolite, trichloroethanol. These three compounds are
transported and distributed to different tissues within the body. Trichloro-
ethylene is commonly found in fatty tissues due to its lipid solubility.
Vesterberg and Astrand (1976) measured the trichloroacetic acid and tri-
chloroethanol concentrations in the blood of three groups of five men each.
The acid content in the blood supply rose for 20 hr after initial exposure.
After exposure, the peak average concentrations of trichloroacetic acid for
these three groups were:
5-9
-------
Group 1-18 mg/kg
Group 2 - 13 to 14 mg/kg
Group 3 - 13 to 14 mg/kg
The highest average concentration of trichloroethanol found in the blood for
the same three groups was considerably lower than the average acid concentra-
tion in the blood, and these peaks occurred only a few minutes after the end
of exposure. Average values reported of trichloroethanol for each of these
groups were 4.5 mg/kg for Group 3, 3 mg/kg for Group 2, and 2.5 mg/kg for
Group 1.
O
Bartonicek (1962) studied nine volunteers who inhaled 1 g/m trichloro-
ethylene for 5 hr; the observed retention rate was 51 to 64%. Within 24 hr,
75% of the retained amount was converted to metabolites, trichloroethanol,
and trichloroacetic acid in the approximate ratio of 1.4 to 1. Trichloroacetic
acid was found at a level of 2.4 ing/100 ml of blood plasma.
Four subjects were subjected to repeated exposures of trichloroethylene
for 4 hr/day for 5 days at 50 ppm (48 + 3 ppm) (Kimmerle and Eben, 1973). It
was noted that trichloroethanol could be detected in the human blood up to 4
days following a single exposure to 50 ppm.
Trichloroethylene, unlike trichloroacetic acid or trichloroethanol, rap-
idly disappears from the blood. Stewart et al. (1962) measured the trichloro-
ethylene concentrations in the blood of subjects exposed to 211 ppm for 190
min, two hours after the experiment began, the blood contained an average con-
centration of 6 ppm. Twenty minutes after the end of exposure, the blood level
concentration of trichloroethylene dropped to 1 ppm.
The concentrations of trichloroethylene in the blood during transport
have been measured by various researchers and usually found in higher concen-
trations in the arterial blood than in venous blood.
In one study, Powell (1945) measured the blood concentration of 12 patients
exposed by inhalation to 1.5 to 2.5 vol % trichloroethylene. It was found that
concentrations in venous blood varied between 6.5 and 12.5 mg/100 ml. The blood
concentration fell to 1 mg % within 2 hr, and to 0.1 mg % within 24 hr.
Trichloroethylene levels in the arterial blood of 15 males were measured
and found to be absorbed from the air at different rates. These rates were not
entirely related to the amount supplied. Astrand and Ovrum (1976) note that a
very thin subject had nearly zero uptake after four, 30-min exposures to 540
and 1,080 rag/m . Vesterberg et al. (1976) measured trichloroethylene in the
arterial blood of the same 15 subjects and found 42 to 45% of the
5-10
-------
trichloroethylene was absorbed. There was also a large scatter in the amounts
of trichloroethanol and trichloroacetic acid in the urine, which indicates in-
dividual differences in the production, as well as elimination of these
metabolites.
Clayton and Parkhouse (1962) mechanically introduced trichloroethylene
into the lungs of human subjects, and monitored arterial and venous (antecubi-
tal fossa) blood samples for the compound. When 1.0% v/v was administered,
trichloroethylene accumulated in the arterial and venous blood. Concentrations
recorded after 20 to 25 min were 12.8 mg/100 ml for the arterial blood, and
11.3 mg/100 ml for the venous blood. Measurements were also recorded for a
0.5% v/v concentration under these same conditions. Arterial blood concentra-
tions ranged from 4.1 to 7.0 mg/100 ml blood, while the concentrations of tri-
chloroethylene varied from 2.2 to 7.0 mg/100 ml in the venous blood. The
authors noted that (after inhalation) by obese subjects, the amount of tri-
chloroethylene was considerably lower in venous than arterial blood. This fact
is attributed to the ability of highly lipid soluble trichloroethylene to be
extracted from the blood by fatty tissue.
Trichloroethylene may be transported across placental barriers in pregnant
women and animals (Beppu, 1968). Laham (1970) showed that trichloroethylene can
pass through the placental barrier and enter the fetal blood system in humans.
The blood taken from 10 pregnant women showed a fetal-to-maternal blood ratio
of trichloroethylene ranging from 0.52 to 1.90. Helliwell and Button (1950)
also demonstrated that trichloroethylene readily passes the placental barrier
in animals (sheep and goats) within a short time period. These animals were
exposed to a range of trichloroethylene vapor varying between 0.53 to 1.51 vol
%. Within a 6-min period, the compound was found in the fetal blood. In sheep,
the fetus concentration was higher than the maternal concentrations; however,
this was not true for the goats. Only one out of the three goats tested showed
a higher concentration in the fetus blood than in the maternal blood.
5.1.1.4 Distribution—
Trichloroethylene may be retained in human and animal tissues. Tissues
from eight humans were examined postmortem by McCpnnell et al. (1975) and
found to contain trichloroethylene in the body fat, liver, kidney, and brain
tissue samples, indicating uptake by these tissues (Table 5-1). It has been
found that animals also build up increasing levels of trichloroethylene in
tissues.
Fabre and Truhaut (1952) studied tissue homogenates from animals exposed
to trichloroethylene. The compound was present in most of the examined tissues;
the greatest concentrations were in the fat, followed by the lungs, spleen,
liver, brain, and kidney. A metabolite, trichloroacetic acid, was found in
the greatest concentrations in the spleen, suprarenal glands, reproductive or-
gans, and urine. After acute exposure to trichloroethylene, the greatest amount
of trichloroacetic acid was present in the spleen, while after chronic exposure
5-11
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TABLE 5-1. OCCURRENCE OF TRICHLOROETHYLENE IN HUMAN TISSUE
Age of
subject Sex Tissue
76 F Body fat
Kidney
Liver
Brain
76 F Body fat
Kidney
Liver
Brain
82 F Body fat
Liver
48 M Body fat
Liver
65 M Body fat
Liver
75 M Body fat
Liver
66 M Body fat
74 F Body fat
ug/kg
32
< 1
5
1
2
3
2
< 1
1.4
3.2
6.4
3.5
3.4
5.2
14.1
5.8
4.6
4.9
Post-mortem samples taken from subjects who had lived in northwestern
England of unreported work history or trichloroethylene exposure, iso-
lation accomplished by solvent extraction and column chromatography;
samples analyzed by gas-liquid chromatography using an electron cap-
ture detector with confirmation by mass spectroscopy (Source:
McConnell et al. (1975).)
5-12
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the largest amount of acid was present in the lungs. A refined analytical meth-
odology has been developed whereby only 50 /il of urine is required to measure
trichloroethylene metabolites in human subjects (Henrich and Lenich, 1977).
The error range for the method is stated to be 5 to 8%.
Metabolites of trichloroethylene were found in in vitro studies of iso-
lated dog and rat tissues. Butler's (1949a) study indicated that trichloro-
ethanol was present in the liver, kidney, diaphragm, brain, testis, spleen,
and whole blood in rats. In dogs, trichloroethanol was found in the liver,
kidney, cortex, cerebral cortex, whole blood (using heparin and oxalate anti-
coagulants) and plasma (heparinized). The other major metabolite, trichloro-
acetic acid, was observed only in the liver and kidney of rats and dogs.
Tissue levels of trichloroethylene in dogs after acute or chronic expo-
sure were recorded by Cohen et al. (1958). Eleven dogs were exposed to tri-
chloroethylene vapors under a variety of conditions ranging from 1 to 289 ex-
posures at concentrations of 7,000 to 20,000 ppm (3.2 to 9.1 w/w %). The
compound was detected in the fat, blood, liver, kidney, adrenal, brain, lung,
muscle, pancreas, spinal cord, spleen, and thyroid of the dogs. Fat tissue
tended to be the biggest depository, although for acute exposure blood con-
tained high levels of the solvent.
Stewart et al. (1964) also found similar results in dogs. They noted that
the highest concentration of trichloroethylene was found in omental fat and
tissue having a high lipid content. These dogs were given 1 or 2 mg/kg orally
and sacrificed 16 hr posttreatment.
A similar study on three guinea pigs and a dog was conducted by Kulkarni
(1944). Trichloroethylene was detected in the following tissues: blood, liver,
and brain in the guinea pigj blood and brain in the dog.
Barrett et al. (1939) reported finding trichloroethylene in the tissues
of rabbits and dogs exposed to the vapor at unreported levels for 20 to 30 min.
Table 5-2 summarizes their findings. With the exception of dog 1, the highest
trichloroethylene concentrations were in the fat.
5.1.2 Metabolism and Excretion
5.1.2.1 Metabolism—
Trichloroethylene is rapidly converted to its metabolites through the
pathway shown in Figure 5-1. It has been hypothesized that trichloroethylene
can be biotransformed into either the oxide (epoxide) or the glycol before
undergoing rearrangement into trichloroacetaldehyde (Waters et al*, 1976).
Trichloroacetaldehyde then forms the known intermediate, chloral hydrate, by
hydrolysis. Chloral hydrate is then either oxidized to trichloroacetic acid
(Cooper and Friedman, 1958) or reduced to trichloroethanol (Friedman and
Cooper, 1960). Trichloroethanol can, in turn, be either oxidized to
5-13
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TABLE 5-2. CONCENTRATIONS OF TRICHLOROETHYLENE IN
TISSUES OF DOGS AND RABBITS
Concentration^/
Tissue
Muse le
Fat
Liver
Blood
Kidney
Lungs
Heart
Rabbit 1
4
44
15
24
12
26
27
Rabbit 2
6
48
17
24
12
26
27
Dog 1 Dog 2
7 10
92
17 43
26 23
12 26
26 31
26 45
a/ Milligrams per 100 g tissue.
Source: Barrett et al. (1939).
5-14
-------
Cl Cl
I I
CI-C-C-H
I I
OH OH .
TRICHLOROETHYLENE
GLYCOL
H
TRICHLOROETHYLENE
MICROSOUAL MIXED FUNCTION OXIDASES
NAOPH/OZ
-H20^
+ H20
1CI-C-C-H
Cl OH
+
OH-
TRICHLOROETHYLENE
0X1OE
INTRAMOLECULAR REARRANGEMENT PRODUCT
*
N
c, H
TRICHLOROACETALDEHYDE
HYDROLYSIS
CI*OH
I I
CI-C-C-H
^ Cl OH -^^
ALCOHOL OEHYOROGENASE/NAOH
Cl H *
I I
CI-C-C-OH
I I
Cl H
TRICHLOROETHANOL
UDf GLUCUftONYL TffANSFERASE
Cl H
C'-C-C-0-C6H906
a H
TRICHLOROETHANOL
GLUCURONIOE
CHLORAL HYDRATE
MIXED FUNCTION
OXIOASES
CHLORAL HYDRATE DEHYDROGENASE/NAD
0
TRICHLOROACETIC ACID
PROPOSED INTERMEDIARY METABOLISM OF TRICHLOROETHYLENE
(Reprint from Waters et al., 1976)
Figure 5-1
5-15
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trichloroacetic acid (by the mixed function oxidase system) or conjugated with
glucuronide to form trichloroethanol glucuronide.
The formation of an epoxide intermediate during biotransformation of tri-
chloroethylene was first suggested by Powell (1945). Daniel (1963) hypothesized
that the epoxide intermediate instantaneously rearranges to trichloroacetal-
dehyde before forming chloral hydrate. Trichloroethylene is a close structural
analog to the carcinogen vinyl chloride (which has also been postulated as hav-
ing an epoxide intermediate); therefore, Van Duuren (1975) and Van Duuren and
Banerjee (1976) theorized that trichloroethylene biotransformation may also
proceed via an epoxide intermediate.
The epoxide intermediate has been confirmed through chemical experiments
by Bonse et al. (1975). The oxirane was synthesized by the chlorine-catalyzed
photooxidation of trichloroethylene. The epoxide is relatively unstable with
a half-life in nonpolar solvents (60°C) of 25 min. A thermal rearrangement oc-
curs with chlorine migration to form dichloroacetyl chloride.
Recent experiments by Uehleke et al. (1976) on liver microsomes incubated
with trichloroethylene show that a 2,2,3-trichlorooxirane metabolite was proved
by spectral investigation of the cytochrome P-450 complex.
In some later experiments, ^C-trichloroethylene was injected into mice,
the liver tissue isolated, and the protein precipitated with trichloroacetic
acid. The protein-associated radioactivity was called "irreversibly bound" and
equated with alkylation of liver macromolecules by the authors (Uehleke and
Poplawski-Taberelli, 1977).
Butler (1949b) first suggested that chloral hydrate is the intermediate
form in the metabolic pathway. The conversion of trichloroethylene to chloral
hydrate was demonstrated by Liebman (1965) and Byington and Leibman (1965).
Leibman (1965) showed that the transformation to chloral hydrate occurs in the
liver microsomes of rats, rabbits, and dogs. This reaction requires NADPH and
oxygen (see Figure 5-1). The existence of chloral hydrate as a transient metab-
olite was also demonstrated by Cole et al. (1974). Samples of venous blood
taken from patients anesthetized with trichloroethylene were analyzed using
a combined system of gas chromatography and mass spectroscopy. The peaks ob-
tained from these blood samples had retention times similar to those of chlo-
ral hydrate, indicating chloral hydrate to be a metabolite of trichloroethylene.
Daniel (1963) showed that chlorine attached to trichloroethylene is not
removed during biotransformation in rats exposed to single doses of 4.0, 7.5,
or 8.6 /xCi 36Cl-labeled compound. Approximately 93% of the 36Cl-labeled tri-
chloroethylene administered by stomach tube was excreted unchanged through the
lungs or in the urine as trichloroethanol and trichloroacetic acid. The spe-
cific activities of metabolic trichloroacetic acid and trichloroethanol were
5-16
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shown to be the same as that of the administered trichloroethylene, thus dem-
onstrating an intramolecular rearrangement of chloride.
Urine samples from dogs exposed to trichloroethylene vapor were tested by
Barrett and Johnston (1939) and found to contain a metabolite which had three
chlorine atoms attached to one carbon atom. They concluded that this metabolite
was trichloroacetic acid. Identification of the acid as a metabolite was con-
firmed by Powell in 1945. Four years later, Butler (1949a) isolated trichloro-
ethanol in the urine of dogs. After an anesthetic dose of trichloroethylene
(1 hr) to two dogs, 1.52 and 0.53 g of trichloroethanol was excreted by the
animals; nearly all was conjugated. The trichloroacetic acid produced by the
same dogs was estimated to be 0*70 and 0.16 g from plasma concentrations and
urinary excretion, respectively.
The metabolic pathway of trichloroethylene has been postulated and re-
viewed in many studies (Butler, 1949b; Uhl and Haag, 1958; Daniel, 1963). One
recent major review was presented by Kelly and Brown (1974) which indicated
that there are three major metabolic biotransformations: (a) oxidation to
chloral hydrate in the microsomal fraction of the liver cells; (b) reduction
to trichloroethanol; and (c) oxidation to trichloroacetic acid.
Minor metabolites have also been reported in the literature. As early as
1939, Barrett and Johnston indicated that when trichloroethylene was metabolized
in dogs, a small amount of chloroform was produced. Steam distillation of urine
from exposed dogs indicated the presence of chloroform. However, there is dis-
agreement as to whether chloroform is a true metabolite of trichloroethylene.
Barrett and Johnston suggested that chloroform did not occur in the urine as
such, but resulted from the decomposition of trichloroacetic acid during dis-
tillation. According to Defalque (1961), there is no substantial evidence that
chloroform is a minor metabolite of trichloroethylene. Soucek and Vlachova
(1954; 1960) noted the presence of a minor metabolite, monochloroacetic acid,
in exposed humans. Ogata and Saeki (1974) reported the presence of monochloro-
acetic acid and chloral hydrate in the blood serum after oral administration
of trichloroethylene to rabbits. However, because of its short half-life (sum-
.marized in Table 5-3), chloral hydrate does not remain in the body for any
length of time. After intensive investigations, Defalque (1961) reported that
chloral hydrate and monochloroacetic acid are the only minor metabolites. More
recently, however, Traylor et al. (1977) found carbon monoxide produced by
liver microsomal cytochrome P-450 in in vitro experiments with isotopically-
labeled trichloroethylene.
5-17
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TABLE 5-3. HALF-LIFE OF CHLORAL HYDRATE
Species Tissue Exposure Half-life Reference
Humans Blood Ingestion, 5 to 30 min Marshall and Owens (1954)
30 mg TCE/kg
Dogs Blood Intravenous 5 min Mackay and Cooper (1962)
injections
Mice Brain Intravenous 10 to 20 min Mackay and Cooper (1962)
injections
A study by Henschler (1977) was reported which proposed a rule of "chemi-
cal reactivity, biotransformation, and mutagenicity/carcinogenicity," based on
in vitro bacterial mutagenesis assays and animal test results and discussed
further in that segment of this document. Henschler's rule of structure-
activity suggests that carcinogenicity requires unsymmetric chlorine substi-
tution which produces an electron withdrawal effect, and "high electrophilic-
ity" is prerequisite for carcinogenic/mutagenic potential of the chlorinated
compounds.
The Henschler theory would suggest that trichloroethylene is carcinogenic,
except that Henschler proposes complete detoxification of the epoxide by rear-
rangement to chloral hydrate under in vivo conditions in mammals (Henschler,
1977). The differences between carcinogenic compounds of similar structure and
trichloroethylene were also emphasized by Bolt and Filser (1977). The binding
to protein of vinyl chloride was compared to the binding properties of tri-
chloroethylene. Unlike vinyl chloride, which had a great affinity for protein
sulfhydryl groups, trichloroethylene bound rather nonspecifically to any free
amino group of protein (Bolt and Filser, 1977).
To summarize the recent work on trichloroethylene metabolism, trichloro-
ethylene was shown to demonstrate a specific binding spectrum with P-450
(Uehleke et al., 1976; 1977), the first substantial (but indirect) evidence
that the compound formed an epoxide. Bonse's experiments with the isolated,
perfused rat liver preparation (Bonse et al., 1975) suggest that the expected
chemical behavior of trichloroethylene did not follow the other chlorinated
ethylenes, in that their in vitro experiment found no dichloroacetic acid, a
predicted metabolite through an epoxide pathway. Henschler (1977) has suggested
5-18
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that intramolecular rearrangement occurs in trichloroethylene. Specifically,
the reaction involves formation of alpha-ketocarbonium ions after C-0 hetero-
lysis, resulting in a single chlorine-substituted carbonium. Henschler's specu-
lation is of considerable significance for the evaluation of the carcinogenic
or mutagenic potential of trichloroethylene, because this intramolecular rear-
rangement represents a deactivation mechanism as opposed to reaction by alkyla-
tion with cellular macromolecules. Henschler et al. (1979) have synthesized a
trichloroethylene epoxide and have studied its metabolic degradation. Defini-
tive tests on the covalent binding of these metabolites are in progress but
unpublished at this date.
The experiments of Van Duuren, on the other hand, suggest that covalent
binding occurs between rat liver microsomal protein and C-trichlorbethylene
(reviewed in Van Duuren, 1977). This binding, demonstrated in vitro, in rat
liver microsome preparations, was enhanced by inducers of mixed function oxi-
dases and inhibited by compounds which depressed the enzymatic activity.
Mechanistic evaluations of the possible pathways of metabolic activation
of trichloroethylene have suggested that the postulated electrophilic inter-
mediate, trichloroethylene epoxide, may be handled differently in different
biological systems. A Lewis acid-type catalytic rearrangement to the nonreac-
tive chloral hydrate may occur in mammalian liver, according to the work of
Bonse and Henschler (1976). This pathway may not be the same as that of the
microorganisms used as tester strains in the in vitro mutagenicity assays.
5.1.2.2 Excretion —
5.1.2.2.1 Biological half-life—Many articles have been published on the
biological half-life (T^i^ ) of trichloroethylene and its metabolites in humans.
Ikeda and Imamura (1973) collected and summarized these previous citations of
biological half-lives; an expanded version of these citations is presented in
Table 5-4. Additional studies on the half-lives in the urine, not cited by
Ikeda and Imamura, have been collected and added.
Ikeda and Imamura noted a wide variance in biological half-lives (26 to
51 hr) of total trichloro-compounds in factory workers exposed to trichloro-
ethylene (Table 5-4). There appears to be no correlation between the number
of exposures and variance in biological half-lives. However, Ikeda and Imamura
observed that the total mean value calculated was about 41 hr. This value
closely correlates to the experimental values of half-lives in subjects not
previously exposed to trichloroethylene vapors.
Two other observations based on data from Table 5-4 were made by Ikeda
and Imamura. First, no related sex differences were observed in the half-life
of total trichloro-compounds; second, the half-life in an "addicted" patient
was higher than in the factory workers.
Few data have been published on the biological half-lives of trichloro-
ethylene in the blood. Table 5-5 summarizes these biological half-lives.
5-19
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TABLE 5-4. BIOLOGICAL HALF-LIFE OF METABOLITES IN THE URINE OF HUMAN SUBJECTS EXPOSED
TO VAPORS OF TRICHLORDETHYLENE
Exposure load
Biological half-life (hr)
Group affected Number of people Sex and time Total trichloro-compounds Trichloroethanol Trichloroacetic acid References
Factory workers 6 M 10 to 150 ppm for 4 hr
1 or 2 times /month
6 M 5 to 170 ppm for 2 hr
1 or 2 times /month
6 M intermittently exposed
to 200 ppm 5 days/week
6 M 20 to 40 ppm for 8 hr/day
for 5 days /week
6 F intermittently exposed
to 50 ppm 5 days/week
I Volunteers 2 F 186 ppm for 5 hr
rO
o
5 M 250 to 380 ppm for 160 min
5 F 250 to 380 ppm for 160 min
5 M 170 ppm for 7 hr
4 M 170 ppm for 3 hr
5 M,F 50 ppm for 6 hr
Addict 1 M -
42.7 + 4.5 3/
(37.3 + 6.2)
48.8 + 11.7
(47.5 + 7.7)
26.1 + 4.8
(22.7 + 4.6)
33.7 + 6.8
(26.9 ± 5.0)
50.7 + 7.7
(38.3 + 7.5)
50.3
31.4
36.1
35.8
48.6
-
72.6
(95.1)
Ikeda and Imamura (1973)
Ikeda and Imamura (1973)
15.3 + 2.2 39.7 + 8.7 Ikeda and Imaraura (1973)
(14.2 ± 2.3) (36.5 + 17.3)
Ikeda and Imamura (1973)
42.7 + 9.1 57.6 + 19.8 Ikeda and Imamura (1973)
(32.6 + 8.9) (50.9 + 22.6)
29.2 55.3 Bartonlcek (1962)t/
19.0 38.0 Nomiyama and Homiyama (1971)t/
25.8 36.1 Nomiyama and Nomiyaraa (1971)-'
Ogata et al. (1971)k/
Ogata et al. (1971)-'
12.0 100.0 Muller et al. (1972)t/
49.7 72.6 Ikeda et al. (1971)t/
(49.8) (95.0)
aY Values are mean + SO calculated from metabolite concentration corrected for a specific gravity of urine of 1.016 together with those corrected for creatinine
concentration in parentheses.
b/ Values are calculated by the present authors from results of referred authors.
-------
TABLE 5-5. BIOLOGICAL HALF-LIFE OF METABOLITES IN THE BLOOD OF HUMAN SUBJECTS EXPOSED
OCCUPATIONALLY OR EXPERIMENTALLY TO VAPORS OF TRICHLOROETHYLENE
Ul
N3
Biological
half-life
Compound Groups
Trichloroethylene Volunteers (5 subjects)
Volunteers (5 subjects)
Type of (hr)
exposure TTCJ*/ TCEt>/
Experimental - 12-'
Experimental - 13.3—
12. 4-'
TCA— ' Reference
Ertle et al. (1972)
85.6-/ Muller et al. (1974)
99.0^'
a_l Total trichloro-compourids.
b/ Trichloroethylene.
£/ Trichloroacetic acid.
d/ 6 lir/day for 5 days at either 50, 100, or 250 ppm for 12 min/hr (high peak concentration, average
50 ppm).
&l 100 ppm trichloroethylene, 6 hr/day for 10 days.
I/ 500 ppm TCE, 6 hr/day for 5 days.
-------
Sato et.al. (1977) has established a mathematical model for urinary ex-
cretion of trichloroethylene, based on data from four men inhaling 100 ppm for
4 hr. The rate constants established should be treated with caution since some
authors point out that trichloroethylene excretion is a variable which depends
on exposure levels as well as duration, and these baseline data are for acute,
low-level exposure.
The biological half-life in the serum and urine of rabbits was reported
by Ogata and Saeki (1974) (Table 5-6). Results show that, except for tri-
chloroethylene and chloral hydrate, the half-lives of metabolites are longer
in urine than in serum.
TABLE 5-6. BIOLOGICAL HALF-LIFE OF TRICHLOROETHYLENE AND
METABOLITES IN RABBITS^'
Half-life (hr)
Compound
Trichloroethylene
Chloral hydrate
Free trichloroethanol
Total trichloroethanol
Conjugate trichloroethanol
Monochloroacetic acid
Trichloroacetic acid
Urine
_
-
30.5
38.0
42.0
36.0
43.5
Serum
3.8
6.4
8.4
8.5
8.5
14.0
18.5
.a/ Rabbits were given 13 moles/kg of trichloroethylene orally.
Source: Ogata and Saeki (1974).
5.1.2.2.2 Effects of drugs—Drugs may promote or retard the excretion
rates of trichloroethylene and its metabolites in man and animals. Glucose
with insulin, ethanol, and phenobarbital increased the excretion rates of both
trichloroacetic acid and trichloroethanol. Disulfiram (tetraethyl thiuram di-
sulfide) and toluene caused decreases in the excretion kinetics of both metabo-
lites, whereas fructose and sodium lactate decreased the formation of trichloro-
ethanol.
After inhalation exposure to 65 to 125 ppm trichloroethylene for 5 hr,
12 g of glucose and 15 units of insulin were given to humans by Soucek and
Vlachova (1960). The excretion rates of trichloroethanol and trichloroacetic
acid were increased. The quantity of trichloroethanol excreted on the first
day was increased 2.6 times; however, no increase in the excretion quantity
5-22
-------
was noted for trichloroacetic acid. By the end of the experiment, excretion
of metabolites increased approximately 22%.
Bartonicek (1962; 1963) singly administered glucose, fructose, or sodium
lactate intravenously, or ethanol orally to eight human volunteers before ex-
posing them to 5 hr of trichloroethylene vapors (186 ppm). The urinary excre-
tion rates were measured over a period of 22 days. Glucose caused a 13% in-
crease in excretion of total trichloro-compounds. The amount of trichloro-
ethanol was increased by 8%, while trichloroacetic acid was increased by 5%.
Monochloroacetic acid was not measured. Similar results were found for orally
administered ethanol; a 6% increase in the final amount of trichloroethanol
and a 3% increase in trichloroacetic acid were noted. However, different re-
sults were observed for fructose and sodium lactate, which increased the for-
mation of the acid while simultaneously decreasing the amount of trichloro-
ethanol. A study by Sukhotina et al. (1973) also indicated that glucose helped
to accelerate the excretion of trichloroethylene.
Disulfiram reduces the excretion kinetics of the metabolites. Bartonicek
and Teisinger (1962) exposed four subjects to 186 ppm trichloroethylene for 5
hr after pretreatment with 3 to 3-1/2 g disulfiram. A noticeable decrease in
both major metabolites (trichloroacetic acid; trichloroethanol) was reported.
All four people showed a 40 to 64% decrease in excretion of trichloroethanol,
and a 72 to 87% decrease in the acid. The excretion of trichloroethylene by
the lungs increased, which indicates that metabolism was blocked. Similar re-
sults---little trichloroacetic acid excretion—were obtained by Forssman et
al. (1955) after giving disulfiram to rats exposed to trichloroethylene.
Other animal studies showed that phenobarbital altered excretion rates.
After pretreating rats with phenobarbital, Leibman and McAllister (1967) found
that trichloroacetic acid and trichloroethanol excretion rates increased. How-
ever, the total cumulative excretion of metabolites was approximately the same
in both the controls and experimental groups. Urochloralic acid (trichloro-
ethanol glucuronide) exhibited the greatest increase after pretreatment with
phenobarbital and, unlike trichloroacetic acid and trichloroethanol, the cumu-
lative output was about twice that of the controls. Analogous results were ob-
tained in 1973 by Ikeda and Imamura, who showed an increase in in vitro oxida-
tion and an enhancement of the in vivo metabolism of trichloroethanol when rats
and hamsters were pretreated with phenobarbital.
In vivo and in vitro studies in rats by Ikeda (1974) demonstrated that
co-administration of toluene and trichloroethylene caused a suppression of
the excretion of total trichloro-compounds.
5.1.2.2.3 Routes and rates of elimination—Trichloroethylene and its me-
tabolites are excreted in urine, by exhalation, and to a lesser degree in sweat,
feces, and saliva. Trichloroethanol, trichloroethanol glucuronide, monochloro-
acetic acid, and trichloroacetic acid appear in the urine immediately after
5-23
-------
exposure begins. The excretion of monochloroacetic acid from the organism pro-
ceeds the fastest, followed by trichloroethanol and trichloroethanol glucuronide
and finally trichloroacetic acid. On the other hand, trichloroethylene is ex-
creted in the urine in small amounts (Soucek, 1959). Most of the trichloro-
ethylene which enters an organism is either metabolized or excreted unchanged
in expired air.
Soucek and Vlachova (1960) examined the excretion time and percent excre-
tion of monochloroacetic acid, trichloroacetic acid, and trichloroethanol in
humans exposed to up to 150 ppm trichloroethylene for 5 hr. Monochloroacetic
acid was shown to be excreted in the first few minutes after exposure. Excre-
tion of monochloroacetic acid was maximal at the end of the exposure and con-
tinued for 48 to 168 hr (average 112 hr). Monochloroacetic acid comprised about
4% of the retained trichloroethylene. Trichloroacetic acid appeared in the
urine immediately after inhalation, and its concentration slowly rose due to
its ability to accumulate in the body. Maximal excretion occurred within 24
to 48 hr and lasted for 520 hr. The fall in the rate of excretion was consid-
ered to be the sum of two exponential rates (phases). The first phase lasted
about 5 days, and the second phase lasted approximately 14 days. Trichloroace-
tic acid comprised 10 to 30% (19% average) of the retained vapor. Trichloro-
ethanol was also excreted within the first few minutes of exposure. Excretion
of trichloroethanol reached its maximum a few hours after exposure and rose
very rapidly. The excretion time was 312 to 390 hr (average 350 hr). A decrease
in the excretion rate appeared as the sum of two exponential rates. The first
phase lasted 3 to 4 days, while the second phase lasted 7 to 9 days. The total
quantity of trichloroethanol excreted was between 32 and 59% of the trichloro-
ethylene retained; the average was 50%. The total quantity of these three me-
tabolites excreted in the urine of humans amounted to from 43 to 100% of the
absorbed trichloroethylene. The ratio of these three metabolites was found to
be monochloroacetic acidrtrichloroacetic acid:trichloroethanol = 1:5:12.
This detailed study performed by Soucek and Vlachova (1960) was generally
confirmed by Bartonicek (1962) and Ogata et al. (1971). Eight volunteers were
exposed to 186 ppm trichloroethylene for 5 hr by Bartonicek (1962). Of the re-
tained trichloroethylene, from 38.0 to 49.7% and 27.4 to 35.7% was excreted as
trichloroethanol and trichloroacetic acid, respectively. Bartonicek, in the
same experiment, found trichloroethanol and trichloroacetic acid were excreted
in the feces, sweat, and saliva for a total of 8.4%.
Ogata et al. (1971) conducted two separate experiments on 13 male subjects
exposed to approximately 170 ppm trichloroethylene. One group of five people
(A) remained in the exposure chamber for 3 hr in the morning and 4 hr in the
afternoon at an exposure of 170 ppm. A second group of four people (B) were
also exposed to 170 ppm, but they remained in the chamber for only 3 hr (in
the morning). Urine was collected for 100 hr after initial exposure. In Groups
A and B, the concentration of trichloroethanol was maximum 1 to 3 hr after ex-
posure, and trichloroacetic acid concentrations were maximum 42 to 69 hr after
5-24
-------
exposure. The excretion rate of trichloroacetic acid and trichloroethanol re-
turned to normal after 92 hr. The total amounts of trichloroethanol and tri-
chloroacetic acid recovered in the urine were 44 and 18.1%, respectively, for
the 7-hr exposure. Fifty-three percent of the trichloroethanol and 21.9% of
the trichloroacetic acid was the final amount recovered in the 3-hr exposure
to 170 ppm.
Rate constants for total trichloro-compounds, trichloroethanol and tri-
chloroacetic acid have been calculated from previous data by Nomiyama and
Nomiyama (1971). A wide variance in the excretion kinetics rate exists. Total
trichloro-compounds have urinary excretion rate constants varying between 0.14
to 0.36 (Prerovska et al., 1958; Bartonicek, 1962; Ogata et al., 1969; Stewart
et al., 1970). Trichloroethanol rate constants ranged from 0.14 to 4.0
(Prerovska et al., 1958; Soucek, 1959; Ohmori, 1960; Bartonicek, 1962; Ogata
et al., 1969; Stewart et al., 1970). Trichloroacetic acid urinary excretion
rate constants as calculated by Nomiyama and Nomiyama (1971) varied greatly
between 0.09 and 0.65 (Powell, 1945; Soucek et al., 1953; Soucek, 1954;
Bardodej et al., 1956; Prerovska et al., 1958; Soucek, 1959; Ohmori, 1960;
Abrahamsen, 1960; Bartonicek, 1962; Longley and Jones, 1963; Tada, 1969; Ogata
et al., 1969).
The levels of trichloroethylene metabolites in the urine of humans have
been recorded by many researchers. Ikeda and Ohtsuji (1972) conducted two sep-
arate experiments on male workers exposed to trichloroethylene vapors, and re-
corded the excretion of the metabolites in the urine. In the first experiment
six workers were exposed intermittently to 10 to 50 ppm of the solvent. Total
trichloro-compounds varied from 38 to 376 mg/liter, trichloroethanol varied
from 11 to 281 mg/liter, and trichloroacetic acid varied from 18 to 95 mg/liter
in the urine. In the second experiment, 14 workers were exposed intermittently
to a range of 120 to 250 ppm trichloroethylene. The urinary metabolites ranged
from 55 to 487 for total trichloro-compounds, 33 to 347 for trichloroethanol,
and 22 to 177 for trichloroacetic acid. The overall time during which these
urinary metabolites were measured was not given.
Surveys were conducted by Ikeda et al. (1972) on 85 male industrial work-
ers exposed to trichloroethylene under working environments. The urinary ex-
cretion of metabolites was recorded as was the total trichloro-compounds. The
results are summarized in Table 5-7 and show that metabolite concentration in-
creased as exposure concentration increased.
Sukhanova and Burdygina (1971) measured the metabolite level in the urine
of students during their 4 months' apprenticeship in a plant which used tri-
chloroethylene. The content of metabolites in the urine increased signifi-
cantly. After 4 months the metabolites found in the urine of students ranged
from 2.3 to 65.6 mg/liter.
5-25
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TABLE 5-7. AVERAGE METABOLITE CONCENTRATIONS IN URINE OF WORKERS EXPOSED TO VARIOUS
CONCENTRATIONS OF TRICHLOROETHYLENE
Metabolite concentrations
Number of
people exposed
36
9
5
6
4
4
5
5
5
4
4
Concentration
(ppm)— Time exposed
0
3
5
10
25
40
45
50
60
120
175
8
8
8
8
•-8
8
8
8
8
8
8
hr/day ,
hr/day ,
hr/day,
hr/day,
hr/day,
hr/day,
hr/day ,
hr/day,
hr/day,
hr/day,
hr/day ,
6
6
6
6
6
6
6
6
6
6
6
days /week
days /week
days /week
days /week
days/week
days /week
days /week
days/week
days /week
days /week
days /week
Total trichloro- Trichloro-
compounds ethanol
1
39
45
60
164
324
399
418
468
915
1,210
.4
.6
.5
.3
.9
.0
.9
.0
.3
.9
0
25
24
42
77
220
256
267
307
681
973
.1
.9
.0
.3
.3
.7
.3
.9
.8
.1
Trichloro-
acetic acid
1
12
20
17
77
90
138
146
155
230
235
.7
.2
.6
.2
.6
.4
.6
.4
.1
.8
_a/ The parts per million of solvent in the air was measured using Kitagawa (1961) detection tubes.
least five determinations were made and the averages were recorded.
Source: Ikeda et al. (1972).
At
-------
Five male volunteers were subjected to 200 ppm trichloroethylene 7 hr/day
for 5'days (Stewart, 1968). Twenty-four-hour urine samples were collected and
analyzed for trichloroacetic acid and trichloroethanol before, after, and dur-
ing exposure. The results are summarized in Table 5-8.
A study conducted by Friberg et al. (1953) showed similar results. Three
people were exposed to trichloroethylene concentrations ranging from 100 to
150 ppm 7 hr daily for 1 week; during the later days of the study, from 250
to 300 mg of trichloroacetic acid per liter of urine was excreted. Frant and
Westendorp (1950) calculated that if people were exposed to 100 ppm of tri-
chloroethylene for several days, they would excrete about 200 mg/liter of tri-
chloroacetic acid in the urine. Grandjean et al. (1955) reported that workers
excreted about 8% of inhaled trichloroethylene as trichloroacetic acid in a
ratio of 3:1 (3 mg/liter trichloroacetic acid in the urine to 1 ppm trichloro-
ethylene in the air). This ratio was larger in younger people (6:1) than in
older people (2:1).
Results from two experiments described below indicate there may be a vari-
ation in the urinary excretion of trichloroethylene metabolites depending on
the sex of the subject. More specifically, there may be a sex difference in
human metabolism of trichloroethylene. However, there is not enough evidence
to substantiate this theory.
Nomiyama (1971) exposed five male and five female students for 160 min
to 250 to 380 ppm trichloroethylene. A difference was noted among males and
females in the excretion of trichloroacetic acid and trichloroethanol during
the first 24 hr after exposure. Females excreted more trichloroacetic acid in
their urine than did males, while males excreted twice as much trichloro-
ethanol as females. Of the retained trichloroethylene in males, 32.6% was ex-
creted as trichloroacetic acid and 48.6% as trichloroethanol, whereas in fe-
males, 43.9% of retained trichloroethylene was excreted as trichloroacetic acid
and 42.7% as trichloroethanol.
Similar results were obtained by Kimmerle and Eben (1973). After exposing
eight volunteers (four male and four female) to either 44+4 ppm or 50 + 7
ppm of trichloroethylene for 4 hr, a difference in the amount of excretion
products was noted. Females showed a higher excretion of trichloroacetic acid
in the urine than males. No other differences between sexes in urinary excre-
tion levels or concentrations of .trichloroethylene and trichloroethanol in the
blood were observed.
The amount of trichloroethylene excreted in expired air also varies de-
pending on the sex of the test subject. Stewart et al. (1974a) reported that
females after being exposed to 20, 100, and 200 ppm trichloroethylene had
lower breath concentrations than males exposed to these same concentrations.
5-27
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TABLE 5-8. URINARY EXCRETION OF TRICHLOROACETIC ACID AND TRICHLOROETHANOL
IN FIVE SUBJECTS DURING AND FOLLOWING TRICHLOROETHYLENE
EXPOSURE-'
Ul
i
ro
oo
Metabolite concentrations (mg/l)
Time
1st Exposure day
2nd Exposure day
3rd Exposure day
4th Exposure day
5th Day following last exposure
12th Day following last exposure
Trichloroacetic acid
51 ( 34- 84)
175 (113-238)
229 (148-416)
306 (249-439)
50 ( 35- 61)
8 ( 2- 22)
Trichloroethanol
308 (179-480)
359 (294-480)
399 (296-546)
538 (294-822)
15 ( 10- 18)
14 ( 1- 37)
ji/ Subjects were exposed to 200 ppm trichloroethylene, 7 hr/day for 5 days.
Source: Stewart (1968).
-------
The current tests for exposure to trichloroethylene (including test limits
and usage) were reviewed for NIOSH (Piotrowski, 1977). Several brief European
studies on trichloroethylene determination in human breath and urine are cited
that were not included in the major reviews. Points that are cited from these
secondary references on excretion include:
A report that the urine/alveolar excretion of trichloro-
ethylene was age dependent, varying from a value of 6 in young
subjects to 2 in elderly people, which means high urinary ex-
cretion in the young.
Urinary excretion of 20 mg/liter trichloroacetic acid
was said to correspond to an air concentration of 0.05 mg/
liter of trichloroethylene.
Several reports demonstrated different slopes to the
urinary excretion curve of trichloroethanol after several
days' exposure to trichloroethylene when compared to excre-
tion of the metabolite after only 1 day exposure at the same
air concentration. A steady state is reached after five con-
secutive days' exposure.
Four volunteers inhaled 70 and 140 ppm trichloroethylene for 4 hr during
exercise and at rest. Monster et al. (1976) reported that exercise increased
the quantity inhaled but not the distribution of metabolism. Analysis accounted
for 67% of the dose: 10% unchanged from lungs and 39% trichloroethanol plus
18% trichloroacetic acid in the urine.
Leibman and Ortiz (1977) hypothesized enzymatic pathways through chloral
hydrate by which trichloroethylene would form an epoxide, but they found none
of the vital intermediates to substantiate the hypothesis. Their tests were
run in vitro in incubation mixtures of rat liver microsomes, trichloroethylene,
and an NADPH-generating system.
Ikeda (1977) reports recent metabolic studies using urine samples from
workers exposed to trichloroethylene. The average urinary half-life of the me-
tabolites was 41 hr. In a case of a single subject who frequently abused the
compound, a longer urinary half-life of 73 hr was seen.
Lehnert et al. (1977) performed 6,000 urine analyses on workers chron-
ically exposed to trichloroethylene and other solvents. The metabolite, tri-
chloroacetic acid, rose significantly during the workweek. Dietary factors and
solvent half-life affected the excretion of other solvents in the study.
Additional excretion studies have been conducted on animals since Barret
and Johnston (1939) discovered trichloroacetic acid in the urine of dogs. The
routes of excretion in animals (urine and breath) are similar to man's. No
studies have been conducted on excretion of trichloroethylene and metabolites
5-29
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through the sweat, feces, and saliva. In animals as in man, trichloroethanol
is excreted in larger volumes than trichloroacetic acid or monochloroacetic
acid. In only one animal species did the relative quantity of trichloro-
ethanol and trichloroacetic acid differ from man's; the rabbit excreted 10
times more trichloroethanol than trichloroacetic acid, and about 50 times
less trichloroacetic acid than man (Bartonicek and Soucek, 1959).
Rats were exposed to 50 ppm trichloroethylene (0.267 mg/liter) 5 days/week,
8 hr daily for 14 weeks (Kimmerle and Eben, 1973). A constant excretion of tri-
chloroacetic acid was noted during the experiment, while trichloroethanol in-
creased until the 10th week before slowly decreasing. Urban and Muller (1974)
subjected in vitro perfused rat liver preparations to trichloroethylene as a
vapor or in solution. The rat liver retained about 60% of the trichloroethylene
vapor (50 ppm); of the 30 ppm retained, 58% was metabolized into trichloro-
ethanol, 40% into trichloroacetic acid, and 17o was found to be excreted by the
bile. Friberg et al. (1953) exposed rats to 640, 1,150, and 2,500 ppm for 4
hr, and showed that excretion of trichloroacetic acid increases up to 24 hr,
and then decreases for up to 6 days.
After feeding radioactive (carbon-labeled) trichloroethylene to rats,
Daniel (1963) found that most of the radioactive compounds were excreted in
the urine up to 18 days after exposure. The half-life of expiration was found
to be 5 hr.
Inhalation studies on rats by Forssman and Holmquist (1953) led to the
observation that rats, exposed for 30 to 60 min by inhalation to trichloro-
ethylene with a variance in exposure level of 11,000 to 16,000 ppm, exhaled
32 to 69% of the inhaled quantity. From 21 to 28% of the retained quantity was
excreted as trichloroethanol and 1.2 to 3.9% as trichloroacetic acid. With
higher exposure concentrations, they found that urinary excretion of trichloro-
acetic acid accounted for up to 7.8% of the inhaled solvent dose.
The excretion and half-life of metabolites found in the urine of rabbits
after oral ingestion of trichloroethylene was reported by Ogata and Saeki (1974).
Monochloroacetic acid was found in the urine 5 min after exposure. Its concen-
tration slowly rose and reached a maximal excretion 20 hr after administration.
Trichloroethanol appeared in the urine 30 min after oral ingestion of trichloro-
ethylene and the concentration increased rapidly until maximal excretion was
attained 12 hr after administration. Ogata and Saeki also noted that a large
amount of conjugated trichloroethanol was present as a glucuronide. Conjugated
trichloroethylene appeared in the urine 30 min after oral administration and
reached maximum excretion 15 hr later. Half-life of trichloroethylene metabo-
lites in the urine was as follows: free trichloroethanol, 30.5 hr; conjugated
trichloroethanol, 42.0 hr; monochloroacetic acid, 36.0 hr; and trichloroacetic
acid, 43.5 hr. Table 5-9 summarizes the finding of Ogata and Saeki (1974).
5-30
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TABLE 5-9. TIME REQUIRED FOR METABOLITES TO REACH MAXIMAL AND
HALF-LIFE EXCRETION
''
Trichloroethylene
Chloral hydrate
Free trichloroethanol
Total trichloroethanol
Conjugated trichloroethanol
Monochloroacetic acid
Trichloroacetic acid
Maximum
(hr)
Urine Serum
2.0
2.0
12.0 4.0
15.0s, 4.0
a/
15.0s 4.0
12.0 4.0
20.0s 6.0
Half-life
(hr)
Urine
.
-
30.5
38.0
42.0
36.0
43.5
Serum
3.8
6.4
8.4
8.5
8.5
44.0
18.5
_a/ Calculated.
Source: Ogata and Saeki (1974).
Mathematical models studying the excretion of trichloroethylene and its
metabolites have been proposed (Sato et al., 1977j Fernandez et al., 1975;
1977).
5.1.3 Biochemical Effects
5.1.3.1 Organ/Cell Effects—
Bloxam (1967a) studied the effect of trichloroethylene on perfused rat
liver; at a perfusate concentration of about five times higher than what nor-
mally would be expected in the blood of an anesthetized rat, glucose and urea
output was inhibited. Liver damage was indicated by water gain, loss of intra-
cellular potassium, and inhibition of bile production. Bloxam (1967b) subse-
quently showed that large doses of trichloroethylene decreased membrane func-
tions by causing a loss of amino acids, impairing the ability of the liver
cells to maintain normal concentrations of some amino acids, and increasing
the concentration gradients of branched chain amino acids.
5.1.3.2 Effects on Enzyme Systems—
Trichloroethylene is capable of increasing or decreasing enzyme levels
in man and animals. Friborska (1969) demonstrated that leukocyte alkaline phos-
phatase levels were increased in humans after repeated exposure. An increase
in the acid phosphatase level in the blood was also noted. The investigator
suggested that these results might have been caused by a response to changing
pH of the blood related to glycogen metabolism in the liver, or an increased
capacity to metabolize alcohols.
5-31
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Szulc-Kuberska (1972) conducted biochemical studies on 32 people who were
chronically exposed to trichloroethylene vapors in industry. Disorders of tryp-
tophan metabolism, which suggested a lowered activity of tryptophan pyrolase
and pyridoxine, were observed. Yamaga and Saruta (1953) examined a worker who
had been exposed to vapors for 7 months and found an increase in serum alkaline
phosphatase.
Grandjean et al. (1955) noted possible age differences in metabolism of
trichloroethylene in man. Workers exposed for an 8-hr workday to 1 to 335 ppm
trichloroethylene (usually about 30 ppm) excreted trichloroacetic acid in the
urine at a level of 84 to 87 mg/liter, which accounts for about 13% of the av-
erage trichloroethylene that was inhaled. The young workers excreted metabolite
in almost three times greater quantities than old workers exposed to the same
levels of trichloroethylene.
Heim et al. (1966a, 1966b) conducted two studies on carbohydrate and en-
ergy metabolism in white mice. The first study examined the carbohydrate and
energy metabolism in the brain, while the second study was concerned with liver
carbohydrate and energy metabolism. Mice were exposed in both experiments to
1.8 vol 7o trichloroethylene for 30 to 60 min. An extreme drop in the body tem-
perature of the mice (38.3 to 25.3°C) occurred. Increases in glucose and
glucose-6-phosphate and decreases in fructose diphosphate, dihydroxyacetone
phosphate, and pyruvate content were considered to be signs of reduced glycoly-
sis in the brain. The glycogen, glucose, fructose diphosphate, dihydroxyace-
tone phosphate, and lactate levels of the mice livers fell, while glucose-6-
phosphate and pyruvate levels were not significantly changed. Adenosine
diphosphate (ADP), adenosine monophosphate (AMP), and creatine phosphate were
also reduced, whereas adenosine triphosphate (ATP) increased. While other
possible causes for these test results could be hypothesized, such as body
temperature effects, the data are also consistent with a disruption of inter-
mediary metabolism in the liver.
Leibman and McAllister (1967) demonstrated that the conversion from tri-
chloroethylene to chloral hydrate could be increased in rat liver preparations.
Approximately 2% (v/v) trichloroethylene was administered to rats for periods
from 15 min to 2 hr. At this concentration the activities of liver microsomal
drug-oxidizing enzyme systems are enhanced by pretreatment with trichloro-
ethylene.
Reductions in the activity of the redox enzymes in the liver and to a
lesser degree in the kidneys were found by Kiseleva and Korolenko (1971) during
the first 24 hr after an anesthetic dose of trichloroethylene (30 min) to rats.
Losses of the enzymes from the peripheral regions of liver lobules and proxi-
mal kidney tubules were also observed. However, the enzymatic functions had
returned to normal 15 days after the single exposure.
5-32
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Rabbits that had been injected with 8.75 to 9 ml/kg (total dose) of
trichloroethylene showed decreased activities of the following enzymes in the
lenses of the eyes: aldolase, glutamic-pyruvic transaminase, glucose-6-
phosphate dehydrogenase, lactic dehydrogenase, and hexokinase. Trichloro-
ethylene elevated the levels of two enzymes in the eye lens of rabbits (Savic
and Hockwin, 1969).
Mazza and Brancaccio (1967) reported that trichloroethylene had a stimu-
latory action on the adrenals from 12 rabbits that had inhaled approximately
2,800 ppm intermittently for over 1,000 hr in 6 weeks. A small increase in
plasma and urinary adrenocortical and adrenomedullary hormones was found,
along with a moderate increase of 3-methoxy-4-hydroxymandelic acid excretion.
Ungar (1965) indicated that trichloroethylene inhibits the brain protease
in the rat brain cortex in vivo. In a study on rats designed to look for the
mechanism of the neurotoxic effects of some solvents, Savolainen (1978) found
that low levels of pure trichloroethylene had little effect on brain lysosomes.
5.1.3.3 Histologic and Pathologic Effects —
A histological study was performed on a worker who suddenly died at work,
apparently from trichloroethylene addiction. Tissue from the liver, lung, heart,
kidney, and brain were examined. Fatty degeneration of the liver and lung hemor-
rhages were noted while the heart, kidney, and brain tissues appeared normal.
Adams et al. (1951) examined the vapor toxicity of trichloroethylene ex-
posures on animals. Histopathological examinations for organic damage were
conducted and recorded. The examinations indicated no histologic effects had
occurred except a slight increase in liver weight of rabbits exposed to 400
ppm, 7 hr/day, 7 days/week for 161 exposures. Adams et al. noted that in ani-
mals no histologic or pathologic effects are observed when the concentrations
of trichloroethylene drop below 3,000 ppm. The grade of material used was 98
to 99.7% pure; the impurities were not identified, but they were not carbon
tetrachloride, ethylene dichloride, tetrachloroethane, perchloroethylene, or
chloroform.
A similar study using the highest purity trichloroethylene available was
conducted by Prendergast et al. (1967). Rats (either Long-Evans or Sprague-
Dawley), Hartley guinea pigs, squirrel monkeys, New Zealand albino rabbits,
and beagle dogs were exposed to either 730 ppm, 8 hr/day, 5 days/week for 6
weeks or to 35 ppm for 90 days continuously. No histopathologic effects were
noted in the group of animals exposed to the latter concentrations; however,
in the former exposure, all animals did show nonspecific inflammation of the
lungs, but it could not be attributed to the exposure.
Wirtschafter and Cronyn (1964) administered subcutaneously (one time only)
0.004 moles/kg (0.5 g/kg) trichloroethylene to rats (Long-Evans strain). Nec-
ropsies were performed at 2, 4, 8, 16, 20, 24, 30, 36, 42, 48, 72, 96, 120,
5-33
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and 168 hr. Mild degenerative changes were found in the hematoxylin and eosin
sections of the livers after 12 hr. However, the liver parenchyma changed back
to normal 12 hr later. The only other notable change was a clumping or granu-
larity in the cytoplasm around the central veins. Ramadan and Ramadan (1969)
exposed rats to anesthetic levels of trichloroethylene, and found no hepatic
parenchymal changes during histochemical examination. None or only slight histo-
logically detectable fatty infiltration of the liver was observed in rats given
a single 4-hr exposure of 6,400 ppm trichloroethylene (Kylin et al., 1962).
Barrett et al. (1938) exposed guinea pigs to 1,200 ppm of commercial grade
trichloroethylene for 7 hr/day, 5 days/week (over 1,100 hr of exposure); no
changes were noted in the lungs, spleen, kidneys, heart, adrenals, or brain.
Mild degenerative changes were noted in the liver.
Herzberg (1934) examined three dogs for histologic changes after exposure
to trichloroethylene (no time or dosage given). The following tissues were ex-
amined: lung, spleen, pancreas, kidney, adrenals, heart muscle, diaphragm,
and pectoral muscle; comparison to controls indicated no marked changes in
these tissues.
5.1.4 Toxicology Data
5.1.4.1 Target Organs —
5.1.4.1.1 Central nervous system—The major effect of trichloroethylene
is on the central nervous system (CNS) (Quadland, 1944). Trichloroethylene
poisoning is characterized by dizziness, nausea, sleepiness, impairment of
behavior, unconsciousness, and death. Irish (1962) stated that trichloro-
ethylene depresses all functions of the central nervous system in decreasing
order from the cortex to the medulla. In most cases the detrimental effects
usually disappear within a few weeks if no further contact occurs.
Buxton and Hayward (1967) described four cases of industrial accidents
which involved trichloroethylene.^Four workers were required to climb inside
tanks containing trichloroethylene and scoop the remaining liquid out with
buckets. All four workers became ill and one subsequently died. The only symp-
toms of trichloroethylene intoxication noted in two of the four men (who spent
less than 30 min inside the tanks) were nausea and headaches. The symptoms ob-
served in the third man who remained inside the tanks for 2-1/2 hr were nausea,
diplopia, and facial diplegia. The fourth man, exposed to trichloroethylene
vapors for the longest time period, died after developing severe multiple cra-
nial nerve palsies 51 days after initial exposure.
A death caused by central .nervous system effects was reported by St. Hill
(1966). A man was exposed to trichloroethylene while bailing out tanks in a
ship's hold, which was filled with condensate from the ship's steam supply.
The ship's condenser had recently been cleaned with trichloroethylene. After
working at this task for over 20 hr, the worker complained of dizziness,
5-34
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headaches, double vision and paralysis of the neck. The paralysis became severe
and within a few weeks the man died. Another worker involved in the incident
complained of weakness and numbness of the face which lasted several months.
Longley and Jones (1963) reported an incident in which two painters be-
came unconscious after reentering an enclosed tank. Both men became comatose
after breathing trichloroethylene vapor fumes from the paint mixture. The
paint contained at least 75% trichloroethylene and was thinned with an equal
amount of thinner containing 98% trichloroethylene. The men regained con-
sciousness a few hours after being pulled from the tank. From this incident,
it was" estimated that a concentration of 3,000 ppm for 10 min would be suffi-
cient to cause unconsciousness.
Six women employed in the cleaning of optical lenses for binoculars used
their fingers to apply trichloroethylene for removal of small spots of wax re-
maining on the lenses. They reported difficulty in the handling of the lenses
because of an inability to feel the lenses properly. Examination showed per-
sistent loss of tactile sense, inability to grasp objects between thumb and
fingers, and loss of motion (McBirney, 1954).
Malaof (1949) reports a worker who, after entering a freshly drained de-
greasing tank, became comatose and had to be treated for first, second, and
third degree chemical burns. Upon awakening, the worker complained of blurred
and double vision. The total recovery period was 31 days.
A man employed as a metal degreaser lost his sense of smell and later de-
veloped trigeminal analgesia (Mitchell and Parsons-Smith, 1969). Boulton and
Sweet (1960) reported that 24 people who received trichloroethylene as an an-
esthetic developed trigeminal palsies. However, it was suggested by the in-
vestigators that the palsy probably resulted from dichloroacetylene which
would have been formed from passing trichloroethylene through soda lime.
Other nervous system effects have been reported in the literature. Borch
(1973) reported neurologic disturbances. Sagawa et al. (1973) discovered trans-
verse lesions of the spinal cord. Szulc-Kuberska (1972) reported perceptive
deafness with labyrinthine disorders and impairment of hearing (Szulc-Kuberska
et al., 1976). Mazza and Cascini (1956) reported an increase in reflex activ-
ity and hypotension. Grandjean et al. (1955) found autonomic nervous system
disorders and neurologic psychiatric symptoms in 73 workers exposed to tri-
chloroethylene vapors. Brancaccio et al. (1966) reported toxic changes in the
CNS and autonomic systems in 80 workers exposed to trichloroethylene in the
dry cleaning industry. Encephalitis was reported in a person who died from
trichloroethylene poisoning (Kossakiewica-Sulkonska, 1971). Matruchot (1939)
reported mental disorders after trichloroethylene exposure, and several papers
report changes found in electroencephalograms (EEGs) of workers exposed to
trichloroethylene (Mellerio, 1969; Konietzko et al., 1973; Roth and Klimkova-
Deutschova, 1963).
5-35
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Rats exposed to 7.9 jumole/liter (200 ppm) trichloroethylene for 6 hr/day
for 4 days were more active than controls in an open field test 1 hr after the
4th day of exposure. The effect was still detectable 17 hr after exposure
ceased. After 5 days exposure, the animals were killed and brain RNA was found
to be significantly decreased, compared to control levels (Savolainen et al.,
1977).
5.1.4.1.2 Liver—Trichloroethylene has been shown to cause hepatic necro-
sis in man following either inhalation or ingestion (Priest and Horn, 1965;
Ossenberg et al., 1972; Chilsura and Gorsi, 1961). However, liver damage does
not always occur in trichloroethylene intoxication. Most occupational studies
on man find an increase in serum transaminases, which indicates damage to the
liver parenchyma (Albahary et al., 1959; Tolot et al., 1964; Lachinit, 1971).
These increases are transient and usually disappear after exposure is termi-
nated.
Toxic hepatitis was observed in a patient who had been cleaning a tank
in which trichloroethylene was used to clean machine parts. Evidence of liver
damage was based on rising serum glutamic-oxalacetic transaminase (SCOT), serum
glut'amic-pyruvic transaminase (SGPT), and lactic dehydrogenase (LDH) levels
(Bauer and Rabens, 1974). These levels returned to normal 6 weeks later.
Kanetaka and Oda (1973) reviewed 88 cases of liver injury caused by organic
solvent or drugs. Liver biopsy and/or autopsy were conducted on these 88 cases.
Only one of the 88 was induced by trichloroethylene poisoning. The examination
showed centrilobular fatty liver and slight pericellular fibrosis in the centri-
lobular and peri portal areas.
Secchi et al. (1968) discovered that two of seven people orally poisoned
by trichloroethylene developed acute liver disease. Analysis of the samples
of the solvents responsible for the poisonings showed that many of the samples
were contaminated with impurities. Liver damage occurred only in those people
who ingested impure trichloroethylene. No liver damage was noted in those peo-
ple who ingested pure trichloroethylene.
Milby (1968) reported a case of chronic trichloroethylene intoxication
of a 39-year-old female employed as a paint-stripping operator. She showed no
signs of liver injury even though she daily complained of nausea and vomiting,
drunkenness, abdominal cramps, flushing, and swelling of the eyes, face, and
hands. Her physician observed an abnormal electrocardiogram and excretion of
780 mg trichloroacetic acid per liter in her urine.
Eight workers were acutely exposed to trichloroethylene in an electro-
plating plant. The concentrations ranged from 115 to 384 ppm. Predominant symp-
toms were headaches, muscle and joint pains, neurological manifestations and
narcosis. All eight subjects showed an increase in X-globulin fraction and a
decreased albumin fraction. It was concluded that liver damage was present as
5-36
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indicated by the cephalin cholestrol flocculation test (CCF) and hyperglobu-
linemia observations (Nomura, 1962).
Guyotjeannin et al. (1958) reported that 18 workers regularly exposed to
trichloroethylene showed signs of liver toxicity characterized by abnormal
cephalin flocculation, total lipids and unsaturated fatty acids. There was
also an increase in P- and \-globulins.
Joron et al. (1955) found massive liver necrosis in a patient exposed to
trichloroethylene vapors. The patient died more than 1 month after the last
known exposure to the trichloroethylene. The last dose received was estimated
to be several hundred parts per million.
Cotter (1950) examined 10 humans who were exposed to trichloroethylene
vapors arising from a spill on board a ship. Cotter suggested that liver dam-
age was present because of a changing globulin level despite absence of biliru-
bin or phosphatase retention or a disturbance of the esterification of serum
cholesterol. A full recovery of the subjects was noted within 2 months.
It was noted that children are highly susceptible to trichloroethylene
liver pathology when compared to adult susceptibility (Kusch et al., 1976).
In a brief report in the Russian literature of a sizable experimental pop-
ulation, Kalashnikova et al. (1976) correlated biochemical (liver) signs and
excretion of trichloroethylene metabolites in 35 experimentally exposed humans
with 35 controls. Individual variability in metabolites occurred.
Animal studies show that trichloroethylene may have a hepatotoxic effect
on the liver. Gehring (1968) indicated that there were no glutamic-pyruvic trans-
aminase (SGPT) increases in rats exposed to single exposures of trichloroethylene
(5,500 ppm). Adams et al. (1951) exposed rabbits, guinea pigs, rats, and monkeys
to 100 to 400 ppm trichloroethylene, 7 hr/day for 132 to 178 exposure periods
and only observed increases in liver and kidney weights. Kylin et al. (1962;
1963; 1965; 1967) studied short-term and long-term exposures of trichloro-
ethylene (< 0.2% impurities) on mice and found that even exposures as high as
6,400 ppm produced only slight fatty liver degeneration.
In contrast to these findings, Seifter (1944) observed degeneration of
liver parenchyma cells in dogs exposed to either 740 ppm trichloroethylene 8
hr/day, 6 days/week for 3 weeks, or 500 to 750 ppm trichloroethylene 6 hr/day,
5 days/week for 8 weeks. It has been suggested that, since the purity of the
trichloroethylene used in these experiments was not known, the results of this
experiment are difficult to evaluate.
Laib et al. (1978) exposed adult female rats to 2,000 ppm trichloroethylene
8 hr/day, 5 days/week for 3 months, and quantitated the presence or focal loss
of two enzymes in the liver: glucose-6-phosphatase and nucleosid-tri-phosphatase.
5-37
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There was no loss of enzymes due to trichloroethylene. The authors suggest
that this means no carcinogenic change occurs, but the in vitro test used is
not standardly accepted as a definitive measure of a chemical's oncogenicity.
Potentiation of hepatotoxic effects of trichloroethylene by drugs such
as phenobarbital, 3-methylcholanthrene, chlorinated biphenyls, hexachloro-
benzene, and pregnenolone-16-a-carbonitrile are known. Pretreatment with one
of these drugs before inhalation can induce components of the liver mixed-
function oxidase system, thereby causing a higher incidence of liver damage
(Carlson, 1974; Reynolds, 1976).
Different components of the drug metabolizing enzymes in rats were stimu-
lated by five different inducers; then anesthesia was induced with trichloro-
ethylene (1% for 2 hr) (Moslen et al., 1977a; 1977b). Acute liver toxicity was
increased 20-fold over uninduced rats exposed to trichloroethylene which indi-
cated the hepatotoxicity was related to metabolites formed by the hepatic mixed
function oxidase system.
Allemand et al. (1978) has recently described experimental results that
may help clarify the mechanism of trichloroethylene!s liver effects. After ad-
ministration of ^C-labeled trichloroethylene to rats, a metabolite became ir-
reversibly bound to the liver microsomal proteins while little was bound to
muscle protein. Trichloroethylene is metabolized by the microsomal mixed func-
tion oxidase system; when these enzymes were induced, more radioactive material
became irreversibly bound, and when the enzymes were depressed, less radioac-
tive material bound the liver. Allemand et al. concluded that the data indicate
trichloroethylene was metabolized by liver microsomes to a chemically reactive
metabolite which reacted irreversibly with liver protein. Tissue necrosis may
result from such irreversible binding to tissue macromolecules.
5.1.4.1.3 Kidney—Toxic effects of trichloroethylene on the urinary sys-
tem in man are not well defined. Only a few incidences of renal damage due to
trichloroethylene intoxication have been reported.
Acute hepatic and renal damage was reported in two patients, and in a
third patient centrilobular hepatic necrosis was found (Baerg and Kimberg,
1970). These effects were attributed to sniffing of Carbona cleaning fluid,
which is 44 to 70% trichloroethylene by volume, but which also contains car-
bon tetrachloride (Hunter, 1975).
Gutch et al. (1965) reported that a needle biopsy test showed acute tubu-
lar degenerative changes in the kidney of a 41-year-old man who inhaled tri-
chloroethylene vapors. The man had been replacing asphalt floor tile in a small,
enclosed room (10 by 20 ft) with only a small ventilation opening in one window.
Trichloroethylene (99.5% pure) was used as a solvent to clean up tile cement.
A gallon container of trichloroethylene remained open during the cleaning op-
erations which lasted over 2 hr. After leaving work, the man complained of
5-38
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headaches, shortness of breath, and vomiting. He admitted himself to a hospital
5 days later and was diagnosed as having acute renal failure. Kidney function
returned to normal after 5 weeks' rest. A case of acute renal failure after
oral ingestion was reported by Kleinfeld and Tabershaw (1954). A patient who
had ingested liquid trichloroethylene developed jaundice and oliguria and died
as a result of acute renal failure.
Conflicting reports which may indicate evidence of renal damage resulting
from trichloroethylene poisoning in animals are present in the literature for
both inhalation and parenteral studies. Inhalation experiments in animals show
that high acute concentrations of trichloroethylene may have caused nephrotox-
icity, while in lower chronic doses no damage to the renal system was noted.
Kidney damage was observed in rats (maintained on a high protein diet) exposed
to 5 mg/liter (935 ppm) trichloroethylene, 5 hr/day for 7 days (Kalashnikova
et al., 1974). Investigators observed focal dystrophic changes in the renal
tubule epithelium. No abnormal signs of kidney toxicity were noted, however,
by Nowill et al. (1954) in animals (rats, rabbits, and dogs) exposed to 0.05
to 0.1% by volume trichloroethylene. A long-term inhalation study on rats,
guinea pigs, dogs, rabbits, and monkeys by Prendergast et al. (1967) showed
that no nephrotoxicity occurred at continuous concentrations of 35 ppm for 90
days and 730 ppm for 8 hr/day, 5 days/week for 6 weeks.
Plaa and Larson (1965) found that after injecting mice intraperitoneally
with 0.6 ml/kg of trichloroethylene, no renal toxicity was observed. However,
renal failure in rabbits attributed to trichloroethylene poisoning resulted
in death (Bartonicek and Soucek, 1959). They injected parenterally from 33
to 55 g of trichloroethylene into six rabbits over a period of 55 to 100 days.
Two of the rabbits died from renal failure.
5.1.4.1.4 Lungs—Few studies have been conducted on the toxic effects
of trichloroethylene on the lungs of man and animals. The most common toxic
effects of trichloroethylene in the lungs are tachypnea, congestive atelecta-
sis, and bronchoconstriction. Defalque (1961) stated in his review on tri-
chloroethylene that tachypnea has been observed for a long time in humans,
but its significance is still undetermined. Meyer (1973) and Jougland and
Vincent (1971) reported that congestive atelectasis occurred in workers ex-
posed to trichloroethylene. Congestive atelectasis also occurred in people
who accidentally drank trichloroethylene (Jougland and Vincent, 1971).
Bianchi et al. (1963) stated that trichloroethylene causes bronchoconstric-
tion and interferes with the cough reflex. Teare (1948) described the case of
a 16-year-old "addict" who died from acute pulmonary edema after inhaling tri-
chloroethylene. Seage and Burns (1971) reported another case of pulmonary
edema following exposure to trichloroethylene and subsequent ingestion of
ethanol.
5-39
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In animal studies, trichloroethylene's toxic effects upon respiration
are brought about by a combination of central nervous system depression as
well as direct effects on the lung itself (Aviado et al., 1976). In an exper-
iment with cats, trichloroethylene reduced the vasoconstrictor action of hy-
poxia (Sykes et al., 1972).
5.1.4.1.5 Heart—Cardiac arrhythmia is the most frequent effect of tri-
chloroethylene on the heart. The most direct proof that trichloroethylene can
cause ventricular fibrillation and cardiac arrest is that these changes can
be demonstrated in electrocardiograms (ECGs) of subjects who have accidentally
ingested the material trichloroethylene. There are also reports of
trichloroethylene-related deaths occurring which were due to ventricular
fibrillation.
Trichloroethylene is believed to sensitize the heart to epinephrine, re-
sulting in ventricular fibrillation; thus, any form of stress would help in-
duce cardiac sensitization. Anesthetic concentrations of trichloroethylene
have been shown to cause changes in the EGG indicating tachycardia and ar-
rhythmias. The EGG changes that occur during trichloroethylene anesthesia in
man usually cease when exposure is terminated.
Konietzko and Elster (1973) recorded a case of increased ventricular
extrasystoles caused by trichloroethylene intoxication in a man who had no
history of heart ailments before initial exposure to the vapor.
Radonov et al. (1973) reviewed the cases of 200,000 women given trichloro-
ethylene as an analgesic during therapeutic abortions. Seven deaths occurred;
the deaths were attributed to cardiac arrest.
Starodubtsev and Ershova (1976) successfully used trichloroethylene-air
anesthesia in 128 cases of dental surgery in all three levels of stage 1 an-
esthesia. The electrocardiograms showed no apparent toxicity. Soboleva et al.
(1976) used trichloroethylene analysis in 208 patients undergoing maxillofacial
surgery in Moscow, and concluded that the cardiovascular changes were insignifi-
cant and rapidly reversible. Morreale (1975), on the other hand, reported one
56-year-old patient who drank 15 ml trichloroethylene and, along with neural
intoxication, suffered a myocardial infarct which was attributed to the tri-
chloroethylene.
The potential toxicity of deep trichloroethylene anesthesia was contrasted
with the relative cardiac safety of light anesthetic levels by Gundy (1976). He
reported a personal observation of ventricular fibrillation in a 3-year-old who
was simultaneously receiving a dilute adrenalin solution. The synergism that
exists between trichloroethylene and the adrenergic hormones released in vivo
(or administered as drugs) was discussed.
Tomasini (1976) reviewed Italian case histories of trichloroethylene-
related toxicity. In about one-fourth of a group of 35 patients, myocardial
5-40
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arrhythmia of some degree had occurred after trichloroethylene exposure. Ac-
cidental, intentional, and industrial exposures were included in the population.
Trichloroethylene levels that produced the fatalities ranged from oral introduc-
tion of 50 cc pure trichloroethylene in a 21-year-old male to a "pitcher" of
Trilene® in a 38-year-old female. The previous cardiac status of the industrial
workers was not described, nor was quantitation reported on levels of trichloro-
ethylene producing cardiac effects. The author suggested that the mechanism of
cardiotoxicity was depression of normal nodal rhythm which permitted any other
ectopic foci present to break the normal myocardial rhythm. The fact was stated
that trichloroethylene as sold is sometimes a mixture of several chlorinated
solvents. The relationship, if any, of specific Italian additives to the cardiac
effects described was not further developed. Canfora et al. (1976) reported case
histories of eight trichloroethylene-exposed patients from another Italian city--
four of which had cardiac arrhythmias.
In another report, electrocardiographic abnormalities were seen in 15 of
30 patients exposed acutely to high levels of trichloroethylene. Arrhythmia
was the most frequent side effect (Pelka and Markiewicz, 1977).
Barni et al. (1968) suggest that two workers employed by a dry cleaning
establishment died suddenly from cardiac failure after chronic exposure to
trichloroethylene, and Vyskocil and Polak (1963) report a death due to primary
cardiac failure from acute trichloroethylene poisoning.
Four deaths were reported by Kleinfeld and Tabershaw (1954) from acute
overexposure to trichloroethylene. Exposure concentrations were unknown for
three of the four cases. However, in one case, the concentrations which were
measured after the incident occurred fluctuated from as low as 200 ppm to as
high as 8,000 ppm. All four workers continued to work at their jobs even though
they complained of nausea and vomiting, drowsiness, and dizziness. They all
died within a few hours after leaving the plant. The mechanism of death was
considered to be ventricular fibrillation.
Bernstine (1954) stated that a 19-year-old marine who underwent trichloro-
ethylene anesthesia suffered cardiac arrest (due to an excessive concentration
of trichloroethylene in the body), but subsequently recovered.
An operator of dry cleaning equipment died of ventricular fibrillation
after coming into contact during the day with exceedingly high concentrations
of trichloroethylene estimated at 4,500 ppm (Bell, 1951).
Animal studies have shown that trichloroethylene causes depression in the
myocardial contractility (Aviado et al., 1976). The minimum inhaled concentra-
tion of 500 ppm caused a depression in the myocardial contractility in dogs.
Transitory arrythmia was observed in the isolated guinea pig heart at a con-
centration of 5,300 ppm.
5-41
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5.1.4.2 Dose-Response—
NIOSH (1977) has compiled dose-response data for trichloroethylene. Table
5-10 is representative of the lowest published doses or concentrations in the
literature.
Dose-response data have been divided into three categories: acute, sub-
acute, and chronic. Defining the time limit for these three parameters is dif-
ficult. A chronic time limit for an animal such as a rat would be considerably
less (in comparison) than the chronic time limit for man. Therefore, a general
grouping of all organisms into a specified time category was established as
follows:
* Acute - Exposure to vapors for 1 day or less, or one injection.
* Subacute - Exposure to vapors or injections for 2 to 90 days.
* Chronic - Exposure to vapors or injections for more than 90 days.
5.1.4.2.1 Acute effects —
5.1.4.2.1.1 Man—A 31-year-old male died approximately 15 hr after
his last known exposure to trichloroethylene (James, 1963). The subject had a
history of trichloroethylene abuse and was known to volunteer to clean tri-
chloroethylene vats which had recently been drained. After one such cleaning
episode he became lethargic. The next day he returned to work but died while
engaging in light physical work.
A 22-year-old lapsed into unconsciousness after drinking approxi-
mately 140 ml of cleaning fluid containing trichloroethylene. He remained coma-
tose for over 24 hr before regaining consciousness. The subject exhibited other
signs of trichloroethylene poisoning—weak reflex responses, paleness, and
intermittent tachycardia (Stentiford and Logan, 1956).
Armstrong (1948) conducted trichloroethylene anesthetic experiments
on 35 patients (ages 18 to 36) checking for liver damage. Anesthesia lasted
from 20 to 95 min (40-min averages). Armstrong demonstrated that 34 out of 35
people showed evidence of transient liver impairment.
Blondal and Fagerlund (1963) investigated the effects of trichloro-
ethylene on hepatic function in order to ascertain whether liver damage could
be detected by abnormal enzyme concentrations. They administered up to 1.3
vol % trichloroethylene by anesthesia machine for 45 min to 36 patients (se-
lected at random), all of whom underwent extraabdominal operations. No liver
damage was observed as shown by normal glutamic acid-pyruvic acid-transaminase
(GPT) and lactic dehydrogenase (LDH) levels.
Stewart et al. (1962) conducted two experiments on seven human sub-
jects at varying concentrations of trichloroethylene vapors. In the first
5-42
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TABLE 5-10. TOXIC EFFECTS OF TRICHLOROETHYLENE ON MAN AND ANIMALS
Species
Human
Human
Human
Human
Rat
Rat
Mouse
Mouse
Mouse
Dog
Dog
Dog
Rabbit
Rabbit
Route
Oral
Inhalation
Inhalation
Inhalation
Oral
Inhalation
Oral
Inhalation
Intravenous
Oral
Intraperitoneal
Intravenous
Inhalation
Subcutaneous
Dose
857 mg/kg
3,000 ppm/lOM
160 ppm/83M
27-81 ppm/4H
4,920 mg/kg
8,000 ppm/4H
351 gm/kg/78WI
3,000 ppm/2H
34 mg/kg
5,860 mg/kg
1,900 mg/kg
150 mg/kg
11,000 ppm
1,800 mg/kg
Effect
LDLo
LCLo
TCLo TFX:CNS
TCLo TFX*
^50
LDLo
TDLo TFX: CAR
LCLo
^50
LDLo
LD50
LDLo
LCLo
LDLo
Key to abbreviations:
LDLo—lowest published lethal dose
LCLo—lowest published lethal concentration
TCLo--lowest published toxic concentration
TDLo—lowest published toxic dose
LD50--lethal dose 50% kill
H--hour
M—minutes
WI--weeks, intermittent dosage
CNS—central nervous system
CAR--cancer
TFX--toxic effects
TFX* = eye irritation 27 ppm, headache 81 ppm
Source: NIOSH (1977); Nomiyama and Nomiyama (1977)
5-43
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experiment, the subjects were exposed to between 160 to 400 ppm (265 ppra time-
weighted average) for a period of 83 min. In the second experiment, subjects
were exposed to between 172 and 332 ppm (211 ppm time-weighted average) for
a period of 190 min. Subjective and physiological responses were recorded as
follows:
* 160 ppm - transient, mild eye irritation in three out of seven
volunteers.
* 160 to 250 ppm - noticeable odor but not unpleasant, no lighthead-
edness, and Romberg's sign and head-to-toe tests normal. (Romberg's
sign involves standing, feet together, eyes closed, arms at sides,
with no movement.)
* 350 to 400 ppm - lightheadedness in two of seven volunteers,
Romberg's tests were normal, no eye irritation, and no unpleasant
odors.
An unusually high concentration of trichloroethylene was administered
to 12 volunteers by Kylin et al. (1967) to study the effects on the CNS, using
optokinetic nystagmus tests. Each subject was exposed to 1,000 ppm trichloro-
ethylene for 2 hr and then tested. A lowering of the fusion limit was observed
in the volunteers. A more marked decrease in this limit was noted in two volun-
teers who also consumed alcohol during these tests.
Manual dexterity tests (Crawford Small Parts Dexterity Test), card
sorting and dial display were conducted on human subjects by Stopps and
McLaughlin (1967). The purpose of the tests was to measure the changes in
psychophysiological functions of subjects exposed to differing concentrations
of trichloroethylene (100, 200, 300, and 500 ppm) for 2.75 hr. No effect was
noted in the 100-ppm tests. In the 200-ppm study there was a slight decline
in the performance tests, with a greater decline in the 300- and 500-ppm tests.
Another psychophysiological test was conducted on eight male volun-
teers by Vernon and Ferguson (1969). Investigators subjected the volunteers to
a 2-hr exposure of trichloroethylene at levels of 0, 100, 300, and 1,000 ppm.
The only significant decrease in performance was noted at the 1,000-ppm level.
The only other noticeable effect was that one volunteer complained of light-
headedness and dizziness after he was exposed to 300 ppm.
Behavior tests (Wechsler Memory Scale, manual dexterity test, com-
plex reaction time test, and perception test with a tachistoscope) were per-
formed by Salvini et al. (1971) on students (110 ppm for two 4-hr exposures,
separated by a 1.5-hr lunch interval). Increasing concentration decreased the
performance efficiency. The authors suggested that 110 ppm is probably the
concentration at which behavioral effects can be noted in humans.
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Stewart et al. (1973) repeated the tests and procedures conducted
by Salvini et al. (1971). Stewart's group exposed three groups of three humans
to either 0, 50, or 110 ppm trichloroethylene for 8 hr. They found that two of
the nine subjects exposed to 110 ppm had low coordination test scores, indi-
cating a CNS-depressant effect by trichloroethylene. However, Stewart et al.
concluded that the high variability among subjects meant that more subjects
were needed before reliable results could be obtained.
A battery of psychological performance tests was given to 168 work-
ers exposed to various common industrial solvents such as trichloroethylene,
perchloroethylene, toluene, etc., and their mixtures (Lindstrom, 1973). These
results were compared with similar tests given to an unexposed control group
of 50 people. The psychological performances of the group exposed to the com-
mon industrial solvents were inferior to those of the control group. For the
exposed group, accuracy in visual perception and left-hand performance in the
dexterity tests were more disturbed, the sensorimotor speed was significantly
slower, motor patterns were enlarged, and disturbances in psychomotor control
were noted (Table 5-11).
Konietzko et al. (1975) also studied the effects of low concentrations
of trichloroethylene on neuro-responses. Psychomotor function in 20 subjects
exposed to trichloroethylene (95 ppm, 4 hr) was tested. No significant impair-
ment of psychomotor behavior was observed.
Ettma et al. (1975) subjected 47 male volunteers to 150 and 300 ppm
trichloroethylene for 2-1/2 hr. They measured a number of performance and
physiological parameters, and found that these exposure levels probably had
a borderline effect on performance and mental capacity.
Gamberale et al. (1976) tested psychological function three times
in 15 healthy males who had been exposed in a random design method to 540,
1,080, or 0 mg/m^ of trichloroethylene for 70-min periods. Reaction time and
short-term memory were not affected, but a statistically significant (p < 0.05)
drop in performance on mathematics trials occurred. The authors suggested cau-
tion in interpreting these data, because the test showing effect had the larg-
est individual variation and a significant learning effect (p < 0.001) occurred
on repeated testing.
o
Triebig et al. (1976; 1977) exposed eight persons to 260 mg/m (50
ppm) trichloroethylene during a simulated workday, 5 days a week, for 6 weeks.
Effects of long-term trichloroethylene exposure on the CNS were demonstrated
by results of a battery of psychological tests. Although blood levels and
urine examination showed uptakes of trichloroethylene, there was no sign of
alteration of the CNS. There were large individual variations in uptake and
metabolism of trichloroethylene. The authors suggest that reports on experi-
mental human exposure should carefully differentiate between results obtained
5-45
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TABLE 5-11. COMPARISON OF PSYCHOLOGICAL PERFORMANCE TESTS BETWEEN
SOLVENT-EXPOSED GROUPS AND CONTROLS
Test
INTELLIGENCE
(Wechsler Adult Intelligence
Scale: similarities, picture
completion, digit symbol)
OTHER ABILITIES
(Boardon-Wiersma vigilance)
(Santa Ana dexterity test)
PERSONALITY
(Rorschach ink blot test: re-
sponse number and time)
PSYCHOMOTOR BEHAVIOR
(Mira test: five measures of
extension and motor distur-
bance)
Behavioral
subtests
1 Sim
2 PC
3 D Sy
4 BW,
5 SA,
6 SA,
7 SA,
8 Ro,
9 Ro,
10 Mi
11 Mi
12 Mi
13 Mi
14 Mi
speed
right
left
coord.
R. #
R. time
1
2
3
4
5
Exposed
group
Mean SDl/
14.
13.
36.
32.
45.
43.
29.
2.
3.
3.
3.
2.
2.
2.
6
5
5
0
4
5
6
6
0
4
2
9
9
9
5
3
12
6
7
6
6
1
1
1
0
1
1
1
.8
.4
.4
.7
.3
.1
.4
.3
.3
.0
.0
.2
.0
.0
Control
Mean
15
15
37
34
49
48
30
3
3
3
2
3
3
3
.5
.5
.3
.9
.4
.2
.5
.1
.1
.0
.7
.4
.3
.2
SD p2/
4
2
9
5
6
6
6
1
1
1
1
1
1
1
.4
.3
.7
.9
.8
.4
.2
.3
.3
.0
.0
.0
.1
.0
NS
0.001
NS
0.01
0.01
0.001
NS
NS
NS
0.01
0.001
0.01
0.01
0.05
a/ SD denotes standard deviation.
b/ Two-tailed risk level as assessed by Student's test.
or, P value, level higher than 0.05.
Source: Lindstrom (1973).
NS denotes risk
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with acute, short-term, and chronic exposure, because their data indicate that
uptake may vary in individuals with length of exposure.
Acute exposure to 0, 27, 81, or 201 ppm (1 to 24 hr) did not change
two-point discrimination or perception of flicker rate in 12 volunteer students
(Nomiyama and Nomiyama, 1977). Further, the level of exposure did not change
the profile of metabolites in these experiments.
5.1.4.2.1.2 Mice — The LD^QQ ^or mice f°r a 2-hr vapor exposure was
reported to be between 7,475 and 8,410 ppm, while the narcotic dose (uncon-
sciousness) was 4,670 ppm (Lazarew, 1929).
Cresutelli (1933; cited by Aviado, 1976) reported the following re-
sults for mice exposed to acute concentrations of trichloroethylene.
* ~ 3,290 ppm for 2.5 hr; death 1 hr after exposure;
* ~ 8,770 ppm for 1.4 hr; death 110 min after exposure; and
* ~ 9,345 ppm for 1.2 hr; death 67 min after exposure.
Friberg et al. (1953) calculated an LD^Q of 8,450 ppm trichloro-
ethylene for mice exposed for 4 hr. Gehring (1968) found the 11)50 in female
Swiss-Webster mice to be 5,500 ppm for 585 min exposure time and an anesthetic
time of 46 min for the same concentrations.
Aviado et al. (1976) determined the 24-hr LC5Q for mice to be 0.220 +
0.099 g trichloroethylene per liter of air (41,000 ppm). The oral LD5Q of Swiss-
Webster mice was shown to be 2.85 + 0.55 g/kg of trichloroethylene. At least two
studies have been published on the 1,050 level of mice injected intraperitoneally
with trichloroethylene. Aviado et al. (1976) reported the 24-hr LD5Q level for
Swiss-Webster mice to be 1.20 + 0.31 g/kg. For the same strain of mice, Klaassen
and Plaa (1966) reported the LD5Q level as 3 g/kg (24 mM/kg). The use of dif-
ferent carriers and trichloroethylene purity levels has often produced differ-
ences in toxicologic studies.
Subcutaneous injections of trichloroethylene (29 to 170 mM/kg) were
administered to mice (Princeton strain) by Plaa et al. (1958). They found the
average LD5Q to be 120 mM/kg or 15.8 g/kg (67-200 mM/kg).
Acute dosage with trichloroethylene may cause slight histological
damage to the liver in animals. Jones et al. (1958) noted that 200 mice (Swiss
strain) orally dosed with trichloroethylene in olive oil developed mild degen-
erative liver changes apparent on histopathological study 72 hr after exposure
at all doses.
5-47
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Female albino mice were subjected to acute inhalation exposure to
98.8% pure trichloroethylene by Kylin et al. (1963). Mice were exposed to ei-
ther 1,600 or 3,200 ppm for 4 hr. The mice were sacrificed 1 hr or 1, 2, 4,
8, and 16 days after exposure. Trichloroethylene did not cause any marked signs
of liver damage. An earlier study by Kylin et al. (1962) showed similar results
in mice at up to 6,400 ppm trichloroethylene.
No acute nephrotoxic results were observed in Swiss strain mice af-
ter intraperitoneal injections of 0.6 ml/kg trichloroethylene (Plaa and Larson,
1965). Phenosulfonphthalein (PSP) excretion, presence of proteinuria and gluco-
suria (Combistix®), and histopathologic tests were used to check for signs of
kidney damage. Higher dosages showed some renal dysfunction for 3 days but on
day 4 no signs were present.
Klaassen and Plaa (1966) intraperitoneally injected Swiss strain
mice with anesthetic grade trichloroethylene (no impurities detected), at a
level of 2,200 mg/kg. No renal dysfunction was observed in the mice. The tests
used to detect kidney dysfunction were urinary PSP, glucose, and protein excre-
tion.
Hepatotoxicity studies on animals are better represented in the lit-
erature than kidney toxicity studies. Klaassen and Plaa (1966) determined the
hepatic function in male Swiss-Webster mice by checking the retention of
sulfobromophthalein (BSP) and serum glutamic-pyruvic transaminase activity
(SGPT). They injected mice intraperitoneally and found the ED^Q which causes
elevation of SGPT levels to be 18 mM/kg (2.4 g/kg) of trichloroethylene. In
the final analysis, Klaassen and Plaa concluded that only mild hepatic dys-
function was obtained when mice were administered trichloroethylene at near
lethal dosages.
White mice exposed to 1.8 vol 7<> concentration of trichloroethylene
for less than 1 hr were reported to develop disturbances in intermediary liver
metabolism (Heim et al., 1966). Gehring (1968) indicated that significant in-
creases in the SGPT levels did not occur in female Swiss-Webster mice until
near lethal concentrations were administered. Female mice (DD strain) were
exposed to 1,100 ppm trichloroethylene vapors in a chamber for 4 hr by Ikeda
et al. (1969). No hepatotoxic effects were observed.
5.1.4.2.1.3 Rats--Acute vapor toxicity studies were conducted on
Sherman rats (Carpenter et al., 1949). Six rats were exposed to 8,000 ppm tri-
chloroethylene for 4 hr. This was the approximate W
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Zahner et al. (1961) reported that exposure to 400 and 800 ppm tri-
chloroethylene vapor for 4 to 8 hr significantly reduced the frequency of spon-
taneous alternating behavior in rats. An increase in running speed was observed
in rats exposed to 400 and 600 ppm trichloroethylene but decreased speed was
observed at 1,600 ppm.
Rats were exposed to 400, 800, and 1,600 ppm trichloroethylene for
6 hr by Grandjean (1963). No significant decrease in the motor performance was
noted for the 400-ppm exposure, but a decrease in the motor performance did
occur in rats exposed to 800 ppm. However, rat behavior had returned to normal
within an hour. Exposure to 1,600 ppm also caused aberrations in motor activ-
ity. Similar results were noted by Zahner et al. (1961). In all cases rat ac-
tivity returned to normal after exposure ceased. In an earlier rat inhalation
study, Grandjean (1960) exposed three rats to 200 and 800 ppm trichloroethylene
for 11 to 14 hr. Using food as a stimulus, it was shown that the rats' psycho-
logical equilibrium was modified such that there was an increase in excitabil-
ity or a sense of disinhibition.
Twelve to sixteen hours after injecting 0.004 moles/kg (M/kg/ 0.5
g/kg) of trichloroethylene, Long-Evans strain rats showed indications of func-
tional liver changes plus microscopic hepatic damage (Wirtschafter and Cronyn,
1964). After 24 hr, the liver began to return to normal.
5.1.4.2.1.4 Dogs—Anesthetic concentrations of trichloroethylene
were administered to five dogs for 3 hr (Richard and Bachman, 1955). Sulfa-
bromophthalein (BSP) tests were utilized to indicate liver damage. The study
showed that BSP retention was not elevated in the five dogs, indicating that
trichloroethylene had no effect on the liver function.
The LD5Q f°r dogs after intraperitoneal injection with trichloro-
ethylene was determined to be 21 mM/kg (2.8 g/kg) (Klaassen and Plaa, 1967).
Dogs were tested for renal damage by using the urinary phenolsulfonphthalein
test. No renal damage was found in dogs at these concentrations. In the same
study, dogs were given a single intraperitoneal injection of trichloro-
ethylene. The dose level which elevated the serum glutamic-pyruvic trans-
aminase (SGPT) levels in half the dogs was 6.3 mM/kg (0.8 g/kg).
Baker (1958) exposed 15 dogs to acute concentrations of trichloro-
ethylene (30,000 ppm). Within 20 min, the dogs became semicomatose and had
difficulty controlling their limbs; death usually followed.
Aviado et al. (1976) studied the myocardial effects of acute doses
of inhaled trichloroethylene in dogs and listed the following results:
* The minimal concentration which caused depression in myocardial
contractility was 500 ppm.
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* A reduction in the pulmonary blood flow occurred at 1,000 ppm.
* Tachycardia and systemic hypotension were noted in dogs exposed
to 2,500 to 10,000 ppm.
* Severe depression of the myocardiac contractility and hypotension
were observed at concentrations of 50,000 ppm.
Smith and Ledingham (1972) found that the hearts of dogs anesthetized
with 0.4% trichloroethylene were capable of responding to hypoxia and hyperoxia
by increasing or decreasing cardiac output.
5.1.4.2.1.5 Rabbits—One of the earlier studies of trichloroethylene
inhalation was conducted by McCord (1932); trichloroethylene levels which caused
death in rabbits were:
20,000 ppm for 2 hr;
10,000 ppm for 2.5 hr;
5,000 ppm for 14 to 28 hr;
1,000 ppm for 28 to 41 hr; and
500 ppm for 19 days.
In the same study, McCord also reported the levels at which death or
illness is caused in rabbits due to absorption through the skin:
7.7 ml/kg 3 times/day for 4 days--death;
6.6 ml/kg 3 times/day for 5 days—death;
3.8 ml/kg 3 times/day for 5 days—death; and
3.6 ml/kg 3 times/day for 14 days —illness.
Bernardi et al. (1956) found the lethal concentration of trichloro-
ethylene in rabbits to be 11,000 ppm for 50 min. Ten rabbits exposed to acute
concentrations of trichloroethylene (7,000 to 14,000 ppm) for 15 to 60 min
showed changes in their EEGs varying from minor to electroclinical epileptic
seizures (Desoille et al., 1962).
5.1.4.2.1.6 Other species--Mikiskova and Mikiska (1966) gave intra-
peritoneal injections of trichloroethylene to guinea pigs. They administered
6.7 mM/kg (0.8 g/kg) trichloroethylene to each animal. Within 30 min, the ner-
vous system was disturbed, resulting in loss of muscular tone, depression of
the righting reflexes and slowness of respiration. In this study, the metabo-
lite, trichloroethanol, as well as trichloroethylene was used. They found that
trichloroethanol had similar effects on the nervous system except that tri-
chloroethanol was three times more effective. Richards (1973) showed that an-
esthetic concentrations of trichloroethylene administered in vitro to slices
of the guinea pigs' olfactory cortex caused depression of the synaptic activity.
5-50
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The results of studies with fish and other environmental species are
given in Section 6.2. Detailed results for fish are given in Section 6.2.1.
5.1.4.2.2 Subacute effects —
5.1.4.2.2.1 Man—Stewart et al. (1970) exposed human subjects to
200 ppm trichloroethylene for five consecutive days. No abnormal results were
obtained on the neurological tests. However, 50% of the subjects required
greater mental effort to.perform the Romberg test. Also, during the exposure,
some of the subjects complained of feeling light-headed with headaches, fa-
tigue, drowsiness, and throat and mild eye irritations.
Forster et al. (1974) studied the electroencephalographic and the
visually evoked recordings (VER) of three women exposed daily to low levels
of trichloroethylene (100 ppm, 7 hr/day for 5 days). They found a reduction
in VER wave amplitude in all three females and suggested that this reduction
(at 100 ppm) is caused by a cortical excitation (desynchronization). Although
trichloroethylene is known to be an anesthetic at high concentrations (4,500
ppm), these studies indicate that at low concentrations (< 100 ppm) trichloro-
ethylene could be a stimulant.
5.1.4.2.2.2 Mice—Slight fatty degeneration, which tended to abate
2 weeks after initial exposure, was observed in all the experiments conducted
by Kylin et al. (1965). Twenty albino mice per experiment were exposed to 1,600
ppm trichloroethylene 4 hr/day, 6 days/week for periods of 2, 4, or 8 weeks.
The only difference observed in the mice from the controls was slight fatty
degeneration.
5.1.4.2.2.3 Rats—Taylor (1936) exposed rats to 3,000, 2,000, 1,000,
and 500 ppm trichloroethylene for 6 hr/day, 5 days/week for 6 months. No ad-
verse effects were noted in the rats exposed to,2,000 ppm or less. However,
three of the six rats in the 3,000-ppm concentration died, one each on days
15, 17, and 32, respectively.
Mild ataxia, marked salivation, restlessness, hyperexcitability, ex-
aggerated reflexes, weight loss and hepatomegaly were observed in Wistar albino
rats exposed to 3,000 ppm trichloroethylene for 7 hr/day; the rats received 27
exposures in 36 days (Adams et al., 1951).
Three rats were exposed to a trichloroethylene vapor concentration
between 0.05 and 0.1 vol % trichloroethylene for 18 hr/day for 90 days by
Nowill et al. (1954). No abnormalities in the rats' liver, kidney, or blood
system were found.
Prendergast et al. (1967) exposed either Long-Evans or Sprague-Dawley
rats to 730 ppm trichloroethylene 8 hr/day, 5 days/week for 6 weeks, or to 35
ppm continuously for 90 days. In the first exposure level (730 ppm), the rats
showed signs of nonspecific pulmonary inflammation, slight leukopenia, and a
5-51
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nasal discharge. The liver was examined microscopically and found to be normal.
The rats examined in the second experiment at concentrations of 35 ppm were
normal except for insignificant growth depression.
Ikeda et al. (1969) injected Wistar strain male and female rats in-
traperitoneally every 2nd day with trichloroethylene. Rats received 40 separate
injections during the experiment. The first three injections contained 0.5 ml/
kg, while the next 37 injections contained 1.5 ml/kg. Investigators were unable
to find significant damage to the liver in any of the mice.
Hepatomegaly has been shown to occur in rats inhaling concentrations
as low as 55 ppm. Twenty Specific Pathogen Free (SPF)-Wistar-II rats were ex-
posed to 55 ppm trichloroethylene 8 hr/day, 5 days/week for 14 weeks (Kimmerle
and Eben, 1973). Liver function and microscopic examination tests proved nor-
mal. The only abnormality observed by investigators was an increase in liver
weight.
Repeated inhalation of trichloroethylene produced an inhibition of
conditioned reflex in rats on the pole-climb performance (Goldberg et al.,
1964a; 1964b). In the 1964a study by Goldberg, female Carworth Farms Elias
(CFE) rats were exposed to concentrations of 200, 500, 1,568, or 4,380 ppm
trichloroethylene for 10 days. The animals receiving 1,568 ppm became slightly
ataxic but not to the point of motor imbalance. Those exposed to 4,380 ppm
were incapable physically of completing the tests. Tolerance developed in the
rats, but 2 days after the final exposure the rats' behavior had returned to
normal. In another study by Goldberg et al. (1964b) rats were exposed to 125
ppm trichloroethylene, 4 hr/day, 5 days/week for 5 weeks. This concentration
caused significant alterations in behavior, i.e., impaired the performance
of rats in a shock-avoidance test.
Silver-man and Williams (1975) observed up to a 24% reduction in to-
tal activity of rats exposed to 100, 200, and 1,000 ppm trichloroethylene,
5 days/week for 5 weeks. At 1,000 ppm, the reduction in activity was noted on
the first day, whereas in the 100-ppm trial, reduction in total activity was
delayed at least 10 days after starting exposure in one group of rats and after
as many as 59 days in another.
5.1.4.2.2.4 Guinea pigs—A study conducted by Barrett et al. (1938)
demonstrated that moderate liver damage occurred in guinea pigs after expos-
ing them to 1,200 ppm trichloroethylene for up to 1,100 hr.
No abnormalities were found in 11 guinea pigs (7 male and 4 female)
exposed to 100 ppm of trichloroethylene 7 hr/day, 5 days/week for 26 weeks
(Adams et al., 1951).
Fifteen guinea pigs (Hartley strain) inhaled either 730 ppm trichloro-
ethylene 8 hr/day, 5 days/week for 6 weeks, or 35 ppm continuously for 90 days
5-52
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(Prendergast et al., 1967). Normal growth was noted in all the experimental
animals. However, in the guinea pigs exposed to 730 ppm of trichloroethylene,
slight leukocytosis and nonspecific pulmonary inflammation was observed.
5.1.4.2.2.5 Cats--Cats were exposed to 20 ppm trichloroethylene va-
por for 60 to 90 min a day for 4 to 6 months. Fatty degeneration of the livers
without inflammation was noted by Mosinger and Fiorentini (1955).
5.1.4.2.2.6 Dogs—Seifter (1944) exposed dogs to differing concen-
trations of 98+% pure trichloroethylene (0.5% trimethylamine as a stabilizer).
Degeneration of liver parenchyma cells was found in dogs exposed to 750 ppm,
7 to 8 hr/day, 6 days/week for 3 weeks, and in dogs exposed to from 500 to 750
ppm, 5 to 6 hr/day, 5 days/week for 8 weeks. Liver injury was based on BSP
tests, glycogen depletion, and histologically observed hydropic parenchymatous
degenerati on.
Baker (1958) exposed 25 dogs to various concentrations of trichloro-
ethylene ranging from 500 to 3,000 ppm, 2 to 8 hr/day, 5 days/week. The 3,000-
ppm exposure caused the cerebellar Purkinje cells to disintegrate.
Beagle dogs were exposed to either 730 ppm trichloroethylene 8 hr/
day, 5 days/week for 6 weeks, or 35 ppm continuously for 90 days (Prendergast
et al., 1967). The results of these experiments show no abnormalities occurring
in the heart, liver, spleen, or kidney. However, nonspecific lung inflammation
was observed in the group of dogs.
5.1.4.2.2.7 Rabbits—Nowi11 et al. (1954) exposed three rabbits to
trichloroethylene concentrations between 0.05 and 0.1 vol % 18 hr/day for 90
days. The only noticeable effect on the rabbits caused by the vapor was an ap-
parent sluggishness. Liver, renal, hematopoietic studies were all normal.
Bartonicek and Soucek (1959) reported that two out of six rabbits
died from renal failure after being injected parenterally with 33 to 55 g to-
tal trichloroethylene for 55 to 100 days.
New Zealand albino rabbits were exposed to either 730 ppm trichloro-
ethylene 8 hr/day, 5 days/week for 6 weeks or 35 ppm continuously for 90 days.
Nonspecific lung inflammation was observed in rabbits exposed to the highest
concentration. No other abnormal effects were noted at either concentration
by Prendergast et al. (1967).
The effects of trichloroethylene on the blood and bone marrow of rab-
bits were reported by Mazza and Brancaccio (1967). They exposed 12 rabbits to
2,790 ppm (15 mg/liter) for 4 hr/day, 6 days/week for 45 days. They concluded
that myelotoxic anemia was caused by the direct action of trichloroethylene
poisoning on the bone marrow.
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Tests of trichloroethylene intoxication were conducted on rabbits
by Bartonicek and Brun (1970). Sixteen female rabbits were divided into three
groups; nine rabbits were injected parenterally with 2.92 g trichloroethylene
twice a week for 41 to 247 days, three rabbits were parenterally injected with
4.38 g twice a week for 29 days, and four rabbits were used as controls. No
severe neurological changes occurred. However, moderate changes in the form
of diffuse chronic-ischemic or toxic nerve cell damage in the majority of the
cranial nerve nuclei, in the Gasserian ganglion, and the cerebellar cortex were
noted in both groups.
5.1.4.2.2.8 Monkeys—Adams et al. (1951) exposed two Rhesus monkeys
to 200 ppm trichloroethylene for 7 hr/day, 5 days/week (148 exposures in 212
days) and one monkey to 400 ppm for 7 hr/day, 5 days/week (161 exposures in
225 days). No toxic effects were observed. In another study, Prendergast et
al. (1967) exposed three squirrel monkeys to 730 ppm trichloroethylene 8 hr/
day, 5 days/week for 6 weeks, and to 35 ppm continuously for 90 days and found
no toxic effects. However, nonspecific lung inflammation was found in the mon-
keys exposed to the 730-ppm level.
5.1.4.2.3 Chronic effects —
5.1.4.2.3.1 Man—Dimitrova et al. (1974) indicated that workers who
were acutely exposed to trichloroethylene vapor showed significant cardiac
changes. Twenty female workers who were exposed to trichloroethylene vapors
(above the maximum allowable concentrations) for periods of from 7 months to
4 years were used in these experiments. Their electrocardiograms, carotid
sphygmograms, and phonocardiograms were recorded and compared to a control
group of 58 healthy persons with no known contact with trichloroethylene. The
female workers showed a shorter cardiac cycle and longer isometric period and
tension phase than the controls.
5.1.4.2.3.2 Rats—A study which showed histological damage of the
liver was conducted by Fonzi et al. (1967). Rats were exposed to trichloro-
ethylene for 30 min/day for 120 days. In addition to slight liver damage, a
decrease in total serum proteins was found.
Depression in the growth of male rats and significant increases in
splenomegaly and hepatomegaly in both sexes were observed in rats exposed to
400 ppm trichloroethylene for 7 hr/day; 173 exposures were received in 243
days. Rats tolerated 151 exposures in 205 days to 200 ppm trichloroethylene
without adverse effect (Adams et al., 1951).
Pelts (1962) exposed rats for 5.5 months to trichloroethylene and
found a reduction in the phagocytic activity of the rat leukocytes. Rats were
exposed to 0.1 mg/liter (19 ppm) for 6 hr/day, 6 days/week for 65 days and
then to 0.2 mg/liter (37 ppm) for the duration of the exposure.
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Chronic exposure of rats to trichloroethylene (75 ppm for 72 to 121
days) caused an increased motor excitation in between signals, a reduction in
the time of latency of a food-motivated reaction, and discrimination disorders
(Formanek and Horvath, 1957).
Battig and Grandjean (1963) exposed rats to 360 to 420 ppm trichloro-
ethylene, 8 hr/day, 5 days/week for 44 weeks. No abnormal behavior responses
were noted in the Hebb test or the test for conditioned avoidance response.
However, swimming speed in water was reduced, while enhancement of the explora-
tory behavior occurred. Battig's study (1964) showed that more physical activ-
ity was observed in rats after being exposed to 400 ppm for 43 weeks than in
the controls.
5.1.4.2.3.3 Rabbits—Heterogeneous albino rabbits were subjected to
three different concentrations of trichloroethylene by Adams et al. (1951).
One group of rabbits exposed to 200 ppm 7 hr/day, 5 days/week for 36 weeks
showed no evidence of poisoning. The second group of rabbits tolerated 32 weeks
at 400 ppm for 7 hr/day, 5 days/week. Slight hepatomegaly was observed in these
rabbits. A third group of rabbits exposed to trichloroethylene concentrations
of 3,000 ppm, 7 hr/day, 5 days/week for 5-1/2 weeks revealed increases in the
liver and kidney weights and minor disturbances of equilibrium and coordination.
Some of the studies of Bartonicek and Brun (1970) also included chronic dosing
schedules to rabbits (see Section 5.1.4.2.2.7).
5.1.4.2.3.4 Guinea pigs--Male and female guinea pigs exhibited signs
of hepatomegaly and growth retardation in both males and females exposed to 400
ppm trichloroethylene for 7 hr/day; 167 exposures were received in 235 days
(Adams et al., 1951). The growth retardation in males was significant, while in
females retardation was slight but not significant. Significant retardation in
males and females was also observed in guinea pigs exposed to 200 ppm trichloro-
ethylene for 7 hr/day; 163 exposures occurred in 227 days.
5.1.4.3 Sensitization—
Sensitization includes two phenomena: increased potency of other agents
and allergic effects. Very little work has been conducted in either area. Bas-
ically, studies of trichloroethylene have only been done on the role in Sensi-
tization to epinephrine of the heart, contribution to Sensitization of the
pulmonary stretch receptors, the synergistic effects of alcohol in man, and
the apparent allergic responses causing contact or dermal eczema.
Trichloroethylene may sensitize the heart to sympathoadrenal discharges
and to epinephrine (Huff, 1971). Reinhardt et al. (1973) indicated that tri-
chloroethylene sensitizes the myocardium of dogs when anesthetized at levels
of 0.5% or higher. Morris et al. (1953) stated that trichloroethylene sensi-
tized the dog heart to epinephrine to a greater extent than did chloroform.
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Decreases in the sensitization of the myocardium with trichloroethylene
in epinephrine-induced arrhythmias by Nethalide-^ (pronethalol, a beta recep-
tor antagonist) was shown by Murray et al. (1963). Another organ, the lung,
showed sensitization of the pulmonary stretch receptors when ventilated with
low concentrations of trichloroethylene (Coleridge et al., 1968).
Potentiation of trichloroethylene toxicity to alcohol has been demon-
strated by various researchers. "Degreasers flush" often appears when tri-
chloroethylene and ethanol are absorbed simultaneously. Stewart et al. (1974b;
1974c) exposed volunteers to 200 ppm trichloroethylene, 7-1/2 hr/day for 5
days. The subjects drank a quart of beer 71 hr after the last exposure and
within 30 min the subjects began to flush; the condition lasted for a period
of 60 min.
Eczema may be a type of allergic response due to sensitization. Workers
whose jobs involve hand-contact with liquid trichloroethylene have reported
relatively high incidences of eczema. Many reports of dermatological effects
of trichloroethylene exposure exist, among them Schirren (1971), Baker and
White (1946), Bauer and Rabens (1974), and Stewart et al. (1974a). Eczema
will disappear within a few weeks if the workers refrain from physical con-
tact with the liquid.
Bauer and Rabens (1977) reviewed reports on true allergy to trichloro-
ethylene and suggest that a few isolated reports on true eczematous allergy
may exist. Four reported human cases were apparently sensitized by vapor in-
halation, after which response to trichloroethylene contact was an erythema
which becomes papular, then blistered, and later exfoliates.
This phenomenon, true allergy to trichloroethylene, is also relevant to
study of trichloroethylene metabolism. An immune response needs a molecule
larger than trichloroethylene as an antigen. It must be assumed that in vivo
covalent coupling of trichloroethylene to a protein or other large molecule
must occur in order for an immune reaction to result.
5.1.4.4 Teratogenic Effects—
Trichloroethylene is not considered to be teratogenic. Euler (1967) ex-
posed rats to 65 ppm (0.34 rag/liter) trichloroethylene and reported that no
adverse effects were observed in the embryonal or fetal development (time
limit not given). Schwetz et al. (1975) reported no teratogenic events oc-
curred in pregnant mice exposed to 300, 875, or 1,250 ppm trichloroethylene,
7 hr/day or days 6 to 15 of gestation.
However, there has been one report which found retardation in the growth
of newborn rats exposed continually to 0.004 mg/liter (1 ppm) of trichloro-
ethylene (Krasovitskaia and Malyarova, 1968), but there has been no confirma-
tion of this adverse effect.
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A teratogenicity-mutagenicity study of trichloroethylene (and perchloro-
ethylene) is in progress at Litton Bionetics (Occupational Health and Safety
Letter, November 8, 1977; Toxic Materials News, 1978). The experimental design
involved exposure of Charles River rats and New Zealand rabbits to trichloro-
ethylene in closed inhalation chambers beginning 3 weeks before impregnation
and continuing through gestation. Both dams and fetuses, sacrificed 1 day be-
fore parturition, were examined for toxicity and teratogenic effects (Beliles
and Brusick, 1977). The study has been in progress during 1978, but no data
are available.
A study by PPG Industries (Chem. Eng. News, 1977) reported no embryqlogi-
cal effect due to trichloroethylene when pregnant female rats inhaled 300 ppm.
In this study, Calandra et al. (1977b) exposed pregnant albino rats to 300 ppm
of stabilized trichloroethylene (PPG: Trichlor 132) during gestation days 6
to 15. No effect was seen in the exposed rats, compared to an unexposed control
group, in the following parameters: fetal (maternal body weight), maternal
body weight gain, mortality of dam, number of corpora lutea, number of implan-
tation sites, number of resorption sites, and number of fetuses.
A recent study exposed female Wistar rats to 100 ppm trichloroethylene in
air for 20 days, 4 hr/day, starting at day 6 of pregnancy. Healy and Wilcox
(1977) described this level of exposure as similar to the waste anesthetic gas
level that is present in the operating room when trichloroethylene is used as
an anesthetic agent. The exposure of the dams reduced fetal weight and increased
the number of fetal absorptions significantly over controls.
5.1.4.5 Mutagenic Effects—
There have been a number of recent studies using various assay techniques
to determine the mutagenic potential of trichloroethylene. Current results are
tabulated (Table 5-12) with both positive and negative results depending on
the test system and whether or not the system was metabolically activated.
Some of these studies are still in progress.
Greim et al. (1975) showed that metabolic activation of the
nonsymmetrically-chlorinated ethylenes (including trichloroethylene) produced
a mutagen in the Ames test, using either S_. typhimurium TA1535 or E_. coli K12;
It was not clearly specified which strain was used with trichloroethylene.
These compounds were not mutagenic when tested with fresh human lymphocytes
in an assay for chromosomal aberrations.
The results of Shahin and vonBorstel (1977) and those of Calandra et al.
(1977a) are in disagreement regarding the mutagenicity of trichloroethylene.
The dominant lethal mutagenic study of Calandra mated male rats, exposed to
inhaled trichloroethylene at 300 ppm for 9 months, with untreated females. No
early deaths, fertility changes, numbers of corpora lutea, implantation sites,
or viable embryo numbers occurred in test rats over control animals. Calandra
et al. report that in this in vivo system trichloroethylene was not mutagenic.
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TABLE 5-12. MUTAGENICITY TESTING—TRICHLOROETHYLENE
Test system
Reaction tested
Result
Reference
Microbial:
£. cyphimurium TA1535
F. colt K12
£. typhimurium. activated
£. Evphimurium. nonactlvated
S. cerevisiae D4, D7
Human lymphocytes
TCE-dosed male rats + untreated
females
TCE-dosed males + untreated
females
Gene mutation in bacteria (Ames
test)
Mitotic recomb.
Mitotic recomb.
Point mutations
Mitotic gene conversion
Chromosomal aberrations
Dominant lethal mutagenicity
assay
Dominant lethal assay
Mutagenic in activated system
Negative
Negative
Positive
Positive
No aberrations
No mutagenic signs in F, generation
No mutagenic signs in reproductive
performance
Greim et al. (1975)
Bartsch et al.
(1976)
Bronzetti et al.
(1977)
Greim et al. (1975)
Calandra (1977a)
Bell (1977)
Microbial:
£. cerevisiae 3V185-14C
Rat embryo cells in culture
S_. typhimurium, five tester
strains, activated and non-
activated
Host-mediated assay: £. pombe
and B6C3F1 mice
Hicrobial:
S_. typhimurium TA100
Drosophlla (fruit fly)
Plant: Tradeseantia
Clone 4430
Microbial
Gene mutation
Cell transformation
Bacterial gene
Mutation
In vivo mutation of yeast cells
in trichloroethylene-dosed
mice
Gene mutation
Recessive lethal traits in F^;
chromosome breakage
Mutagenicity
Mutagenicity
Frameshift mutagen and base substi-
tution mutagen
Positive mutagen
Positive: stabilized trichloro-
ethylene
Negative: pure trichloroethylene
Weakly positive with one of six
strains tested
Study as yet unpublished (1979)
Positive: at 0.5 ppm/6 hr
Positive
Shahin and
Von Borstel (1977)
Price et al. (1977)
Margard (1978)
Positive: stabilized trichloro- Loprieno et al.
ethylene (1979)
Negative: pure trichloroethylene
Simmons et al. (1977)
Abrahamson (1978)
Sparrow (1976), (un-
published)-'
Ramel (1976) (unpub-
lished)^
a/ Cited in Infante (1977) and by personal communication.
5-58
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The results of Shahin and vonBorstel (1977) indicate that in a bacterial
test system (S_. cerevisiae strain XV185-14C) following metabolic activation
with mouse liver enzymes trichloroethylene appeared to induce frameshift as
well as base substitution mutations.
Price et al. (1977) tested trichloroethylene and the other subject com-
pounds by adding low levels to Fischer rat embryo cells and counting cellular
transformation. All three compounds, trichloroethylene, methyl chloroform, and
perchloroethylene (tested at 99.9% or better purity) produced transformation
of the cells in culture. It is relevant to these results that the Fischer rat
embryo cell line carries an oncogenic virus, and there has been some question
as to the use of these screens for mutagenicity/carcinogenicity testing.
The dominant-lethal tests reported by Bell (1977) exposed 15 male rats
to 300 ppm trichloroethylene for 6 hr/day, 5 days/week for 9 months. The ex-
posed rats were mated to two unexposed females a week for eight consecutive
weeks. The reproductive performance of the trichloroethylene-exposed rats was
not different from control rats. No chromosomal data were reported, but the
author concluded that no dominant-lethal mutagenic effect had occurred on the
basis of the reproductive performance.
The nonvolatile metabolites of trichloroethylene—chloral hydrate, tri-
chloroacetic acid, and trichloroethanol--were tested for mutagenicity in the
Ames assay using microsotnal activation and S. typhimurium strains TA98, TAlOO,
TA1535. The negative results (except for a weak positive with one bacterial
strain using chloral hydrate) were unacceptable to the author who plans to use
more metabolic activation next time (Waskell, 1978). Simmon et al. (1977) re-
port that trichloroethylene incubated in a desiccator with S* typhimurium TAlOO
for 7 hr showed a weakly positive mutagenic response. No data were furnished
on results from six other bacterial strains used for mutagenic testing in the
study.
The mutagenic potential of trichloroethylene in the fruit fly, Drosophila
melanogaster, is being investigated in an ongoing study. Male fruit flies are
exposed to trichloroethylene, mated to females, and the offspring examined for
recessive lethal traits and for chromosome breakage/rejoining. Results are not
yet available (Abrahamson, 1978).
Infante (1977) reviewed the positive bacterial mutagenicity tests on tri-
chloroethylene, citing personal communications from C. Ramel and A. H. Sparrow
as well as Greim et al. (1975). Waters et al. (1977) included some of the same
research on trichloroethylene mutagenicity studies in the review. A preprint
outlining results of a host-mediated assay was obtained from the Laboratorio
Di Genetica of the University of Pisa in Italy (Loprieno et al., 1979). The
laboratory is conducting both yeast cell mutation tests with S_. pombe, and
host-mediated assays where the yeast cells are injected into the abdominal
cavity of trichloroethylene-dosed B6C3F1 mice to test for in vivo production
5-59
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of mutagenic metabolites. Loprieno reports that pure trichloroethylene was non-
mutagenic, but when the compound was stabilized with 0.09% epichlorohydrin it
showed mutagenicity. This work was also reported in Chem. World (February 14,
1979) and Chem. Reg. Reporter (Vol. 3, p. 455, June 22, 1979).
Degreaser operators (28) with different levels of trichloroethylene expo-
sure during the workday were measured for toxic effects on chromosomes by
lymphocyte culture. Nine workers exposed to trichloroethylene at higher levels
but not for longer times showed abnormal numbers of hypodiploid cells but nor-
mal caryotypes; one of the nine had a small metacentric extra chromosome. The
makeup of the control group, the years/months of trichloroethylene workplace
exposure, and the ambient levels of chemical inhaled were not presented
(Konietzko et al., 1978).
5.1.4.6 Carcinogenic Effects--
NCI (1976a; 1976b) reported that trichloroethylene induced cancer in mice.
Trichloroethylene was administered by oral gavage five times per week for 78
weeks. The doses were 1,169 and 2,339 mg/kg for male mice and 869 and 1,739
mg/kg for female mice. These tests were conducted using industrial grade (99%
pure) trichloroethylene on Osborne-Mendel rats and B6C3F1 mice. A complete
necropsy and microscopic evaluation were conducted on all the animals (except
7 out of the 480 who died at unscheduled times).
No significant difference was noted in neoplasms between experimental
and control groups of rats. However, in both male and female mice, the higher
dose induced primary malignant tumors of the liver. For males, 26 of 50 mice
who received the low dosage and 31 of the 48 mice who received the high dosage
developed hepatocellular carcinomas while only 1 out of 20 of the controls
showed neoplasms. In female mice, 4 of the 50 receiving the low dosage and 11
out of 47 receiving the high dosage developed neoplasms as compared to 0 out
of 20 of the controls. Followup studies are now being conducted to confirm
these results.
Oral doses were administered by gavage to 28 NLC mice (age not specified).
Dosages of 0.1 ml of a 40% solution of trichloroethylene in oil were adminis-
tered twice weekly for an unspecified time. No liver lesions or hepatomas were
observed (Rudali, 1967). A summary of carcinogenic data is presented in Table
5-13.
Weisburger (1977) reviewed the NCI cancer trials on trichloroethylene.
Several factors important to the final results were denoted, which showed that
trichloroethylene had little or no effect on rats but produced hepatocellular
carcinomas in mice. These factors were: the rat (Osborne-Mendel) was chosen
because it was highly susceptible to chlorinated solvents, but it neverthe-
less failed to get tumors; analysis of the trichloroethylene used in the tests
showed 0.19% 1,2-epoxybutane; and normal human exposure will be likely to be
through inhalation, not ingestion. This review singled out three of the 12
5-60
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TABLE 5-13. SUMMABY OF CARCINOGENIC DATA
I
a\
Species
Dogs
Rats
Guinea pigs
Monkeys
Rabbits
Ho.
16
12
11
2
4
Exposure
Inhalation
150-750 ppm in. air 20-48 hr/wk
for 7-16 wk
Inhalation
3,000 ppm, 27 exposures
100 ppm, 132 exposures
200 ppm, 148 exposures
200 ppm, 178 exposures
Results
No tumors
No deaths
3 rats died,
No tumors
Reference
Seifter (1944)3/
Adams et al. (1951)3/
Cats
Mice
Mice
Rats
28
Inhalation
200 ppm 75 min/day for 6
months
Intragastric
0.1 ml in 40% oil solution 2/wk
Intragastric
2,339 mg/kg (M) 5/wk for 78 wk
1,739 mg/kg (F) 5/wk for 78 wk
1,169 mg/kg (M) 5/wk for 78 wk
869 mg/kg (F) 5/wk for 78 wk
No tumors,
No tumors,
No deaths
Hepatocellular
carcinoma,
Mestastases, mainly
lung
Mosinger and Fiorentini (1955)-
Rudali (1967)2/
NCI Carcinogenesls
Technical Report
Number 2
Intragastric
1,097 mg/kg (M,F) 5/wk for 78 wk No hepatocellular
549 mg/kg (M,F) 5/wk for 78 wk carcinoma, many
deaths from toxic
experiment
NCI Carcinogenesis
Technical Report
Number 2 (1976)^
j»/ Survey of Compounds Which Have Been Tested for Carcinogenic Activity (1957-1971).
J>/ NCI Carcinogenesis Technical Report No. 2 (1976).
Source: Waters et al. (1976).
-------
halogenated hydrocarbons tested by the NCI carcinogenesis bioassay program as
chemicals that "could pose a hazard to humans on continued exposure." Tri-
chloroethylene, methyl chloroform, and perchloroethylene were not included on
the list, although all three were among the 12 halogenated hydrocarbons tested
in the bioassays.
With respect to the NCI bioassay program results on trichloroethylene,
it is possible that when carcinomas are produced in mice but not rats, some
species or strain susceptibility may be responsible, as was indicated by
Weisburger. Further, Oesch (1973) reports that mice, as a species, have a com-
paratively low activity of epoxide hydrase. This enzyme detoxifies epoxides,
which is the form suggested for tumor induction by trichloroethylene.
A 2-year inhalation toxicity study using 960 Charles River albino rats
and 1,120 B6C3F1 mice is being sponsored by trichloroethylene producers. Ex-
posure to trichloroethylene is at 100, 300, 600, and 0 ppm, 7 hr/day, 5 days/
week. Ten mice per sex per exposure group are killed to check effects at 1,
3, 6, and 12 months; the same number of rats are sacrificed at 6 and 12 months.
Preliminary data indicate no tumors are reported grossly in the rats and the
difference in number of tumors found between test and control animals is not
statistically significant (Clark, 1977).
The NIOSH special occupational hazard review of trichloroethylene cited
a communication from Tola (1977) which details a current cohort epidemiologi-
cal study in Finland on the carcinogenicity of trichloroethylene to 1,868 work-
ers exposed to trichloroethylene from 1965 through 1976. There were 10 cases
of cancer of mixed site which have occurred in the 47 deaths in this group.
There is no indication of an increased risk of cancer, but the group is young
with half under 40 years of age. The epidemiologic study will continue for sev-
eral more years.
A recent Swedish cohort study comprised of 518 men revealed no excess can-
cer deaths in a population exposed to 30 ppm or more of trichloroethylene when
compared to a subcohort with lower levels of exposure (Axelson et al., 1978).
The study records allowed 10 years of latency time between exposure and effect,
and the exposure levels were estimated by records of trichloroacetic acid ex-
cretion in urine, assuming 100 mg/liter trichloroacetic acid equaled a tri-
chloroethylene exposure of over 30 ppm. The authors suggest that a very strong
tumorigenic effect would have been detected by this study, and none was found.
Van Duuren et al. (1979) report, in a study on mouse skin initiation/
promotion, that trichloroethylene produced local papillomas in 4 of 5 mice
treated with 1.0 mg in 0.1 ml acetone three times weekly. One of 30 ICR Ha
Swiss mice treated developed a squamous cell tumor at the application site at
264 days.
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Bell et al. (1978) have issued a report on the reanalysis of a trichloro-
ethylene inhalation study done at IBT. Reanalysis of all the pathology slides
shows a "significant difference in tumor incidence between groups Tl (100 ppm
trichloroethylene) and T2 (300 ppm trichloroethylene) combined with T3 (600
ppm trichloroethylene) in both male and female mice" (Bell et al., 1978). This
important result cannot be evaluated with scientific accuracy because of the
lack of a concurrent control group; only "historic" controls must be used.
5.1.4.7 Factors Affecting Toxicity—
5.1.4.7.1 Synergistic effects with other chemicals—Only minor research
efforts have been undertaken on chemical synergisms of trichloroethylene. Very
few chemical compounds have been considered synergistic: acetone, isopropyl
alcohol, Aroclor 1254, hexachlorobenzene and pregnenolone-16-a-carbonitrile
may increase hepatotoxicity when administered with trichloroethylene. Siegel
et al. (1971) indicated that mixtures of dichloroacetylene (DCA) and trichloro-
ethylene are more toxic than pure trichloroethylene. The 4-hr LC5Q of tri-
chloroethylene was estimated to be 12,500 ppm in rats and the 4- to 6-hr LC^Q
of DCA alone was 19 to 20 ppm in two rodent species. The combined
trichloroethylene-DCA LCso was 55 ppm with a trichloroethylene-to-DCA ratio
of approximately 7:1.
Certain chemical compounds may change the effect of trichloroethylene.
These effects are described in the following paragraphs.
Evreux et al. (1967) reported that 0.1 and 0.2 mg/kg dosages of pro-
pranolol, a p-adrenergic antagonist, prevented cardiac arrhythmia (produced
by trichloroethylene) in dogs.
Acetone and isopropyl alcohol increase serum glutamic pyruvic transami-
nase (SGPT) levels as demonstrated in a study by Traiger and Plaa (1974) in
which male Swiss-Webster mice were given either acetone or isopropyl alcohol
orally 18 hr prior to intraperitoneal injections of trichloroethylene. The
potentiation of these compounds was measured by recording the increases in
SGPT levels (hepatotoxicity).
Ethanol potentiation of trichloroethylene toxicity was noted in Sprague-
Dawley rats after exposure to 5,000 ppm of trichloroethylene for 4 hr
(Cornish and Adefuin, 1968); however, the toxicity was not increased by
ethanol when the rats were exposed to only 100 ppm. Experiments conducted on
rabbits by Desoille et al. (1962) show that chronic ethyl alcoholism aggra-
vates trichloroethylene poisoining.
In a recent report, Cornish et al. (1977) could not demonstrate potentia-
tion of trichloroethylene toxicity by prior ethanol treatment. A large i.p.
dose (20 ml) of trichloroethylene increased liver enzyme activity (SCOT); pre-
treatment with ethanol did not modify this response. Although chronic alcohol
dosage causes increased enzyme synthesis by the microsomal oxidase system,
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there was no potentiation of solvent toxicity by this induction. The earlier
study (Cornish and Adefrein, 1966) showing ethanol-trichloroethylene synergism
in rat liver cannot, therefore, be explained by microsomal enzyme induction.
Phenobarbital may potentiate the hepatotoxicity of trichloroethylene.
Rats were injected with enzyme-enhancing levels of phenobarbital and, 24-hr
later, exposed to 10,400 ppm of trichloroethylene for 2 hr (Carlson, 1974).
Increased hepatotoxicity was shown by measurements of serum enzymes and hepatic
glucose-6-phosphatase and histological observations of liver sections. 3-Methyl-
cholanthrene also increased the hepatotoxicity of trichloroethylene. Cornish et
al. (1973) reported an opposite effect by phenobarbital. A single dose of pheno-
barbital (50mg/kg) administered intraperitoneally 1 or 2 days prior to tri-
chloroethylene exposure had no effect on the toxicity of trichloroethylene to
Sprague-Dawley rats.
Other drugs also increase hepatotoxicity when administered with trichloro-
ethylene. Reynolds (1976) noted an enhancement by pretreating animals exposed
to trichloroethylene (1%) for 2 hr with chlorinated biphenyl (Aroclor 1254),
hexachlorobenzene, or a synthetic steroid (pregnenolone-16-a-carbonitrile).
Kluwe et al. (1978) also reported that the exposure of mice to polybrominated
biphenyls (PBBs) made the animals more sensitive to the effects of trichloro-
ethylene exposure, as measured by the decrease in para-aminohippurate accumu-
lation. The authors suggested that PBB ingestion may "sensitize" humans and
other animal species to chlorinated hydrocarbon-induced toxicity.
Brautbar et al. (1977) suggested that renal failure, which occurred in a
post-surgery patient, was due to penicillin (12 million units i.v.) and the
trichloroethylene anesthesia. The anesthesia was administered 5 days before
the penicillin treatment. No studies of trichloroethylene metabolites or liver
damage were done, nor was the dosage of trichloroethylene estimated. A physio-
logical rationale for this proposed synergism was not presented.
5.1.4.7.2 Stabilizer toxicity--The following chemicals are used in various
combinations for stabilizing trichloroethylene: butylene oxide, diisobutylene,
epichlorohydrin, esters such as ethyl acetate, nitromethane, N-methyl pyrrole,
tetrahydrofuran, three to four carbon alcohols, and selected amines.
Trichloroethylene requires some degree of stabilization due to the nature
of the chemical bond between the carbon and the chlorine and the structure of
the molecule. Normally, these stabilizers are effective at concentrations of
less than 1% by weight.
Margard (1978) reported the results of Ames tests on several different
trichloroethylene (and perchloroethylene) stabilizer formulations in a propri-
etary, unpublished industrial study. A statement regarding the tests was of
particular interest: two common stabilizer chemicals (antioxidants), when
added to a mutagen-positive chlorinated solvent, reversed the results of the
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Ames tests to negative. These data emphasize the desirability of a more com-
plete screen of in vitro tests before classifications of toxic effects are
made.
Henschler et al. (1977) analyzed and identified the components in tech-
nical grade trichloroethylene, a sample believed to be the same as that used
for the NCI bioassay experiment for carcinogenicity. Two of the contaminants
were epichlorohydrin and 1,2-epoxybutane, both shown to be mutagenic in the
Ames in vitro test with S. typhimurium TAlOO, and mutagenic or carcinogenic
by other published studies (Fishbein, 1976; van Duuren, 1977). The contaminants
and stabilizers are as follows:
Compound % w/w
Epichlorohydrin 0.22
Epoxybutane 0.20
Carbon tetrachloride 0.05
Chloroform 0.01
1,1,1-Trichloroethane 0.035
Diisobutylene 0.02
Ethyl acetate 0.052
Pentanol-2 0.015
Butanol-2 0.051
At a trichloroethylene dosage of 135 g/kg for 27 weeks, mice were reported
to show neoplastic changes. None of these compounds, at the level of contamina-
tion listed above, would be present in amounts which have been reported carcino-
genic to mice for that specific compound.
As an example, epichlorohydrin was carcinogenic to mice at a dosage of
720 mg/kg for 18 weeks (NIOSH, 1977). If epichlorohydrin is added to trichloro-
ethylene at a level of 0.2270 and the mixture given to mice at a dosage of 135
g/kg for 27 weeks (the neoplastic dose for trichloroethylene), the level of
epichlorohydrin stabilizer received by the mice is far below the amount re-
quired to produce tumors. However, any possible synergisms of these multiple
contaminants are completely unknown.
5.1.5 Human Epidemiology
5.1.5.1 Occupational Exposure--
Several studies have been conducted on the health of workers occupationally
exposed to trichloroethylene vapors. Signs and symptoms of trichloroethylene
poisoning observed in workers are characterized by dizziness, headaches, nausea,
vomiting, disturbances of vision, impairment in hearing, alcohol intolerance,
5-65
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bradycardia, unconsciousness, and death. When trichloroethylene comes into con-
tact with the skin, eczema, blisters, and, in severe cases, chemical burns may
result.
5.1.5.2 Medical Surveillance--
Four different methods of measuring the environmental concentrations of
trichloroethylene by biological methods have been proposed. The four biological
methods are measurements of: (a) trichloroethylene in the breath, (b) tri-
chloroacetic acid in the urine, (c) total trichloro-compounds in the urine,
and (d) trichloroethylene and trichloroacetic acid in the blood.
Stewart et al. (1974) indicated that breath analysis is a rapid and repro-
ducible method of evaluating humans who have recently been exposed to trichloro-
ethylene vapors. Twenty volunteers (10 men and 10 women) were exposed daily to
20, 100, or 200 ppm trichloroethylene for 1, 3, or 7.5 hr. Breath samples were
taken after exposure, analyzed, and found to be reproducible. In order to
achieve the most accurate results, monitoring of the trichloroethylene concen-
tration in the expired air should be completed within a few hours after exposure.
The urinary excretion of metabolites has been suggested as an exposure in-
dex for trichloroethylene (Teisinger, 1961; Tada, 1969; Ogata et al., 1971;
Ikeda et al., 1971; Nomiyama and Nomiyama, 1971; Ikeda et al., 1972). Nomiyama
(1971) has formulated equations to estimate the environmental concentrations of
trichloroethylene from urinary excretion or respiratory elimination. Nomiyama
indicated that the ratio between environmental trichloroethylene and trichloro-
acetic acid shows too much variation to allow its use as an exposure index.
Muller et al. (1974) stated that formation of trichloroacetic acid continues
for a long period after exposure and is excreted after a long delay, thereby
making trichloroacetic acid a poor index for exposure.
Total trichloro-compounds also have been used to estimate previous expo-
sure to trichloroethylene (Soucek and Vlachova, 1960; Tanaka and Ikeda, 1968;
Nomiyama, 1971; Ikeda et al., 1972). Nomiyama (1971) suggested that total
trichloro-compounds would be a more reliable parameter than trichloroacetic
acid. Stewart et al. (1970), after exposing subjects to 100 or 200 ppm tri-
chloroethylene 1 to 7 hr for 5 days, stated that there was a wide fluctuation
in the total quantity of metabolites excreted. Muller et al. (1974) indicated
that the different elimination rates of the two major trichloroethylene metab-
olites complicate the calculation of trichloroethylene in the body.
The final proposed method to biologically monitor trichloroethylene con-
centrations is measurement of blood and plasma concentrations of trichloro-
ethylene and trichloroacetic acid. Muller et al. (1974) and Pfaffli and Backman
(1972) estimate that by measuring these two compounds in the blood or plasma,
a more predictive value can be reached (i.e., it is better than measuring tri-
chloroethanol and trichloroacetic acid in the urine). More research needs to
be done to ascertain the reliability of this method.
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For all biological monitoring methods, it is imperative to remember that
ingested alcohol will bias results from any of the previously mentioned tests.
5.1.5.3 Epidemiology/Other Human Exposure Studies—
Szulc-Kuberska et al. (1976) examined 40 workers chronically exposed to
trichloroethylene vapors (from 1 to 23 years) and found that most workers
exhibited impairment of auditory and vestibular nerves. Examination revealed
the impairment of hearing to be perceptive deafness and the disorders of ves-
tibular apparatus of mixed central peripheral type. Complaints involved ex-
cessive somnolence, dizziness, headaches, and sexual impotency.
Twenty-four subjects with miscellaneous medical complaints (nausea, head-
aches, etc.) reported their symptoms to NIOSH representatives (Okawa et al.,
1973). NIOSH physicians then examined the urine of 20 workers exposed to tri-
chloroethylene and nine other people serving as controls. The physicians noted
that the workers excreted 17 to 196 mg/liter trichloroacetic acid and 38 to
121 mg/liter trichloroethanol in the urine. Control subjects' urine ranged from
0 to 29 mg/liter for the acid and Q to 27 mg/liter for trichloroethanol.
Measurement of trichloroethylene metabolites and ambient air levels of
trichloroethylene were performed in several industries by NIOSH Health Hazard
Determinations. Upper respiratory tract irritation is the most frequent com-
plaint registered by industrial workers (Roper, 1978; Kominsky, 1978; Gilles
and Philbin, 1978).
In Japan, trichloroethylene (undetermined purity and concentration) pro-
duced changes in the blood cells of an electronics plant staff according to
the report of Henmi and Nagata (1976).
Unconsciousness with cardiac arrhythmias occurred in a female dry cleaning
worker while pouring 40 liters of trichloroethylene into a vat. Liver function
tests were normal after 1 month, and no toxicity to the respiratory tract oc-
curred (Zaninovic, 1977).
In an industrial accident, an 18-year-old male worker died from inhalation
of trichloroethylene fumes. Upon autopsy, trichloroethylene concentration in
the victim's brain was 7.6 rag % (Fischer et al., 1978).
Jindrichova (1970) reported that 72 workers were examined a total of 130
times over a 12-year period (1956 to 1968). Over that time span, trichloro-
ethylene concentrations exceeded the permissible concentration of 400 mg/nr
(~ 75 ppm) up to 25-fold. Their symptoms were characterized by dizziness,
transitory narcosis, narcolepsy, and intolerance of alcohol. Subacute poison-
ing was found in eight of the subjects. Also, 462 urine samples taken during
these 12 years showed that the workers excreted up to 48 mg/liter trichloro.-
acetic acid and 1,750 mg/liter trichloroethanol.
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Lilis et al. (1969) studied 70 workers (83% under age 30) who had been
exposed to trichloroethylene for up to 6 years. At the plant investigation,
40% of the 214 air samples exceeded 50 mg/rrP (approximately 9.3 ppm), and 12%
were over 200 mg/nP, or approximately 37 ppm. Urinary trichloroacetic acid
exceeded 200 mg/liter in 46% of the employees exhibiting effects. Many of the
symptoms reported were similar to previously mentioned studies. The following
incidences of symptoms were recorded: headache, 74%; fatigue, 68%; irritabil-
ity, 56%; loss of appetite, 50%; disturbed sleep, 46%; nausea, 43%; excessive
sweating, 39%; dizziness, 31%; euphoria, 31%; palpitations, 29%; sleepiness
at end of shift, 29%; anxiety, 27%; disturbances of vision, 21%; and alcohol
intolerance, 21%.
Takamatsu (1962) studied 50 workers in a machine factory who were contin-
uously exposed to varying concentrations of trichloroethylene. Workers were
divided into three groups (A, B, and C) depending upon the average exposure.
Group A was exposed to 150 to 250 ppm, while Groups B and C were exposed to
50 to 100 and below 50 ppm, respectively. Of the 20 symptoms noted in these
workers, Group A complained of headache, dizziness, giddiness, drunken feel-
ing, flushing of the face, burning of the throat, skin effects, and fatigue.
Group B reported headaches, burning of the eyes, flushing of the face, and
fatigue; no symptoms were reported in Group C. Takamatsu also reported that
38% of the workers had slight or moderate visual disturbance, while 15% had
diplopia.
Andersson (1957) reported the predominant symptoms of 104 workers en-
gaged in metal, rubber, and dry cleaning industries, which use trichloro-
ethylene, were dizziness, vertigo, headache, tremors, nausea and vomiting,
fatigue, sleepiness, light-headed feelings, coma, and death. The number of
deaths was not reported. Approximately two-thirds of the 104 workers showed
signs of CNS effects. A follow-up study conducted on a few of the workers for
3 to 7 years after their last known exposure to trichloroethylene showed little
evidence of intoxication. Some workers reported that the symptoms disappeared
4 or 5 months after they had quit working.
Bardodej and Vyskocil (1956) divided 75 workers in dry cleaning and de-
greasing operations into four groups (depending upon years of exposure), and
studied the long-term effects of trichloroethylene. The four groups consisted
of workers exposed for less than 1, 1 to 2, 2 to 9, and > 10 years. The ambient
concentrations within these plants varied from 5 to 630 ppm. Bardodej and
Vyskocil recorded the symptoms found in both dry cleaning and degreasing work-
ers, and discovered that many of these workers complained of headaches, fatigue,
sleepiness, lacrimation, and an intolerance of alcohol.
Grandjean et al. (1955) studied 73 workers in 24 different workshops. They
collected a series of 96 air samples during the tests and found environmental
levels of trichloroethylene ranging from 1 to 335 ppm, with most samples be-
tween 20 and 40 ppm. However, the authors said that the air measurement tests
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did not indicate the total exposure. The workers displayed a relatively high
incidence of subjective complaints, alterations of the autonomic nervous sys-
tem, and neurological and psychiatric symptoms. These symptoms appeared to in-
crease with the length of time exposure to trichloroethylene. Since no signifi-
cant changes in the hepatic function were noted, Grandjean et al. could not
conclude if there were any relationships between liver toxicity and exposure.
Ahlmark and Forssman (1951) examined 122 workers and found 50% of the
workers had subjective disorders such as abnormal fatigue, irritability, head-
ache, and an intolerance of alcohol. These symptoms were related to the excre-
tion levels of trichloroacetic acid. Ahlmark and Forssman indicated that 50%
of the subjective disorders occurred in workers who excreted 40 to 75 mg tri-
chloroethanol per liter of urine. Those workers who excreted less than 20 mg/
liter trichloroethanol showed no signs of intoxication. However, these symptoms
appeared in all of those workers who excreted 30 mg/liter or more of trichloro-
acetic acid.
An editorial (JAMA, 1977) reported an American Cancer Society analysis
of 768 anesthesiologists who died during a 17-year period. The results showed
no high levels of liver disease, or any unique profile of cardiovascular or
cancer involvement. The anesthesiologists had been exposed to the more recently
used halogenated anesthetics in addition to the older anesthetics, such as tri-
chloroethylene, ether, or chloroform.
5.1.5.4 Accidental Ingestion and Addiction and Abuse--
5.1.5.4.1 Accidental ingestion—Ingestion of trichloroethylene is not
common, but when it does occur it can result in comas (Stentiford and Logan,
1956), liver toxicity (Secchi et al., 1968), kidney malfunction (Cohen-Solal,
1963), and cardiac arrhythmias (Meyer, 1966).
Accidental oral ingestion by a 4-1/2-year-old boy was reported by Gibitz
and Ploechl (1973). The child drank from a fruit-juice bottle containing tri-
chloroethylene and detergent. After consumption of approximately 7.6 g, as
estimated by trichloroacetic acid excretion, the only major effect noted was
a narcotic reaction lasting about 3 hr. Naish (1945) reported that a girl who
had ingested trichloroethylene became dazed, had numbness of the hands and
feet, and became incoherent. Two cases were reported by Stephens (1945) in
which about 1/2 oz was taken mistakenly for cough medicine, both patients be-
came comatose for a few hours. Stentiford and Logan (1956) reported another
case of accidental uptake by a 22-year-old man who accidentally drank cleaning
fluid containing trichloroethylene. He became comatose and remained in the
hospital 4 days before regaining his orientation and rationality.
Aviado et al. (1976) suggested that the comatose dosage of trichloro-
ethylene would be between 50 to 150 ml in an average adult. Kleinfeld and
Tabershaw (1954) found centrilobular necrosis of the liver, severe lower-
nephron necrosis, and acute pancreatitis in a patient who ingested an unknown
quantity of trichloroethylene; the patient died from hepatorenal failure*
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Meyer (1965) reviewed 15 cases of trichloroethylene ingestion; eight of
these cases proved fatal. All 15 cases showed CNS disturbances with cerebral
edema, central respiratory paralysis, and psychosis.
General anesthesia resulting from oral trichloroethylene poisoning was
observed in a patient by Fleishhacker et al. (1956). Narcotic effects and burns
in the pharynx and gastrointestinal tract were noted in three patients who in-
gested 50 to 150 ml of trichloroethylene (Natanzon et al., 1972). Other cases
of oral poisoning were reported by Puschel (1944); Abrahamsen (1960); Secchi
et al. (1968); Yacoub et al. (1973); and Cohen-Solal (1963).
Generalized dermatitis has appeared in workers who have come into contact
with liquid trichloroethylene. Four case histories were reported by Bauer and
Rabens (1974) which indicated that trichloroethylene caused dermatitis in work-
ers who hand-cleaned machine parts with this solvent; each of the four workers
showed other signs of poisoning.
"Accidental" ingestion of trichloroethylene has occurred from its use in
food products. Page and Charbonneau (1977) reported quantitative gas chromato-
graphic determination of trichloroethylene and found nine samples of instant
coffee contained no detectable levels. Four of 12 samples of ground roasted
coffee contained trichloroethylene, but the highest residue was only 1.67
Mg/g«
5.1.5.4.2 Misuse/abuse--The literature reveals that incidences of tri-
chloroethylene abuse (sniffing) have been increasing since the 1950's. The
most commonly abused product is cleaning fluid; the most common lesions found
during postmortem examination of abusers are hepatic necrosis and nephropathy.
James (1963) reported a fatality in a worker who frequently misused tri-
chloroethylene. The worker developed paresis of the olfactory nerves with inter-
mittent gastric disturbances over a 9-year period. His death occurred 17 hr af-
ter the last known exposure. Fatty degeneration of the liver and lung hemorrhage
were noted in the autopsy report. The urine contained a large amount of tri-
chloroacetic acid (55.5 mg/100 ml urine).
Alapin (1973) observed 20 cases of "addiction" in which two fatal cases
occurred. Alha (1973) also reported that deaths were caused by people sniffing
trichloroethylene mixtures found in paint thinners and cleansing agents. Baerg
and Kimberg (1970) found centrilobular hepatic necrosis and acute renal fail-
ure in three teenagers who sniffed Carbona® cleaning fluid (40% trichloro-
ethylene ).
Manasiev and Iliev (1976) studied 22 workers who were exposed to trichloro-
ethylene on their jobs. The exposure was confirmed by measuring trichloroacetic
acid in their urines. Twelve of the workers were reported to exhibit symptoms
of dependence and had symptoms of inebriation when the subjects inhaled tri-
chloroethylene. Manasiev and Iliev report that the apparent "need" to inhale
5-70
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the material was suggestive of psychic if not physical dependence on the inha-
lation of trichloroethylene.
One case of intentional exposure to trichloroethylene is reported in clin-
ical detail by Auzepy et al. (1976) along with a review of 17 other cases of
solvent exposure in France. The complications seen in the hospitalized patients
were as follows: two cardiac arrhythmias, eight respiratory problems, seven
inebriation and CNS symptoms, three comas, three delayed pneumonias, and one
delayed severe renal problem.
A 19-year-old sniffed industrial trichloroethylene for 30 min before swim-
ming. After climbing out of the swimming pool, he collapsed and died a few min-
utes later; death was attributed to heart failure (Cragg and Castledine, 1970).
A 16-year-old boy who frequently misused trichloroethylene was found dead
on the floor with his head over a bucket filled with the liquid. Postmortem
examination showed superficial burns of the left side of his face, acute in-
flammation of all the air passages and hemorrhagic edema of the lungs; death
was attributed to acute pulmonary edema (Teare, 1948).
5.1.6 Anesthetic and Analgesic Use
Trichloroethylene is used in the medical field as an anesthetic and anal-
gesic and is required by the National Formulary to be not less than 99.5% pure.
The anesthetic grade contains from 0.008 to 0.0127,, (w/w) of an antimicrobial
agent, thymol, and a blue dye.
The use of trichloroethylene as an anesthetic and analgesic became quite
popular during the 1940's, especially in England, but declined shortly there-
after as more effective and versatile anesthetic agents became available
(Waters et al., 1976). It has been demonstrated that, in use as an anesthetic,
it is bacteriostatic (Consorti and Giomarella, 1968; Mehta et al., 1974).
As an anesthetic, trichloroethylene usage has decreased primarily because
it does not produce sufficient skeletal muscle relaxation and tends to induce
postoperative complications. A recent survey by NIOSH (1975), however, indi-
cated that 5% (63 of 1,254) of hospitals with more than 100 beds in the United
States still use trichloroethylene. Another study reported in Chemical and En-
gineering News (1975) estimated that a maximum of 60,000 patients a year re-
ceive trichloroethylene during anesthetic procedures. In Great Britain and the
USSR, for example, the lack of a depressing effect on blood pressure and breath-
ing makes a small amount of trichloroethylene a common addition to a general
anesthetic combination.
Anesthetic induction and recovery are said to be both pleasant and slow
because of the high solubility of trichloroethylene in the blood (Huff, 1971).
Irritation of the local respiratory tract and mucous secretions are minimal;
the chemical may stimulate the pulmonary stretch receptors governing lung
5-71
-------
deflation, which would result in the shallow, accelerated breathing
(Whitteridge and Bulbring, 1944). Ventricular fibrillation resulting from sen-
si tization of the heart to epinephrine and other catecholoamines has been re-
ported earlier in this section.
The use of trichloroethylene as an analgesic has been recommended and is
still used for short operative procedures in obstetrics, burn dressing, cystos-
copy, and dentistry. However, trichloroethylene is contraindicated in toxemia
of pregnancy, anemia, and disease of the heart, lung, and kidneys. It is not
recommended for use with children or together with epinephrine because of the
high risk of ventricular fibrillation (Osol and Pratt, 1973). In obstetrics,
it is effectively used as an analgesic for women in labor, where less than 10
min of light anesthesia is required. Self-administration for obstetrical anal-
gesia has proved to be effective and safe. The easy access to pure trichloro-
ethylene and the development of special inhaler devices have increased the us-
age of vapors for obstetrical analgesia.
British use appears to be considerable, in spite of the cited danger of
trichloroethylene producing ventricular fibrillation when (a) used as sole
agent for deep anesthesia, or (b) when adrenaline solutions are given simul-
taneously (Farman, 1977).
Most of the early deaths reported during trichloroethylene anesthesia
have been attributed to the production of dichloroacetylene, a neurotoxic
agent. Formation of dichloroacetylene resulted from passage of trichloro-
ethylene over soda lime (used as a carbon dioxide absorber in a closed-system
rebreathing apparatus).
In dentistry, the use of trichloroethylene is sporadic. The Council of
Therapeutics has reevaluated trichloroethylene and no longer considers it a
product to be used regularly; the compound was formerly included and discussed
in the Council's book, Accepted Dental Therapeutics, but it has been omitted
since 1970. The apparent reasons for reevaluating the use in dentistry and
recommending that it no longer be used were the incidences of cardiac ar-
rythmias and the episodes of apnea (Mitchell, 1977, private communication).
The use of trichloroethylene in dental surgery patients in conjunction
with other anesthetic agents has apparently increased in the USSR. Starodubtsev
et al. (1976) reported a significant rise in respiration rate of patients ad-
ministered trichloroethylene in conjunction with flothane.
Multiple anesthetic agents including 0.4% trichloroethylene were used on
50 dental surgery patients in a recent trial (Allen et al., 1976). Detailed
cardiorespiratory measures were made; the trichloroethylene-halothane combina-
tion produced fewer cardiovascular depressant effects than other anesthetic
combinations and was considered to be "useful for general anesthesia in oral
surgical procedures in outpatients."
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5.2 METHYL CHLOROFORM (1,1,1-TRICHLOROETHANE)
5.2.1 Uptake and Absorption
In assessing the relationship of absorption to the overall health effects
of methyl chloroform (MC), one needs to consider the types of action involved
in the chlorinated hydrocarbons in general. They are all anesthetics; they are
all affected by the rate of absorption during exposure by inhalation, the most
common route of exposure in man.
Differences in the rate of absorption, reflected in the partition coef-
ficients, could account for the approximately tenfold greater toxicity of the
1,1,2-isotner over the toxicity of 1,1,1-trichloroethane (Fairchild et al.,
1977). The blood/air partition coefficients are 1.4 for methyl chloroform and
44.2 for 1,1,2-trichloroethane (Morgan et al., 1972). The body content of the
latter will increase much more rapidly than the former during exposure to equal
concentrations of vapor. Following exposure, the body content of methyl chloro-
form will decrease much more rapidly by excretion in breath than that of its
1,1,2-isomer, leaving less in the body for metabolism.
Cutaneous absorption, according to Stewart and Dodd (1964), depends on
the area of exposure. Methyl chloroform is more readily absorbed through the
skin than is trichloroethylene. Because continuous immersion of both hands in
methyl chloroform for 30 min has been estimated to be equivalent to a 30-min
vapor exposure to 100 to 500 ppm of the compound, skin absorption would pre-
sent only a limited health hazard. In Stewart and Dodd's experiments, both
male and female subjects ranging in age from 25 to 62 years were used. Three
kinds of hand exposure were tested: thumb immersion; total hand immersion;
and topical hand application, which consisted of brief immersion, withdrawal,
solvent evaporation, and reimmersion. Alveolar air samples were-measured dur-
ing and following exposure. Methyl chloroform in the alveolar air increased
rapidly during immersion and dropped off slowly following exposure. The re-
sults are shown in Table 5-14. Considerable effort was taken that the exposure
through the skin was not confounded by vapor inhalation. Periodically, during
the skin exposure, samples of breathing zone air were analyzed. Inhalation,
as a source of the methyl chloroform in this experiment, was not a factor
(Stewart and Dodd, 1964).
Fukabori et al. (1976) report initially rapid skin absorption in humans.
Methyl chloroform was either applied to the forearm skin (2 hr/day for 5 days)
or both hands were dipped in the solvent (seven times, per day for 4 days). The
compound appeared in the breath as early as 30 min after arm application, and
the concentration reached 3 to 7 ppm in the breath after 2 hr. On the 5th day,
blood concentrations were 6 to 9 ^g of methyl chloroform per milliliter. When
hands were dipped in methyl chloroform, concentrations in expired air ranged
from 5 ppm on the 1st day to 11 ppm on the 4th day.
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TABLE 5-14. ABSORPTION OF 1,1,1-TRICHLOROETHANE
PPm
Length of Average peak Average breath
exposure Type of breath concentration
(min ) exposure concentration 2 hr post exposure
30 Thumb 1.0 0.31
30 Hand (immersion) 21.5 1.55
30 Hand (topical) 0.65 0.31
Source: Stewart and Dodd (1964).
A study of the absorption of methyl chloroform vapors through human intact
skin has recently been performed by Riihimaki and Pfaffli (1978); however, no
data from the work are available at this time.
Apparently, many of these experiments provide only estimated data. In
practice, the net rate of absorption for prolonged exposure will be reduced
as the concentration of dissolved vapor builds up in the blood stream. This
effect was demonstrated very clearly by Riley et al. (1966) who showed that
when a subject is exposed to a chlorinated hydrocarbon vapor in uniform con-
centration, the concentration in expired air increased fairly rapidly during
the first hr, after which time there was little change. After exposure to
methyl chloroform, excretion of the unmetabolized compound in breath may con-
tinue for many hours or even days (Stewart et al., 1969); see subsection 5.2.4.
Morgan et al. (1972) prepared -^Cl-labeled methyl chloroform and admin-
istered it by a single breath inhalation of vapor to five human male volunteers.
The subjects held their breath 20 sec to ensure maximum absorption. Exhaled air
was trapped for 1 hr and the methyl chloroform concentration measured. Total
excretion in breath after 1 hr equaled 4470 of the original dose of methyl chloro-
form, the second highest excretion rate observed in the study of 13 halogenated
hydrocarbons.
The uptake of methyl chloroform from air containing 0, 100, 350, and 500
ppm of the compound was studied in 20 male and female subjects by Stewart et
al. (1975). Subjects were exposed for 1, 3, and 7.5 hr at each concentration.
Breath samples were taken from 1 min to 71 hr after exposure, and were analyzed
for unmetabolized compound. Curves of the methyl chloroform remaining in the
5-103
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breath were plotted to estimate the magnitude of exposure. Breathing 350 ppm
methyl chloroform for 1 hr, for example, produces a breath level of about 165
ppm, which drops off to under 1 ppm at 23 hr. On the other hand, breathing
the same concentration (350 ppm) for 7.5 hr gives a breath concentration of
~ 244 ppm which has dropped to ~ 7 ppm 16 hr later.
Stewart et al. (1961a) measured human urine samples 15 min after exposure
to methyl chloroform; some samples contained up to 2 ppm of the compound, some
contained only a trace, and some urine samples, none at all.
MacEwen and Vernot (1974) measured absorption of methyl chloroform into
the blood of 8 dogs, 4 monkeys, and 40 rats after continuous inhalation expo-
sure at 250 and 1,000 ppm for 100 days. Although fatty livers in mice given
1,000 ppm methyl chloroform were seen in preliminary experiments, none of the
animals exhibited lesions which could be related to exposure. Levels of un-
changed methyl chloroform in blood of these animals is shown in Table 5-15.
TABLE 5-15. METHYL CHLOROFORM CONCENTRATIONS IN BLOOD
Exposure
level
(ppm)
Control
250
1,000
Animals and exposure time
3
0
11. 3^
75
Dogs
5
0
' 16
46
(weeks )
9
0
9.2
38
13 3
0 0
17 4.0
75 33
Monkeys
5
0
14
48
(weeks )
9 13
0 0
3.2 4.4
17 30
Source: MacEwen and Vernot (1974).
a/ Quantities in micrograms per gram.
Morgan et al. (1972) demonstrated that in man, the amount of absorption
of methyl chloroform is increased by inhaling the vapor and holding the breath.
5.2.2 Transportation and Distribution
Regardless of the exposure of a substance, there is no harm possible unless
there is some interaction with the organism. Astrand (1975) has reviewed the
uptake of several solvents (including methyl chloroform) into the blood and
tissues of man. Figures 5-2a and 5-2b show the time course of methyl chloroform
in the lungs and blood after exposure by inhalation (Astrand et al., 1973).
5-104
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I
Q.
ai
METHYLCHLOROFORM
A styrene
• aromat. white spirit
O toluene
A methylene chloride
O aliphat. white spirit
• methylchloroform |
time after the
\ end of exposure
5 10 30mJ 2 5 10 20hoor,
Figure 5-2a. Exposure to methyl chloroform by inhalation of 250 and 350 ppm
in five subjects at rest and during work (from Astrand, 1975).
100
75
50
25
quotient
A styrene
• aromat. white spirit
O toluene
A methylene chloride
Q aliphat. white spirit
• methylchloroform |
Figure 5-2b.
50 100 150 Watt
Quotient between arterial blood concentration and alveolar air
concentration after 30 min exposure during rest (N=20) and
exercise (N=4-5). The poor solubility of methyl chloroform
is evident (from Astrand, 1975).
5-105
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Partition coefficients for methyl chloroform in the body are: blood/gas =
1.4; oil/gas = 139; oil/blood = 100 (Morgan et al., 1970; 1972). These figures
are based on measurements in vitro made at 40 and 25°C. The "oil" measurement
is a model of the amount of methyl chloroform that subcutaneous fat would hold.
Of seven solvents measured by Astrand (1975), methyl chloroform was least solu-
ble in blood (followed by methylene chloride^ trichloroethylene, and toluene).
Four male Sprague-Dawley rats were exposed to 955 ppm of methyl chloro-
form for 73 min, and the concentration measured in the expired air until it
was undetectable (Boettner and Muranko, 1969). Stewart et al. (1961) had ex-
posed humans to similar levels and compared the data. One hour following expo-
sure, human breath contained 1.85 times the concentration of methyl chloroform
as in rat breath; 10 hr following exposure, human breath contained four times
the concentration in rat breath. These results showed that humans and rats dif-
fer in any or all of the parameters of absorption, elimination, or retention.
Concentrations of methyl chloroform in the breath of rats and man were
compared at 1 hr following different exposure indices, usually calculated as
the product of concentration and time (Stewart et al., 1961a). The results
indicated that the concentration of the compound was of greater importance
than the time of treatment in determining postexposure breath concentration.
Further studies with concentrations from 100 to 1,000 ppm confirmed that when
the concentration of the chlorinated hydrocarbon is sufficient to cause rapid
saturation, the concentration of methyl chloroform or total chlorinated hydro-
carbon in expired air is proportional to the concentration of the compound
rather than the time of treatment, once the saturation limit is reached.
5.2.3 Metabolic Effects
5.2.3.1 Biotransformation—
The primary metabolites of methyl chloroform are trichloroethanol and tri-
chloroacetic acid (TCA) as shown in Figure 5-3 (Hake et al., 1960; Ikeda and
Ohtsuji, 1972).
On the basis of in vitro experiments with normal gut flora, it appears
that microbial degradation is not an important process in metabolic degrada-
tion (McConnell et al., 1975).
Hake and co-workers (1960) injected one female and two male rats (170 to
183 g) intraperitoneally (i.p. ) with 700 mg/kg of methyl chloroform-1-^C.
About 50% of the urinary radioactivity occurred as 2,2,2-trichloroethanol in
the form of glucuronide conjugate. The other 50% volatilized at room tempera-
ture and was probably the parent compound. It was suggested that methyl chloro-
form metabolized by an initial oxidation to trichloroethanol and subsequent
oxidation to small quantities of trichloroacetic acid. In this study, 98.7%
of the injected radioactivity was exhaled as unchanged compound, and 0.5%
5-106
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METHYL
CHLOROFORM TRICHLOROETHANOL
CC,3_CH3 »» CCI3-CH2OH
/ \
glucuronide \^
conjugation oxidation
. . ' \
CCI3 - CH20 - glue. TR,CHLOROACET|C AC|D
CCI3COOH
Sources: Hake et al. (1960); Ikeda and Ohtsuji (1972).
Figure 5-3. Metabolic route suggested for methyl chloroform.
as C02« Only 0.8570 of injected radioactivity was recovered in urine, and
only half of that was identified as a metabolite.
The studies on metabolism by Ikeda and Ohtsuji (1972) compared the metabo-
lism of methyl chloroform using both inhalation dosage (a route of greater in-
terest to human work) and i.p. injection. Eight studies of six rats per study
were made, using 50-g Wistar rats and a concentration of 200 ppm for 8 hr. All
urine excreted in 48 hr was collected. Trichloroacetic acid (0.5 mg/kg body
weight) and trichloroethanol (3.1 mg/kg body weight) were found. A dose of
2.78 mmol/kg body weight of methyl chloroform was also injected i.p. into a
similar group of rats to check the effects of dosage route. The results of
urine analyses following i.p. injection were essentially the same as those ob-
tained on the inhalation experiments. The relative levels of trichloroethanol
and trichloroacetic acid seen in Ikeda1 s experiments may indicate that the
acid is derived from the alcohol.
Fukabori and co-workers (1976) reported the metabolism of methyl chloro-
form in humans after skin application to two sites.
Site I
Forearm skin, 2 hr/day for 5 days
Metabolites in urine: Trichloroethanol, 2 to 6 mg/day (Day 1)
Trichloroacetic acid, slight increase with in-
creased exposure
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Site II
Dip both hands, seven times per day for 4 days
Metabolite in urine: Trichloroethanol, 5 to 15 mg/day
It should be noted that most of the methyl chloroform was in the expired air;
concentrations of unchanged solvent ranged from 5 to 11 ppm (days 1 and 4),
respectively, when hands were dipped in the solvent.,
5.2.3.2 Detoxification and Activation—
Stewart (1968) exposed five male volunteers to 500 ppm methyl chloroform,
7 hr/day for five consecutive days. The 24-hr urines collected before, during,
and after this exposure were analyzed for trichloroethanol and trichloroacetic
acid. Results were as follows, and show that trichloroethanol concentrations
in urine are higher than trichloroacetic acid levels, but the persistence of
trichloroacetic acid is greater.
Control value (mean)
1st exposure day
2nd exposure day
3rd exposure day
4th exposure day
5th day after last exposure
12th day after exposure
Trichloroacetic
acid (mg/24 hr)
14.2
7.5
10.9
12.3
14.1
18.0
17.5
Trichloroethanol
(mg/24 hr)
< 1
20.1
30.1
29.3
46.6
7.0
< 1
Mikiskova and Mikiska (1966) report that the metabolites of this chlori-
nated hydrocarbon have physiological effects. Trichloroethanol, which is ex-
creted after repeated exposure, is a central nervous system depressant even
when it is conjugated with glucuronic acid. The effects, particularly the toxic
effects, of trichloroacetic acid (the major urinary metabolite) are low.
5.2.4 Excretion
Pulmonary excretion rates in man in the first hr following exposure to
methyl chloroform were 447» (Morgan et al., 1970). In a series of compounds,
excretion rates were inversely proportional to the lipid solubility of the
compound.
A summary of the excretion of methyl chloroform in exhaled breath is given
in Table 5-16.
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TABLE 5-16. METHYL CHLOROFORM EXCRETION IN EXHALED BREATH
Route
Species
% Dose exhaled
unmetabolized
Reference
Skin contact Humans
Inhalation Humans
Injection (i.p.) Rats
Peak breath level = Stewart and Dodd (1964)
14% of estimated
150-ppm dose
44% in 1 hr
> 99% of 700 mg/kg
Morgan et al. (1970)
Hake et al. (1960)
In the studies of Hake et al. (1960), over 99% of the i.p.-injected
methyl chloroform was excreted by rats via the pulmonary route (98.7% un-
changed, 0.5% metabolized) and less than 1% via the urine (0.85% of dose,
half identified as the glucuronide of trichloroethanol). Boettner and Muranko
(1969) have used animal breath excretion data for estimation of exposure in
humans.
Ikeda and Ohtsuji (1972) gave methyl chloroform to rats by two routes:
inhalation and i.p. injection. Alveolar air was the main route of excretion
in both series of studies. Urinary excretion was as follows:
Metabolites in urine (48 hr)
Dosage
Inhalation
(200 ppm, 8 hr)
Injection, i.p.
(2.78 mmol)
Trichloroacetic acid
(mg/kg body weight)
0.5 + 0.2
0.5 + 0.2
Trichloroethanol
(mg/kg body weight)
3.1 + 1.0
3.5 + 1.4
Ikeda suggested that the tendency of a compound to be excreted into al-
veolar air was related to vapor pressure. Although methyl chloroform has a
high vapor pressure and is excreted by the breath (over 99%) (Hake, 1960),
the principle does not apply equally well to a series of chlorinated solvents,
probably because metabolism is highly important to excretory rates.
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O Q
Morgan et al. (1970) measured pulmonary excretion of QCl-labeled methyl
chloroform and trichloroethylene in man following a single breath administra-
tion; the former was excreted more rapidly than the latter: 44 and 10% of
the inhaled dose, respectively, were excreted in the breath in the first hour.
The rate of excretion varies inversely with the serum/air partition coefficient!
With low level exposure of 1 mg/liter (or about 183 ppm), Monzani (1969)
found that (a) only one of 18 workers excreting trichloroacetic acid in the
urine, and (b) that excretion was at a level of 9.72 mg/liter of urine.
Table 5-17 summarizes the intake and excretion of methyl chloroform as
reported by several different studies, and shows that most of the compound
is excreted by the lung.
In 1968, Tada and co-workers exposed two male subjects by inhalation to
a series of chlorinated hydrocarbons. The urinary excretion of trichloroacetic
acid was increased by repeated exposures (see Figure 5-4). However, the in-
crease was not proportional to vapor concentration and exposure duration.
Tada (1969) repeatedly exposed humans to 200 to 400 ppm methyl chloro-
form. There was an increase in urinary excretion of trichloroacetic acid with
a maximum reached in 4 to 5 days; the urinary acid levels fluctuated during
the day, but the authors suggested that the total 24-hr excretion was related
to time and intensity (vapor concentration) of exposure.
Methyl chloroform was still found at a level of 0.1 ppm in the breath of
an individual 1 month after exposure to a mixture of 370 ppm of the compound
and 130 ppm trichloroethylene, 7 hr/day for 5 days (Stewart et al., 1969).
Methyl chloroform was also present in alveolar air 1 month after exposure for
6.5 to 7 hr/day for 5 days at 420 to 612 ppm concentration (Stewart et al.,
1961a).
5.2.5 Biochemical Studies
5.2.5.1 Organ/Cell Effects--
Most of the biochemical and clinical chemistry reported concerns the ef-
fects on the liver and kidney, or the urinary signs of these effects in both
man and experimental animals.
In a study by Platt and Cockrill (1969), rats were orally dosed for 7 days
with 1.25 ml/kg body weight (1.675 g/kg) of methyl chloroform in paraffin oil.
Increases in protein of both microsomal and cell sap fraction were seen. En-
zyme activity of NADPt^-cytochrome C reductase and glutamic dehydrogenase also
increased. Seven other enzymes in the treated rats did not differ from controls.
The unchanged enzymes were:
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TABLE 5-17. FATE OF METHYL CHLOROFORM
Intake
Inhalation ~ 5 mg
Hand
Man,
Man,
Man,
Man,
Man,
Man,
Man,
Man,
immersion/30
inhalation
inhalation
inhalation
inhalation
inhalation
inhalation
inhalation
inhalation
(1 breath)
rain
37
184
210
350
350
420
460
496
ppm
ppm
ppm
ppm/
ppm
ppm
ppm
ppm
Retained by
body
44%
22
Lung
per
Excretion
Unchanged
Urine Blood
dose
ppm at
10 min
(daily)
(work place )
2
1
hr (x 6)
hr
7-1/2 hr
2
2
3
hr (x 3)
hr
hr
Metabolized
Lung^ Urine
3.4 mg/f
9.7 mg/f
urine
urine
3.1 mg/TCA/day
I 98
I 1
I 165
I 7
ppm
ppm
ppm
ppm
at
at
at
at
1 min
23 hr
1 min
16 hr
7.2 mg/TCA/day
23
38
ppm
ppm
at
at
1 hr
1 hr
<0.01%
total
dose/min
Man,
Man,
(Rat
(Rat
inhalation
inhalation
) injection
) inhalation
500
632
700
370
ppm
PPm
78
2
min
hr
mg/kg
ppm
7
hr (x 5)
70
41
98
<100 ppb at
1 month
ppm
ppm
.7%
at
2 ppm 3-4 ppm
1 hr
0.5% 0.85%
Summarized from several tables.
Source: Criteria Document, NIOSH (1976),
-------
Trichloroacetic Acid
mg/l
Merhyl Chloroform
Exposures
)5
~ 5
Source: Tada et al. (1968).
Figure 5-4. Increase in urinary excretion of trichloroacetic acid metabolite by repeated
exposure to vapor.
-------
Aminopyrine demethylase
NADH2-cytochrome C reductase
Glucose-6-phosphatase
Lactic dehydrogenase (LDH)
Glutamic dehydrogenase
6-Phosphogluconate dehydrogenase
Glucose-6-phosphate dehydrogenase
Lazarew (1929) saw depression of contractility in the frog heart after
methyl chloroform exposure, and Belej and Aviado (1975) saw the phenomenon in
the canine heart-lung preparation.
Herd and Martin (1975) inhibited rat liver mitochondrial respiration in
in vitro with methyl chloroform. Herd et al. (1974) also studied the effect
on isolated papillary muscles from rat hearts. There was a 10% decrease in
the time to develop maximum tension after solvent exposure. Addition of cal-
cium ions assisted the isolated heart preparation to recover after the methyl
chloroform exposure.
Rats, pretreated (2 ml/kg; 2.68 g/kg) with methyl chloroform 24 hr before
sacrifice were used for measurement of hepatic blood flow. The pretreatment
had no effect on hemodynamic measurements, but some slight inflammation of the
treated rat livers was seen (Rice et al., 1967).
Krantz et al. (1959) anesthetized rats with methyl chloroform, then re-
moved the hearts after 1-hr exposure and measured oxygen uptake by cardiac ven-
tricle tissue. Oxygen uptake of the exposed heart tissue was reduced by one-
third over controls. Other in vitro work reported in the same study included
blood clotting time and hemolytic action of methyl chloroform used as an anes-
thetic agent. Methyl chloroform exposure produced no change in clotting time
or hemolysis production.
5.2.5.2 Effects on Enzyme Systems—
Van Dyke and Wineman (1971) made an in vitro dechlorination study on Cl-
labeled methyl chloroform. Less than 0.5% of the -^"Cl was enzymatically re-
moved in 30 min. A 7-hr daily exposure of rats to 500 ppm had no effect (e.g.,
no induction) on their liver microsomal dechlorination of methyl chloroform
when tests were run in vitro. It was noted that the more toxic isomer of
methyl chloroform, 1,1,2-trichloroethane, acted as a good substrate for the
liver dechlorinating system. Dechlorination of 1,1,2-trichloroethane could
be induced by exposing rats to methoxyflurane, while the dehalogenation of
methyl chloroform could not. This basic study on the mammalian cleavage of
the carbon-halogen bond is of interest as a possible mechanism of toxicity.
Carlson (1973) studied the toxicity of methyl chloroform by inducing liver
enzymes with both 3-methylcholanthrene and phenobarbital. These compounds dif-
fer in the spectrum of enzymes induced; the former protects against
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toxicity and the latter potentiates CCl^ toxicity. Pretreatment of rats with
phenobarbital (50 mg/kg/day for 4 days) before exposure to a massive dose of
methyl chloroform by inhalation (11,600 ppm/2 hr) produced increased liver
weights, decreased glucose-6-phosphatase, a sixfold elevation in serum gluta-
mic pyruvic transaminase (SGPT) and a fourfold elevation in serum glutamic
oxaloacetic transaminase (SCOT). There was no interaction between 3-methyl-
cholanthrene induction and methyl chloroform, in spite of the high concentra-
tion (13,070 ppm) used; from the results it was not possible to show protection
because of the lack of ability of the 1,1,1-trichloroethanol to cause signifi-
cant hepatotoxicity. It could be stated that enzyme induction by phenobarbital
allows expression of a hepatotoxicity that otherwise (a) does not occur, or
.(b) if it occurs is not measurable without phenobarbital enzyme induction.
Methylcholanthrene had no effects on the test system.
Pretreatment of male Swiss Webster mice with either isopropyl alcohol (2.5
ml/kg) or acetone (2.5 ml/kg) 8 hr before i.p. injection of methyl chloroform
(3,500 mg/kg) had no effect on serum glutamic pyruvic transaminase (SGPT) lev-
els (Traiger and Plaa, 1974).
Intraperitoneal injection of methyl chloroform, given in corn oil (2.8
ml/kg; 3.76 g/kg), to Sprague-Dawley rats produced no changes in liver enzymes,
specifically glucose-6-phosphatase, and no change in liver lipoperoxidation.
Levels of triglycerides were also not changed (Klaassen and Plaa, 1969).
Gehring (1968) reported SGPT levels of over 54 units in female Swiss
Webster mice given an LD^Q dose of 99.5% pure methyl chloroform (16.8 ml/kg;
22.5 g/kg).
The liver function of dogs has been studied by Krantz et al. (1959) and
Klaassen and Plaa (1967). Krantz gave methyl chloroform for 1 hr as an anesthe-
tic (no dose levels stated) and found no change in liver function as tested by
sulfobromophthalein (BSP) retention immediately, 24, and 72 hr later. Klaassen
and Plaa found no BSP changes with doses of 2.5 to 3.5 ml/kg i.p., but found
SGPT activity changed at 24 hr with an ED5g of 0.87 ml/kg. Slight subcapsular
liver necrosis was found later in these dogs.
Cornish et al. (1973) measured the serum glutamic oxaloacetic transaminase
(SCOT) activity in rats given 0.3 to 2.0 ml/kg body weight (400 to 2,700 mg/kg)
of methyl chloroform. Rats had received two 50 mg/kg i.p. doses of phenobarbital
1 and 2 days before. A methyl chloroform dose-dependent rise was seen in SCOT
values which was not changed by the phenobarbital, which is the opposite of
Carlson's data (Carlson, 1973). Cornish, however, administered phenobarbital
at 50 mg/kg for 2 days, and Carlson gave the same dose for 4 days.
Klaassen and Plaa (1966) gave mice 3,700 mg/kg of methyl chloroform and
got the following results on liver function tests:
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Phenolsulfopthalein (PSP) excretion - Not changed
BSP retention - Not changed
Oral administration to rats of 1,650 mg/kg (1.25 ml/kg) of methyl chloro-
form for 7 days produced the following effects on enzyme systems (Platt and
Cockrill, 1969):
Glutamate dehydrogenase - Significant increase
NADPH2-cytochrome C reductase - Significant increase
Aminopyrine demethylase - Not changed
NADH2-cytochrome C reductase - Not changed
Glucose-6-phosphatase - Not changed
Glucose-6-phosphate dehydrogenase - Not changed
6-Phosphogluconate dehydrogenase - Not changed
Dornette and Jones (1960) measured serum transaminase in five patients
who had been anesthetized with methyl chloroform for up to 2 hr and found no
significant effects on the enzyme.
Kramer's extensive study of human enzyme levels in long-term exposure to
methyl chloroform is described under the section on epidemiology (Kramer et
al., 1976). Measurements on 151 exposed and 151 unexposed workers were made.
No statistically significant differences were found in the following enzymes:
SCOT, SGPT, gamma glutamyl transpeptidase, LDH, and alkaline phosphatase.
Griffiths et al. (1972) reported on serum enzymes of a single subject
who inhaled a methyl chloroform/trichloroethylene mixture. SCOT and LDH were
greatly elevated, but due to the mixture inhaled, the effects of methyl
chloroform alone cannot be assessed.
Torkelson et al. (1958) studied the effect of single exposure of human
subjects to methyl chloroform at 900 to 1,000 ppm for 75 min. The SGPT was nor-
mal (as were a series of other clinical chemical tests).
5.2.6 Toxicologic Data
5.2.6.1 Target Organs—
In man, the first effects of methyl chloroform exposure are seen on the
central nervous system (CNS) with effects on reaction time and manual dexterity
after 1 hr of exposure at 350 ppm (Gamberale and Hultengren, 1973) and dis-
equilibrium at 900 to 1,000 ppm for 20+ min (Torkelson et al., 1958; Stewart
et al., 1961). Animal experiments have shown CNS responses and behavioral
changes with exposure but at higher concentrations than those necessary to pro-
duce subtle effects in man. Although these effects are those of any reversible
anesthetic agent, their occurrence after exposure to methyl chloroform in in-
dustry or the environment are considered toxic effects.
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The heart is one of the organs most vulnerable to the effects of methyl
chloroform. Aviado et al. (1976) elicited a significant depression of cardiac
contractility with exposure to 1,000 ppm in the dog, although Reinhardt et al.
(1973) found that the minimal concentration that causes sensitization in the
dog to be 27.8 mg/liter or 5,000 ppm. Effects on the electrocardiogram, myo-
cardial contractility, cardiac output, pulmonary and systemic vascular resis-
tance in experimental animals have been studied (Somani and Lum, 1965; Lucchesi,
1965; Herd et al., 1974; Belej et al., 1974; Aviado and Belej, 1975; Krantz et
al., 1959; Rennick et al., 1949). The sensitization of the heart to the effects
of epinephrine is discussed in a later section.
The liver is susceptible to toxicity from all the chlorinated hydrocarbons
in one degree or another so it could be classified as a methyl chloroform tar-
get organ. The susceptibility of the liver varies between animals and man. In-
halation of ~ 2,600 ppm for 15 min produces clinically detectable effects on
the liver in man, but in mice the hepatoxic dose is close to the lethal inhala-
tion dose (Aviado et al., 1976).
Local irritation of the respiratory tract is a common human complaint and
on chronic inhalation studies in animals, lung irritation was occasionally the
only effect seen.
5.2.6.1.1 Brain, CNS effects—Dahlberg (1972) suggests the greatest haz-
ard of methyl chloroform is its "narcotic nature" although damage to other
organs (liver, kidney) has occurred. According to Dahlberg, methyl chloroform
is only 40 to 50% as hazardous as trichloroethylene in its narcotic effect.
A Russian report without control data describes pathological changes in
nerve cells of rats after 120 exposures to methyl chloroform (Tsapko and
Rappoport, 1972). Perivascular brain changes were also reported after 50 ex-
posures in the same study.
Most CNS effects of methyl chloroform reported in the literature lie some-
where between the two reports above, one of which suggests methyl chloroform
produces minimal narcosis and the other which suggests serious pathological
effects. In man, 1,000 ppm for 30 to 70 min will produce narcosis symptoms
by most any measure.
Since the compound produces no excitation and much less fluid and saliva-
tion in the mouth/respiratory tract than agents such as diethyl ether, methyl
chloroform was considered a superior anesthetic in the last century (Von
Oettingen, 1964). Its problems lie with the cardiovascular system, not the
CNS; it is an effective functional depressant of the CNS.
Dornette and Jones (1960) used 1 to 2.6% methyl chloroform (10,212 to
26,550 ppm) with 80% nitrous oxide for anesthesia induction in 50 human sub-
jects. The volunteers were kept anesthetized up to 2 hr, maintained with
5-116
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increased methyl chloroform levels of 0.6 to 2.25% (6,127 to 22,982 ppm), ad-
ministered with decreased nitrous oxide-oxygen. The authors attributed 75% of
the anesthetic effect to methyl chloroform and the remaining to the nitrous
oxide-oxygen mixture. Light anesthesia was induced within 2 min, and recovery
of reflexes occurred 3 to 5 min after discontinuing the anesthetic agent.
Siebecker et al. (1960) looked at the human EEC in methyl chloroform (plus
nitrous oxide) anesthesia and found patterns similar to halothane.
Krantz et al. (1959) induced methyl chloroform anesthesia in dogs with
0.45 g/kg and produced respiratory failure with 0.8 g/kg. A single human volun-
teer, who was anesthetized for 30 min, complained of slow recovery from anes-
thesia and of "feeling tired" for several hours after the anesthesia.
Complete narcosis in experimental animals has been calculated to occur
at 8,280 ppm and death from overexposure at 11,960 ppm (Lazarew, 1929). Expo-
sure time is also a factor; when the air is saturated with methyl chloroform
(16.7% or 167,000 ppm), dogs become unconscious in 7 to 8 min (Dubois and Roux,
1887); at 18,000 ppm rats become helpless in 5 min and unconscious in 1 hr;
monkeys exhibit ataxia in 1 hr and show serious depression after 5 hr of inha-
lation at 5,000 ppm (Adams et al., 1950). The studies of Adams indicate these
central effects are characterized by functional disturbance, not tissue in-
sult. CNS depression constituted the only acute effects. Signs of this depres-
sion, stupor, locomotor problems, and unconsciousness, were totally reversible
if the animals were removed from exposure before respiratory failure and cardiac
arrest occurred.
Savolainen et al. (1977) exposed adult male rats by inhalation to 20
/Ltmole/liter (500 ppm) methyl chloroform 6 hr/day for 5 days and found no be-
havioral changes in an open field test. The animals, killed after the 5th day
of exposure, had a slight decrease in brain RNA content. (The RNA changes were
greater with trichloroethylene, which was tested in a concurrent group.)
Larsby et al. (1978) measured central nervous system function in rabbits
infused i.v. with a lipid emulsion of methyl chloroform. This animal model
showed that 75 ppm produced vestibular disturbances. The authors feel the
model may have application to human industrial exposure levels.
The Romberg test (a neurological test that measures proprioceptive con-
trol with a subject standing, feet together, eyes closed) has been used to
measure the narcotic or anesthetic-like CNS effects of methyl chloroform.
Stewart et al. (1961a) found four-fifths of the men failed to perform a nor-
mal test after 15 min exposure at 2,650 ppm (starting at zero concentration),
but saw no CNS effects at 500 ppm. Torkelson et al. (1958) found positive
Romberg tests in all subjects exposed to methyl chloroform at 1,740 to 2,180
ppm. Lightheadedness occurred in three of four subjects exposed to 1,000 ppm
for 70 to 75 min.
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Simple tests of motor control have demonstrated reversible narcotic ef-
fects by methyl chloroform in human subjects exposed to 250 ppm (Gambarale and
Hultengren, 1970), 450 ppm (Salvini et al., 1971), 1,000 ppm for 70 to 75 min
(Torkelson et al., 1958), and at 900 ppm for 20 to 73 min (Stewart et al.,
1961a). Stewart et al. (1961a) found no CNS effects with balance and coordi-
nation tests following methyl chloroform exposure at 500 ppm for 3 hr, but ob-
served CNS effects in four of five subjects exposed at the same level for a
longer time (6.5 to 7 hr) (Stewart et al., 1969).
Stahl et al. (1969) reviewed six fatal cases of exposure; brain analysis
showed the concentration of solvent to be: 0.32; 2.7; 9.3; 50.0; 56.0; and
59.0 milligrams per 100 g tissue. Kleinfeld and Feiner (1966) noted high, but
unquantitated, levels in brain after a death from methyl chloroform.
A recent exposure to 7,000 ppm of methyl chloroform occurred in industry;
one worker died, five were hospitalized, and 10 others were treated for inhala-
tion. Investigators from the local health department indicated that all victims
exhibited classic effects of narcosis with full recovery, except those having
preexisting cardiac and/or circulatory dysfunction (W. Gleary, personal com-
munication). In the opinion of the investigators, the full recovery aspect in-
dicates that no residual CNS effects occurred, which is consistent with nearly
all the reports reviewed.
5.2.6.1.2 Cardiovascular toxicity—Griffiths et al. (1972) reported
clinical data on two subjects who died after exposure to a combination of
methyl chloroform and trichloroethylene. The investigators suggested that the
heart was the actual source of abnormal enzyme levels (SCOT, LDH), which are
normally considered signs of liver involvement.
In 50 cases of human anesthesia with methyl chloroform, Dornette and
Jones (1960) found the blood pressure depression but no consistent change in
EGG pattern. The changes included premature ventricular contractions and a
change in electrocardiogram (specifically, depressed S-T segments). There was
one case of cardiac arrest, but it was not known if the anesthesia was a con-
tributing factor. Anesthetic doses used had a maximum level of 26,000 ppm.
Dogs exposed to methyl chloroform at 8,000 ppm for 5 min or less had an
abrupt drop in total peripheral resistance and transient compensatory cardiac
responses. The stroke volume, heart rate, and myocardial contractility dropped
within seconds (Herd et al., 1974). This drop in blood pressure, common with
inhalation of the volatile halogenated hydrocarbons, was stated to be due to
interference with the ability of norepinephrine to antagonize peripheral vas-
cular depression (Griffiths et al., 1972). According to Griffiths et al., even
on very high experimental doses, the EGG was unchanged for several minutes af-
ter the blood pressure drop. Herd et al. (1974) found that peripheral vasodila-
tion induced by methyl chloroform could be reversed by phenylephrine hydro-
chloride, and further, that injection of calcium prevented methyl chloroform-
induced hypotension and depression of myocardial contractility.
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There have been several studies on tissue/organ effects and the heart.
In 1929 Lazarew showed depression in contractility of the perfused frog heart
by methyl chloroform. Aviado and co-workers have shown contractility depres-
sion in both an in vitro dog heart test and the primate heart (Belej et al.,
1974; Aviado and Belej, 1975). Herd et al. (1974) reported that heart muscle
from unexposed rats developed impaired contractility when exposed in vitro to
methyl chloroform. Krantz et al. (1959) showed that heart muscle from rats,
which had been anesthetized for 1 hr with methyl chloroform, had impaired oxy-
gen consumption. They also showed that in both monkeys and dogs exposed to
methyl chloroform, the T-wave of the EGG was flattened or inverted. This seg-
ment of the EGG is involved with repolarization of the cardiac ventricle after
firing. Aviado's studies showed that changes in the QRS potential and duration
was most correlated with lethality to mice (Aviado et al., 1976). The QRS por-
tion of the EGG is involved with impulse transmission across the ventricle.
The death of a young seaman due to methyl chloroform abuse resulted in
cardiac changes (Travers, 1974). Progressive hypotension and bradycardia and
several instances of cardiac arrest resulted in death 24 hr after collapse.
Autopsy showed right atrial and ventricular dilation.
The death of one victim and serious effects in a second victim of a recent
industrial methyl chloroform exposure were both possibly related to the car-
diovascular effects of the solvent (W. Cleary, personal communication). A
worker exposed to an estimated 7,000 ppm of methyl chloroform became uncon-
scious. Two of his rescuers (both having preexisting cardiac and/or circula-
tory problems) suffered cardiovascular effects. One died of cardiac arrest
and the second suffered a heart attack at the scene of the rescue. No infor-
mation was available on the cardiac status of four other workers hospitalized
in the same incident, or on 11 others treated at the plant but not hospitalized
(Michigan Department of Public Health, 1977). No further information is avail-
able (Cleary, 1979).
Inhalation of high levels of methyl chloroform produces a decrease in
heart rate and blood pressure during the first few minutes of exposure. These
effects have been reported at 6,250 ppm for rabbits (Truhaut et al., 1972);
8,000 ppm for dogs (Herd et al., 1974); 25,000 and 50,000 ppm for monkeys
(Belej et al., 1974); air saturated with methyl chloroform for dogs (Griffiths
et al., 1972); and at 10, 212 to 226 and 550 ppm for humans (Dornette and
Jones, 1960).
Congestion in the tissues following methyl chloroform exposure (which
is a sign of cardiovascular toxicity) has been reported in several studies
(Griffiths et al., 1972; Adams et al., 1950; Horiguchi and Horiguchi, 1971;
Tsapko and Rappoport, 1972; Rice et al., 1967). Human autopsy reports have men-
tioned tissue congestion following deaths due to methyl chloroform, especially
after prolonged abuse or high exposure (Hall and Hine, 1966; Stahl et al.,
1969; Hatfield and Maykoski, 1970).
5-119
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Many questions remain concerning the cardiovascular toxicity of methyl
chloroform. Published studies agree that hypotension occurs with methyl chloro-
form exposure, and a normal physiological response to a rapid hypotension (as
with a large dose of the solvent) would be a reflex sympathoadrenal discharge.
There have been no studies that satisfactorily answer whether or not chronic
methyl chloroform exposure affects the levels of the catecholamine-raetabolizing
enzymes. The suggestion that the heart itself is sensitized to the effects of
catecholamines is addressed later in this subsection.
Mice inhaling high levels of methyl chloroform (50,000 to 250,000 ppm)
showed a dose-related drop in heart rate, followed by rebound increase 15 to
25 min after the end of exposure. EGG changes lasted for 24 hr after inhala-
tion of methyl chloroform; a decrease and widening of the QRS complex remained
after the heart rate and other cardiac changes had returned to normal. The QRS
complex of the EGG detects exclusively the nerve transmission across the mus-
cle of the main chambers of the heart (ventricular depolarization) (Aviado et
al., 1976).
Figure 5-5 summarizes several studies which have shown methyl chloroform
effects at specific cardiac sites as measured by EGG change.
Normal ECG» man
Species Dose
Man Anesthetic
Man Anesthetic
Man 115 ppm, 1-6 years
Monkey 20,500 ppm
Monkey 0.59 ml/kg
Dog 5,000 ppm 5 min
Dog 2,500 ppm 5 min
Effect
Widened QRS
Depressed ST
Abnormal QRS/ST in 10
of 121 persons exposed,
1 of 121 unexposed group
Arrhythmia
Depressed ST
Epi. sensitization
No cardiac effect
Sources: Aviado et al. (1976); Jensen (1976).
Figure 5-5. Gardiotoxicity of methyl chloroform^
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5.2.6.1.3 Liver and kidney effects--Liver cell damage produces an increase
in cytoplasmic transaminase, followed by lactic dehydrogenase (LDH) from the
mitochondria. To determine the organ source of these enzyme level changes after
methyl chloroform exposure, the LDH must be electrophoretically fractionated.
Damaged heart cells can also release LDH.
Prothrombin activity is a very useful parameter of liver damage resulting
from inhalation of methyl chloroform or related solvents. This test is useful
because (a) many clotting factors are supplied by the liver, and (b) some of
these factors have short half-lives--under 1 day--so a rather rapid change in
reactivity would occur if synthesis is affected (Hamilton and Hardy, 1974).
Of seven enzymes measured, Platt and Cockrill (1969) found increases in
only two in rats dosed orally with methyl chloroform (1,650 mg/kg) in liquid
paraffin for 7 days. The NADPH2~cytochrome C reductase and glutamate dehydro-
genase activity of rat liver were significantly increased in the treated ani-
mals.
Klaassen and Plaa (1969) found no elevation in liver triglycerides within
the first 36 hr after dosage of rats with methyl chloroform at 3,800 mg/kg (75%
of the
Six controlled human experiments produced a conclusion that urinary uro-
bilinogen was the most sensitive test of liver stress if subjects inhaled methyl
chloroform at ~ 500 ppm or above (Stewart et al., 1961a). The SCOT values and
the 15-min PSP excretion deviated somewhat from preexposure values, but re-
mained within normal limits.
The lowest dose of methyl chloroform that resulted in hepatic effects was
reported by McNutt et al. (1975) who found significantly elevated triglycer-
ide levels in mice exposed 4 and 13 weeks at 250 ppm. MacEwen et al. (1974),
however, failed to produce elevated liver triglycerides in mice continuously
exposed to 250 ppm for 100 days, but observed the effects at 1,000 ppm.
Krantz et al. (1959) found no effects from methyl chloroform on BSP re-
tention time in an anesthetized dog, but repeated administration of the anes-
thesia resulted in hepatic pathology in one of four rats.
Horiguchi and Horiguchi (1971) reported congestion of the liver and bile
duct inflammation in male mice exposed to 1,000 ppm of methyl chloroform (2 hr,
nine times).
Plaa (1976) has summarized work on trichloroethylene, methyl chloroform,
and perchloroethylene with respect to liver toxicity (Table 5-18). The table
shows that toxicity is a function of the test used for all the subject com-
pounds.
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TABLE 5-18. LIVER EFFECTS OF METHYL CHLOROFORM AND
OTHER CHLORINATED HYDROCARBONS
Relative potency rankings of the subject halogenated
hydrocarbons in miceg'
24-Hr LD BSP Retention ED SGPT Elevation ED
Trichloroethylene Trichloroethylene Methyl chloroform
Perchloroethylene Methyl chloroform Trichloroethylene
Methyl chloroform Perchloroethylene Perchloroethylene
Potency ratios of the three subject solvents for
SGPT elevation or BSP retention in
BSP Retention potency SGPT Elevation potency
Compound ratio (LD /ED ) ratio (LD /ED )
Methyl chloroform 1.4 1.5
Trichloroethylene 101 1.4
Perchloroethylene 0.9 1.0
Severity of liver injury induced by minimal lethal doses of the
three subject solvents; SGPT elevation being used as
the index of hepatic dysfunction^/
SGPT (R-F units)
Compound Dogs Mice
Perchloroethylene 400 Nil
Methyl chloroform 350 65
Trichloroethylene 250 90
j!/ The ranking is: most potent first and least potent last,
Source: Plaa (1976).
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Hanasono et al. (1975) dosed (i.p. ) male rats with methyl chloroform (1.0
ml/kg) 3 days after a dose of alloxan which produced diabetes symptoms but no
SGPT or triglyceride change. The hepatotoxic effects of methyl chloroform on
control and diabetic rats are shown for SGPT levels and hepatic triglyceride
levels.
SGPT Triglyceride in liver
(units/ml) (mg/g tissue )
Controls 42+2 5.7+0.5
Diabetic 65 + 19 21.6 + 13.1
Rice et al. (1967) gave rats methyl chloroform (2 ml/kg) 24 hr before
performing hemodynamic measurements on the isolated, perfused livers. Under
those in vitro conditions, hepatic blood flow was not changed by the pretreat-
ment, although carbon tetrachloride did change blood flow characteristics in
the same experimental series. A subcapsular inflammatory reaction was found
in the livers of animals pretreated with methyl chloroform.
Fuller et al. (1970) reported an increase in the in vitro metabolism of
hexobarbital, meprobamate, and zoxazolamine following the inhalation by rats
of methyl chloroform for 24 hr (2,500 to 3,000 ppm). There was an increase in
vitro of the metabolism of these three compounds by hepatic microsomal enzymes
under the influence of methyl chloroform.
The inhalation of methyl chloroform at a level of approximately 10,000
ppm for 4 to 6 hr had no effect on liver function of ethanol-dosed rats, al-
though other chlorinated hydrocarbons exhibited increased hepatotoxicity
(Cornish and Adefuin, 1966). Cornish et al. (1973) also failed to demonstrate
increased hepatotoxicity due to methyl chloroform in rats pretreated with
phenobarbital. Carbon tetrachloride was more hepatotoxic in the phenobarbital-
treated rats.
In laboratory animals, liver function appears to be readily influenced
by methyl chloroform. Klaassen and Plaa (1967) reported disturbances in liver
functions in dogs; liver function change was also reported in rabbits (Truhaut
et al., 1969).
The guinea pig is probably the species most sensitive to liver injury.
Adams et al. (1950) reported no organic effects after 1,500 ppm of methyl chloro-
form at 7 hr/day for 3 months; in contrast, Torkelson et al. (1958) reported
liver effects in animals exposed at both 1,000 and 2,000 ppm levels of methyl
chloroform for 30 to 90 min/day for 3 months. Klaassen and Plaa (1966) report
enlargement of hepatocytes with cellular infiltration and vacuolation following
5-123
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methyl chloroform treatment of mice. Slight necrosis occurred only when the
dosage was in the lethal range. The mechanism of these cellular changes has
been suggested by Von Oettingen (1964) to be a function of the lipid solubil-
ity of the methyl chloroform.
Signs of hepatic effects include retention of BSP and change in SGPT ac-
tivity following injection or inhalation of methyl chloroform. Gehring (1968)
found the EDgg for SGPT activity was 2.91 g/kg in mice; Klaassen and Plaa
(1966) report 3.34 g/kg for the same effect. The inhalation ED5g for SGPT
activity in mice was 13,662 ppm for approximately 10 hr (Gehring, 1968).
Truffert et al. (1977) developed a cell culture technique which tests the tox-
icity of chlorinated solvents on liver DNA; short-term, low level exposure to
methyl chloroform in vivo inhibits synthesis of hepatic DNA. The assay may
prove valuable as a mutagen/carcinogen screen.
Plaa and Larson (1965) reported that only one of nine mice given (i.p.)
methyl chloroform (3,400mg/kg) exhibited significant proteinurea. In another
trial, five of five mice exhibited swelling of the convoluted tubules of the
kidney after a similar dose of methyl chloroform. No necrosis was observed.
Renal toxicity (tubular damage) in mice was also observed in another study
(Klaassen and Plaa, 1966). These authors have studied renal function in dogs
exposed to methyl chloroform and report renal changes as measured by PSP, glu-
cose, and protein excretion data, but no histopathological changes (Klaassen
and Plaa, 1967). According to these data, the kidney is less affected by methyl
chloroform than the liver.
Stewart et al. (1971) reported several instances of apparent kidney tox-
icity related to methyl chloroform exposure in humans. Following a case of
human ingestion, elevated serum bilirubin and evidence of kidney injury (red
blood cells (RBC) and protein in the urine) were seen. In experimental expo-
sures to the solvent, elevated urinary urobilinogen was found in one subject
following 20 min at 900 ppm, and some evidence of adverse effects on kidneys
(dye clearance rate, RBC in urine) was observed in six subjects after exposure
to 500 ppm for 78 min. Five of seven subjects exposed to methyl chloroform
for 15 min at 0 to 2,650 ppm had a few RBC in the urine and/or a positive uri-
nary urobilinogen (Stewart et al., 1961a).
5.2.6.1.4 Lung-respiratory tract effects—Irritation of the lungs and
respiratory tract as a result of methyl chloroform inhalation has been re-
ported for man and other species in both industrial exposures and in experi-
mentally controlled exposure (Stewart et al., 1961a; 1969; Salvini et al.,
1971).
Humans occupationally exposed for prolonged periods to methyl chloroform
by inhalation and skin contact (Weitbrecht, 1965) complained of irritation of
the upper respiratory tract. American industrial workers who were chronically
5-124
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exposed at low levels also have complained of respiratory tract irritation
(Rosensteel, 1974; Vandervort and Thoburn, 1975; Hervin, 1975; others).
Nearly all the NIOSH "Health Hazard Evaluation Reports" on methyl chloroform,
when instituted by worker complaint, were due to strong solvent odor and
throat irritation. In nearly all cases the levels in ambient air were far be-
low the maximum allowable concentrations. There is no indication in the lit-
erature that the lungs of man or animals become hypersensitive following re-
peated inhalation, but the irritation is apparently grounds for concern. As
of January 16, 1978, "new drug" status is required for any aerosol drug product
using methyl chloroform as a solvent or drug carrier. Approved products which
use this delivery form must file and receive approval under a standard new drug
application (Federal Register 63386, 1977).
In animal exposure studies, lung changes were seen in guinea pigs exposed
to 1,000 ppra for 72 min/day for 69 exposures, and to 2,000 ppm for 12 min/day
for 69 exposures; 1,000 ppm for 36 min/day and 69 exposures produced no lung
irritation (Torkelson et al., 1958). Prendergast et al. (1967) exposed several
species to 370 ppm of methyl chloroform continuously for 90 days but observed
only nonspecific inflammatory changes in the lungs*
MacEwen and Vernot (1974) reported that the most significant effect seen
in rats continuously exposed to methyl chloroform for 100 days was respiratory
disease. Lung changes were seen in approximately half of the rats exposed to
250 and 1,000 ppm.
Congestion of the lungs in animal inhalation experiments has been widely
reported, particularly for chronic or high-level exposures to methyl chloroform
(Tsapko and Rappoport, 1972; Horiguchi and Horiguchi, 1971). Pulmonary edema
and congestion, however, are consistent with cardiovascular insufficiency rather
than primary lung effects. The lung effects appear to be limited to irritation,
and are reported to be transitory in humans, even following moderately high
exposure (Weitbrecht, 1965)
A summary of the clinical effects, primarily liver and kidney, of methyl
chloroform in man is shown in Table 5-19.
5.2.6.2 Dose-Response Data--
5.2.6.2.1 Acute toxicity—
5.2.6.2.1.1 Human (inhalation)—Stahl et al. (1969) reported four
cases of acute inhalation exposure to methyl chloroform in human males. A 20-
year-old died after working with "paint remover" for an unknown period of time.
There were 2.7, 2.4, 9.8, and 4.9 mg of methyl chloroform per 100 g of brain,
kidney, liver, and muscle, respectively. Liver, lungs, spleen, kidney, and
brain were congested. The brain was anoxic (283 mg lactic acid per 100 g brain).
No evidence was found of other drugs or pathology.
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TABLE 5-19. EFFECTS ON CLINICAL CHEMISTRY OF METHYL CHLOROFORM IN MAN
Dose if known Effects Reference
2,650 ppm, 15 min 2/7 Increased urinary urobilinogen Stewart et al. (1961a)
1-31 ppm 0/13 Had urine hippuric acid change Rosensteel (1974)
A "narcotic dose" Increased urinary urobilinogen at 96 hr Stewart (1971)
"Fatal doses" ~ 30 mg MC^ per 100 g brain (average 6) Stahl et al. (1961)
Anesthetic dose 0/5 Effects on serum transaminase Dornette and Jones (1960)
Ui
(L ~ 1 oz, orally Elevated serum bilirubin at 48 hr Stewart (1968)
(S3
OS ____________^___________________________________^_______^____________________^
_a/ MC = methyl chloroform.
-------
In Case 2, a 17-year-old died 3.75 hr after cleaning metal parts for
4 hr in a closed area. Methyl chloroform levels found were: 0.15, 0.32, 0.26,
0.49, 0.26, and 0.18 mg/100 g blood, brain, kidney, liver, muscle, and lung,
respectively. Urine concentration was 0.1 mg/100 ml. The brain lactic acid was
226 mg/100 g. No other drugs or pathology were found.
A 24-year-old was found dead 2 hr after cleaning metal parts for 4
hr. Cleaning rags were found at his head. The head and neck were markedly cya-
notic. Brain, spleen, and kidneys were congested, the lungs were congested and
edematous, and the liver showed prominent fatty changes. Tissue concentrations
of methyl chloroform were 9.3, 7.8, 13.2, and 2.2 mg/100 g brain, kidney, liver,
and lung, respectively. No other drugs or pathology were apparent.
In another case, three men died after cleaning metal parts in closed
areas. Upon autopsy, their lungs were found to be congested and edematous, and
burn-like lesions were apparent on the buttock skin where prolonged contact
had occurred. Methyl chloroform concentrations in the three victims were as
follows:
Methyl chloroform
(mg/100 g tissue)
Blood
Brain
Liver
Seven subjects were exposed for a total of 15 min to methyl chloro-
form in concentrations increasing from 0 to 2,650 ppm. One became lightheaded
at 2,600 ppm; two could not stand at 2,650 ppm, and three others became very
lightheaded at 2,650 ppm (Stewart et al., 1961a). Between 900 and 1,000 ppm,
the subjects experienced eye irritation, coordination difficulty, and light-
headedness. Equilibrium was restored in all subjects 5 min after exposure
ceased (Stewart et al., 1961a). No toxic effects, biochemical or behavioral,
were reported at exposure levels of 500 ppm for 1 to 3 hr. A summary of the
effects is as follows:
12
59
22
6
56
11
6
50
12
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Exposure
time Concentration Expected human
(min) in air (ppm) effect on CNS
60 100 Apparent odor threshold.
500 No detectable effect but odor is obvious.
1,000 Very slight equilibrium loss.
2,000 Loss of coordination.
30 1,000 Eye and nasal discomfort, slight equilibrium loss.
2,000 Loss of equilibrium.
15 1,000 Beginning of equilibrium loss.
5 2,000 Disturbance of equilibrium.
Source: Stewart (1968).
A summary of acute methyl chloroform GNS effects is shown in Table
5-20.
Methyl chloroform was used as an anesthetic agent in both animals
and humans in the 1800's. Its use as an anesthetic agent was discontinued due
more to its lack of potency than to its toxicity. The anesthetic use of methyl
chloroform is included under "acute toxicity," however, since the CNS depres-
sant effects are considered toxic manifestations of environmental and indus-
trial exposure.
Dornett and Jones (1960) used methyl chloroform as a coanesthetic
agent with 4:1 nitrous oxide-oxygen. In 50 administrations, induction of
anesthesia necessitated methyl chloroform concentrations of 10,000 to 26,000
ppm. Both biochemical and cardiovascular effects were seen in the patients re-
ceiving the methyl chloroform-nitrous oxide anesthesia. An average drop in
systolic blood pressure of 5 to 10 mm mercury in about half of the patients
was reported. In one patient, a drop of 66 mm Hg was seen, and three had large
blood pressure drops that returned to preoperative levels when the concentra-
tion was reduced. ECGs taken on 13 of 32 patients showed aberrancies (six
changes in nodal rhythm, five cases of premature ventricular contractions, and
two cases of S-T depression) and one case of cardiac arrest. In five of the
patients, serum transaminase was measured before and 2, 4, and 6 days after
the methyl chloroform anesthesia (Dornette and Jones, 1960). Two of five showed
a slight transaminase increase, but the increase was low enough that 2 hr of
methyl chloroform anesthesis was considered insufficient to cause liver damage.
Experimental anesthesia using methyl chloroform alone was induced
in another study (Krantz et al., 1959). Recovery was slower than that reported
by Dornette, and blood pressure dropped to 70% of the preanesthetic level. No
EGG pathologies were reported in this subject.
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TABLE 5-20. ACUTE CNS EFFECTS OF METHYL CHLOROFORM
Dose
CNS effect
Reference
1,000 ppm, 70-75 min
1,000 ppm, 30 min
500 ppm, 450 min
900 ppm, 20 min
450 ppm, 8 hr
250 ppm
350 ppm
450 ppm
550 ppm
500 ppm, 7 hr
Equilibrium disturbed, light-headedness,
positive Romberg—'
Equilibrium good, reflexes disturbed
No effect
One of three positive Romberg, two of
three lightheaded
Possible subtle behavioral effects
Manual dexterity and perceptual defi-
ciencies at 350 ppm and above
Two of five subjects showed impaired per-
formance on Romberg after 2 to 3 hr
Torkelson et al. (1958)
Torkelson et al. (1958)
Torkelson et al. (1958)
Stewart et al. (1961a)
Salvini (1971)
Gamberale and Hultengren (1973)
Stewart et al. (1969)
al A positive Romberg test is evidenced by unsteadiness on standing, feet close together, eyes closed.
-------
Siebecker et al. (1960) studied mice and human subjects with methyl
chloroform anesthesia; they found it less potent than chloroform or Fluothane®
alone, and less potent than trichloroethylene at supplementing nitrous oxide-
oxygen anesthesia. The methyl chloroform produced hypotension, little brain
wave (EEC) change, and "considerable" liver toxicity to test mice.
Lazarew (1929) studied the anesthetic effects of methyl chloroform
and 11 other compounds on mice, and assigned toxicity ratings based on the
concentration required to produce prostration or loss of righting reflex. A
dose of methyl chloroform of 7,350 ppm for 2 hr was required to produce "prone-
ness"; 8,270 ppm for 2 hr produced loss of reflexes; and 11,950 ppm for 2 hr
produced death.
The effects on clinical chemical measurements of acute exposure may
reflect liver or kidney toxicity, but these effects, in general, occur follow-
ing repeated exposure. A tabulation (Table 5-19) of some biochemical effects
of methyl chloroform exposure was made earlier in this subsection.
5.2.6.2.1.2 Human (oral)—A 47-year-old male accidentally drank
methyl chloroform (~ 670 mg/kg, an estimate based on body weight of 60 kg) and
immediately felt a burning sensation in the upper gastrointestinal tract. Nausea
occurred at 30 min, and diarrhea with vomiting occured at 1 hr. Subsequently,
the urine showed 1+ protein, glucose traces, and some red cells, indicating
kidney pathology. Symptoms eased after 6 hr, and the man was asymptomatic after
12 hr. Serum bilirubin was elevated 50 hr later, but a large series of kidney
and liver function tests were normal, as were the heart and blood profile
(Stewart and Andrews, 1966).
5.2.6.2.1.3 Animal data--A summary of the acute toxicity data found
for animals is as follows:
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Species
Dog
Dog
Rats
Rats
Monkey
Rats
Mice
Mice
Rats
Rats
Mice
Rabbits
Guinea pigs
No.
5
5
30+
30+
1
20+
40+
-
35
35
16
16
16
Sex
M,F
M,F
-
-
F
M
M
F
M
F
F
F
M
Route
•^MMMH
l.p.
l.p.
Inhalation
Inhalation
Inhalation
l.p.
l.p.
l.p.
Oral
Oral
Oral
Oral
Oral
Effect
LD50
Liver
dysfunction
LD50
LD50
Ataxla
LD5Q
LD50
LD50
LD50
LD50
LD50
LD5Q
LD50
Dose
4,200 rag/kg
1,400 mg/kg
18,000 ppm, 3 hr
14,000 ppm, 7 hr
5,000 ppm, 1 hr
5,100 mg/kg
5,300 mg/kg
4,700 mg/kg
12,300 mg/kg
10,300 mg/kg
11,240 mg/kg
5,660 mg/kg
9,470 mg/kg
Reference
Klaassen and Plaa (1967)
Klaassen and Plaa (1967)
Adams et al. (1950)
Adams et al. (1950)
Adams et al. (1950)
Klaassen and Plaa (1969)
Klaassen and Plaa (1969)
Gehrtng (1968)
Torkelson et al. (1958)
Torkelson et al. (1958)
Torkelson et al. (1958)
Torkelson et al. (1958)
Torkelson et al. (1958)
These data indicate that the dosage required to achieve an
,«
level is dependent upon the route of administration. In general, 4,000 to 5,000
mg of methyl chloroform per kilogram of body weight are required for injected
doses; oral dose administration requires almost twice the injection level to
achieve the same results. For inhalation, between 3 and 7 hr exposures to
~ 16, 000 ppm are required for 50% mortality.
5.2.6.2.2 Subacute toxic! ty—
5.2.6.2.2.1 Humans— Stewart et al. (1969) exposed 11 human males,
31 to 62 years old, to methyl chloroform by inhalation at 500 ppm for 6.5 to
7 hr/day for 5 days. Subjective reports included the following:
Occasional headache 11/11
Occasional nose and throat irritation 11/11
Occasional sleepiness 11/11
Lightheaded during 1st hr 2/11
Loss of equilibrium after 1 hr exposure 2/11
After methyl chloroform exposure, the following 12 common clinical chemistry
parameters were normal: RBC count; white blood cell (WBC) count; SCOT; cre-
atine; LDH; FBI (protein-bound iodine); RBC fragility; cholesterol; bilirubin;
and blood electrolytes. "Complete urinalysis" also yielded normal results.
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Salvini et al. (1971) exposed six males to methyl chloroform by in-
halation of 450 ppra for 2- to 4-hr periods, with each period being separated
by a 90-min interval. The subjects were given the following psychophysiological
tests after the inhalation:
Perception test with tachistereoptic presentation
Wechsler Memory Scale
A complex reaction time test
Manual dexterity test
The subjects had also been given the tests prior to inhalation of methyl chloro-
form. No differences in motor function, coordination, equilibrium, or behavior
patterns between the two tests (one pre-exposure and one post-exposure) were
seen. Some eye irritation accompanied methyl chloroform exposure.
The National Institute for Occupational Safety and Health (NIOSH)
issued a report in August 1978 which reviewed the toxicity of nine chloro-
ethanes, including methyl chloroform (NIOSH, 1978). The purpose of this tox-
icity review was to alert workplace personnel to new information on four chloro-
ethanes (not methyl chloroform). Methyl chloroform was discussed because of its
structural similarity to compounds which are "to be handled as if they were.
human carcinogens."
An unreferenced table listed the adverse effects on humans and ani-
mals. The report concluded that methyl chloroform and the five other chloro-
ethanes structurally related to the four carcinogens should be handled with
caution in the workplace.
Axelrod and Huffaker (1979), New York State Department of Health,
have reviewed the health effects of methyl chloroform for an in-state regula-
tory group as has Frost (1978) for the Texas Air Control Board. Both of these
evaluations emphasize the desirability of control of methyl chloroform; animal
and human health effects were a contributing reason.
5.2.6.2.2.2 Animals—MacEwen et al. (1974) exposed eight monkeys
to 14 weeks of continuous inhalation of methyl chloroform: four at 250 ppm
and four at 1,000 ppm. The authors analyzed for the following: hemoglobin;
RBC and WBC counts; Na; K; alkaline phosphatase; SCOT, SGPT; creatinine; chlo-
ride; glucose; blood urea nitrogen; albumin globulin; total protein; calcium;
cholesterol; total bilirubin; and serum triglycerides. All fell in the normal
range. No pathology occurred at either dose level.
Adams et al. (1950) exposed one female monkey by inhalation to 3,000
ppm of methyl chloroform for 7 hr/day for 53 exposures over 74 days. The mon-
key was necropsied and no pathology was found in the following tissues: lung;
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heart; liver; kidney; lymph nodes; spleen; adrenal; pancreas; stomach; small
and large intestines; bladder; thyroid; and skeletal muscles.
Prendergast et al. (1967) exposed nine squirrel monkeys (three per
dose) to inhalation of methyl chloroform as follows:
Dose 1: 6 weeks, 2,700 ppm, 8 hr/day, 5 days/week
Dose 2: 90 days, 450 ppm, continuous
Dose 3: 90 days, 165 ppm, continuous
The monkeys on dose 1 lost 3% of body weight, but no microscopic pathology
was reported; dose 2 produced a 4% weight loss and lung inflammation; dose 3
monkeys gained weight normally but showed lung congestion.
MacEwen et al. (1974) exposed 16 dogs (eight per dose) to 14 weeks
continuous inhalation of 250 or 1,000 ppm of methyl chloroform. The measure-
ments taken on all dogs included: WHB count; reticulocyte count; electrolytes;
serum triglycerides; total protein; alkaline phosphatase; SCOT; and SGPT. The
clinical chemistries were normal, and no pathology could be ascribed to the
exposure.
Prendergast et al. (1967) exposed six beagle dogs (two per dose) to
inhalation of methyl chloroform as follows:
Dose 1: 6 weeks, 2,700 ppm, 8 hr/day, 5 days/week
Dose 2: 90 days, 450 ppm, continuous
Dose 3: 90 days, 165 ppm, continuous
Dogs on dose 1 lost 2% of their body weight, showed blood leukopenia, but had
normal lungs; dose 2 dogs gained weight (5% less than controls) and had lung
inflammation. Dose 3 dogs gained weight normally, had no blood pathologies,
but showed sporadic lung congestion.
Adams et al. (1950) exposed two female albino rabbits to 5,000 ppm
of methyl chloroform by inhalation for 7 hr/day for 31 exposures over a total
of 44 days. The exposed rabbits had a slight depression in growth rate compared
to the unexposed animals but no other pathologies were reported.
Prendergast et al. (1967) exposed nine New Zealand albino rabbits
(three per dose) to inhalation of methyl chloroform as follows:
Dose 1: 6 weeks, 2,700 ppm, 8 hr/day, 5 days/week
Dose 2: 90 days, 450 ppm, continuous
Dose 3: 90 days, 165 ppm, continuous
5-133
-------
Rabbits on dose 1 lost 0.5% body weight but showed no other pathology; dose 2
produced significant leukopenia, lung inflammation, and fluid-filled growths
in the peritoneal area of one of the three rabbits. Dose 3 produced only
sporadic lung congestion.
Adams et al. (1950) exposed 11 male and 12 female Wistar rats to
inhalation of methyl chloroform under the following conditions:
Dose 1: 44 days, 5,000 ppm, 7 hr/day, 5 days/week, for 31 exposures,
10 rats
Dose 2: 66 to 67 days, 3,000 ppm, 7 hr/day, 5 days/week, for 47 to
48 exposures, 13 rats
Dose 1 temporarily retarded growth in the female rats (2 weeks), but no effects
were seen at the end of the tests in organ weights, clinical chemistry, and
gross or microscopic pathology. No effects were seen in dose 2.
Prendergast et al. (1967) exposed 45 Sprague-Dawley or Long-Evans
rats (15 per dose level) to inhalation of methyl chloroform as follows:
Dose 1: 30 exposures, 2,700 ppm, 8 hr/day, 5 days/week
Dose 2: 90 days, 450 ppm, continuous
Dose 3: 90 days, 165 ppm, continuous
Rats receiving dose 1 were normal in blood, gross pathology, and microscopic
pathology of the brain, heart, lung, liver, spleen, and kidney. Dose 2 pro-
duced a normal blood profile, but lung nodules in one animal occurred, with
nonspecific lung inflammation in all. At dose 3 (lower than dose 2) 13 of 15
rats died, apparently of disease, and not due to exposure-related causes.
Two groups (40 each) of rats were exposed by inhalation to 250 or
1,000 ppm of methyl chloroform continuously for 14 weeks (MacEwen et al.,
1974). Growth rate of the exposed rats was not significantly different from
controls, but the liver weight, as a function of total body weight, signifi-
cantly increased at the 1,000-ppm dose.
Twenty male SPF Wistar II rats were exposed by inhalation to 204 ppm
of methyl chloroform 8 hr/day, 5 days/week, over 14 weeks. The following param-
eters were normal: symptoms; weight gain; hematology; organ weights; liver
and renal function tests; and gross and microscopic pathology (Eben and
Kimmerle, 1974).
Prendergast et al. (1967) exposed 45 Hartley guinea pigs (15 per
dose level) to methyl chloroform by inhalation as follows:
5-134
-------
Dose 1: 6 weeks, 2,700 ppm, 8 hr/day, 5 days/week, for 30 exposures
Dose 2: 90 days, 450 ppm, continuous
Dose 3: 90 days, 165 ppm, continuous
Guinea pigs exposed at dose 1 were all normal. Dose 2 animals had nonspecific
lung inflammation, but clinical chemistry and blood were normal; dose 3 animals
showed sporadic lung congestion, but, as with dose 2, clinical chemistry and
blood were normal. All animals at all doses survived.
Adams et al. (1950) exposed 71 mixed strain, mixed sex, guinea pigs
(roughly divided into male/female dose groups) to methyl chloroform as follows:
45 days, 5,000 ppm, 7 hr/day, 5 days/week, 32 exposures
29 days, 3,000 ppm, 7 hr/day, 5 days/week, 20 exposures
60 days, 1,500 ppm, 7 hr/day, 5 days/week, 44 exposures
92 to 93 days, 650 ppm, 7 hr/day, 5 days/week, 65 to 66
exposures
Dose 5: 57 to 58 days, 650 ppm, 7 hr/day, 5 days/week, 40 to 41
exposures
Dose 1:
Dose 2:
Dose 3:
Dose 4:
exposures
Significant decreases in growth rate (or weight loss, compared to controls)
occurred at all doses. Organ weights and clinical chemistry were normal at all
dose levels. Microscopic pathology was normal at 1,500 ppm or less (doses 3,
4, and 5). At 5,000 ppm (dose 1), there was slight centrilobular fatty infil-
tration in the livers but no necrosis; slight testicular degeneration also
occurred. At 3,000 ppm (dose 2), the livers showed slight centrilobular fatty
infiltration, with small fat-staining globules in central hepatocytes.
MacEwen et al. (1974) exposed 360 mice (180 per dose level) to in-
halation with methyl chloroform at 250 or 1,000 ppm continuously for 14 weeks.
At the 1,000 ppm level, there was a significant increase in fat in the centri-
lobular hepatocytes and the liver triglycerides were elevated throughout ex-
posure but returned to normal 2 weeks postexposure. No hepatic necrosis, in-
flammation, or fibrosis occurred at either the 250- or 1,000-ppm level.
McNutt et al. (1975) exposed 20 CF-1 or CP-1 male mice (10 per dose
level) to methyl chloroform by inhalation at 250 or 1,000 ppm continuously for
14 weeks. At 250 ppm, the only pathology was elevated triglycerides at weeks
4 and 13. At 1,000 ppm, triglycerides were elevated all 14 weeks of inhalation,
liver weights were significantly increased all 14 weeks, and microscopic pathol-
ogies were seen. Centrilobular hepatocyte hypertrophy occurred, with peak fat
accumulation in the liver at week 7. Focal necrosis occurred at week 10 with
acute inflammation. Vacuolization and fat clearance occurred at week 12. Toxic-
ity data for fish and other aquatic species are presented in Section 6.2.
5-135
-------
5.2.6.2.3 Chronic toxicity--Quast et al. (1975) exposed weanling rats
to methyl chloroform by inhalation for 52 weeks. Ninety-six males and 96 fe-
males were used at each dose level (875 and 1,750 ppm) with 192 males and 192
female controls. Observations were made at 52 and 104 weeks. Weight gain was
normal for both groups, and mortality of the exposed rats did not differ from
controls at either dose level. Hematology showed sex differences: 67o neutro-
philia and ~I°L lymphocytopenia occurred in males at 1,750 ppm, and females had
137o lymphocytosis at both dose levels. A single tumor arising at 15 months in
one female receiving the 1,750-ppm dose was reported.
Bell (1978b) reported preliminary findings from a chronic vapor inhalation
toxicity study which exposed groups of 50 to 200 Charles River COG-CD rats
(both sexes) to methyl chloroform. The methyl chloroform exposure levels were
200, 440, and 875 ppm of stabilized chemical for 18 months, 7 hr/day, 5 days/
week. Other exposure groups received unstabilized methyl chloroform or no test
chemical. Clinical chemical studies and hematology were performed. There was
no indication during initial audit results of a carcinogenic response. Bell
summarized the data on hematologies and clinical chemistries, as well as the
pathology completed to date: no suggestion of carcinogenic response and ex-
cellent animal survival.
Table 5-21 summarizes both the acute and chronic toxic effects of methyl
chloroform for all species discussed in this subsection.
5.2.6.3 Sensitization—
5.2.6.3.1 Delayed effects—Possible cumulative effects on the CNS were
seen in mice by exposure to inhibited methyl chloroform (Horiguchi and Horiguchi,
1971). Mice were exposed to 1,000 ppm for 2 hr every other day for 3 weeks (to-
tal of 18 hr). Activity of the mice was measured 2 hr before, during, and 2 hr
after exposure. Activity increased during and after exposure for the last 7
days, whereas the activity in exposed and unexposed mice had been similar on
the first 2 days.
Bass (1970) studied 18 of 110 cases of sudden death which occurred follow-
ing sniffing abuse of methyl chloroform in conjunction with exercise. The author
suggested Sensitization of the heart to endogenous catecholamines as a possible
cause.
A case of apparent abuse of a methyl chloroform-trichloroethylene mixture
was reported by Griffiths (1972). The subject was found in respiratory arrest
and died 3 days after hospitalization. The heart-derived lactic dehydrogenase
was elevated (LDH normal = 200 to 500 Wroblewski-LaDue units; reading = 1,690
units on day 3 after exposure). On autopsy, fatty liver and heart cell necroses
were seen. The investigator suggested that cardiac Sensitization contributed to
this fatality.
5-136
-------
TABLE 5-21. TOXIC EFFECTS OF METHYL CHLOROFORM
Exposure Dosage
Organism route In organism In air Exposure Lime
Mice Oral 9.7-11.24 g/kg
Oral 14.08 g/kg
l.p. 4.7-4.9 g/kg
l.p. 2.34 g/kg
Inhalation - 11,900 ppm
Inhalation - 148,230 ppm 5 min
Inhalation - 164,700 ppm
Inhalation - 51,240 ppm 5 min
l.p. 11.2 g/kg
i.p. 3.34 g/kg
Inhalation - 13,600 ppra 595 min
Inhalation ' - 3,020 ppin
Inhalation - 8,240 ppm
l.p. 2.5 ml/ks
l.p. 1 ml/kg
Inhalation - 250-1,000 ppm Continuous 1-14
weeks
Innalacion 4UU rol beaker ' Under 1 min
saturated
Oral 207. solution - 72 hr after dose
Inhalation - 300-1, 2,'iU ppm 7 lie/day; days 6-
by mother 15 of gestation
Inhalation - 13,500 ppm 16 min
Si Le
-
-
-
-
•
-
Heart
Heart
l.i ver
Liver
Liver
Liver
Brain
Kidney
Liver
Liver
II f iir t
Liver
Offspring
Brain
Toxic effect
LD50
LD50
LD50
LD50
L%
'•°50
No arrhytlimia; no epinephrine sensi-
tivity
Depression
Liver toxicity, ED
Liver toxicity, ED n
Liver toxicity, ED -
Liver enzyme induction
CNS depression
Swelling of tubules
Liver enzyme depression
Liver toxicity
cardiac drugs
Fatty infiltration
Mo tetratogenic effects or fetal tox-
Iclty
Anesthesia
Reference
Torkelson et al. (1958)
Aviado et al. (1976)
Cehrlng (1968);
Klaassen and Plaa (1966)
Aviado et al. (1976)
Lazarew (1929)
Aviado et al. (1976)
Avlado and Belej (1974)
Avlado et al. (1976)
Plaa et al. (1958)
Klaassen and Plaa (1966)
Lai and Shaw (1970) '
Lazarew (1929)
Plaa and Larson (1965)
Shaw and Lai (1976)
McNutt ei: al. (1975)
Hermans 6 n ( 1970 )
Slebecker et al. (I960)
Schwetz et al. (1975)
Gehring (1968)
(continued)
-------
TABLE 5-21. (continued)
Exposure Dosaee
Organism route In organism
Mice Inhalation
(cont inued )
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Rats Oral 10.3-14.3 g/kg
l.p. 5.08 g/kg
<-" Inhalation
1
I—1
W Inhalation
00
Oral 1.65 g/day
l.p. 3.74 g/kg
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation . ' -
-4
Incubation, 1 x 10 molar
liver, mi-
cros omes
In air
1,000 ppm
1,000 ppra
1,000 ppm
1,000 ppm
875 ppm
1,750 ppm
250 ppm
-
-
18,000 ppm
14,250 ppm
-
-
30,000 ppm
8,000 ppm
10,000 ppm
2,500-3,000 ppm
18,000 ppm
18,000 ppm
10,000 ppm
8,000 ppm
100-1,000 ppm
-
Exposure time
2 hr/day (x 9)
2 hr/day (x 9)
2 hr/day (x 9)
Continuously 90 days
52 weeks
52 weeks
Continuously 100 days
-
-
3 hr
7 hr
Daily/7 days
-
7 hr
7 hr
1 hr/day/3 months
24 hr
12 hr
0.3 hr
3.0 hr
7.0 hr
1-20 hr
-
Site
Brain
Lungs
Liver
Liver
White cells
White cells
Liver
-
-
-
Liver
Liver
Liver
Liver
Liver
Liver
Kidney
Brain
Brain
Brain
-
Liver
Toxic effect
Increased ambulatory activity
Congestion
Congestion; Inflammation
Increased liver weight; necrosis, In-
flammation
Lymphocytopenia
Hematologic effects
Mild Inflammation, no Increased weight
LD50
"'so
LD50
LD50
Liver enzyme induction
No effects
Weight Increase
Fatty liver
Weight increase
Liver enzyme Induction
Weight Increase
CNS depression
CNS depression
CNS depression
Detected on breath proportional to In-
haled dose
Liver enzyme Induction
Reference
Horlguchl (1971)
Horlguchl (1971)
Horlguchl (1971)
MacEuen and Vernot (1974)
Quast et at. (1975)
Quast et al. (1975)
MacEwen and Vernot (1974)
Torkelson et al. (1958)
Klaassen and Plaa (1969)
Adams et al. (1950)
Adams et al. (1950)
Platt and Cockrlll (1969)
Klaassen and Plaa (1969)
Adams et al. (1950)
Adams et al. (1950)
Torkelson et al. (1958)
Fuller et al. (1970)
Adams et al. (1950)
Adams et al. (1950)
Adams et al. (1950)
Adams et al. (1950)
Boettner and Muranko (1969)
VanDyke and Rlkans (1970)
(continued)
-------
TABLE 5-21. (continued)
Exposure
Organism route
Rats i«p«
(continued)
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Ut Inhalation
C
V0: Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Dosage
In organism In air
0.3-2.0 ml/kg
200 pom
10,000-15,000
ppra
2,000-3,000 ppm
220-440 ppm
204 ppra
180-190 ppm
- ' 73 ppm
135 ppm
135 ppra
370 ppm
2,200 ppra
2jO ppm
1,000 ppin
73 ppm
73 ppm
1,500 ppm
8,000 ppm
12,000 ppm
18,000 ppm
Exposure time
8 hr
2 hr
24 hr
4 hr
14 weeks (8 hr/day)
4 hr
50 days (4 hr/day)
Continuous 90 days
Continuous 90 days
Continuous 90 days
6 weeks (8 hr/day)
Continuous 100 days
Continuous 90 days
50 days (4 hr/day)
120 days (4 hr/day)
3 months (7 hr/day)
7 hr
7 hr
2 hr
Site
Liver
Liver
Liver
-
Brain
Cardiovascular
Liver
Lung
Liver, kidney
Lung
Liver, kidney
Liver
Liver
Lung
Lung
Kidney, liver
Liver
Liver, kidney
Kidney
Toxic effect
No effect: liver enzymes
Poorly metabolized. Major metabolite:
trlchloroeLhanol
No toxicity potenttation by ethanol
Liver enzyme Induction
S Blood, liver, and kidney all normal
in both tests. Trichloroethanol in
(urine Increased lo week 10, then
decreased slightly and stabilized
Changed conditioned reflex threslihold
Venous, heart microscopic pathology,
with time of exposure
Cellular toxicity
Congestion
No effects
Inf Lammat ion
No effects
Increased Uver weight, slight cellu-
lar changes
More pronounced changes
Empliysenui-like changes
Effect increased with increased expo-
sure
No effects
Fatty changes
Increased weight
Increased weight
Reference
Cornish et al. (1973)
Ikeda and Ohtsuji (1972)
Cornish and Adefuin (1966)
Fuller et al. (1970)
F.ben and Kimmerle (1974)
Ebnn and Klmroerle (1<>74)
Tsapko and Rappoport (1972)
Tsapko and Rappoport. (1972)
Tsapko and Rappoport (1972)
Prendergast et al. (1967)
Prendergast et al. (1967)
Prendergast et al. (1967)
PrenJergast et al. (1967)
MacEwen and Vernot (1974)
MacEwen and Vernot (1974)
Tsapko and Rappoport (1972)
Tsapko and Rappoport (1972)
Adams et al. (1950)
Adams et al. (1950)
Adams et al. (1950)
Adams et al. (1950)
(continued)
-------
TABLE 5-21. (continued)
Exposure Dosage
Organism route In organism
Rats Inhalation
(continued)
Inhalation
Guinea pigs Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Oral 8.6-9.47 g/kg
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Dogs Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
10
In air
,000 ppm
500 ppm
1,
2,
I,
000
000
ppm
ppm
000-2,000 ppm
500 ppm
650 ppm
135 ppm
-
500 ppm
2,
2,
5,
3,
1,
I,
2,
000
000
000
000
000
000
200
ppm
ppm
ppm
ppm
ppm
ppm
ppm
125,000 ppm
125,000 ppm
125,000 ppm
8,
a.
000
000
ppm
DIYTI
0.
7
1.
12
Exposure time
05, 0.2, and 0.5
hr/day (x 70)
hr (x 126-130)
2 hr/day (x 69)
min/day (x 69)
Under 12 min/day
(x 69)
7
7
hr (x 126-130)
hr/day/3 months
Continuous 90 days
7
0.
0.
7
7
1.
1.
8
I.
1.
1.
5
-
hr/day (x 126)
05-5 hr (x 64)
05-5 hr (x 64)
hr/day (x 32)
hr (x 20)
2 hr/day/1 months
2 hr/day/3 months
hr/day (x 30)
5-6 min
5-6 min
5-6 min
min
min
Site
Liver
Liver, kidney
hung
Lung, liver
Liver
Liver, kidney
Kidney, liver
Kidney, liver
-
-
Lung
Liver
Liver
-
Liver
Lung
Liver
Heart
Cardiovascular
Lung, kidney
Cardiovascular
Heart
Toxic effect
No increase In weight
No effects
Irritaf ion
Irritation, weight fatty changes
No pathology
No effects
No effects
No pathology
LD50
No effects
Lung Irritation
Fatty liver
Fatty liver
Growth retardation
Liver pathology
Inf Innmntlon
No effects
Ventricular fibrillation
Drop in blood pressure
Congestion
Sharp decrease In peripheral resis-
tance
Decreased henrt rate; decreased rayo-
Reference
Torkelson
Torkelson
Torkelson
Torkelson
Torkelson
Torkelson
Adams et
et
et
et
et
et
et
al.
Prendergast
Torkelson
Torkelson
Torkelson
Torkelson
Adams et
Adams er.
Torkelson
Torkel son
et
et
et
et
al.
al.
et
et
Trendorgast
Griffiths
Griffiths
Griffiths
et
et
et
Herd et a I.
Herd et al.
al.
al.
al.
al.
al.
al.
(195
et al
al.
al.
al.
al.
(195R)
(1958)
(1958)
(1958)
(1958)
(1958)
0)
. (1967)
(1958)
(1958)
(1958)
(1958)
(1950)
(1950)
al.
al.
et al
al.
al.
al.
(1950)
(1950)
. (1967)
(1972)
(1972)
(1972)
(1974)
(1974)
cardial contracLility
(cont iitued)
-------
TABLE 5-21. (continued)
Exposure -Dosage
Organism route In organism in air Exposure time Site
Dogs Inhalation - 2,500 ppm 5 rain Heart
(continued)
Inhalation - 5,000 ppm 5 mln Heart
Inhalation - 2,200 ppm 6 weeks (R lit/day) Liver, kidney
Inhalation - 135 ppm Continuously 90 days Lung
Inhalation - 370 ppm Continuously 90 days Lung
Inhalation - 250 ppm Continuously 100 days
Inhalation - 1,000 ppm Continuously 90 days
l.p. 4.14 g/kg -
l.v. 0.33-0.53 g/kg - - Heart:
Inhalation - 5,090 ppm - ((cart
Inhalation - 50,700 ppm - Heart
Inhalation - 510 ppm - Heart
Inhalation - 2,860 ppm - Heart
Inhalation 800.0 rag/kg -
Inhalation 0.45 g/kg -
Inhalation - 0.8-2.5 vol 7. 5 mln
Perfusion 1% -
through
limb
Inhalation - 200 and 1,000 ppm Continuous 3-13 weeks
Rabbits Oral 5.6 ing/kg -
Inhalation - 16,850 ppm 5 mln Brain
Inhalation - 16,850 ppm Q^,. 5 m)n Braln
Inhalation - 6,250 ppm I hr Brain
Inhalation - 6,250 ppm 10 rain Cardiovascular
(continued)
Toxic effect
No effects
Cardiac sensit ization to epinephrine
No effects
Congest: ion
Inf tairanat ion
No effects
No effects
LD50
Arrhythmia
Sensitized to epinephrine
Depress contractility
No effect
Depressed
Respiratory failure
Anesthesia
Cardiovascular depression
Hypotension, v.-icular reflex depression
Blood chemistry: no effect
LD50
Increased EEC activity
Incrased F.EG activity
Sustained increased EEC activity
Depression
Re fe rence
Reinhardt et al. (1971)
Reinhardt et al. (1973)
Prendergast et al. (1967)
Prendergast et al. (1967)
Prendergast et al. (1967)
MacEwen and Vernot (1974)
MacEwen and Vernot (1974)
Klaassen and Plaa (1967)
Rennick et al. (1949)
Keinhardt et a I. (1971)
Aviado and Belej (1975)
Aviado et al. (1976)
Aviado et al. (1976)
Krantz et al. (1959)
Krantz et al. (1959)
Herd et al. (1974)
Siraaan and Aviado (1976)
MacEwen and Vernot (1976)
Torkelson et al. (1958)
Truhaut et al. (1972)
Truhaut et al. (1972)
Truliaut et a I. (1972)
Truhaut et al. (1972)
-------
TABLE 5-21. (continued)
Exposure
Organism route
Rabbits Inhalation
(continued )
Inhalation
Cats Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Monkeys Inhalation
Inhalation
Ul Inhalation
f-*
.£> Inhalation
N>
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Man Inhalation '
Inhalation
Inhalation
Inhalation
Inhalation
Dosage
In organism • In air
500 ppm
135 ppm
0.4 mg/ liter
0.4 rag/liter
0.4 mg/ liter
0.4 rag/liter
0.4 ing/liter
25,400 ppm
25,400 ppm
3,000 ppm
500 pjm
250 and 1,000 ppm
5,000 ppm
5,000 ppm
3,000 ppm
500 ppm
1,000 ppm
135 ppm
250 ppm
13-75 mg/100 ml
6,090-22,860 ppm
5,050 ppm
2,650 ppm
6,090-22,860 ppm
Exposure t tme
7 hr (x 126-130)
Continuous 90 days
4 hr/day/4 months
4 hr/day/4 months
4 hr/day/4 months
4 hr/day/4 months
4 hr/day/4 months
•
-
7 hr/day (x 53)
7 hr/djy/6 months
Continuous 3-13
weeks
1 hr
5 hr
7 hr/day (x 20)
7 hr (x 126-130)
Coni inuous 90 days
Continuous 90 days
Continuous 100 days
-
-
-
15 min
.
Site
Liver, kidney
Liver, kidney
Liver ^
Kidney \
Myocardium^
Blood
Brain
Heart
Lung
Liver
Liver
-
Brain
Brain
Kidney, liver
Kidney, liver
Kidney, liver
Kidney, liver
Kidney, liver
-
Heart
Liver
Liver
„
Toxic effect
No changes
No pathology
! Reversible
Distrophic
Changes
No changes.
Reflex changes
Depress contractility; hypotension
Respiratory depression; broiichodllat ion
No effects
No effects
Blood chemistry; no effect
Slight ataxla
Trembling hands, arms
No effect
No effect
No lesions
No evidence of pathology
No lesions
Lethal dose
Arrhythmia
No effect
Decreased urobilinogen
Anesthesia
Reference
Torkelson et al. (1°58)
Prendergast et al. (1%7)
Tsapko and Rappoport (1972)
Tsapko and Rappoport (1972)
Tsapko and Rappoport (1972)
Tsapko and Rappoport (1972 )
Tsapko and Rappoport (1972)
Pelej et al. (1974)
Aviado and nelej (1975)
Adams et al. (1950)
Torkelson et al. (1958)
MacEven and Vernot (1974)
Adams ec al. (195")
Adams et al. (1950)
Adams el al. (1950)
Torkelson et al. (1958)
MacKwen and Vernol (1974)
Prendergast et al. (1967)
MacEwen and Vernot (1974)
Hall and Mine (1966)
Dornettc and Jones (1960)
Stewart et al. (I961a)
Stewart et al. (I96ia)
Dornette and Jones (1960)
(conti nut-.d)
-------
TABLE 5-21. (continued)
Ln
1
£
Exposure . Dosage
Organism route In organism In air Exposure time Site
Man Inhalation - 450 ppm 4 hr Brain
(continued)
Inhalation - 500 ppm 7 hr Brain
Inhalation - 500 ppm 7 hr/day/5 days Brain
Inhalation - 1,000 ppm 15 mln
Inhalation - 1,000-1,100 ppm 15 mln Fye
Inhalation - 1,910-2,100 ppm 15 min Tliro.it
Inhalation - 2,620-2,750 ppm 15 min Brain
Inhalation - 2,710 ppm 15 mln Brain
Inhalation - 450-710 ppm 90 rain
Inhalation - 900-1,190 ppm 30 mln
Inhalation - 900-1,000 ppm 75 min Fyc, brain
Inhalation - 1,750-2,200 ppm 5 min Drain
Inhalation 1 part drug/4 - One deep breatli
parts air —
about 2.6 mg
Skin exposure 0.65-21.5 ppm - 30 min
Inhalation 9.3-59 mg/100 g -
brain
Inhalation 0.49-22 mg/100 - -
g liver
Oral 0.6 g/kg
Inhalation - 20,000 ppm 5 min
Inhalation - 10,000 ppm 5 min
Inhalation - 5,000 ppm 5 min
Inhalation - 2,000 ppm 5 min
Toxic effect Reference
No behavioral effect. Salvini et al. (1971)
Dizziness Stewart et al. (1969)
No CNS effects Rowe et al. (1963)
Expired air smells of drug Stewart et al. (1961a)
Eye irritation Stewart et al. (I961a)
Throat irritation Stewart et al. (I961a)
"Light, head" Stewart et al. (I96la)
Disequilibrium Stewart et al. (196la)
No breath smell of drug Torkelson et al. (1958)
Expired air smells of drug Torkelson et al. (1958)
Eye irritation, light head Torkelson et al. (1958)
Disequilibrium Torkelson et al. (1958)
Poor llptd deposition in vivo Morgan et al. (1970)
Breath concentration reflected exposure Stewart and Dodd (1964)
Stahl et al. (1969)
Six fatalities; all lungs congested
Stahl et al. (1969)
Vomiting, diarrhea Stewart and Andrews (1966)
Expected effects: complete incoordtn-
atioti
Toxlcity Committee, Amerl-
Expected effects: pronounced coordin- cal) industrial Hyglenlsts
ar.ton loss •% Association (1964);
quoted by Stewart (1968)
Expected effects: Incoordlnatlon
Expected effects: equilibrium disturbed^
(continued)
-------
TABLE 5-21. (continued)
Exposure
Organism route
Man Inhalation
(continued )
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Ui
1 Inhalation
h-1
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Dosace
In organism In air
10,000 ppro
2,000 ppm
1,000 ppm
10,000 ppm
5,000 ppra
2,000 ppm
1,000 ppm
20,000 ppro
10,000 ppro
5,000 ppm
2,000 ppm
1,000 ppm
500 ppra
100 ppm
36,000-62,000
ppra
272 ppm, breath
199 ppm, breath
~ 250 ppm,
breath
Exposure time
15 min
15 min
15 min
30 min
30 mln
30 min
30 min
1 hr
1 hr
1 hr
1 hr
1 hr
1 hr
1 hr
_
1 hr
1 hr
3 hr
Site Toxic
Expected effects:-
tion loss
Expected effects:
Expected eftects:
problems
Expected effects:
tion loss
Expected effects:
Expected effects:
Expected effects:
comfort
Expected effects:
possible death
Expected effects:
tion loss
Expected effects:
loss
Expected effects:
Expected effects:
rium loss
Expected effects:
ous
Expected effects:
Death: braln/luii
effect Reference
pronounced coord ina-
loss of equilibrium
possible equilibrium
pronounced coordina-
Incoordl nation
loss of equilibrium
mild eye/nose dis-
surgical anesthesia,
pronounced coord ina-
obvi ous coord i na t i on
loss of coordination
very slight equillb-
no effect; odor obvi-
breath odor apparent
Toxiclty Committee, Ameri-
can Industrial Hygienists
Association (1964);
Quoted by Stewart (1968)
B edema Hatfield and Maykoski (1970)
Brain Pronounced coordination loss Stewart (1971)
Brain, liver Unconscious: depressed urinary uro- Stewart (1971)
bllinogen
Nausea, dizziness
Stewart (1971)
(continued)
-------
TABLE 5-21. (continued)
Exposure Dosaee
Organism route In organism In air
Han Inhalation 3*5 ppm, 17 hr
(continued) after exposure
Inhalation
Inhalation
Inhalation - > 5,000 ppm
Inhalation - Anesthesia
Inhalation - 250 ppm
Ul
1 Skin,
£* inhalation
in
Inhalation - 115 ppm
Inhalation - 115 ppm
Inhalation - 115 ppm
Inhalation - 115 ppm
(and skin
contact?)
Inhalation - 2,400 ppm
(and skin
contact?)
Exposure time Site. Toxic effect
7 hr - Nausea, vomiting, dizziness
Repeated Liver, brain "Clue sniffing" - 5/10 = hepatotox-
icily, 2/10 = CNS effects (tinnitis,
ataxia, paresthesla)
"Clue sniffing" - deaths more likely
with sniffing plus physical activ-
ity, review, 110 cases
10 min - Oeatb
Blood, circula- Depression, EEC changes
tion, brain
Unspecified toxicity
Months Eye, lung Cniijunct.iv.-iL Irritation, respiratory
Irritation, insomnia, unspecified
R.-istrointest inal complaints
7 hr/day, 1-6 years Heart ECC abnormality: five expected; eight
found
7 hr/day, 1-6 years Liver No evidence of toxicity
7 hr/day, 1-6 years Kidney Occurrence of blood in urine of ex-
posed group is twice that of con-
trols
7 hr/day, 1-6 years Blood No pathologies
(6/196)
8 hr/day, 1 week - Steady increase in urinary metabolite
excretion
Reference
Stewart (1971)
Litt and Cohen (1Q69)
Bass (1970)
Kleinfeld and Feincr (1966)
Siebecker et al. (I960)
BJnaschi et al. (1969)
Weltbrecht (1965)
Kramer et al. (1976)
Kramer et al. (1976)
Kramer et a I. (1976)
Kramer et al. (197S )
Seki et al. (1975)
Sekl et al. (1975)
Inhalation Not determined
Inhalation Not determined
"Solvent sniffing" Heart
for undetermined
time
"Solvent sniffing" Kidney
for undetermined
time
(continued)
Ventricular fibrillation widened Q,P,S Travers (1974)
complex
HematurJa
Travers (1974)
-------
TABLE 5-21. (continued)
Exposure Dosage
Organism route . In organism In air Exposure time Site
Man Inhalation - 39 ppm Dally at workplace
(continued)
Inhalation - Many solvents Dally in workplace Eyes
plus MC
Unknown Occurrence in - - Body fat
postmortem
samples (8)
range 1-32
Unknown Occurrence In - Kidney
postmortem
samples (8)
range 1-32
M3/kg
Unknown Occurrence in - - Liver
postmortem
samples (8 )
range 1-32
Hg/kg
Inhalation - >5,000 ppm 10 rain
Inhalation Workplace expo- - - -
sure, New York
Toxic effect Reference
No effects Apol (1973)
"Burning" reddening of conjunctival Vandervort
mucos.i and/or pharyngeal mucosa and Thoburn (1975)
Range of 2-32 w;/kg McConnell et al. (1975)
Range of 1-2 ng/kg McConnell et al. (1975)
Range of 2-5 Mg/kg McConnell et al. (1975)
Death Kleinfeld and Feiner (1966)
'[wo deaths, eight hospitalized with Kleinfeld and Feiner (1966)
toxic symptoms during 5-year per-
iod
-------
5.2.6.3.2 Allergic effects—Vandervort and Thoburn (1975), reported that
one worker in a printing plant exposed to Ottoson No. 9 solvent by hand con-
tact (a mixture of methyl chloroform and naptha) had "broken out" and had to
wear gloves for protection. Another worker showed a "rather severe reaction"
on exposure to the solvents, which required "systemic medication." There was
no indication that the skin reactions were due to methyl chloroform exposure,
but since the apparent causative solvent mix included this compound, the inci-
dents are included here.
Stewart (1971) included a report of human toxicity that had allergic-type
symptoms, although the article did not suggest the possibility that allergy
was the toxic cause. Two hours after leaving work, a worker experienced a sud-
den onset of nausea, vomiting, explosive diarrhea, and dizziness. The man had
worked close to a cleaning operation that used methyl chloroform during the
workday, and he had been aware of its odor throughout the day. The plant phy-
sician found the patient normal the next morning.
According to Stewart (1968), prolonged or repeated contact of methyl
chloroform with the skin results in a transient erythema and slight irritation.
In accidental contact with the cornea of the eye, the compound produces a "mild
conjunctivitis which subsides within a few days." Depending on the intensity
of the repeated response, these cases could demonstrate simple irritation or
sensitization.
Torkelson et al. (1958) stated that the Dow Chemical Company had received
reports of a few cases of skin irritation associated with the use of stabilized
methyl chloroform. No reports diagnosed as true allergic hypersensitivity to
this compound in either man or animal models were found in the literature.
5.2.6.4 Teratogenic Effects—
Schwetz et al. (1975) assayed for reproductive and teratogenic outcomes
in Sprague-Dawley rats (250 g) and Swiss Webster mice (25 to 30 g) exposed by
inhalation to 875 ppm of methyl chloroform for 7 hr/day from gestation day 6
to gestation day 15. The compound was a commercial grade preparation and con-
tained 5.570 inhibitors, or about 50 ppm. Caesarian sections were performed on
gestation day 21 (rat) and 18 (mouse). Maternal livers in the 13 rats exposed
exceeded liver weights for control rats (p < 0.05), but no significant findings
were reported for mice. No teratogenic effects were seen in all exposed rats
and mice for the following parameters: weight gain; percent fetal resorptions;
average litter size; fetal body measurements; fetal gross anomalies; skeletal
anomalies; microscopic assay; and maternal carboxyhemoglobin content.
One mouse litter included an occurrence of a short tail and another mouse
litter had an occurrence of cleft palate. Two different litters of rats in-
cluded embryos with vertebral anomalies. These findings were not statistically
significant. Since no additional studies were found, it was concluded that the
teratogenicity of methyl chloroform has not been established.
5-147
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Bell (1978a) reported on the preliminary results of a one-generation
vapor inhalation study in rats exposed to dioxolane, a stabilizer used in
methyl chloroform for industrial use. Five male rats had been exposed to
125 ppm dioxolane for 120 7-hr exposures (5 days/week). The males were sub-
sequently mated to females during a 15-day period, during which they both
received exposure; the females continued to receive dioxolane until 1 or 2
days before delivery. Results indicated that the mating and fertility indices
of the exposed animals were lower than for untreated controls. No statisti-
cally significant differences were found in number of pups delivered, number
stillborn, cannibalized, or the number living at 1, 4, 12, or 21 days.
5.2.6.5 Mutagenic Effects—
The mutagenicity of 1,1,1-trichloroethylene has been evaluated in the
B6G3F1 mouse using the host-mediated assay with £• pombe. Using 3, 6, and 16
hr exposure to 5,000 ppm methyl chloroform, triplicate assays showed fewer
forward mutants than was seen in control plates at all exposure times.
Loprieno et al. (1979) concluded that in the experimental conditions em-
ployed in the present study 1,1,1-trichloroethane was not mutagenic.
Seventy-one compounds identified in drinking water were assayed for muta-
genicity in bacterial systems: S. typhimurium (five strains), E. coll WP2,
or Sj. cerevisiae D3 to assay for mitotic recombination (Simmon et al., 1977).
Methyl chloroform and trichloroethylene were both weakly mutagenic in one
trial system. Simmon's work showed a dose-response curve, but the number of
revertant colonies was only twice the number in control plates at the highest
methyl chloroform dose (750 /nl of solvent in an open dish in a 9-liter closed
chamber).
In a recent industry-sponsored chronic inhalation study, 96 male and 96
female rats were exposed to methyl chloroform at levels of 1,750 or 875 ppm
for 6 hr/day, 5 days/week, for 12 months (Quast et al., 1978). Cytogenetic
examination of bone marrow cells from rats sacrificed after the 12 months
indicated no chromosome damage nor chromatid aberrations in the male rats.
The number of scorable chromosome spreads for the female rats was very low
overall; consequently data on female rats were not presented.
A test of cell transformation using the Fischer rat embryo cell line
F170 was performed on methyl chloroform (and the other subject solvents).
These cells carry an oncogenic virus, as discussed in the section on tri-
chloroethylene, and were transformed by methyl chloroform. These transformed
cells produced fibrosarcomas in rats when they were inoculated. The potency
of the methyl chloroform-induced transformation was similar to the transfor-
mation produced by trichloroethylene (Price et al., 1978).
Farber, in a communication to Merenda of EPA (October 20, 1978)
(Anderson, 1979), reported on the test of methyl chloroform by Litton Bio-
netics. Methyl chloroform gave the following results with activated Salmonella
strains:
5-148
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TA 1535 - Positive response
TA 1537 - "Equivocal" response
TA 1538 - Negative response
The test methods, material used for activation, and possible results with other
tester strains were not discussed.
Henschler (1977) tested methyl chloroform in the Ames test for mutagenic-
ity using Salmonella tester strain TA 100 (a highly sensitive strain). Methyl
chloroform was nomutagenic in both activated and unactivated tests.
Frost (1978), in a report to the Texas Air Control Board, reviewed the
positive data on methyl chloroform and two other compounds in producing cellu-
lar effects: the positive Ames test by Simmon et al. (1977) and the cell
transformation test by Price et al. (1978). A list of nine recommendations used
by the Science Committee of the Food Safety Council for judging the mutagenic-
ity of a chemical was presented. His summary, favoring regulation, stated that
methyl chloroform (and other chemicals) "had been subjected to insufficient
testing to allow unregulated dissemination. . ." Publications in referenced
journals, using a screen of scientifically-acceptable tests, are not available
on these compounds.
5.2.6.6 Carcinogenic Effects—
The bioassay of methyl chloroform for carcinogenicity under the Carcinogen
Bioassay and Program Resources of the National Cancer Institute has been pub-
lished (National Cancer Institute, 1977).
Rats of the Osborne-Mendel strain and B6C3HF1 mice (50 of each sex of each
rodent) were given methyl chloroform orally in corn oil at each of two dose
levels 5 days/week for 78 weeks. Survivors were killed in the 110th week for
rats and in the 90th week for mice.
Rats on chronic studies received high and low doses of 1,500 and 750 mg/kg;
mice received adjusted (increasing) doses averaging 5,615 and 2,807 mg/kg. The
methyl chloroform used in the carcinogenicity studies was technical grade, con-
taining 95% 1,1,1-trichloroethane, 3% £-dioxane, and 2% of several minor impuri-
ties and inhibitors. Male and female weanlings were started on the test at 5
weeks of age and killed at 96 weeks of age. Initially, the doses for male and
female mice were 4,000 and 2,000 mg/kg body weight. During the 10th week of the
study, doses were increased to 5,000 and 2,500 mg/kg. During the 20th week of
the study, doses were again increased to 6,000 and 3,000 mg/kg and maintained
at these levels to the end of the study.
Carbon tetrachloride was used as a positive control compound because it
is a known carcinogen in this rat strain (Reuber and Glover, 1970). Body weights
and food consumption were monitored. Necropsies were performed on all animals,
5-149
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and microscopic examination was done on H&E slides of the following tissues:
brain; pituitary; adrenal; thyroid; parathyroid; trachea; esophagus; thymus;
salivary gland; mesenteric lymph nodes; cervical lymph nodes; heart; nasal pas-
sages; lung; spleen; liver; kidney; stomach; small intestine; large intestine;
pancreas; urinary bladder; prostate or uterus; seminal vesicles and testis with
epididymis or ovary; skin with mammary gland; muscle; nerve; bone; bone marrow;
and "tissues masses."
There was no significant weight loss during the study in the rats, but
both sexes of mice had depressed body weights in the methyl chloroform-treated
group as compared to controls. The survival time of treated mice was also sig-
nificantly decreased. In females, survival time was dose-related, with survival
numbers at 90 weeks in the order: controls; low dose; and high dose. In male
mice, however, the control group had an unusually high death rate (higher than
either dosed group).
Of the malignant neoplasms, the following four occurred only in test
groups. Papillary cystadeno carcinoma (subcutaneous) occurred once in 50 high-
dose females. One urinary bladder transitional-cell carcinoma in 1 of 50 high-
dose males; a brain malignant glioma in 1 of 48 low-dose males; and a mesenteric,
metastatic osteosarcoma in 1 of 50 high-dose females. Each type of neoplasm rep-
resented had been encountered previously in a spontaneous lesion in this rat.
No relationship of type or incidence to chemical treatment was apparent.
Among the mice in the study, all tumors seen in exposed groups were also
seen in the control group. Each type of neoplasm described was stated to have
been encountered previously as spontaneous occurrences in aging laboratory mice.
No relationship in type or incidence to chemical treatment was apparent.
The B6C3F1 hybrid strain of mouse was susceptible to chlorinated
hydrocarbon-induced carcinogenesis, as shown by the incidence of hepatocellu-
lar carcinoma in the positive control mouse group which received carbon tetra-
chloride. These data are summarized in Table 5-22.
The Osborne-Mendel rat is a specific choice of strain for production of
carcinoma of the liver. They are more resistant than other strains such as
Sprague-Dawley to cirrhosis, an acute toxic effect of hepatocarcinogens; they
therefore survive longer periods so are more likely to develop carcinomas.
The NCI report summarizes what was described as a "fractured experiment"
in that the abbreviated life spans of both rats and mice confound the study.
The neoplasms seen, however, were not believed attributable to methyl chloro-
form exposure, since no relationship was established between the dosage groups,
the species, sex, type of neoplasm, or the state of occurrence (Federal
Register, 1977).
5-150
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TABLE 5-22.
COMPARISON OF THE INCIDENCE OF HEPATOCELLULAR
CARCINOMA IN CONTROL GROUP MICE
Group
Methyl chloroform
Carbon tetrachloride
Male
Control
Low dose
High dose
Female
Control
Low dose
High dose
2/19
0/47
1/49
1/20
0/48
0/50
2/19
49/49
47/48
1/20
40/40
43/45
Source: National Cancer Institute (1977).
Work is in progress on a replication of these tests. A new protocol (see
Table 5-23) has been prescribed for the new tests. One of the major changes
in the protocol provides limits on dose-related weight loss and deaths early
in the study. The definition of maximum tolerated dose (MTD) which allows any
number of deaths in the high dose group is being revised (Federal Register,
1978). The maximum tolerated dose for the repeat carcinogenesis bioassays is
in keeping with the proposed regulations and is based on animal growth rate
instead of lethality. The completion and evaluation of the new carcinogenesis
assay is scheduled for 1980-1981.
An industry-sponsored study (Quast, 1975) that reported no tumors on
chronic methyl chloroform exposure is discussed in Section 5.2.6.2.3, "Chronic
Toxicity."
A recent review by Schlossberg (1979) quoted several symposia and con-
gresses that suggest a major carcinogenic effect of the chlorinated hydrocar-
bon solvents could "be indirect. By mechanisms of atmospheric ozone depletion,
and indirectly through higher ultraviolet ray exposure, both melanoma and
nonmelanoma basal cell carcinoma incidence are theorized to increase with de-
pletion of the ozone layer.
5.2.6.7 Factors Affecting Toxicity--
5.2.6.7.1 Cardiac hypersensi tivity—Methyl chloroform was considered by
Lucchesi (1965) to be a very effective cardiac sensitizer in the dog; it was
used as a model for producing arrhythmias to test unknown compounds. A dose
5-151
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TABLE 5-23. NCI EVALUATIVE CARCINOGENESIS BIOASSAYf/
Objectives
To assess the carcinogenicity of methyl chloroform in rat strains other
than the Osborne-Mendel.
To investigate the correlation between hepatotoxicity and hepatocarcinogen-
icity in the B6C3F1 mouse. (Is hepatotoxicity resulting in liver damage a
necessary precursor of hepatocarcinogenicity, or can a chemical of this
type--chlorinated hydrocarbon—produce hepatocellular carcinoma at dose lev-
els wnere no other significant liver toxicity can be detected?)
To correlate dosage with blood levels in the various strains and species.
Protocol
Gavage in corn oil, five times per week. Subchronic study in the following
rat species: Fischer 344, Long-Evans, Wistar, and Sherman. Groups will in-
clude 10 rats per sex at each of five dose levels. Vehicle and untreated
control groups will include 10 rats per sex. Blood will be drawn from three
rats of each sex at terminal sacrifice for quantitative analysis of test
compound and trichloroacetic acid, a major metabolite.
The subchronic study in B6C3F1 mice (13 weeks) will have six dose levels of
10 mice per sex, which will be sacrified in groups at 30, 60, and 90 days
for a total of 360 animals. Appropriate vehicle and untreated controls will
be sacrificed at the same times. A total of 460 mice are included. The liv-
ers of all of these will be examined histopathologically, and the following
will be performed on all 460 mice at sacrifice: record liver weight and
liver fat; take blood sample and measure sorbitol dehydrogenase, fructose-
1-phosphate aldolase, and SCOT. Blood will also be taken from three mice of
each sex at each of the six dose levels and vehicle controls at the 30- and
90-day (terminal) sacrifices for quantitative analysis for test drug and
trichloroacetic acid.
Chronic studies at maximum tolerated dose and MTD/2 for all the rat strains
(2,000 animals) and 540 of the B6C3F1 mice will be done for 2 years.
iil Abbreviated from the protocol.
5-152
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of methyl chloroform (133.6 mg/kg) was added to a dog tracheal cannula and fol-
lowed in 15 sec by epinephrine (10 Mg/kg); arrythmias were invariably produced.
Somani and Lum (1965) also used this model and consistently produced ventricu-
lar fibrillation in dogs, except for animals pretreated with beta-adrenergic
blocking agents. Hermansen (1970) has used methyl chloroform to produce car-
diac fibrillation in mice.
Reinhardt et al. (1973) found the minimal concentration of methyl chloro-
form to cause cardiac sensitization in the dog was 5,000 ppm for 10 min; 2,500
ppm was ineffective. Clark and Tinston (1973) found that sensitization of the
dog heart was produced by methyl chloroform at about 7,500 ppm (40.7 mg/liter)
for 5 min. Rennick et al. (1949) showed that the heart became sensitized to
epinephrine-induced arrythmias after inhalation of methyl chloroform (330 to
530 mg/kg) in barbital-anesthetized dogs. In this situation, Rennick et al.
concluded that methyl chloroform was more effective than chloroform at produc-
ing cardiac arrhythmias.
Changes in the electrocardiogram produced by methyl chloroform have been
measured by several workers. Kramer et al. (1976) measured several parameters
in industrially exposed human workers and reported finding no significant pat-
terns in chronically exposed as compared to unexposed persons. (This study is
described later in Section 5.2.7.) Dornette and Jones (1960) saw EGG changes
of depressed S-T segments, nodal rhythm change, and premature ventricular con-
tractions in a case of cardiac arrest resulting from anesthesia with methyl
chloroform at 12 to 26,000 ppm.
Aviado and Belej (1974) reported that methyl chloroform acutely admin-
istered will induce cardiac arrhythmias in mice and sensitize the hearts of
mice to epinephrine. Mice, however, require a very high inhalation dosage com-
pared to the dog. In anesthetized mice exposed to 400,000 ppm of methyl chloro-
form epinephrine (6 Mg/kg) produced two-degree A-V blocks. It was also reported
by Aviado et al. (1976) that the effects on the QRS potential in exposed mice
lasted for 24 hr after inhalation, unlike the other cardiac changes (heart
rate, PR interval), which were quickly reversible when exposure ceased. This
observed decrease in QRS potential and widening of the QRS complex reflect
methyl chloroform effects on the ventricles.
Belej et al. (1974) studied the effects of several aerosol propellants
on the heart of the monkey, dog, and mouse. Methyl chloroform was included in
Class 1, a group that produced arrhythmia and myocardial depression at 2.5 to
5% concentration in the monkey. The dog heart was particularly sensitive to
epinephrine-induced arrhythmia after exposure to methyl chloroform.
5-153
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In a study of the cardiac-sensitizing properties of the compound, an aero-
sol product containing'70% methyl chloroform and 29% Freon 12 was tested in 12
beagle dogs at a methyl chloroform concentration of 5,000 ppm. The heart was
monitored during 15 min of inhalation, then afterward during stress-induced or
intravenously administered epinephrine. The dog heart was not sensitized to
epinephrine by this treatment (Borzelleca and Egle, 1974).
Strosberg et al. (1973) protected against methyl chloroform-induced fi-
brillation in mice with propranolol and also with reserpine. Propranolol is
a beta-adrenergic blocking drug that acts on effector organs and is known to
block the cardiac effects of both epinephrine and norepinephrine beyond the
nerve ending. Reserpine also blocks sympathetic activity but by another mech-
anism. Treatment of the mice to remove sources of endogenous catecholamines
did not protect the mice from methyl chloroform effects.
The mechanism for the cardiac arrhythmias observed with methyl chloroform
has been investigated by several groups. One hypothesis is that the cardiac
malfunction is adrenergically mediated (Krantz et al., 1959; Strosberg et al.,
1973). Another group has suggested the effect is direct (Rennick et al., 1949),
and a third group believes both spontaneous and adrenergically mediated effects
contribute to the arrhythmogenic properties (Aviado and Belej, 1974).
5.2.6.7.2 Misuse/Abuse—There exists a history of both intentional and
unintentional misuse of products containing methyl chloroform. There is there-
fore a concern due to the potential cardiac sensitizing effects associated with
the use of this compound.
In 1973, 21 deaths resulted from the use of a decongestant aerosol spray
that contained 44% methyl chloroform. All but one case apparently resulted from
the abuse or misuse of the product (Federal Register, 1973). The Food and Drug
Administration (FDA) has since required registration of drugs containing this
compound and several products have been removed from the market.
Bass (1970) reported 29 cases of sudden death during a 5-year period from
sniffing methyl chloroform. In the review (covering several volatile hydrocar-
bons and halocarbons) of 110 cases, 18 deaths resulted from solvent-sniffing
plus exercise. Bass suggested these deaths occurred following cardiac sensiti-
zation to endogenous catecholamines. The Bass cases overlap to an unknown de-
gree with the case histories listed in Table 5-24, and, due to a lack of data
on individual cases, they are not listed separately.
A report by Stewart and Andrews (1966) stated that a 47-year-old worker
drank 1 oz of stabilized methyl chloroform. Nausea began 30 min after ingestion,
and vomiting and diarrhea continued for 6 hr although gastric lavage was per-
formed 2 hr after drinking the solvent. The man was hospitalized, and the clin-
ical findings showed no adverse effects on the CNS, EGG, SGPT, blood urea
nitrogen, SCOT, hematocrit, and hemoglobin. The urine showed 8 to 10 red cells
5-154
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with protein. Increased bilirubin was detected 48 hr after ingestion of the
solvent.
Hall and Hine (1966) reported two deaths by intentional abuse of methyl
chloroform. Acute passive congestion of brain and marked congestion of lepto-
meninges were found at autopsy. The kidneys showed marked vascular congestion
around the pyramids, especially on the periphery. Lungs of both victims were
congested, as were the bronchi. Small hemorrhagic areas were reported in one
case, thick dark blood in the parenchyma in the other. The heart was not dis-
cussed in either case report.
Griffiths et al. (1972) studied the serum enzymes of two patients who had
inhaled a methyl chloroform-trichloroethylene mixture. One of the two showed
greatly elevated LDH and SCOT activities; the major source of the LDH was de-
termined to involve cardiac pathology. The authors suggested that the SCOT
elevation may have been secondary to cardiac causes because prothrombin (which
should have been affected with liver damage) was normal on day 5 when the pa-
tient died.
An annual summary of the reported human fatalities is shown in Table 5-24.
TABLE 5-24. HUMAN FATALITIES WITH METHYL CHLOROFORM-''
Year
1966
1966
1969
1970
1973
1974
1976
1977
Industrial
4
5
1
1
1
Abuse/accidental
2
1
21
1
Reference
Hall and Hine (1966)
Kleinfeld and Feiner
Stahl (1969)
Hat fie Id and Makoski
Aviado (1974)
Travers (1974)
Caplan et al. (1976)
Toxic Materials News
(1966)
(1970)
(1977)
af Listing may include the same data sources cited in the review by Bass
(1970).
5.2.6.7.3 Stabilizers/Inhibitors--Starting mainly with the work of
Torkelson et al. (1958), it was noted that the toxicity to experimental ani-
mals differed when pure methyl chloroform, as opposed to the "inhibited" or
"stabilized" compounds, was used. In 1966, methyl chloroform was introduced
with a different inhibitor system than that tested for toxicity by Torkelson.
The new system provided the stability needed under vapor degreasing condi-
tions; the precise stabilizer package used by each producer is proprietary.
5-155
-------
The various stabilizers and inhibitors employed with methyl chloroform
were discussed in Section 3. In the following list, the LD5Q is provided for
each compound in rats and mice; data were taken from the 1976 Registry of Toxic
Effects of Chemical Substances. It is readily seen that all these inhibitors
are more toxic than methyl chloroform, which has an LD5Q (oral) in rats of
10,000 to 14,300 mg/kg (Torkelson et al., 1958).
Lowest LD5Q (rats
Compound or mice, mg/kg)
1,4 Dioxane 5,600
416 g/kg = carcinoma
N-methyl pyrrole 418
Dioxolane 7,400
Butylene oxide 500
Acrylonitrile 82
Nitromethane 940
Toluene 1,640
Ketones Varies with specific chemical
Three to four carbon alcohols Varies with specific chemical
It is apparent that the inhibitors presently found in methyl chloroform
at 3 to 8% (allowable up to 10% in U.S. military specifications) could have
toxic effects at very high test levels in animals. At the level of 350 ppm in
the human workplace, however, the inhibitor levels would be at the micrograms
per liter level. Given the LD5Q of most inhibitors, this exposure level should
not produce toxicity. A different situation exists with respect to dioxane.
In 1971, 1,4 dioxane was placed in a "new carcinogen category" by the American
Conference of Governmental Industrial Hygienists (ACGIH). It is a highly effi-
cient inhibitor and has been used at the 3 to 4% level in commercially stabi-
lized methyl chloroform (Llewellyn, 1972). Since there is no standard for a
safe exposure level to a chemical defined as a carcinogen, a problem could
exist in using 1,4 dioxane as an inhibitor unless new research changes the
status of the compound, or new standards for carcinogens are defined. The
ACGIH, for example, has suggested that the hepatocellular and nasal tumors
resulting from dioxane in mice, dosed at 1,015 mg/kg/day, should be reevalu-
ated on the basis of their standards of dosage limitations. The ACGIH considers
as occupational carcinogens only substances which react by the respiratory
route only at doses below 1,000 mg/m^ for the mouse and 2,000 mg/irr for the
rat (ACGIH, 1976).
A one-generation mating study on a stabilizer used in methyl chloroform
was discussed in Section 5.2.6.4 (Bell, 1978a).
5-156
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5.2.7 Human Epidemiology
5.2.7.1 Occupational Exposure—
Most available reports on occupational exposure came from the health haz-
ard evaluations/toxicity determinations of the NIOSH.
Apol (1973) reported an analysis of the air at the Lorain, Ohio, Ford
Motor plant after employees complained 'of solvent-induced upper respiratory,
eye, and skin irritation. They found the average concentration of methyl
chloroform (TWA) was 39 ppm at the user site. No measurements of worker
breath and urine were made.
Frost et al. (1972) collected breath samples from 12 workers at the end
of a day of methyl chloroform contact. The workers exposed to higher levels
had higher breath levels (25 ppm in an unventilated room compared to 3 to 5
ppm with ventilation). They reported that trichloroacetic acid excretion by
workers was less reliable than breath analysis for determining exposure.
Weitbrecht (1965) studied several compounds for toxicity to workers.
Seven workers were exposed to methyl chloroform, both through hand contact
and inhalation of an estimated 10 to 20 ppm. The urinary excretion of tri-
chloroacetic acid (20 to 60 mg/kg) was difficult to relate to exposure, since
the workers had their hands in methyl chloroform for variable times.
After a preliminary experimental exposure to establish a standard curve
on exposure-trichloroacetic acid excretion, Tada (1969) performed a field sur-
vey on 15 plant workers exposed to methyl chloroform. With an average exposure
in air of 37 ppm for 7 hr/day, urinary trichloroacetic acid averaged 3.4 mg/
liter of urine for a 3-day test.
Binaschi et al. (1969) reported on an undetermined number of Italian shop
workers exposed to 250 ppm of stabilized methyl chloroform. The complaints about
the solvent began when methyl chloroform was added to other solvents already in
use.
A study was performed on employees of Japanese plants using methyl chloro-
form in printing. Urinary metabolites were determined in 46 subjects, and a
medical questionnaire was given. The investigators suggest that methyl chloro-
form may accumulate in the body, since one of the workers showed a steady in-
crease in urinary metabolite concentrations toward the end of the workweek.
Metabolites were found in urine even on Sunday when no exposure occurred (Seki
et al., 1975).
Hervin and Lucas (1973) evaluated the health.effects resulting from methyl
chloroform exposure in a plant employing 170 workers in the production of auto-
motive parts. Twenty-two samples of air were analyzed for methyl chloroform
5-157
-------
o
and the concentrations ranged from 30 to 1,660 mg/m (about 6 to 306 ppm). No
hazard was said to exist with regard to the exposure.
Hervin (1975) determined that the total daily exposure to methyl chloro-
form was not at a personally hazardous level after an evaluation of 35 employees
in a textile dye plant• Breath and area air were sampled and the highest level
found was 220 mg/nr (40.5 ppm) in a 1.3-liter breath sample.
Gilles and Rostand (1975) measured air levels, interviewed 15 employees,
and studied the plant insurance records in another evaluation of an industrial
site. The breathing zone and area samples obtained showed 7 to 18 ppm for the
former and a maximum of 14 ppm for area samples. No hazard was seen with this
exposure. NIOSH has investigated additional workplace sites to evaluate worker
exposure to methyl chloroform and determine its hazard status. Methyl chloroform
levels were below those allowed in the workplace (Gilles and Philbin, 1978;
Markel, 1978; Gilles, 1977).
Stewart (1961) reported urinary urobilinogen elevations in two of nine
women after they had worked with methyl chloroform for several months. Uro-
bilinogen levels are used commonly to check for liver function.
5.2.7.2 Detection of Exposure—
The diagnosis of exposure to methyl chloroform depends on detection of
the compound in the expired air, blood, or tissue of the individual, or of
metabolites in the urine. Several detection methods are available (Binaschi
et al., 1969; Stewart, 1971; Stewart et al., 1961; Stewart and Dodd, 1964;
Astrand, 1975; Astrand et al., 1973).
Behavioral measurements are known to be very sensitive tests of exposure
to CNS-active agents. Salvini et al. (1971) tested humans before and after
8-hr daily exposure to 350 and 450 ppm of methyl chloroform by a perception
test, Wechsler memory scale, O'Connor manual dexterity test, reaction time
test, and an aspiration test. Salvini et al. reported that the 450 ppm level
significantly decreased only perception test results.
Gamberale and Hultengren (1970) administered performance tests (simple
reaction time, choice reaction time, manual dexterity, and two perceptual
speed tests) to 12 subjects breathing methyl chloroform vapors at 250, 350,
450, and 550 ppm. While individual test performance varied according to train-
ing, there were adverse effects on performance of all tests at 350 ppm and
above when compared to control conditions.
Postmortem levels of methyl chloroform to evaluate solvent exposure have
been reported. Hall and Mine (1966) suggest that 35 to 100 mg/100 ml of methyl
chloroform in the blood could be expected in fatal cases; Stahl et al. (1969)
believe that the fatal blood level is considerably below 35 mg/100 ml blood.
Caplan (1976) reported a fatal case with a blood level of only 2 mg/100 ml,
5-158
-------
but ethanol was also found. Stewart's experiments (1961) demonstrated that
human subjects who reached a blood concentration of 0.7 to 1.0 mg/100 ml dis-
sipated the chemical in 30 min. They further suggested that the blood concen-
trations of persons overcome by the solvent would be in the range of 1.0 to
1.5 mg/100 ml.
The results of several studies investigating excretion of methyl chloro-
form and its metabolites have been discussed in the Excretion subsection
(5.2.4). These data are relevant to surveillance for exposure.
5.2.7.3 Epidemiological and Other Controlled Studies—
Few long-term studies on the effects of methyl chloroform in man have been
conducted due to experimental design problems in finding a suitable population.
Kramer et al. (1976) of Dow Chemical Company furnished a publication pre-
print and limited background data for the only paired-control research found
on human subjects exposed to methyl chloroform. The study utilized 151 matched
pairs of employees, and was conducted in two adjacent textile plants, one of
which used stabilized methyl chloroform as a general cleaning solvent. The
main purpose of the study was to evaluate health effects due to methyl chloro-
form exposure in an industrial population, with particular attention paid to:
1. Whether or not chronic exposure resulted in any effect on the heart
detectable by EGG;
2. Evaluation of general health; and
3. Determination of hepatoxic and CNS effects.
Study subjects were selected from the study plant (486 employees) on the basis
of four priorities: (a) individuals exposed to current levels in excess of
100 ppm; (b) individuals with past exposure at over 100 ppm; (c) individuals
with minimal exposure; and (d) individuals who had cooperated in an earlier,
uncontrolled study.
Pairmates were selected from the control plant, matched to the study sub-
jects on the basis of age (+ 5 years), race (white or nonwhite), sex, job de-
scription, shift worked, and socioeconomic status. The pairing of the first
three parameters was never relaxed, but the latter three criteria were occa-
sionally "eased" to obtain enough pairs for the study.
The physical parameters studied were height, weight, blood pressure, and
pulse. From a venipuncture, the following tests were run on blood and serum:
hematocrit; hemoglobin; RBC and WBC counts; and three tests on the state of
the RBC. Clinical chemical tests included alkaline phosphatase, SCOT, SGPT,
gamma glutamyl transpeptidase, total bilirubin, urea nitrogen, LDH, uric acid,
total protein, albumin/globulin serum ratio, albumin, calcium, and phosphorus.
5-159
-------
Expired air samples and ECGs were also taken. The EGG reading was computer-
interpreted on-line using the Smith-Mayo program. Jtl
Employees were grouped according to a methyl chloroform personal exposure
index of one to five, which ranged from a job with index one (1 to 14 ppm) to
five (150 to 249 ppm). The employees in the exposed group had exposure to
methyl chloroform for up to 6 years. The concentration range at the air return
to the air conditioner was 11 to 838 ppm during a 5-day period sampled, aver-
aging 115 ppm.
For quantitative variables, t-tests and tests of homogeneity of variables
were made. Paired differences with respect to environmental and demographic
variables were analyzed by multiple regression analysis. The authors concluded
that no differences existed between control and subject population with respect
to EGG change, hepatic dysfunction, or other recognizable clinical patterns.
There were statistically significant differences between groups in isolated
cases. Some or all of these statistical differences may have been due to random
variation or causes other than methyl chloroform exposure. Differences between
clinical chemical values of the exposed and control population that were seen
in the limited data and papers furnished by the investigators (and which need
additional clarification) are included in Tables 5-25 and 5-26.
The QRS-T wave EGG data are shown in Table 5-26 because there is an indi-
cation in the literature that this portion of the EGG is most frequently af-
fected by high experimental doses of methyl chloroform (Aviado et al., 1976),
and since a stated primary purpose of the study by Kramer et al. was to look
at effects on the heart. One subject, with one of the highest breath levels
of methyl chloroform, had a T-wave that deviated significantly from normal.
Table 6 of the published study (Kramer et al., 1978) noted 31 "abnormali-
ties" in the circulatory systems of exposed workers and 24 in the control
group. Of the seven systems studied (circulatory, gastrointestinal, genito-
urinary, nervous, musculoskeletal, dermal, respiratory), only the circulatory
system showed more abnormalities in the exposed group.
A commentary by Kuhar (1979) on the matched pair study (Kramer et al.,
1978) made the following points: no EGG data were collected on 20% of the
population, which suggests caution in evaluation of the remaining data; the
population used, which did not include all exposed individuals, should be
checked for bias in selecting a subset; data were not furnished on job ex-
posure matching criteria; exposure data were not adequately characterized
in the report; and the conclusion that fluorocarbon exposure was not relevant
to the study is not borne out by animal experiments.
5-160
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TABLE 5-25. EPIDEMIOLOGIC EFFECTS OF METHYL CHLOROFORM
Subjects
151 Chronically
exposed workers
Exposure
time Exposure level
!< 5-30 ppm on
breath
Average 115 ppm
Parameters that appear to differ in
exposed versus control populations-
Liver: A SGPT associated with cumulative ex-
posure
Heart: EGG abnormalities: five expected, eight
Statistical
significance
of effect
p < 0.05
p < 0,05
151 Controls (no
methyl chloro-
form in work-
place)
in workplace air
found
Blood: BUN showed high variances in exposed com-
pared to control workers
Blood: Serum albumin significantly different in
exposed compared to control workers
Blood: A hemoglobin levels in exposed workers
associated with exposure duration
p < 0.05
p < 0.05
a/ This summary was made on raw data from the pre-publlcation copy furnished by Kramer. In the published paper, the
authors concluded there were no solvent-related health effects (Arch. Environ. Health, November-December 1978,
pp. 331-342).
Source: Kramer, C. C., et al., "Health of Workers Exposed to 1,1,l-Trichloroethane: A Matched Pair Study," unpub-
lished study from Dow Chemical Company, Midland, Michigan, 30 pp. (1976).
-------
TABLE 5-26. COMPARISON OF COMPUTER-READ EGG IN METHYL
CHLOROFORM EXPOSURE STUDY
N>
Propram alROril.hm
QRS - T wave
No specific QRS-T abnormalities noted
Abnormal QRS voltage
No other qualifications
Probably from LVll
QRS measurements outside normal li.mi.Ls
without known clinical significance
Prolonged QT duration
High voltage R wave
Nonspecific ST changes with early repolar-
ization
ST segment deviation
Normal T wave
Low voltage with CW rotation
Horizontal CW rotation
Abnormal T wave
T wave abnormality
(Anterior ischemia)
(Low voltage lateral ischemia)
(Inferior ischemia)
T wave deviation from normal limits
T wave measurements outside normal limits
without known clinical significance
Variant T wave
Anterior direction
Postero-lateral direction
High voltage
Exposed
3
8
i
5
8
3
3
1
1
1
1
3
4
3
1
0
4
1
0
3
0
Control
0
5
1
4
I
7
2
0
0
0
0
6
1
0
0
1
5
2
1
1
I
Average rank
breath level
79.3
57.2
74. :i
44.4
65.2
71.7
25.2
81
33
62.5
49
32.2
76.3
69.3
97
9.5k/
109
55.3
Average rank
career dose
54.7
52.3
46.7
55.7
66.5
60.0
38.5
1202/
33
91
115
35.7
51.3
51.3
51
15.5k/
61
33.0
a/ P < 0.05.
b/ P < 0.01.
Source: Kramer ct al. (1976).
-------
Urinary metabolites, vibrational sense, a medical health questionnaire,
and unreported laboratory tests were performed in a limited epidemiologic
study by Seki and co-workers (Seki et al., 1975). The subjects, 196 people in
four Japanese printing factories, were exposed to methyl chloroform as the
sole organic solvent at average concentrations of 4, 25, 28, and 53 ppm. Six
of 196 subjects had a slight decrease in the ability to feel vibration, but
this was independent of concentration. The scores on medical questionnaires
were also independent of exposure intensity. The authors did find a linear
relationship between vapor concentration and level of urinary metabolites
(trichloroacetic acid and trichloroethanol). The increased level of urinary
metabolites towards the end of the workweek, together with the biological
half-life of 8.7 hr, suggested to Seki et al. that methyl chloroform was
stored in the body after repeated exposures. Metabolite concentrations found
in the workers are summarized in Table 5-27.
TABLE 5-27. METABOLITE CONCENTRATIONS IN URINE SAMPLES FROM
METHYL CHLOROFORM EXPOSURE
Exposure
concentration
(ppm)— '
0
4.3
24.6
53.4
No.
subjects
30
10
26
10
Trichloroethano 1
(mg/^ average)
0
1.2
5.5
9.9
TCA^/ (mg/^
average )
0
0.6
2.4
3.6
Source: Seki et al. (1975).
a/ Eight hours per day; 5-1/2 days/week.
b/ TCA = trichloroacetic acid.
5-163
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5.3 PERCHLOROETHYLENE (TETRACHLOROETHYLENE)
The sources utilized for this review on the health effects of perchloro-
ethylene include original literature sources and four reviews (NIOSH, 1976;
EPA, 1975; Walter et al., 1976; and Fuller, 1976). A part of the report was
taken from the undated prepublication copy of the Information Center complex
of the Oak Ridge National Laboratory's report to the National Science Founda-
tion. Industry sources have furnished unpublished data, and governmental agen-
cies (e.g., National Cancer Institute) have furnished information for specific
sections of the review. In general, reviews of the published literature cov-
ered early 1979 with some papers included from mid-1979.
5.3.1 Absorption, Transport, Distribution
Perchloroethylene (tetrachloroethylene; C^C = CCl2) is absorbed mainly
through the lungs and the gastrointestinal tract with very little absorption
through the skin. Lamson, Robbins and Ward (1929) stated that in ingested
food, the presence of fat was required for perchloroethylene absorption through
the intestine of dogs. However, the chemical (in concentrations sufficient to
produce narcosis) was absorbed by rats and mice, and to a lesser extent in cats
and puppies without the presence of fat. Schwander (1936) reported that mice
absorbed perchloroethylene to a moderate extent through the skin.
In studies on rabbit skin, Rowe et al. (1963) used a dermal dose of 30
g/kg. This dose produced chemical burns but no lethality, indicating very low
skin penetration.
A study of the absorption of perchloroethylene vapor through intact human
skin (Riikimaki and Pfaffli, 1978) demonstrated that only insignificant amounts
of the chemical would be absorbed at exposure levels of 600 ppm for 3.5 hr
(pulmonary absorption was experimentally eliminated). Using the blood and ex-
haled air values, it was calculated, assuming nearly total alveolar excretion,
that about 7 ppm was absorbed.
An example of transport across "respiratory" surfaces and tissue deposi-
tion is furnished by a study on fish. Neely et al. (1975) reported that rain-
bow trout muscle contained perchloroethylene at 36.9 times the water concentra-
tions.
Stewart and Dodd (1964) exposed five human subjects to pure perchloro-
ethylene by immersing one thumb in the solvent for 40 min. Perchloroethylene
concentrations were measured in the breath both during and after exposure. The
compound penetrated human skin slowly and was very slowly lost from the body.
The subjects reported a mild burning sensation 5 to 10 min after immersion,
the intensity of which increased to a moderate burning sensation within 15 to
20 min. This sensation continued for 10 min after, removal from the bath and
subsided gradually within an hour; the accompanying marked erythema subsided
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within 1 to 2 hr after exposure. The highest mean peak breath concentration
occurred less than 15 min after completing a 30-min dermal exposure. Peak
breath concentration was 0.31 ppm and the mean breath concentration 2 hr af-
ter exposure was 0.23 ppm.
5.3.2 Metabolism and Excretion
5.3.2.1 Biological Half-Life--
Stewart et al. (1961a) postulated a long biological half-life and a rapid
blood clearance for perchloroethylene because humans exposed to the compound
at 194 ppm for either 187 or 83 min or at 101 ppm for 183 min had no detectable
levels in their urine or blood after 30 min. It required 94 hr for clearance
of the vapor from the expired air after an 83 min exposure at 194 ppm and 400
hr after a 393 ppm exposure for 210 min. Morgan et al. (1972) have shown that
the elimination rate of a chlorinated hydrocarbon is related to its lipid solu-
bility. Using a single breath of 3°Cl-labeled perchloroethylene, the authors
measured serum/gas partition coefficients (32 for perchloroethylene) and olive
oil/gas partition coefficients (490 for perchloroethylene). When the ACGIH
threshold limit values were plotted against the serum/gas partition coeffi-
cients, an inverse relationship was seen. Stewart (1969) related the concen-
tration of perchloroethylene in the expired air to the total amount of solvent
absorbed, the duration of the exposure, the time elapsed following exposure,
the individual rate of lung excretion, the whole body blood concentration, and
the whole body lipid repository. Fernandez et al. (1976) stated that perchloro-
ethylene was primarily eliminated via expired air and that very little was me-
tabolized by humans; however, 2 weeks were required to completely eliminate
the perchloroethylene which was retained during a 8-hr exposure to 100 ppm of
the chemical.
Bolanowska and Golacka (1972) reported that humans exposed to perchloro-
ethylene at 390 mg/m^ (~ 57 ppm) for 6 hr with two 1/2-hr interruptions elim-
inated 25% of the absorbed chemical via expired air, 0. 02%/hr percutaneously,
less than 10% via the urine, and retained 62% in their bodies. For the first
few days after cessation of exposure, perchloroethylene disappears from the
breath with a half-time of about 70 hr. They presumed this percentage of the
dose then undergoes biotransformation in the body. A major metabolite, how-
ever, trichloroacetic acid, accounted for only 2% of the inhaled perchloro-
ethylene over a 67-hr collection period. [This ~ 60% human absorption figure
can be compared to the mouse data of ~ 90% absorption (Yllner, 1961).]
Ikeda and Imamura (1973) reported the half-time of perchloroethylene in
humans measured by urinary excretion of metabolites was 144 hr, after exposure
8 hr daily, 5 days weekly, at 10 to 100 ppm.
After repeated exposure, an increase of perchloroethylene can be de-
tected on the breath. The data of Bolanowska and Gloacka (1972), however,
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indicate that much of the perchloroethylene is metabolized or excreted by
routes other than the breath.
Experimentally, Stewart et al. (1970) showed that the breath excretion
of perchloroethylene increased only 10% on day 2 exposure. On an average, when
100 ppm was inhaled for 7 hr, the breath concentration was 20 ppm (Stewart et
al., 1970). Using the methods of Bolanowska and Golacka (1972) for calculat-
ing perchloroethylene kinetics, it was determined that alveolar excretion oc-
curred at the rate of 15 mg/hr after a 6-hr exposure to 390 mg/m (about 56
ppm).
Tada and Nakaaki (1969) stated that after exposure to perchloroethylene,
the net excretion of the metabolite trichloroacetic acid in the urine in-
creased daily to a maximum in 3 or 4 days.
Van Dyke and Wineman (1971), using rat liver microsomes in a closed in-
cubation system, found that less than 170 of the ^"Cl was enzymatically re-
moved from °Cl-labeled perchloroethylene in 30 min thereby indicating a very
slow degradation rate.
Moslen et al. (1977) pretreated rats with phenobarbital or Arochlor-1254
which are inducers of the mixed function oxidase system, followed by one oral
dose of 0.75 ml/kg perchloroethylene. A significant increase in the urinary
excretion of total trichlorinated compounds and trichloroacetic acid (per-
chloroethylene metabolites) resulted, giving evidence for involvement of the
mixed function oxidase system of liver microsomes in the in vivo metabolic
pathway.
Henschler (1977) has presented some hypotheses for the breakdown paths
of perchloroethylene in man, which includes forming highly electrophilic epox-
ides which may react with nucleophilic tissue constituents. However, the route
is incompletely understood and experimental data to test the hypotheses are
sparse.
Products identified after metabolism of perchloroethylene are as follows:
Metabolite Species Reference
Trichloroacetic acid Man, animals Piotrouski (1977);
Ikeda (1977)
Urinary chlorine "Animals" Daniel (1963)
Ethylene glycol Not specified Dmitrieva (1967)
Oxalic acid Not specified Dmitrieva (1967)
Trichloroethanol Man Ikeda (1977)
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Figure 5-6 summarizes some current theories on the pathways involved in
perchloroethylene metabolism.
5.3.2.2 Routes and Rates of Elimination--
Exposure of five female mice to ^C-perchloroethylene vapor (1.3 mg/g
body weight) in a sealed flask for 2 hr resulted in 90% absorption of the
solvent; during subsequent 4-day measurements, 70% was expired in the air,
20% was excreted in the urine, and 0.5% was excreted in the feces (Yllner,
1961). Fractionation of urinary metabolites resulted in the identification
of trichloroacetic acid (52%), oxalic acid (11%), dichloroacetic acid (trace),
and other unidentified, polar labeled compounds (18%). Monochloroacetic acid,
formic acid, and trichloroethanol were not identified as metabolites. There-
fore a metabolic pathway in which perchloroethylene was converted to trichloro-
acetic acid via an epoxide intermediate was postulated.
x
Cl C=CC1 - >Cl C_J"CC1 - >Cl CCOC1 - >C1 CCOOH + Cl"
^ £m £. £ 3 J
Perchloroethylene Epoxide Trichloroacetic Trichloroacetic
acid chloride acid
Studies by Daniel (1963) confirmed a similar pathway in Wistar rats which
had been dosed by stomach tube with 1.34 or 10 mmoles of ^^Gl-labeled per-
chloroethylene. At the lower dose level, 97.9% of the ^"Cl had been recovered
in the expired air after 48 hr; the half-life of respiration for the compound
was about 8 hr. The expired air contained no metabolites of perchloroethylene
and, after 18 days, the urine contained only 2% of the Cl, of which 0.6%
was trichloroacetic acid. This investigator concluded that the compound was
transformed to trichloroacetic acid via an epoxide intermediate. The absence
of trichloroethanol and oxalic acid was explained by the fact that the acid
chloride is rapidly hydrolyzed to trichloroacetic acid and chloride ion.
The metabolism of perchloroethylene in humans, rats, and mice was com-
pared by Ikeda and Ohtsuji (1972). After inhalation exposure, trichloroethanol
and trichloroacetic acid as well as other unidentified trichloro compounds
were found in the urine of exposed subjects as summarized in Table 5-28.
Rats and mice were also injected intraperitoneally with the chemical (2.7
mmoles/kg body weight) to eliminate the possibility of variation in results
due to differences in the efficiency of pulmonary uptake. In these studies a
metabolite profile similar to earlier work cited above was obtained except
that in the 1972 Ikeda and Ohtsuji study, less trichloroethanol was found.
5-179
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PERCHLOROETHYLENE epoxFdotjon
Cl2C=CCI2
SYMMETRICAL
OXIRANE TRICHLOROACETYL
/Ov intramolecular CHLORIDE
-^ CChCOCI
rearrangement °
00
o
REPORTED METABOLITES
OXALIC ACID
C2H2O4 • 2H2O (Rodents)
D1CHLOROACETIC ACID
CHCI2COOH (Mice)
ETHYLENE GLYCOL
HOCH2CH2OH (Rats)
TRICHLOROETHANOL
CCI3CH2OH (Man)
Greim et al. (1975)
Ikeda and Ohtsuji (1972)
Dmitrieva (1967)
UNKNOWN
CHLORINATED
PRODUCTS
TRICHLOROACETIC ACID
CCI3COOH
Figure 5-6. Metabolic route suggested for perchloroethylene.
-------
TABLE 5-28. EXCRETION OF URINARY METABOLITES BY HUMANS, RATS,
AND MICE AFTER EXPOSURE TO PERCHLOROETHYLENE
Species
HumanS/
Human
Rat
Mouse
Ol
M Rat
oo
h-1
Mouse
No.
subjects
4
66
48
20
35
20
Exposure
Route
Inhalation
Inhalation
Inhalation
Inhalation
i.p. injection
i.p. injection
Dosage
20-70 ppm
200-400k/ ppm
200 ppm/8 hr
200 ppm/8 hr
2.78 mmol/kg
2.78 mmol/kg
Urinary metabolites
Trichloroacetic acid
4-20 mg/jG
21-100 mg/4
5.3 mg/kg body weight
20.7 mg/kg body weight
5.5 mg/kg body weight
23.3 mg/kg body weight
Trichloroethanol
4-35 mg/4
32-97 mg/4
3.2 mg/kg body weight
4.3 mg/kg body weight
0.08 mg/kg
0. 1 mg/kg
_a/ Workers subject to daily intermittent exposure.
_b/ Worker receiving 400 ppm was also in direct skin contact with the liquid.
Source: Summarized from the tables of Ikeda and Ohtsuji (1972).
-------
Ikeda et al. (1972) have measured the exposure and subsequent urinary ex-
cretion of perchloroethylene metabolites in 85 male workers using perchloro-
ethylene as a dry cleaning solvent. In one study, workers exposed 8 hr/day,
6 days/week to 10 to 400 ppm furnished urine samples. A plateau rate of metab-
olite excretion was reached when the perchloroethylene concentration in work-
place air approached 100 ppm; this urinary metabolite excretion did not increase
even when perchloroethylene in the workplace air rose to 400 ppm. The authors
conclude that the data show that human ability to metabolize perchloroethylene
is limited, and metabolism patterns differ in acute and chronic exposure. No
data were furnished on whether or not larger amounts of perchloroethylene are
deposited in lipid tissue in the body with increased exposure, but accumula-
tion is implied.
When humans were exposed by inhalation to perchloroethylene (87 ppm) for
3 hr, trichloroacetic acid and unidentified trichloro compounds were found in
the urine (Ogata et al., 1971). The concentration of trichloroacetic acid in
the urine increased during exposure but had returned to nearly normal 64 hr
after exposure as shown in Figure 5-7. The total trichloro compounds recovered
in the urine were equivalent to only 2.8% of the retained perchloroethylene,
1.8% of this being trichloroacetic acid. Only 4% of the retained dose was me-
tabolized (Ogata et al., 1971). The concentrations of trichloroacetic acid
and the unknown organic chloride were determined by the chromium oxidation
method.
04
'-•» •' unknown orqanic chloride
--o-- trichloroaceTic acid
lExpoiure
O IO 2O 3O 4O 5O 6O 7C
Hourj
Figure 5-7. Urinary excretion of trichloroacetic acid,
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Fernandez et al. (1976) have shown that trichloroacetic acid appeared in
the urine of humans during exposure and the excretion rate rose slowly although
the' total urinary excretion after 72 hr was only 1.85% of the total dose re-
tained. Their results are tabulated in Table 5-29.
TABLE 5-29. HUMAN URINARY EXCRETION OF
TRICHLOROACETIC ACIDl/
Time of collection TCA~ excreted
Subject postexposure (hr) (rag)
E.G.
B.H.
0-8
8-24
24-48
48-72
0-8
8-24
24-48
48-72
4.54
7.19
9.68
3.63
3.05
8.50
8.95
3.70
_a/ Exposures to perchloroethylene vapor for 8 hr to 150
ppm.
_b/ TCA = Trichloroacetic acid.
Source: Fernandez et al. (1976).
Moslen et al. (1977) reported studies in which the mixed function oxi-
dase enzymes in rat liver were stimulated by in vivo dosing of phenobarbital
or Aroclor 1254 (four rats for each drug). Perchloroethylene, 0.75 ml/kg body
weight, was dosed orally mixed with mineral oil. Controls received vehicle
only. The rats were kept in metabolism cages for 24 hr.
Perchloroethylene was metabolized primarily to trichloroacetic acid. Uri-
nary metabolites increased five- to seven-fold over controls in phenobarbital-
and Aroclor-treated groups. Aroclor pretreatment enhanced the toxicity of per-
chloroethylene; SCOT enzyme tests were doubled and histological liver pathology
was also increased in Aroclor-pretreated, perchloroethylene-dosed rats.
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Moslen concluded that the magnitude of cytochrome P-450 induction corre-
lated with the extent of liver damage by perchloroethylene, which strongly sug-
gests a perchloroethylene metabolite is involved in the liver effects.
Henschler (1977) has reviewed the toxicity of several chlorinated solvents,
emphasizing trichloroethylene and perchloroethylene. The metabolite, trichloro-
acetic acid, was formed in human volunteers at the same level when exposure oc-
curred to either 50 to 100 ppm trichloroethylene or 100 to 200 ppm perchloro-
ethylene. Henschler suggested that the most plausible route for the metabolism
of these solvents was through an electrophilic epoxide step, which would also
be responsible for the biochemical lesions produced by perchloroethylene (and
trichloroethylene).
Leibman and Ortiz (1977) studied the enzymatic breakdown of perchloro-
ethylene by an in vitro system. They hypothesized that perchloroethylene formed
the corresponding oxide, followed by hydration of the oxide to trichloroethylene
glycol. Either of these would form only one product, trichloroacetyl chloride,
which would rapidly hydrolyze to trichloroacetic acid. Trichloroacetic acid is
the only metabolite which has been detected in vitro after perchloroethylene
liver perfusion. The data suggest that the microsomal drug-metabolizing enzymes
are not involved in perchloroethylene metabolism to the extent they are in
other related compounds (like trichloroethylene). For example, Mg-H- (at the
level which enhances chloral hydrate production by trichloroethylene) will in-
hibit perchloroethylene metabolism. When a key enzyme, epoxide hydrase, was
inhibited by adding cyclohexane, no differences in perchloroethylene metabo-
lites were seen. This study means that further research is necessary to ex-
plain the increased liver toxicity seen in perchloroethylene-dosed rats with
Aroclor-stimulated enzyme systems, as reported by Moslen et al. (1977).
Ikeda (1977) reported on the urinary half-life of perchloroethylene metab-
olites in humans who were occupationally exposed to the vapor. The urinary half-
life of total trichloro compounds averaged 144 hr; 190.1 +32.9 hr for females
(six subjects exposed 8 hr/day, 5 days/week, 10 to 20 ppm) and 123.3 +23.5 hr
for males (six subjects exposed 8 hr/day, 5 days/week, 30 to 100 ppm).
The half-life of metabolites expired into alveolar breath was calculated
to be 65 hr and for urinary metabolites the mean biological half-life is 144
hr (Ikeda, 1977). Estimated biological half-life for fat stores of perchloro-
ethylene is 71.5 hr, using the theoretical methods of Guberan and Fernandez
(1974).
By two exposure routes, Ikeda noted that perchloroethylene remained in
humans about three times longer than trichloroethylene, indicating about a
three-fold greater rate of body accumulation of perchloroethylene.
A summary of the fate of perchloroethylene taken from data in the litera-
ture and discussed here is found in Table 5-30.
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TABLE 5-30. FATE OF PEKCIILOROETIIYLENI::
Species
Man
Man
Man
Man
Man
^ Man
oo
Ln
Mice
Rats
Rats
Dog
Cat
Route
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Thumb immersion
Inhalation
Inhalation
Oral
Injection
Injection
Acutely retained
Intake by body (%)
1 breath (5 mg)
87 ppm/3 hr 50
194 ppm/ 18 7 min
390 ppm/6 hr 62
395 ppm/3. 5 hr
1.3 mg/kg
200 ppm/8 hr
1.75 and 13 MCi
5.36 g/kg
5.36 g/kg
Excretion
Unchanged Metabolized
Lung Urine Skin Feces
15%/1 hr 2.8%
<50%
<30 ppm at 1 hr
25% <10% 0.02%
85 ppm at 1 hr
Maximum 6.6 ppm
70% 20% <0.5%
5.3 mg/kg
97.9% 1.6-2.1 (18
days )
(2 days)
Source: MRI compilation of various sources found in this text.
-------
5.3.3 Biochemical Interactions
Medical World News'contained a report of a 6-week-old baby with jaundice
and an enlarged liver; the baby was breast-fed by a mother who frequently in-
haled perchloroethylene in a Canadian dry cleaning establishment (Anonymous,
1978a). The mother's milk contained perchloroethylene levels up to 1 mg%. The
child's symptoms vanished when breast feeding was discontinued. It was noted
that while adults metabolize and excrete these chlorinated solvents readily
at low levels, the enzyme systems in a 6-week-old child would not be adequate
for detoxification.
Ogata et al. (1968) reported a decrease in hepatic ATP levels with a pro-
portional increase in total hepatic lipids and triglycerides in mice exposed
to perchloroethylene. In another study, mice were exposed to perchloroethylene
at 200, 400, 800, and 1,600 ppm for 4 hr. Upon histological examination of the
liver, fatty infiltration but not cellular necrosis was seen at all dose levels
(Kylin et al., 1963). Rowe et al. (1952) reported a slight increase in total
liver lipid content. Daniel (1963) and Ikeda et al. (1969) found, however, that
there was no significant effect of perchloroethylene on liver lipid content in
rats. Data from Daniel (1963) are shown in Table 5-31.
TABLE 5-31. THE EFFECT OF EXPOSURE OF RATS TO THE
VAPOR OF PERCHLOROETHYLENE ON LIVER
LIPID CONTENT
Dose: 3-6 hr exposures at 1,000 ppm
No. of
animals
7
7
7
7
Sex
Male
Male
Female
Female
Series
Control
Test
Control
Test
mg Lipid/100 mg
dry weight liver
11.2 + 1.4
10.3 + 2.2
10.7 + 2.2
8.0 + 1.5
Source: Daniel (1963).
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Experiments by Mazza (1972) showed that mitochondrial damage resulted
when rabbits were exposed to approximately 2,790 ppm perchloroethylene for
4 hr daily, 5 days/week, for 9 weeks. Measurement of the activity of glutamic-
oxalacetic transaminase, glutamic-pyruvic transaminase and glutamic dehydro-
genase, before and at 15, 30, and 45 days after initiation of the experiments,
showed a significant increase for all enzymes by 45 days. Further tests demon-
strated damage to cytoplasmic and mitochondrial structures of the liver paren-
chyma with the mitochondrial damage being greater (see Table 5-32 ).
TABLE 5-32. EFFECT OF INHALATION EXPOSURE OF RABBITS TO PERCHLORO-
ETHYLENE ON THE ACTIVITY OF LIVER ENZYMES
GOT-2/ GPT-2/ Schmidt
(mU/ml) (pmol/ml) (ymol/ml)
Before exposure-'' 0,10+0.06-/ 0.37+0.03 0.33+0.03 6.70+0.37
After 15 days 0.10+0.05 0.38+0.04 0.33+0.03 6.72+0.26
After 30 days 0.49+0.05 0.49+0.05 0.44+0.03 1.92+0.06
After 45 days 0.81+0.07 0.74+0.09 0.71+0.10 1.79+0.09
aj GDH = Glutamic dehydrogenase.
GOT = Glutamic-oxaloacetic transaminase.
GPT = Glutamic-pyruvic transaminase.
Schmidt Index = GOT + GPT/GDH.
b_/ Exposure was at 15 mg/liter of air with a constant air flow of 750 liters/hr.
c/ Mean plus standard deviation for N equal 15.
Source: Mazza (1972).
Tarasova (1975) found that following inhalation exposure of rats to per-
chloroethylene (7 days at 185 ppm) there were morphological changes in mast
cells characterized by increased vacuolization of the cytoplasm and conforma-
tional changes in the granules.
Klaassen and Plaa (1966, 1967) estimated the £059 for liver and kidney
damage in dogs and mice. The ED^Q values for organ dysfunction were measured
by BSP, SGPT, glucose, protein and phenolsulfonphthalein (PSP). They also de-
termined the potency ratio, or, the ratio of the LD5Q to the ED^Q. All effects
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were observed after single intraperitoneal (i.p.) doses. After administration,
effects on the liver and kidneys were determined by microscopic examination
and by clinical tests for liver and kidney function: SGPT elevation, and BSP
or PSP excretion. The data in tabular form (Table 5-33) are summarized as
follows :
TABLE 5-33. 24-HR MEDIAN LETHAL AND EFFECTIVE DOSES
OF PERCHLOROETHYLENE
EDCA for clinical tests (ml/kg)
Species
Mouse
Dog
(ml /kg)
2.9 i.p.
2.1 i.p.
BSP Retention
2.9
ND
SGPT
2.9
0.74
PSP Retention
ND
1.4
Note: ND = Not determined.
Source: Summarized from Klaassen and Plaa (1966; 1967),
Effects of perchloroethylene on the adrenal gland were measured in rab-
bits inhaling 2,790 ppm 4 hr/day, 5 days/week for 9 weeks (Mazza and
Brancaccio, 1971). Urine and plasma levels of adrenal cortical and adrenal
medullary hormones were measured, as well as excretion of a hormone metabo-
lite. Although no statistically significant differences were found, both
cortical and medullary hormones were increased with perchloroethylene expo-
sure. The adrenal hormone-related 3-methoxy-4-hydroxymandelic acid was also
eliminated in larger quantities in treated rabbits.
5.3.4 Toxicological Data
5.3.4.1 Target Organs--
In January of 1978, the National Institute for Occupational Safety and
Health published a "Current Intelligence Bulletin" on perchloroethylene
(NIOSH, 1978a). The purpose of these Intelligence Bulletin documents is to
review, evaluate, and supplement new information received on occupational
hazards that are either unrecognized or are greater than generally known.
This Intelligence Bulletin summarized no additional, new hazard. The main
hazard to workers stressed in the document was based on results of positive
5-188
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animal tests on perchloroethylene carcinogenicity and teratogenicity. An ad-
ditional suggested workplace hazard was slow elimination in man of inhaled
perchloroethylene.
The most characteristic response of an acute exposure to perchloroethylene
is depression of the central nervous system. Like all the chlorinated hydrocar-
bon solvents, there is the potential of cardiac sensitization to epinephrine
by perchloroethylene. With exposure at toxic levels, liver effects are diag-
nosed by changes in enzyme profiles. Chemical burns can occur with skin contact,
and there is an apparently local (as opposed to target organ) effect of eye
and respiratory tract irritation on inhalation of perchloroethylene at 75 to
80 ppm for 1 to 4 min (Stewart et al., 1961b).
5.3.4.1.1 Central nervous system (CNS)—The chronic studies found in the
literature were at industrial sites with uncontrolled exposure; often the dose
was unreported.
A case report by Gold (1969) suggests serious nervous system effects in
one exposed subject. A 47-year-old male, who owned a dry cleaning establish-
ment, worked daily for 3 years around the fumes. On Sunday he would clean the
tanks, apparently being subjected to high exposure levels, after which he
would literally stagger home and sleep or pass out for a couple of hours,
during which time he could not be roused. His acute symptoms included nausea,
vomiting, dizziness, staggering gait, and disorientation. Chronically he ex-
hibited difficulty remembering recent events, mild disorientation, mood labil-
ity, and fatigue, with symptoms persisting at least 1 year after exposure
ceased. The clinical picture suggested both basal ganglia involvement and
cerebral cortical damage.
The only animal study found in the literature that could be related to
this type of pathophysiology was the selective destruction of the Purkinje
layer of the cerebellum and myelin sheath swelling seen with chronic per-
chloroethylene exposure in dogs (Baker, 1958).
Published citations of chronic exposure to perchloroethylene show CNS
effects but often the dosage information is not reported. Nine workers ex-
perienced vertigo, headache, nausea, and vomiting with intermittent exposure
for 3 weeks to 8 months at 75 ppm of perchloroethylene. When the exposure
was as long as 2 to 4 years, two workers had neurological symptoms. One had
difficulty in walking, and trembling of the extremities, and the other ves-
tibular problems (Lob, 1957).
A single worker was exposed for 2 months to perchloroethylene at levels
which led to confusion and eventually produced unconsciousness. No discussion
was made of any neurologic effect that persisted following removal from ex-
posure (Eberhardt and Freundt, 1966).
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Coler and Rossmiller (1953) found neurologic responses to perchloroethylene
exposure in seven workers exposed to approximately 300 ppm.for 2 days a week.
Staggering and inebriation-like symptoms were reported, as were lightheadedness
and memory impairment. The symptoms disappeared when exposure ceased.
Nine firemen responding to a leak of perchloroethylene were exposed to
high levels of fumes for approximately 3 min. All nine became lightheaded, un-
coordinated, and reported a sensation "as though they wanted to reach out and
touch an object but somehow could not reach it." The high levels of exposure
produced liver function changes as many as 63 days later. No neurological or
behavioral follow-up was made, and there was no subject report of any nervous
system problems beyond acute exposure (Saland, 1967).
Franke and Eggeling (1969) in a clinical-statistical study on cleaning
plant workers, recorded symptoms that could have been signs of hyperactivity
of the autonomic nervous system. Forty percent of the workers had hyperhidro-
sis, dermographism, or fine tremors, plus miscellaneous subjective complaints.
These three symptoms were also cited as effects seen in 50% of workers in
another study of the dry cleaning industry (Munzer and Heder, 1972). In the
Franke study, the concentration of perchloroethylene in the air was a maximum
of 400 ppm with 75% of the 326 random samples measuring 100 ppm or less. Munzer
and Heder's report cited concentrations between 25 and 400 ppm.
Irreversible neurologic effects on humans (peripheral neuropathies) pro-
duced by unknown levels of perchloroethylene have been described by E. Baginsky
(cited by NIOSH, 1976).
The effects of alcohol and an antidepressant (diazepam) on workers addi-
tionally exposed to perchloroethylene were studied in six male and six female
subjects (Stewart et al., 1977). Potential synergistic effects of perchloro-
ethylene and these drugs were measured with a battery of neurological and be-
havioral tests. Blood levels of drugs confirmed the doses in all subjects.
Drug doses used in the trials were: perchloroethylene - 0, 25, or 100
ppm for 5.5 hr; diazepam - 0, 6, or 10 rag/day; and 50% ethanol - 0, 0.75, or
1.5 ml/kg body weight. The alcohol or diazepam were dosed 2 hr into exposure,
two additional hours into exposure, and 30 min postexposure to perchloro-
ethylene.
Behavioral test batteries included: Michigan eye-hand coordination; ro-
tary pursuit; Flanagan coordination; Saccade eye velocity; and dual-attention
tasks. In addition, the EEC was recorded during perchloroethylene exposure.
Data analysis revealed that subjects had decreased performance on at
least one test while on each drug alone at the highest dose level, but no
synergistic interaction with perchloroethylene was seen in any test with
either drug.
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Alcohol consumption decreased performance in three of the tests. Diaze-
pam showed significant performance effects only on the rotary pursuit test.
Perchloroethylene, at 100 ppm, repeatedly gave decreased performance only on
the Flanagan coordination test. This 7-min test is designed to assess memory
together with two related forms of manual dexterity (Buros, 1972).
Unconsciousness due to overexposure occurred in two cases reviewed by Hake
and Stewart (1977), and in both cases reversibility of all narcotic symptoms
occurred. One exposure involved a patient on a respirator who was anesthetized
when a workman washed the hospital respiratory air vent with perchloroethylene.
The clinical condition did not otherwise change, and temporary anesthesia was
the only toxicity.
A dry cleaning operator also became unconscious and lay in a pool of per-
chloroethylene for 12 hr. He underwent a seizure and exhibited some temporary
renal and liver toxicity. After 21 days, the CNS, liver, and kidney tests were
negative but the breath analysis continued to show perchloroethylene.
The effects of perchloroethylene on behavior and neurological status of
18 exposed workers from the dry cleaning industry were measured (Tuttle et al.,
1977). On an average, these workers were exposed daily to 18 ppm perchloro-
ethylene, calculated on an 8-hr time-weighted average over the 5 days of test-
ing. Nine members of this group had a mean exposure to 32 ppm. Eight tests were
administered as part of an experimental test battery:
1. Feeling tone checklist
2. Wechsler digit span
3. Wechsler digit symbol
4. Neisser letter search
5. Critical flicker fusion
6. Santa Ana dexterity test
7. Choice reaction time
8. Simple reaction time
The reaction time tests were added since some neurotoxins slow nerve conduc-
tion velocity and movement time, and these tests should quantitate such effects.
There was a difference (p less than 0.10) between neurological ratings for the
perchloroethylene-exposed workers versus controls. Statistical analysis, how-
ever, showed these test results correlated better with earlier exposure to a
Stoddard solvent instead of the current perchloroethylene exposure (Tuttle et
al., 1977). Results on the behavioral performance tests did correlate better
with work fatigue than with the level of exposure that occurred during the
workshift.
Short-term exposure to perchloroethylene in man has produced many reports
of reversible narcotic or anesthetic effects on the central nervous system.
These have been quantified in human volunteers at various concentrations by
Carpenter (1937), Rowe et al. (1952), and Stewart et al. (1961b).
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Carpenter (1937) reported that the short-term exposure of human subjects
to 1,500 ppm resulted in behavioral and neurological effects, and ringing of
the ears was reported by subjects exposed to 2,000 ppm for 7.5 min. The
author reported no neurological effects when four subjects were exposed to
500 ppm perchloroethylene for 70 min. Rowe et al. (1952), on the other hand,
exposed four subjects to 216 ppm perchloroethylene for 45 min to 2 hr. All
four had eye irritation within 30 min. When exposure was to 280 ppm for as
long as 2 hr, central nervous system effects were reported, such as light-
headedness, impaired motor coordination. Three of four found 1,060 ppm for
1 min intolerable.
In summary, the data indicate that there was no motor coordination effect
at 100 ppm; lightheadedness and dizziness began to appear at 200 ppm; nausea
and loss of inhibition appeared at 475 ppm. Between 1,000 and 1,500 ppm,
acute central nervous system effects were noted immediately upon exposure.
These are narcotic or anesthetic effects, and have been shown by medically
measurable parameters to be reversible on cessation of exposure, as opposed
to toxic effects which infer pathological change.
Another case of acute industrial exposure was described by Eberhardt and
Freund (1966). Two months' exposure while cleaning metal parts with perchloro-
ethylene produced symptoms of confusion, dizziness, and anorexia in a 65-year-
old female. The concentration inhaled and extent of skin contact were undis-
closed in the report. Recovery occurred following 8 days absence from exposure.
Stewart et al. (1974) exposed 19 volunteers to varying concentrations (20
to 150 ppm) of perchloroethylene for a 5-week period. EEC analysis and be-
havioral tests were run. A single behavioral measure showed a change related
to exposure level: the Flanagan coordination test registered lower scores on
males exposed to 150 ppm 7-1/2 hr/day, 5 days/week. Most subjects showed in-
creased delta wave activity on the EEC after 7-1/2 hr exposure to 100 ppm,
but not at 20 ppm. The delta wave is part of the normal sleeping EEC.
This experiment is another indication of the slow elimination of per-
chloroethylene from the body. With repeated daily exposure, perchloroethylene
builds up in the blood and tissues, especially in lipids (Stewart et al.,
1974; Guberan and Fernandez, 1974).
Tso (1975) reanalyzed the data of Stewart et al. (1974) and suggested
that the sample sizes were too small to permit firm conclusions on behavioral
tests and EEC results as related to exposure. The re-analysis of Stewart's
work was based on a subtask group of four subjects.
A review by Fuller (1976) indicates that intermittent acute exposure to
perchloroethylene may, in fact, represent a chronic exposure, due to reten-
tion of the compound in the body. Since this chemical is stored in fatty tis-
sue and is slowly metabolized, a single, high-level exposure may subject the
organs to continuous exposure over a period of 2 weeks.
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Savolainen et al. (1977) report very subtle effects—no statistical
aiialysis—on 10 Sprague-Dawley rats exposed to 200 ppm perchloroethylene 6
hr/day for 4 days. Marked sequestration of the solvent occurred in fat and
brain. The effects included an apparent diminishing of brain RNA content on
the 5th day and behavioral differences from controls (increased preening).
Liver levels of cytochrome P-450 did not exhibit consistent change.
Lazarew (1929), using 151 experimental animals, determined the concen-
tration of perchloroethylene to cause unconsciousness was 2,211 ppm (15 mg/
liter). Complete narcosis with loss of reflexes occurred at 2,948 ppm (20
mg/liter), and the minimal fatal concentration of the solvent was 5,896
ppm (40 mg/liter).
Animal studies that emphasize perchloroethylene toxicity to the central
nervous system are largely studies from the USSR. Dmitrieva and Kuleshov
(1971) reported aberrancies of the EEC in rats exposed for 1 month to 15 ppm
perchloroethylene. Histologic examination of the brains showed swelling of
some cerebral cortical cells with isolated cells containing vacuoles in the
protoplasm. Electrical conductivity and cerebral tissue impedance changes
that were seen in the exposed animals apparently returned to normal 1 month
after cessation of exposure; only the EEC pattern remained different.
A review of personal communications and translations of USSR literature
was made on the peripheral neuropathies produced by perchloroethylene (NIOSH,
1976). Fifteen cases of diagnosed peripheral neuritis correlated with exposure
to perchloroethylene or unspecified chlorinated hydrocarbons were cited from
U.S. reports, and 145 cases of various peripheral neuropathies from unspeci-
fied chlorinated hydrocarbons were cited from the USSR literature.
An apparent effect on the peripheral nervous system was reported in the
Russian literature. Chronic inhalation of perchloroethylene by mice at 15 or
75 ppm, 5 hr/day for 3 months, decreased electroconductance by 5 to 10% and
the muscular contraction of the hind leg by 8, 12, and 24% at 1, 2, and 3
months, respectively. After a month's absence from perchloroethylene exposure,
the electroconductance returned to control levels (Dmitrieva, 1968).
5.3.4.1.2 Liver—Reports of controlled human exposure to perchloro-
ethylene including liver function tests as a follow-up have not been found.
Liver damage as a result of accidental exposure has been reported by Stewart
et al. (1961b), Stewart (1969), and Saland (1967). Coler and Rossmiller (1953)
reported one case of cirrhosis of the liver and three cases of suggested liver
damage in nine workers who had used a solvent containing 99% perchloroethylene
for over a year. The liver damage was diagnosed by significant sulfobromo-
phthalein (BSP) sodium dye retention at 30 min, urinary urobilinogen, and pos-
itive cephalin flocculation test. It was also indicated that none of the work-
ers had histories of high alcohol consumption. Hughes (1954) reported a single
5-193
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case of liver toxicity with nausea, jaundice, and grossly abnormal liver func-
tion tests (undescribed) in a young man exposed approximately 3 months to high
levels of perchloroethylene. Recovery occurred after 4 weeks, but 10 months
after the illness, the man experienced nausea on brief perchloroethylene expo-
sure. Two women working with perchloroethylene as long as 10 hr/day for 2.5
months (no measure of workplace air concentration) were reported to have liver
toxicity by Meckler and Phelps (1966). Diagnosis was made by alkaline phos-
phatase, SCOT, bilirubin, and cephalin flocculation measurements which were
consistent with liver disease. Liver biopsy 2 weeks after exposure showed
degeneration of parenchymal cells, focal collections of mononuclear cells,
and exaggeration of liver sinusoids. The liver was still enlarged 6 months
later.
The death by cardiovascular failure of a 33-year-old man reported by
Trense and Zimmerman (1969) followed 4 months working with perchloroethylene.
At autopsy, an enlarged liver with some hepatic cell necrosis was found.
Chlorinated hydrocarbons were not found in the liver.
Patel et al. (1977) report a case of overexposure to perchloroethylene.
The patient was so depressed on hospital entry that reflexes were absent and
mechanical ventilation was necessary. Cardiovascular signs were normal through-
out, in spite of a calculated exposure for an unknown time to 1,500 ppm. Liver
and kidney function tests were normal during the 4-day hospitalization and re-
mained normal when tested "several weeks" after discharge.
A single case report by Larson et al. (1977) described a woman who wore
clothing (shortly after removed from a self-operated dry cleaning washer) con-
taining perchloroethylene. The woman was hospitalized comatose with a grand
mal seizure and elevated bilirubin, SCOT, and LDH (which returned to normal).
Moeschlin (1964) reported only slight liver damage in a worker (diagnosed
by serum bilirubin and BSP retention) after 6 years perchloroethylene exposure
at unknown levels. The test results returned to normal 20 days after removal
from exposure.
A case report (Stewart et al., 1961b) involved a workman exposed to 1 gal.
of perchloroethylene and 50% Stoddard Solvent for 3.5 hr; this exposure produced
unconsciousness. Liver function impairment occurred after 9 days with urinary
urobilinogen and serum bilirubin elevation; alkaline phosphatase became elevated
at 2 weeks, and SGPT was elevated on the 18th day after exposure. Stewart et al.
simulated the exposure conditions and estimated the. concentration of perchloro-
ethylene to range from 25 to 1,470 ppm.
Liver function as diagnosed by bilirubin and thymol turbidity determina-
tions was significantly affected in 113 perchloroethylene-exposed workers when
compared to 43 unexposed workers (Franke and Eggeling, 1969). About 75% of the
measurements showed exposure to be under 100 ppm; no data on exposure duration
were reported.
5-194
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In a review of central nervous system effects of perchloroethylene, only
one of the 10 subjects also had liver involvement (Lob, 1957).
Mazza (1972) administered perchloroethylene to 15 rabbits at 2,790 ppm
for 45 days and measured serum transaminase and glutamic dehydrogenase as
markers of liver toxicity; both were increased. Liver pathology included both
mitochondrial and cytoplasmic damage from the exposure.
Kylin et al. (1965) exposed groups of 20 mice to 200 ppm perchloroethylene
by inhalation. Fatty degeneration of the liver occurred, and liver extractable
fat correlated with histological evaluations. Liver cell necrosis was not seen,
so no abnormal values were reported for conventional liver function tests.
These authors conclude that fatty degeneration and liver cell necrosis are
independent of each other. In producing fatty degeneration, they suggested
that perchloroethylene was approximately 10 times worse than trichloroethylene.
Carpenter (1937) produced liver damage in rats with 230 ppm for 8 hr/day,
5 days/week for up to 150 days. Lamson et al. (1929), however, looked for liver
necrosis and found none in a series of 400 animals (dogs, cats, rabbits, and
mice) given perchloroethylene in doses up to 25 ml/kg or after 5 to 6 hr inha-
lation at anesthetic concentrations. Liver toxicity after acute exposure does
not always appear on tests if liver function is measured immediately.
An industry study (Watanabe and Schumann, 1978; Schumann and Watanabe,
1979) reported an evaluation of perchloroethylene metabolism and hepatic
binding in rats and mice following exposure to 10 or 600 ppm C-perchloro-
ethylene vapor for 6 hr, as well as oral dosage of 599 mg/kg. The mouse me-
tabolized 7 to 9 times more perchloroethylene per kilogram than did the rat,
when exposed at the 10 ppm dose, and 1.6 times as much at the high dose. The
authors hypothesized (Watanabe and Schumann, 1978) that the mechanism of
perchloroethylene-induced carcinogenesis in mice is related to the tissue
binding in liver and the resulting injury, not to a genetic event. The data
to substantiate the hypothesis were not presented with the study.
Results of some liver function tests after exposure are found in the sec-
tion on biochemical interactions.
5.3.4.1.3 Kidney—Plaa and Larson (1965) report necrosis of the proximal
convoluted tubules in one of six mice given 4,100 mg/kg perchloroethylene in-
traperitoneally and swelling of the tubules in four of six. Only one of the
six demonstrated significant proteinuria after 24 hr with the 4,100 mg/kg
dose, but two of four mice given 8,200 mg/kg perchloroethylene had high pro-
teinuria.
A chronic inhalation study with a stabilized commercial perchloroethylene
formulation (Dowper®) demonstrated an increase in mortality from the 5th to
the 24th month of the study in male Sprague-Dawley rats exposed to 600 ppm for
5-195
-------
5 days/weekf 6 hr/day for 12 months (Rampy et al., 1978). The mortality in-
crease appeared to be associated with an earlier onset of "spontaneous ad-
vanced chronic renal disease" in the males only, according to this report.
The extensive pathology reports (on 30 tissues from the exposed and control
animals) described increased numbers of inflammatory cells in the kidneys
and focal progressive nephrosis in the solvent-exposed rats of both sexes,
especially at the high (600 ppm) inhalation dose.
Brancaccio et al. (1971) measured renal function in 12 rabbits treated
by inhalation of perchloroethylene at 2,280 ppm for 45 days. By measuring
creatinine clearance and para-amino hippuric acid, the authors concluded that
the renal tubular function was more affected than the glomerular capacity by
chronic perchloroethylene exposure.
Dumortier et al. (1964) reported a human case of nephritis (and liver
involvement) that was diagnosed as perchloroethylene toxicity, although the
subject had a history of alcoholism. Vomiting and kidney failure (anuresis)
occurred 1 week after using perchloroethylene to clean metal. Albuminuria and
uremia, as well as oliguria, were diagnosed; treatment was by blood dialysis
with an artificial kidney machine. Kidney function improved after 1 month.
Carpenter (1937) reported that damage occurred more readily to kidney
than to liver in rats with chronic exposure to perchloroethylene. After 150
exposures at 130 ppm and a 20-day rest, kidney congestion was found. At 230
ppm, some kidney changes were found after 21 exposures, and in most rats,
no liver pathology was found.
5.3.4.1.4 Adrenals—Mazza and Brancaccio (1971) report that perchloro-
ethylene is stimulatory to the adrenals. They exposed 10 rabbits for 45 days
to concentrations of 2,200 ppm perchloroethylene and measured gradually--
increasing levels of both adrenocortical and adrenomedullary hormones. Uri-
nary excretion of 3-methoxy-4-hydroxy mandelic acid (the principal catechola-
mine metabolite) also increased slightly during this time.
5.3.4.2 Dose-Response Data~-
5.3.4.2.1 Acute/subacute toxicity in animals—Schlingman and Gruhzit
(1927) stated that horses are less tolerant to the effects of perchloroethylene
than cattle, which are less tolerant than sheep, which are less tolerant than
chickens, cats, and other carnivores, respectively. Inhalation of or subcutane-
ous injection with the chemical can cause a decrease in blood pressure (Lamson
et al., 1929). Narcosis in cats is characterized by marked irritation, saliva-
tion, sneezing, and frequently convulsions (Lehmann and Schmidt-Kehl,. 1936;
Lamson et al., 1929). Dogs demonstrate cardiovascular effects on exposure to
perchloroethylene, just as observed when exposed to the other two subject
solvents--methyl chloroform and trichloroethylene (Christensen and Lynch,
1943; Fiedler, 1939). The toxic effects of perchloroethylene in mice, rabbits,
5-196
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cats, and dogs as reported in early studies and summarized by Von Oettingen
(1964) have been summarized in Table 5-34. Some human and guinea pig data
have been added to Von Oettingen's tabulation.
Klaassen and Plaa (1966) found the intraperitoneal 24-hr LDcQ in mice
to be 28 mmoles/kg. Lethal doses produced anesthesia and death within a few
hours. Histological examination revealed enlargement of hepatocytes, cellular
infiltration and vacuolation, and slight necrosis in the liver. Minimal necro-
sis of the convoluted tubules and hydropic degeneration with increased phenol-
sulfonphthalein clearance occurred in the kidney. These changes, which are of
an inflammatory nature, were accompanied by trace accumulation of lipid and
occurred only at near lethal doses. Shaipak (1976) reported respiratory tract
irritation resulting from inhalation of unstated levels of perchloroethylene.
When two groups of 10 mice were intraperitoneally dosed at a very high
(2.5 ml/kg) level and a moderate dose level (0.5 ml/kg) three times on alter-
nate days, there was still no significant kidney dysfunction as determined by
lack of protein or glucose in urine (Plaa and Larson, 1965). Perchloroethylene
was judged, on the basis of prolonged pentobarbital sleeping time, to have a
very low hepatotoxicity (Plaa et al., 1958). Gehring (1968) reported severe
writhing and massive peritonitis on intraperitoneal injection of mice with
perchloroethylene. He found the 24-hr LD
-------
TABLE 5-34. SUMMARY OF TOXICOLOGICAL EFFECTS OF PERCHLOROETHYLENE
ON MAN AND, ANIMALS
Animal
Mouse
Mouse
Mouse
Mouse
Mouse
Mouse
Mouse
Mouse
Mouse
Mouse
Mouse
Mouse
Mouse
Mouse
Mouse
Mouse
Mouse
Route
Intraperi-
toneal
Oral
Inhalation
Inhalation
Inhalation
Inhalation
Intraperi-
toneal
Inhalation
Intraperi-
toneal
Inhalation
Inhalation
Inhalation
Oral
Inhalation
Inhalation
Inhalation
Inhalation
Dose
3.2 ml/kg;
2.9 ml/kg
5.0 ml/kg
5,218 ppm
3,700 ppm
3,700 ppra
3,700 ppm
3.98-4.64
ml/kg
200 ppm
2.5-2.9
ml/ kg
300 ppm
20 mg/j
U.S50
ppm')
40 rag/ 2
(5,900
ppm)
4-5 ml/kg
15 Eg/i
(2,400
ppmi
17 mg/,;
C2.500
ppra)
13 Bg/.i
(2,600
ppn)
23 ral/i
(3,400
ppm)
Length of exposure:cffects
1 dose: 50% death In 24 hr
1 dose: 50% death in 24 hr
24 hr:50% death
730 min:50% death in 24 hr
24 min: anesthetization
470 min: liver dysfunction
1 dose: liver dysfunction; enlargement of
hepatocytes; vacuolization; slight
necrosis
4 hr/day, 6 days/week, 1-8 week:fatty de-
generation of the liver
1 dose: kidney dysfunction
7 hr/day, days 6-15 of gestation: increased
liver weight; decreased fetal body weight;
increased subcutaneous edema (fetal tox-
icity); minor skeletal abnormalities
Minimal narcotic effect
Minimal fatal concentration
Death in 2-9 hr from central nervous system
depression
Disturbed equilibrium in 64 ain and rest in
134 min but no narcosis in 160 min
Disturbed equilibrium in 42 min and rest in
67 min but no narcosis in 120 min
Disturbed equilibrium in 17 min and rest in
30 min, narcosis occurred in 47 min and
recovery regained 150 rain
Disturbed equilibrium in 11 min and rest in
33 min, narcosis occurred in 54 min, death
of one-third of the animals within 190
Reference
Klaassen and Plaa (1966);
Schuhmacher and Grand jei
(1960)
Wenzel and Gibson (1951)
Friberg et al. i 1952)
Gehring (1968)
Gehring (1968)
Gehring (1968)
Gehring (1968); Klaassen
and Plaa (1966)
Kylin et al. (1965)
Klaassen and Plaa (1966)
Moolenaar (unpublished)
(1975)
Lazarew '.1929)
Lamson et al. (1929)
Lamson et al. (1929)
Crescitelli (19331
Crescitelli (1933)
Crescitelli (1933)
Crescitelli (1933)
rain after exposure
(continued)
5-198
-------
TABLE 5-34. (continued)
Aninal
Mouse
Mouse
Mouse
Route Dose
Inhalation 25 mg/2
(3,700
ppm)
Inhalation 40 ng/l
(5,900
ppm
Inhalation 200-1,600
ppm
Leneth of exoosurei iff ects Reference
Disturbed equilibrium in 12 min and rest in Crescitelli (1933)
21 min, narcosis occurred in 31 min and
death of two-thirds of the animals within
164 min after exposure
Disturbed equilibrium in 4 rain and rest in Crescitelli (1933)
3 min, narcosis occurred in 14 min and
death of all animals by 49 min after ex-
posure
3 hr/day, 3 days :increase in mortality and Schumacher et al. (1962)
inhibition of growth
Mouse
Inhalation
15-74 ppm
Suocutaneous 1.5 ml/kg
injection
Mouse
Oral
Oral
Oral
Inhalatiap
i-.5 nil/kg
in cil
o nil/kg
in ?il
0.109 .-nl +
O.OU trl
0. U^ mi
(in oil)
+ 0.011 ml
3,000-6,000
DOM
•.Sherman) Inhalation i.,000 ppm
?.at Inhalation '*{•• 2 ppm
?.at Inhalation 300 pprr.
Rat Inhalation 1,600 ppm
Rat Inhalation 2,500 ppm
Rat Inhalation 600 ppm
Rat Inhalation 230 ppm
Rat Inhalation 470 ppm
5 hr/day, 3 months Decreased electroco-
ductance of muscle and amplitude of
.muscular contraction
Alternate days fcr 20-40 days idecre.ised
serum albumin level, increased
globulin levels
LD
5Q
LDjQ for mice 19-23 g
LDjQ for mace 19-23 ?
Up to 3 hrrincreasa in liver veight, in-
crease in t?tal lipid concent o£ liver
accompanied by a few diffusely dis-
tributed fac globules
i hr:LD5Q
Entire gestation period:decreased levels
of DNA and total nucleic acids in the
liver, brain, ovaries, and placenta
7 hr/day, days 5-15 of gestation:decreased
maternal weight gain; increased incidence
of fetal rescrption
13 7-hr exposures:drowsiness, stupor, in-
creased salivation, axtreme restlessness,
Jisturbance j£ equilibrium and coordina-
tion, biting and scratching reflex
1-13 7-hr exposures:loss of consciousness
and death
6 hr/day, 5 days/week, 12 months:increased
mortality over controls
8 hr/day, 5 days/week, 7 months:ccngestion
and light granular swelling of kidneys
3 hr/day, 5 days/week, 7 months:increased
secretion, cloudy swelling and ^asquama-
tion of kidneys, congestion and ciouc'y
swelling of liver; congestion of spleen
(continued)
5-199
Dmetrieva (1%3)
Ogata and rluroda (1962)
Xb'hne (1940)
Kohne (1940)
Dvbing and Dyeing (1946)
Sybing Ir.d Dybinz '1946)
Soue et al. (1952)
Carpe-ter ec -il. (1949)
Anar.ina (1972)
MooUnaar (1975)
Rova et al. (.1952)
Rowe et al. (1952)
Leong ec al. (1975)
Caroentar (1937)
Carpenter (1937)
-------
TABLE 5-34. (continued)
Animal
Route
Dose
Length of exposure.'effects
Reference
Rabbits Inhalation 2,211 ppra
Rabbit Inhalation 15 ppm
Rabbit Inhalation 2,211 ppra
Rabbits Oval 5 ml/kg
Rabbits Inhalation 2,500 ppm
Rabbits Inhalation 2,212 ppm
Rabbi-s Inhalation 15 ppm
45 daysisignificant reduction of glomerular
filtration rate and the renal plasma flow;
decrease of highest excretory tubular ca-
pacity (kidney damage)
3-4 hr/day, 7-11 months:depressed agglutinin
formation
45 days:increased plasma levels of adrenal
cortical and adrenal medullar hormones;
increased excretion of principal cate-
cholamine metabolite
1 doseideath within 24 hr
28 7-hr exposures:central nervous system
depression without unconsciousness
45 days:liver damage indicated by elevated
SGPT, SCOT, SGLDH; marked reduction of
Schmidt index
3-<* hr daily, 7-11 monthsimoderately in-
creased urinary urobilinogen; patho-
racrphological changes in the parenchyma
of liver and kidneys
Rabbit
Rabbit
Flatfish
Cat
Cat
Cat
Cat
Cat
Cat
Dog
Dog
Dog
Cog
Dog
Oral in oil
Subcutaneous
in oil
Dissolved in
water
Oral
Oral in
oil
Oral in milk
or water
Oral in milk
or watar
Oral in ailk
or water
Oral in milk
or water
Inhalation
Oral in oil
Intravenous
Intraperi-
tor.eal
injection
Intraperi-
toneal
injection
5 ml/kg
2.2 g/kg
737 ppm
4 ml/kg
4 mg/kg
0.5 T.l/kg
1.0 ml/kg
4.5 ml/kg
5 ml /kg
9,900 ppir.
4-25 ml/kg
85 mg/kg
2.1 ml/kg
1.23 ml /kg
Death in 17-24 hr
Death in 24 hr
Letnal to 50% of fish in 96 hr
Death in 36 hr
Death within hours
No effect
Drowsiness and unsteadiness of hind legs,
recovery in 3 days
More severe symptoms
Death in 24 hr
i-Jarcosis, marked salivation, narrow margin
of safety
Death in 5-43 hr
Death in 30 min
Lethal to 50% cf animals in 24 nr
Liver dysfunction (as measured by increase'
SGPT levels in 50% of animals) in 24 hr
Brancaccio ei Jl. (1971)
Mazza (1972)
Mazza and Brancaccio (1971)
Von Oettinsen (1937)
Sowe *t al. (1952)
Mazsa (1972)
Mavrotskii et al. (1971)
Lamson et al. (1929)
Barsoum and Saad (1934)
McCor.nell et al. (19V5)
Von Oettinger. (1937)
Lanson et al. (1929)
Maplestone and Ch<;ora (1933)
Maplestone and Chopra (1933)
Miplestone and Chopra C1935)
Maplestone and Chopra (1933)
Lamscn ec al. (1929)
Lair.son ec al. (1929)
Barsoum and Saaci (1934)
KUassen and Plaa (1967)
Klaassen and Flaa (Ia67)
(continued)
5-200
-------
TABLE 5-34. (continued)
_Aaima_JL__
Route
Dose
.Length o£ exposuretef facts
Reference
Dog
Guinea
Pig
Guinea
pig
Guinea
Hurr.an
Human
Human
Human
Human
Intraperi- 2.32 ml/kg
toneal
injection
Inhalation 2,500 ppm
Inhalation 400 ppm
Inhalation 100 ppm
Oral 3 ml
Inhalation 75-80 ppm
Inhalation 100-120 ppm
Inhalation 1,500 ppm
Inhalation 475-600 ppT.
Inhalation 1,000 ppm
Inhalation 230-385 ppm
Inhalation High
Inhalation High
Human Skin contact Liquid
Human Inhalation High
Ir.halaticn High
Kidney dysfunction (as measured by increased
retention of PSP in 50% of animals) in 24 hr
18 7-hr exposuresiloss of equilibrium, coordi-
nation and strength
169 7-hr exposureslincrease liver weight, in-
crease in neutral fat and esterified cho-
lesterol in the liver and moderate central
fatty degeneration with slight cirrhosis
132 7-hr exposures:slight increase in liver
weight, in lipid content, and several
small fat vacuoles in liver
Mild transient gastrointestinal reactions
1-4 minislight transient eye irritation
1 hr:soft palats irritation accompanied by
dryness; mild eye irritation
Immediate:faincness, aching facial muscles;
dyspnea upon exertion, mental sluggishness,
slight inebriation and slight effect upon
physical balance noted after exposure
2 hr:increased salivation, increased perspi-
ration of hands, increased secretion of
mucous from the nasal passages, numbness
about mouth, mental effort needed for good
~otor coordination
1 hr, 35 min:marked irritation to eyes and
upper respiratory tract; lassitude, mental
fogginess, anesthetization of lips and tip
of nose, exhilaration, congestion of the
eustachian tubes
2 days/week, 2-1/2-6 years:severe gastric
hemorrhage and cirrhosis of the Liver;
signs of liver dysfunction
1 year:hemoptysis, coughing, sweat attacks,
jaundice, oliguria, hematemesis, cardio-
vascular failure and death
Unconsciousness; death
30 min:burns, erythema, blistering
Acute:transient liver damage
Acuteipulnonary edema
Klaassan and Plaa (1967)
Rowe et al. (1952)
Rowe et al. (1952)
Rowe et al. (1952)
Mutalik and Gulati (1972)
Stewart et al. (I96lb);
Carpenter (1937); Kowe
et al. (1952)
Stewart et al. (1961b);
Carpenter (1937); Rowe
et al. (1952)
Stewart et al. (1961b);
Carpenter (1937); Rowe
et al. (1952)
Stewart et al. (I961b);
Carpenter (1937); Rowe
et al. (1952)
Stewart et al. (196tb);
Carpenter (1937); Rowe
et al. (1952)
Coler and Rossmiller (1953)
Trense and Zimmerman (1969)
Stewart et al. (I961b); Lcb
(1957); Ling and Lindsay
(1971); Morgan (1969);
Stewart (1969); Saland
(1967); Braddock (1965);
Patel at al. (1973).
Ling and Lindsay (1971);
Morgan (1969)
Stewart et al. C1961b);
Stewart (1969); Saland
(1967)
Lob (1957); Patel et al.
(1973)
Source: Adapted from Von Oettir.gen (1964) and Fuller (1976).
5-201
-------
TABLE 5-35. PERCHLORDETHYLENE INHALATION BY RATS
Concentration
(ppm)
20,000
12,000
6,000
2,500
1,600
"No effect"
time (hr)
-
0.2
0.4
3.0
5.0
Acute effect
time (hr)
-
0.6
0.6
5.0
7.0
Time to 50%
death (hr)
0.8S/
2.0
1.0-5.0
8.0
-
a/ At 20,000 ppm - First death: 0.08 hr
All dead: 1.6 hr
Source: Adapted from Rowe et al. (1952).
The most characteristic effect of exposure to perchloroethylene in rats
was depression of the central nervous system manifested by drunken behavior,
stupor, unconsciousness, and respiratory failure. Cardiac failure possibly
occurred. Unconsciousness was not observed at 2,000 ppm, but occurred at 3,000
ppm within a few hours and at 6,000 ppm within a few minutes. Deaths occurred
during or immediately after exposure. Those animals which survived exhibited
a slight transient whole body weight loss and liver damage characterized by
an increase in total lipid content, in liver weight and slight cloudy swelling.
5.3.4.2.2 Acute/subacute toxicity in humans—Rowe et al. (1952) studied
the effects of single inhalation exposures by perchloroethylene on humans. The
first symptoms of excessive exposure, which occurred at concentrations greater
than 200 ppm, were mild eye irritation and central nervous system disturbances.
The effects seen and doses which produced them are inset below. All data are
from Rowe et al. (1952). Exposure to concentrations less than 100 ppm generally
do not result in any disturbances.
5-202
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Exposure concentration Affects
83-130 ppm Concentration was reported to be unobjectionable;
odor was immediately apparent to individuals; one
out of six people experienced congestion of frontal
sinuses; transient eye irritation.
206-235 ppm Odor was immediately apparent but acclimation readily
occurred; eye irritation developed in 20 to 30 min
and persisted; congestion of frontal sinuses and
nasal discharge noted; slight dizziness and sleepi-
ness noted by some individuals.
206-356 ppm General dislike of exposure; light-headedness; burning
sensation in eyes; congestion of the frontal sinuses;
"thick tongue" and tight mouth; transient nausea in
some individuals; impaired motor coordination such
that mental effort was required; recovery was gen-
erally within 1 hr.
513-690 ppm General dislike of exposure (10 min); eye and nasal
irritation; dizziness; tightness and numbness of
mouth; loss of inhibitions; motor coordination only
with mental effort; recovery complete in 1 hr.
930-1,185 ppm Markedly irritating to eyes and upper respiratory
tract; dose tolerated for 1 min with no effects;
dizziness following exposure for 2 min; recovery
rapid.
Stewart (1969) reported that persons exposed to the solvent had a charac-
teristic chloroform odor on their breath, and exhibited subclinical hepatitis,
as indicated by an increase in urinary urobilinogen levels 7 to 10 days after
exposure. Subjects recovered completely if organ damage due to anoxia (result-
ing from central nervous system depression) was avoided. Stewart's graphic
presentation of perchloroethylene in the expired air of humans exposed at four
different levels is shown in Figure 5-8.
Tada and Nakaaki (1969) experimentally exposed subjects to perchloro-
ethylene. Approximately 50 ppm (4 hr/day, 4 days) produced a urinary excretion
of the metabolite trichloroacetic acid (TCA) of 3.2 mg/liter; approximately
100 ppm exposure for the same time produced 6.7 mg/liter, and 160 ppm exposure
for half the time (2 hr/day, .4 days) produced 3.5 mg/liter in the urine. Tada
suggests that these data show the urinary TCA excretion over 24 hr is fairly
proportional to the perchloroethylene vapor inhaled although there are hour-
to-hour variations. He noted that trichloroethylene produced 10 times as much
TCA in urine as did perchloroethylene when workers were exposed to similar con-
centrations.
5-203
-------
Ul
N>
O
395 ppm, 210 mln
19A ppm, 187 min
0 101 ppm, 183 mln
~~ -"• 194 ppm, 83 mln.
100.0
1000.0
10.0
Time in hours
Source: Stewart (1969)
Figure 5-8. Tetrachloroethylene expired air concentrations following vapor exposure.
-------
Table 5-36 summarizes the human effects of perchloroethylene described
in 5.3.4.2.2. A scale of + to NI I has been designated by MRI and employed to
represent a judgment of the reported effects of perchloroethylene. The single
plus indicates that an effect on that organ was detected, and four-plus means
effects were severe or that death occurred as a result. Two- and three-plus
ratings are made from effect descriptions in the articles; "moderate, serious"
would rate -H-f as an organ effect, whereas "slight or occasionally seen" ef-
fects would rate -H-.
5.3.4.2.3 Chronic toxicity—Since so few lifetime exposure (chronic) tox-
icity studies have been performed with perchloroethylene, all available tests
which exceed an acute testing period have also been included in this section.
Data on the chronic and other long-term toxicity of perchloroethylene are lim-
ited by the available published information.
Carpenter (1937) found that rats exposed to 70, 230, 470, and 7,000 ppm
perchloroethylene for 150 days (8 hr/day, 5 days/week) showed no adverse ef-
fects on reproduction or mortality. Histological examination, however, revealed
kidney damage with congestion, cloudy swelling, and increased secretion and
desquamation of the renal tubules. Joachimoglu (1921) stated that no pathologi-
cal changes were found in the livers of dogs given daily oral doses of per-
chloroethylene (0.7 ml/kg) for 19 days.
Navrotskii et al. (1971) reported increased urinary urobilinogen and patho-
morphological changes in the parenchyma of the liver and kidneys of rabbits af-
ter inhalation exposure to 100 mg/m^ perchloroethylene for 3 to 4 hr/day for
7 to 11 months. Brancaccio et al. (1971) also reported kidney function distur-
bances characterized by statistically significant reductions in the glomerular
filtration rate and the renal plasma flow, and a decrease in excretory tubular
capacity.
Although not discussed in the summary documents of Rampy et al. (1978),
the data indicate that chronic (12 months) inhalation of a perchloroethylene
formulation probably produced some anemia in the female rats at both the 300
and 600 ppm dose levels. The data that suggest this toxic effect include a
low number of cells found in the bone marrow smears in females and a total
white blood cell count of 7.5 x 10^ and 7.2 x 10-* per cubic millimeter after
12 months exposure (seven animals, high and low dose respectively). The de-
pressed hematologic values were difficult to evaluate in this study because
the controls for these experiments also had quite low white cell counts.
Normal Sprague-Dawley rat white cell counts should be about 14 x 10 per
cubic millimeter and never much below 12 x 10-> per cubic millimeter (Ringle
and Herndon, 1976; Ralston Purina Company, 1977).
Rowe et al. (1952) have performed more extensive studies on the chronic
toxicity of perchloroethylene, as seen in Table 5-37.
5-205
-------
TABLE 5-36. EFFECTS OF PERCHLORQETHYLENE ON HUMANS
Concentration
20-70
75-80
106
100
100-120
150
10-400
216
50-250
50-250
50-250
210-244
280
232-385
200^400
25-1,470
475-680
513-690
934-1,140
930-1,185
2,000
Exposure time Eyes
Occasionally daily
1-4 min 4
4 hr 4
7-1/2 hr/day
4-6 min
7-1/2 hr/day
8 hr/day, 5 days/week
2 hr 4
Occasionally daily
Daily, 4 months
Daily, 5 months
30 min
2 hr 44
8 hr, 2 times/week
Occasionally daily
3-1/2 hr 444
30 min 4
10 min 44
95 min 444
1-2 min 4444
7-1/2 min
Reported effects Urinary
CNS Resp. Liver Heart metabolites
4
-
+
44
44
44
44 4
444
4
+ 4_1rl -i^Jj-l.-r III 1
in ~n n i i i i
44
444 44
4444
444
444 444
444 +
444 44
4444 44
4444 44
4444
a^l Reported effects summarized in Section 5.3.4.2.2.
Source: MRI evaluation of reported data.
-------
TABLE 5-37. CHRONIC AND SOME SUBACUTE INHALATION TOXICITY OF PERCHLOROETHYLENE TO LABORATORY ANIMALS2
a/
Animal
Species
Sex
Dose
Effects of treatment
Guinea pigs Female
and
male
100 ppmj 132
exposures
in 185 days
No adverse effects as judged by appearance, behavior, mortality
growth and body weights; there was a significant increase in
female liver weights (p = 0.01); few small fat vacuoles in
some livers.
Female
and
male
N>
o
Female
and
male
Male
Female
and
male
200 ppmj 158
exposures
220 days
400 ppm; 169
exposures
in 236 days
1,600 ppmj 8
exposures
in 10 days
2,500 ppmj 18
exposures
in 24 days
No adverse effects on appearance, behavior, mortality, blood
urea nitrogen, blood nonprotein nitrogen, or serum phosphate
plasma prothrombin clotting time. There was a significant de-
crease in growth and liver weights in females, an increase
in liver lipid and esterified cholesterol with moderate his-
tological changes characterized by central fatty degeneration.
Effects were as stated above but the liver had also begun to be
slightly cirrhotic.
No animals died but there was a considerable weight loss and an
increase in liver weight with fatty degeneration and slight
degenerative changes in the germinal epithelium of the testes.
Animals displayed considerable loss of equilibrium, coordination,
and strength but never lost consciousness; they lost weight
rapidly, showed an increased liver weight with moderate to
marked fatty degeneration in the liver and an increase in
kidney weight with moderate cloudy swelling of the tubular
epithelium.
(continued)
-------
TABLE 5-37. (continued)
Animal
Species
Sex
Dose
Effects of treatment
Rabbits
Oi
o
oo
Monkeys
Rats
Female
and
male
Male
Male
Female
and
male
Female
and
male
400 ppm; 159
exposures
in 222 days
2,500 ppm; 28
exposures
in 39 days
400 ppm; 179
exposures
in 250 days
400 ppm; 130
exposures
in 183 days
1,600 ppmj 18
exposures
in 25 days
No adverse effects.
Marked depression of the central nervous system such that ani-
mals were helpless but not unconscious, slight parenchymatous
degeneration in the liver of one of the two animals.
No adverse effects.
No adverse effects.
Slight growth depression and slight organic injury, during the
first week rats were stuperous, the second week they displayed
behavior indicative of irritation of cholinergic nervous tissue
characterized by marked salivation, extreme restlessness, ner-
vousness, continuous movement, snapping stuperous state, dis-
turbances of coordination and equilibrium, scratching, the in-
tensity decreased but continued throughout the experiment. In-
jection of atrophine sulfate prior to exposure prevented the
response, decrease in body weights, enlargement of the liver
and kidneys but no histological changes.
(continued)
-------
TABLE 5-37. (continued)
Animal
N>
o
IO
Species Sex Dose Effects of treatment
Female 2,500 ppm; 13 Rapid deaths, only one rat of each sex survived all exposures;
and exposures severe depression of the central nervous system with loss of
male 18 days consciousness, no abnormalities except slight cloudy swelling
in the liver with a few fat vacuoles.
a_l All exposures were for 7 hr.
Source: Rowe et al. (1952).
-------
Among the animals studied in 7-hr exposure periods to perchloroethylene at
varying concentrations for up to 250 days, guinea pigs were found to be the
most susceptible to the chemical. Exposure of rabbits, monkeys, and rats to
400 ppm perchloroethylene produced no adverse effects whereas exposure of rats
and rabbits to 2,500 ppm resulted in rapid deaths and marked narcosis, respec-
tively. Rats exposed to 1,600 ppm perchloroethylene exhibited behavior indica-
tive of cholinergic nervous tissue irritation which was reversible by an injec-
tion of atropine sulfate.
5.3.4.3 Sensitization on Chronic Use--
5.3.4.3.1 Tolerance, resistance, and dependence—Lassota (1975) has sug-
gested that a dependency for perchloroethylene may develop when the solvent is
misused as a drug (e.g., to "get high"). He reported on a patient who had
sniffed the chemical two to three times per week, as much as a 200-ml bottle
each time. The patient reported that his desire for the chemical increased af-
ter alcohol consumption. After an extended period of use, he reported blood
in the mouth, trouble concentrating, trembling hands, sensory disturbances
(sight, hearing, smell, touch), talking to himself in a critical manner, and
an increased desire for the chemical. In the hospital he was trembling and
showed antisocial behavior. He had a bottle of perchloroethylene hidden in
his room. In experimental chemical intoxication, he hallucinated and exhibi-
ted equilibrium disturbances. A second patient reported in Lassota's study
was also given perchloroethylene experimentally. While intoxicated with the
chemical, he hallucinated but did not exhibit any equilibrium disturbances.
In the hospital, he had dilated pupils, a decrease in muscular tension, quick
reactions, and a fear of sleep.
5.3.4.3.2 Allergic effects—Munzer and Heder (1972) reported a case of
eczema as a direct effect of exposure to perchloroethylene by a man in a dry
cleaning plant. Erythema, not necessarily allergic, but possibly this type of
reaction, has been reported in workers contacting perchloroethylene by Gold
(1969), Ling and Lindsay (1971), and Morgan (1969).
Effects on the immunologic system of perchloroethylene-exposed experimen-
tal animals have been reported. Chinchillas', exposed at 1.5 or 15 ppm by inha-
lation 3 hr/day, 6 days/week, for 8 to 10 months, exhibited significant changes
in antibody production to a Salmonella typhosa antigen challenge. At 2.8 ppm
only the 7-S antibody titer increased, but at 15 ppm, both total antibody pro-
file and the 7-S globulins were changed (Shmuter, 1972).
Palecek (1970) reported asthma induced by exposure to perchloroethylene.
After each of two massive exposures in a 2-year period, a 55-year-old woman
experienced an acute reaction. After one exposure, she became unconscious, and
both exposures were accompanied by asthmatic coughing attacks. After these two
incidents, she developed asthmatic attacks whenever she was in the shop. The
diagnosis of asthma was made by: (a) the rate of exhaled air decreased from
5-210
-------
4.6 to 2.8 liters/sec, and (b) a positive reaction obtained from an acetylcho-
line test.
Navrotskii et al. (1971) report that the rabbit showed depressed capabil-
ity to form agglutinins (an immune system effect) after 1.5 months exposure
to 15 ppm for 3 to 4 hr/day for 7 to 11 months. No effects were seen at 1.5
ppm.
Hake and Stewart (1977) exposed 12 subjects to 25 to 100 ppm perchloro-
ethylene for 16.5 hr/week and measured central nervous system effects. One of
the subjects was particularly susceptible to the solvent with a high level of
subjective complaints, exposure-related EEC signs, and behavioral test results.
Breath analysis appeared to show no greater solvent absorption in this subject,
and hypersensitivity to perchloroethylene (even allergy) was suggested.
Ogata and Kuroda (1962) injected perchloroethylene subcutaneously in mice
(1.5 ml/kg, 10 and 20 injections every other day) and increased the gamma glob-
ulin content in the mouse serum. This appeared to be a direct effect on serum
protein and not a dilution effect.
5.3.4.4 Teratology—
Schwetz et al. (1975) assayed for reproductive and teratogenic outcomes
in Sprague-Dawley rats and Swiss Webster mice exposed to 300 ppm perchloro-
ethylene by inhalation for 7 hr/day from gestation day 6 to gestation day 15.
Caesarian sections were done on day 21 (rats) and day 18 (mice).
The authors reported a significant reduction in the body weights of ex-
posed pregnant rats (about 5%), but not exposed pregnant mice. Pregnant mice
did, however, exhibit a significant increase in the mean relative liver weights
and their fetuses weighed significantly less than the controls.
In the reproductive performance study, the number of resorptions per im-
plantation site was over two times the control level in exposed dams (rats),
and the average fetal body weight in exposed groups was below control values
(mice), both significant at the 0.05 level.
In the mouse pups, significant subcutaneous edema, delayed skull ossifi-
cation, and the presence of split sternebrae were seen following maternal per-
chloroethylene exposure as described above. No other anomalies in controls or
with the other solvents were seen. Details are found in Table 5-38.
Ananina (1972) (cited by Fuller, 1976) exposed female rats to 44 ppm
perchloroethylene for the entire gestation period and found decreased DNA and
total nucleic acids in the liver, brains, ovaries, and placenta.
In a study of tangential interest to this section because of the very
young mice used for exposure, Shumacher et al. (1962) exposed 3-week-old mice
5-211
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TABLE 5-38. EFFECT OF INHALED PERCHLORDETHYLENE ON THE INCIDENCE OF
i
10
FETAL ANOMALIES AMONG MOUSE AND RAT LITTERS^
a/
Anomaly
Solvent concentration, ppm
Number of litters examined
Control
_
26
Mouse
Perchloroethylene
300 ppm
17
Control
.
30
Percent of litters aftected (number of
Gross
Short tail
Runts (wt. < mean If - 3 SI))
Soft tissue
Dilated cere-bra! ventricles
Dilated esophagus
Dilated renal pelvis
Dilated ureters
Dilated urinary bladder
Cleft palate
Rotated kidney
Displaced kidney
Hemorrhage in esophagus
Hemorrhage in cerebral
ventricles
Undescended testicles
Subcutaneous edema
Skeletal
Delayed ossification
Skull bones
Lumbar ribs or spurs
Delayed occification
Sternebra
Split sternebra
Extra sternebra
Malaligned sternebru
Supernumerary vertebra
(0)
3:i (10)
8 (2)
-
-
8 (2)
-
(0)
8 (0)
-
-
(1)
(0)
27 (7)
69 (8)
31 (8)
4 (1)
(0)
(0)
(0)
(0)
59 (10)
6 (1)
-
-
(0)
-
(0)
(0)
-
-
(0)
(0)
59 (lO^/
100 (i7>£/
35 (6)
24 (4)
24 (4)
(0)
(0)
3 (1)
3 (1)
-
(0)
(0)
(0)
7 (2)
-
-
(0)
(0)
3 (1)
-
17 (5)
33 (10)
13 (4)
30 (9)
(0)
-
-
(0)
Rat
Perchl oroethylene
300 ppm
17
litters)
6 (1)
12 (2)
-
(0)
(0)
6 (1)
(0)
-
-
(0)
12 (2)
(I)
-
(0)
29 O)
6 (1)
24 (4)
(0)
-
-
(0)
a/ Adtni rii stere«l by inhalation / hr daily on days 6-15 of gestation*
b/ Significantly different from control by Hie Fisher Exact Probability Test, p< 0.05.
Source: Adapted from Schwetz et al. (1975).
-------
for 8 hr/day, 3 days each, to 200, 400, 800, and 1,600 ppra perchloroethylene.
The exposure produced significant mortality and growth inhibition in survivors.
Effects on fertility were studied by Carpenter (1937), exposing rats to
70, 230, or 470 ppm perchloroethylene for 8 hr/day, 5 days/week for 28 weeks.
The number of litters conceived was analyzed by an index value defined as the
actual number of litters divided by the possible number of litters. Carpenter's
data indicated the solvent stimulated reproductive performance, especially at
higher doses.
Perchloroethylene inhalation toxicity studies were conducted at Litton
Bionetics on Charles River rats and New Zealand rabbits (Tox Tips, 1977;
Belisles, Niemeier, and Brusick, Litton Industries, sponsored by NIOSH). Ex-
posure began 3 weeks before impregnation and continued through gestation.
Both dams and fetuses are to undergo morphological and histopathological ex-
amination for perchloroethylene related toxicity in addition to teratogenicity.
No reports from this study were available to us at this time.
5.3.4.5 Mutagenicity—
Only one laboratory has reported bacterial (or other) assays showing
mutagenic activity for perchloroethylene, but several articles are related
to the mutagenic potential of the chemical. Yllner (1961) suggested his data
showed perchloroethylene metabolized through an epoxide structure with rec-
ognized mutagenic potential when it is formed in other chemicals. Greim et
al. (1975) measured the activity of perchloroethylene on the rate of spon-
taneous mutation of E. coli Kj^ following incubation with rat liver micro-
somal enzymes (an activated system). Perchloroethylene did not induce mutations
in the test system, either when activated or not activated, and Greim et al.
suggest that it is because the chemical forms a very stable oxirane and there-
fore does not have the alkylating activity of some related compounds. No chem-
ical intermediates of perchloroethylene were isolated as part of this study.
Henschler (1977) synthesized and studied the epoxides of chlorinated eth-
ylenes, in an attempt to find a reactive structure that yielded potential
mutagenicity. Perchloroethylene was shown to be symmetric, relatively stable,
and, using Henschler's scheme of intromolecular rearrangement, nonmutagenic.
Henschler and Bonse (1978) have presented a theory of mutagenesis for a
series of chlorinated ethylenes including perchloroethylene. They suggested
that since the epoxides of these chemicals confer the alkylating and mutagenic
effects, a symmetric structure, such as perchloroethylene, would not be muta-
genic. A modified Ames assay, using activation with mouse liver microsomes and
E_. coli K]^ as the test organism, showed no mutagenicity for perchloroethylene.
Margard (1978) tested both stabilized and unstabilized perchloroethylene
in the Ames assay for mutagenicity. Both activated and unactivated bacteria
gave a positive (mutagenic) response in three of five tester strains with 0.1
5-213
-------
ml stabilized perchloroethylene per plate. Unstabilized, purified perchloro-
ethylene was not mutagenic in the activated system.
Two in vitro test systems were used in the mutagenicity tests on per-
chloroethylene (and other solvents) by Greim et al. (1977). Both microsome-
activated and unactivated TA1538 and IE. coli K^ were used for measuring
frequency. Peripheral human lymphocytes (microsome activated) were used as
target cells to evaluate for chromosomal aberrations. Perchloroethylene was
not activated to a mutagenic form in these tests.
The negative mutagenicity tests by Greim on perchloroethylene were re-
viewed by Infante (1977) who evaluated the risk of exposure to several halo-
genated olefins. No new data were added, but the author stressed that the
positive hepatocellular carcinomas in mice seen in the NCI bioassay as well
as the structural similarity to vinyl chloride was a source of concern.
Rampy et al. (1978) reported on cytogenetic analysis in bone marrow
smears from male rats exposed to 300 or 600 ppm perchloroethylene 6 hr a
day, 5 days a week for 12 months. Three rats from each exposure level were
sacrificed and the bone marrow cells were examined for chromosome or chroma-
tid aberrations. No cytogenic effects were detected in the male rats. Low
numbers of available marrow cells made interpretations impossible in the
female rats.
Table 5-39 summarizes the tests for mutagenicity on perchloroethylene.
5.3.4.6 Carcinogenic Effects—
The National Cancer Institute Carcinogenesis Bioassay report for per-
chloroethylene was released in October 1977 (NCI, 1977).
This report presented test results of a 2-year bioassay for possible
carcinogenicity of perchloroethylene using Osborne-Mendel rats and B6C3F1
mice. USP grade perchloroethylene in corn oil was administered by gavage--
oral dosage--to groups of 50 male and 50 female animals at the following
average (TWA) dose levels: male rats, 517 and 1,034 mg/kg; female rats,
521 and 1,042 mg/kg; male mice, 536 and 1,072 mg/kg; and female mice, 386
and 772 mg/kg. These doses were administered 5 days/week for 78 weeks. Un-
treated controls and vehicle control groups consisted of 20 animals of each
species and sex; the vehicle control animals were dosed with the corn oil
only in the amounts given the high dose animals. After the 78-week period,
rats were observed for 32 additional weeks (a total of 110 weeks) and mice
were observed for 12 additional weeks (a total of 90 weeks). About 30 tis-
sues from all animals were subjected to microscopic evaluation.
Under these conditions, NCI determined that perchloroethylene was a
liver carcinogen in B6C3F1 mice. The data do not indicate that perchloro-
ethylene causes cancer in rats. A significant increase in hepatocellular
5-214
-------
TABLE 5-39. SUMMARY OF MUTAGENICITY STUDIES ON PERCHLOROETHYLENE
Test/organism/strain Result of exposure
Comment
Reference
E. coli K12
TA 1538; TA 1535
Peripheral human lympho
cytes
Rat bone marrow smears
No mutagenesis
No mutagenesis
Microsomal, activated and un-
activated
Rat liver microsomal activa-
tion
No chromosomal aber- Microsomal, activated and un-
rations activated
Bonse et al., 1975;
Greim et al., 1975
Bonse and Henschler, 1976;
Henschler, 1977
Greim et al., 1977
IS3
(-•
(Jt
Free of chromatid and Perchloroethylene inhalation Rampy, 1978
chromosome aberra- exposure in vivo, 300 or 600
tions ppm, 6 hr/day, 5 days/week,
1 year
TA 1535; TA 1537; TA 98;
TA 100
Nonmutagenic in all Unknown activation status
four tester strains
Taylor, 1977
Host-mediated assay using Positive mutagenicity Activated in vivo
tester strains TA 1950;
TA 1951; TA 1952
TA 100
Frameshift mutations No metabolic activation used
and base substitu-
tion
Cerna and Kypenova, 1977
Cerna and Kypenova, 1977
Ames test using a desic- No mutagenesis
cat or
Transformation of F1706 Observed transforma-
Fischer rat embryo cell tion
system
Unrepeated, tests negative
activated and unactivated
Purity of test compound,
unknown
Mortelmans as cited by
Canter, 1978
Price et al., 1978
-------
carcinoma was seen in both sexes of treated mice when compared to control ani-
mals. At both high and low dosage levels, over 50% of the treated males, and
40% of the treated females developed liver cancer. Tumors were seen in 12% or
less of the untreated or vehicle-dosed control mice.
The perchloroethylene doses used were toxic to the kidneys of the Osborne-
Mendel rats in this study. The final report (NCI, 1977) noted toxic nephropathy
and death as early as week 20 of the study. This toxic effect was dose-related;
half the high dose male rats were dead by week 44 and half the females by week
66.
It can be concluded that these tests show no tendency for perchloro-
ethylene to form cancer in the rats that survived the doses. Because of the
difference in death rates in the controls and experimentals, there does exist
a statistical possibility that a result would be different had survival been
equal in the groups. Partly because of this possibility, the bioassays are
being repeated. On the other hand, there was early death in the mice on bio-
assay, and survivors of both sexes showed statistically significant tumor
incidence.
Analysis of the mouse data gives the early mortality shown below, which
suggests that the optimum dose was exceeded. Nevertheless, specific liver tumors
were found in a substantial number of the mice that died early in the experiment.
Mice(B6C3F1 strain); Median survival time
Hij>h dose Low dose Controls
Male 42 weeks 78 weeks Over 90 weeks
Female 50 weeks 61 weeks Over 90 weeks
(the termination of
the experiment )
A review of the NCI data indicates that the response of male mice ap-
peared to be greater than that of female mice not only in total incidence but
in shorter latency.
Weeks to first hepatocellular tumor
High dose Low dose Controls
Male 40 27 90 and 91
Female 50 41 91
5-216
-------
This sex difference in toxicity may not be a real onej control males also
had a higher tumor incidence and latency.
There were several design features that furnish potential weaknesses in
these bioassay results. Several of these potentially-modifying or contributing
features are acknowledged in the NCI report, such as:
I
* Mice exhibited clinically evident toxicity during most of the study,
particularly toxic tubular nephropathy.
* Clinical signs of toxicity were seen in all dosed rats, and very high
death losses occurred.
* Rats had chronic respiratory disease.
* Groups of animals which had received other volatile chemicals were
housed in the same room, presenting the possible chance of animal
exposure to very low levels of other compounds.
* Unique species differences in susceptibility were seen, with high
sensitivity of the B6C3F1 mouse and low sensitivity of the NCI
Osborne-Mendel to perchloroethylene (and most chlorinated aliphatic
compounds). A strongly-evident species difference in metabolism may
indicate aberrancies in the toxification or detoxification pro-
cesses. Species differences in tissue binding, inactivation,
clearance, or epoxide-forming enzyme levels could all vitally in-
fluence the experimental data relevance.
* Dose levels, the maximum tolerated doses, MTD, has been further
clarified since the protocol was established. The very high levels
(the highest consistent with long-term survival) have been criti-
cized as possibly producing unique metabolites in animals through
metabolic paths that are not normally functional. Further, the toxic
effects of such high doses could either enhance or inhibit carcino-
genesis by several potential means.
* Route of exposure for perchloroethylene was by oral gavage, allow-
ing the liver portal transport system to reach and biotransform
the dose before blood and tissue circulation of the type that would
be more likely with inhalation exposure.
Some other work has been done on the carcinogenicity of perchloro-
ethylene. Theiss et al. (1977) dosed A-strain mice intraperitoneally with
perchloroethylene at total doses of 80, 200, or 400 mg/kg administered three
times weekly for 5 to 8 weeks. The survivors, sacrificed 24 weeks after the
last dose, did not show an increased incidence of lung tumors over controls.
5-217
-------
An unpublished chronic inhalation study by Dow Chemical Company (Rampy
et al., 1978) has also studied the carcinogenicity of perchloroethylene.
This study found that 300 and 600 ppm perchloroethylene (a commercial stabil-
ized formulation) when inhaled 6 hr/day, 5 days/week for 12 months produced
no statistically significant increase in tumors in Sprague-Dawley Spartan
substrain rats (at both inhalation dose levels) when compared to control rats
when they were observed for their lifetime. Hematology and urinalysis were
done at 12 and 24 months. At the end of the experiment, 30 different tissues
were examined for each animal. The only tumor observed in higher incidence was
adrenal pheochromocytoma in female rats and only at the low exposure level.
Increased mortality occurred in male rats at the high dose level.
Van Duuren et al. (1979) have summarized the results of a carcinogenicity
study using 15 olefinic/aliphatic hydrocarbons including perchloroethylene.
The compound was tested as an initiator, as a promoter of carcinogenesis, and
as a complete carcinogen by repeated skin application to ICR/Ha Swiss mice of
both sexes. Perchloroethylene was not included in the group of halohydrocarbons
that were additionally dosed orally and subcutaneously. Perchloroethylene
tested negative for initiation/promotion; after a total dose of 163 mg, four
of seven mice had papillomas, the first of which appeared at 229 days. Treat-
ment with the tumor promoter only (phorbol myristate acetate 2.5 ,ug) gave
9 of 10 mice papillomas in 141 days minimum. In summary, the Van Duuren bio-
assay results showed perchloroethylene was not an initiator nor promoter when
repeatedly applied to the shaved skin of mice, and no distant tumors resulted
from this skin application.
Two, 2-year carcinogenesis bioassays of perchloroethylene are being spon-
sored by NCI, according to R. Wheeler (Tracer Jitco, Inc., Rockville, Maryland).
The chronic gavage, or oral dosage study, is being run on four rat strains
and one mouse strain, as outlined on the protocol in Table 5-40.
According to D. Lindberg (Tracer Jitco), the second study is an inhala-
tion dosage study. Perchloroethylene is currently under test in the Battelle-
Columbus Laboratories for this carcinogenesis bioassay, begun in October
1978. The species used: Fischer 344 rat, B6C3F1 mouse, and Syrian golden
hamster, 50 animals per species per sex at each dose level. Maximum tolerated
dose levels have been completed in prechronic tests, and design limits have
been detailed. No study results can realistically be expected before 1981.
• A personal communication indicated that the maximum tolerated dose (MTD)
in these new chronic studies will be modified somewhat from the dose used in
the earlier carcinogenesis bioassays in that the new MTD is based on animal
growth rate (Detrex, 1977). The adjusted MTD is in keeping with the proposed
guidelines outlined for some related hazard testing (Federal Register, 1978).
5-218
-------
TABLE 5-40. NCI PERCHLOROETHYLENE (C04580) EVALUATIVE
CARCINOGENESIS BIOASSAY
Objectives
To assess the carcinogenicity of perchloroethylene in rat strains
other than the Osborne-Mendel. Perchloroethylene did not show car-
cinogenic activity in the Osborne-Mendel rat in the first study.
To investigate the correlation between hepatotoxicity and heptocar-
cinogenicity in the B6C3F1 mouse. (Is hepatotoxicity resulting in
liver damage a necessary precursor of hepatocarcinogenicity, or can
a chemical of this type--chlorinated hydrocarbon—produce hepato-
cellular carcinoma at dose levels where no other significant liver
toxicity can be detected?)
To correlate dosage with blood levels of perchloroethylene in the
various strains and species.
Protocol
Gavage in corn oil, 5 times/week. Subchronic study in the following
rat species: Fischer 344, Long-Evans, Wistar, and Sherman. Groups
will include 10 rats per sex at each of five dose levels. Vehicle
and untreated control groups will include 10 rats per sex. Blood
will be drawn from three rats of each sex at terminal sacrifice for
quantitative analysis of test compound and trichloroacetic acid, a
major metabolite.
The subchronic study in B6C3F1 mice (13 weeks) will have six dose
levels of 10 mice per sex, which will be sacrificed in groups of 30,
60, and 90 days for a total of 360 animals. Appropriate vehicle and
untreated controls will be sacrificed at the same times. A total of
460 mice are included. The livers of all of these will be examined
histopathologically, and the following will be performed on all 460
mice at sacrifice: record liver weight and liver fat; take blood
sample and measure sorbitol dehydrogenase, fructose-1-phosphate
aldolase, and serum glutamic oxaloacetic transaminase. Blood will
also be taken from three mice of each sex at each of the six dose
levels and vehicle controls at the 30- and 90-day (terminal) sacri-
fices for quantitative analysis for perchloroethylene and trichloro-
acetic acid.
Chronic studies at maximum tolerated dose and MTD/2 for all the rat
strains (2,000 animals) and 540 of the B6C3F1 mice will be done for
2 years.
(abbreviated from protocol)
5-219
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Federal legislation or action dealing with the ranking of perchloro-
ethylene as a .carcinogen is in the process of change in mid-1979. The Con-
sumer Product Safety Commission has withdrawn a proposed policy to classify
and evaluate the carcinogenic hazard of perchloroethylene, since other inter-
agency groups were doing similar evaluations (Toxic Material News, 1979a).
5.3.4.7 Factors. Affecting Toxicity—
5.3.4.7.1 Cardiac sensitization--Epinephrine, a compound released from
the adrenal cortex, particularly in stress, has a variety of cardiovascular
effects. In man,, the.mean blood concentration is approximately 0,06 Mg/liter;
excesses are rapidly eliminated by enzymes found in high levels in the liver,
primarily through 0-methylation. When the human is stressed, the adrenal may
secrete 0.004 mg/kg/min epinephrine which must be broken down in the usual
pathway (Best and Taylor, 1955).
The main effect of epinephrine on the cardiovascular system is vasocon-
striction, which increases the blood pressure and heart rate and cardiac out-
put. Many hydrocarbons, particularly halogen-substituted hydrocarbons, are
known to sensitize the heart to the effects of epinephrine. Among the most
dangerous is the effect of ventricular fibrillation resulting from the car-
diac response to epinephrine-induced arrhythmia (Reinhardt et al., 1973;
Aviado et al., 1976; Hays, 1972; Reinhardt et al., 1971).
The specific effects of perchloroethylene on cardiac sensitization were
investigated by Reinhardt et al. (1972). Beagles were injected with epinephrine
(0.008 mg/kg intravenously) followed by inhalation of perchloroethylene (for 5
min), and then a challenge injection of epinephrine (0.008 mg/kg intravenously).
Concentrations of .perchloroethylene up to 1% by volume (10,000 ppm) failed to
produce cardiac, sensitization to epinephrine, although 5,000 ppm methyl chloro-
form produced marked sensitization in some of the dogs. The depressive effect
of perchloroethylene on the central nervous system precluded further testing
at higher concentrations.
Lob (1957) reported that a worker exposed chronically to perchloroethylene
experienced nausea, vomiting, a feeling of inebriation, and fainting. He died
when, after reexposure to the chemical, he was given an injection of phenyl-
ephrine hydrochloride. It has been recommended that epinephrine or phenylephrine
should not be used to improve blood pressure (Von Oettingen, 1964), due to the
possible cardiac sensitization. The effects of endogenously-released (stress
increased) epinephrine and the effects of injected epinephrine have both been
experimentally investigated for effects on the heart of the dog. There is a
species difference in regard to cardiac sensitivity between dogs and primates
that was noted in inhalation studies by VanStee and Back (1969), with the dog
much more prone to cardiac arrest and ventricular fibrillation at doses that
have only transient effects on monkeys and baboons. This difference may have
importance when assessing the hazard to man based on data obtained from dog
experiments. However, the arrhythmic response to epinephrine has not yet been
5-220
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completely defined and the role of perchloroethylene at the molecular level
is little understood. The more sensitive animal models are probably desirable,
therefore, because extrapolation of their data to man offers a better safety
margin than use of data from the more resistant species.
5.3.4.7.2 Synergistic effects-^The inhalation toxicity of a solvent con-
taining 25% perchloroethylene and 75% methyl chloroform was determined by Rowe
et al. (1963) in guinea pigs and rabbits. Synergism was not seen in these ex-
periments because the LCcg of the mixture superimposed on the "expected" LCcQ
plot of the data for each separate constituent. Death resulted from respiratory
failure. Gross examination of the parenchymatous organs revealed only mild ef-
fects on the liver and kidneys. Application of the solvent on ocular membranes
of the rabbits resulted in a response interpreted as pain and slight conjunc-
tival irritation which had cleared within 48 hr. Rats exposed in single inha-
lation experiments exhibited central nervous system depression. Minor liver
changes occurred with chronic (6 months) exposure. Rats died acutely from
either cardiac or respiratory failure. The single oral dose LDcn in rats was
5.7 to 14.8 g/kg. The single inhalation toxicity for rats (iX^g) was also low;
exposures of 0.5, 1.0, 2.0, 4.0, and 7.0 hr were required for concentrations
of 24,000, 20,000, 16,500, 14,000, and 12,000 ppm, respectively. Inhalation
toxicity studies with the solvent mixture showed guinea pigs to be the most
sensitive to the perchloroethylene/methyl chloroform mixture. These effects
are summarized in Table 5-41.
Rowe et al. (1963) also exposed rabbit skin to a solvent mixture of 75%
methyl chloroform and 25% perchloroethylene (nine exposures in 11 days), and
they found the toxicity of the mixture to be no greater than that which would
be expected from its constituents. Exposure of the skin to the chemical mixture
resulted in slight erythema and exfoliation, the response being greater when
the skin was abraded and the solvent-soaked pad bandaged to the skin. Healing
was, however, complete and without scarring.
Under conditions that had enhanced the toxicity of carbon tetrachloride
and trichloroethylene, Cornish and Adefuin (1966) administered ethanol to rats
16 to 18 hr before exposing them to perchloroethylene. Exposures were at 4,000
ppm (6 hr), 5,000 ppm (4 hr), 10,000 ppm (2 hr), and 15,000 ppm (2 hr). Serum
enzymes SCOT, SGPT, and isocitric dehydrogenase, liver lipids and histology
of liver, kidney, lung, adrenal, and spleen were studied. Alcohol ingestion
did not potentiate the toxicity of perchloroethylene in any of these param-
eters at the levels studied.
In a somewhat related study, Cornish (1973) induced the liver microsomal
enzymes in rats by phenobarbital injections (50 mg/kg, i.p., administered 1
and 2 days before perchloroethylene). Perchloroethylene toxicity was not en-
hanced by this enzyme induction, but the toxicities of carbon tetrachloride
and chloroform were both increased.
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TABLE 5-41. EFFECTS OF CHRONIC EXPOSURE TO A SOLVENT MIXTURE CONTAINING 75% METHYL CHLOROFORM
AND 25% PERCHLOROETHYLENE OF LABORATORY ANIMALS
Animal
Dose
Effects of treatment
Rat
ui
i
NJ
hO
S3
Guinea pig,
male
Rabbits
500 ppmj inhaled;
130 7-hr exposures
in 186 days
1,000 ppm; inhaled;
130 7-hr exposures
in 186 days
500 ppm; inhaled;
35 7-hr exposures
in 35 days (5
days/week)
1,000 ppm; inhaled;
35 7-hr exposures
in 49 days (5
days/week)
500 ppm; inhaled;
126 7-hr exposures
in 182 days
1,000 ppm; inhaled;
126 7-hr exposures
in 182 days
No adverse effects as judged by mortality, general appearance behavior,
hematologic examination, urinalysis, alkaline phosphateas, urea ni-
trogen levels, organ weights and organ to body weights.
No adverse effects as judged by the above standards but histological
examination revealed moderate diffuse cloudy swelling, occasional
vacuolization, scattered foci and of focal necrosis, and some en-
larged cells in the liver and moderate degenerative changes in the
epithelium of the kidney convoluted tubules.
Liver weights were slightly elevated which although statistically sig-
nificant could not be substantiated by histological examination.
A significant increase in liver weights with moderate hydrolysis de-
generative changes and a few foci of focal necrosis and degenerative
changes in the epithelial lining of the convoluted tubules and cell
infiltration around the glomeruli.
No adverse effects except milder versions of that reported for rats.
No adverse effects except for milder versions of those reported for
rats.
(continued)
-------
TABLE 5-41. (continued)
Animal
Dose
Effects of treatment
Dogs
500 ppm; inhaled;
131 7-hr exposures
in 189 days
1,000 ppm; inhaled;
131 7-hr exposures
in 189 days
Ul
i
to
OJ
No adverse effects.
No adverse effects as judged by appearance, behavior, mortality, growth,
hematologic data, urinalysis organ weights, serum glutmic-pyruvic
transaminase, alkaline phosphatase, urea nitrogen or bromsulfalein
retention; however, histology revealed liver cells to be large, dis-
tended with hyperchromatic nuclei and there was an increase in the
connective tissue; male dogs were normal and no other changes were
noted.
Source: Adapted from Rowe et al. (1963).
-------
Withey and Hall (1975) mixed perchloroethylene with benzene and toluene
in the following ratios for LD5Q studies in rats: 100:0, 80:20, 60:40, 40:60,
20:80, and 0:100. Mixtures containing perchloroethylene/benzene gave LDcQ val-
ues which were slightly less than additive while mixtures containing both per-
chloroethylene and toluene had inconsistent LD^g values.
Smyth et al. (1969) studied the synergistic action of perchloroethylene
and 26 other solvents, administered orally to rats. The results followed a pre-
dictive additive toxicity model except for the data on polyethylene glycol
400, butyl ether, dioxane, and acetophenone. These four substances showed a
greater than additive toxicity.
5.3.4.7.3 Stabilizer toxicity — N-Methyl pyrrole, epichlorohydrin, epi-
bromohydrin, amines such as allyl amine or methylmorpholine, and allyl glyci-
dol ether have been used as stabilizers in various combinations in perchloro-
ethylene. A comparison of the rodent LD^g levels for these additives to the
LD5Q level for perchloroethylene shows that most of the stabilizers are more
toxic than perchloroethylene. The exception, N-methyl pyrrole, is less toxic;
it takes a dose 9.3 times larger than a perchloroethylene dose to kill the same
number of mice (Sax, 1975; Christensen et al., 1975). The other known stabil-
izers are much more toxic. Epichlorohydrin and epibromohydrin are 63 and 57
times more toxic than perchloroethylene, respectively. Allyl amine is 53 times
more toxic and allyl glycidol ether is 15 times more toxic. The patent litera-
ture and communications from industry indicate that these stabilizer packages
are constantly changing.
Perchloroethylene is usually stabilized by N-methyl pyrrole as an anti-
oxidant. The other compounds on the list are added according to different
formulations to inhibit the reactions which occur if some oxidation does take
place. Epichlorohydrin and epibromohydrin are skin irritants and sensitizers.
Epichlorohydrin has recently been implicated as a suspect carcinogen (Anonymous,
1978b). An industrial epidemiology study found a higher-than-expected rate of
respiratory cancer deaths in workers previously exposed to epichlorohydrin.
Another industry report suggested that epichlorohydrin workers had twice as
many chromosomal aberrations as did controls. It is possible that this stabil-
izer has far more detrimental health effects than perchloroethylene. The allyl
glycidol ethers have been associated with radiomimetic effects, presumably
reflecting biological alkylation (Kotin and Falk, 1963). The amines are basic
and can produce chemical burns of the skin. Some sensitive individuals show
hypersensitivity dermatitis and asthma-like reactions from exposure to the
pure compounds, but their presence in small amounts as stabilizers probably
does not present this hazard.
An unpublished report (Margard, 1978) on the mutagenicity of several
trial stabilizer formulations was obtained. Since the data involved propri-
etary information, sufficient information to interpret the studies was un-
available. The bacterial assays (Ames tests) appeared to be well done,
5-224
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however. The document recognized (p. 25) that a broader assay profile (e.g.,
tests in addition to the Ames) would be desirable to demonstrate mutagenicity
or the lack of it. Perchloroethylene and stabilizers, however, reacted with
the plastic in the sterile labware used to perform the tests; the mammalian
cell cultures were many times more responsive to toxicity than were the bac-
terial cell systems.
Considering the many effects of the stabilizers, it would be of consid-
erable interest to have carcinogenesis assays run simultaneously on the
stabilizer products found in the USP grade perchloroethylene used for the
NCI bioassay tests. A personal communication from a user company (Detrex,
1978) reported that, using five Salmonella tester strains for Ames bacterial
mutagenesis assays, perchloroethylene showed no mutagenic activity when it
was free of added stabilizer and epichlorohydrin.
5.3.4.7.4 Medical surveillance; signs of overexposure—Perchloroethylene
is slowly eliminated from the body (Guberan and Fernandez, 1974; Stewart et
al., 1961; 1974) With repeated exposure, it is known to build up in blood
and tissue, especially lipid-containing tissue, and is slow to metabolize.
The most common way to determine acute exposure is to measure trichloroacetic
acid in urine (Ikeda et al., 1972; Ogata et al., 1971; Ikeda and Ohtsuji,
1972).
The narcotic effects of perchlordethylene have been quantitated af.ter
acute exposure by coordination tests, EEC tracings, and common behavioral
tests (Stewart et al., 1970; 1974). The Romberg test is simple and has been
used frequently in experimental exposure studies. Stewart et al. (1970)
noted a positive Romberg after 3 hr exposure to 100 ppm perchloroethylene.
Urinary urobilinogen reactions, SCOT and SGPT have been commonly reported
as positive in workers after exposure to perchloroethylene (Lob, 1957; Stewart,
1969). Aberrant levels of liver enzymes (SCOT, SGPT), however, are indicators
of toxicity rather than of simple exposure.
Some serious symptoms have been recorded in the literature in workers
exposed for long periods to high levels of perchloroethylene. Irreversible
neurologic effects have been reported by Gold (1969) and Lob (1957). Russian
cases were cited in the NIOSH review (Antoniuzhenko and Palkin, 1973). The
neurologic effects included exaggerated dertnographism, vestibular dysfunction,
and various muscular symptoms that appeared on neurological examination. Most
signs and symptoms persisted for extended periods after exposure ceased.
Pulmonary symptoms (initially diagnosed as tuberculosis) were apparently
produced by perchloroethylene in one fatal case (Trense and Zimmerman, 1969).
Liver symptoms of jaundice and renal failure followed, 9 days after the onset
of pulmonary symptoms. Patel et al. (1973) describe a case of exposure to
5-225
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excessive perchloroethylene in which acute pulmonary edema was the predomi-
nant symptom.
5.3.5 Human Epidemiology
5.3.5.1 Occupational Exposure—
Because perchloroethylene is used as a dry cleaning agent, a commercial
solvent, and a degreasing solvent, exposure of workers to low level concen-
trations frequently occurs. The acute and chronic toxicity has been extensively
studied (Von Oettingen, 1964; Rowe et al., 1952). Stricoff (1979) has reviewed
the epidemiological exposure studies and suggested that the hazard of per-
chloroethylene inhalation was mostly unrecognized in the dry cleaning indus-
try, and work practices for safety are largely unimplemented.
There have been several reports of dermal response to perchloroethylene
contact in occupational situations. These chemical burns vary in severity.
Foot et al. (1943) described skin irritation resulting from the vapors con-
tacting the skin under a respiratory mask. Ling and Lindsay (1971) described
a case of extensive erythema and burn blisters (first and second degree sol-
vent burns) on a laundry worker who, after being overcome by perchloroethylene
fumes, fell and lay for 5 hr in the liquid solvent which had accumulated on
the floor. Consciousness returned in 24 hr.
Patel et al. (1973) reported survival from another industrial exposure
to perchloroethylene at an unknown concentration level in which a worker
lost consciousness and lay for 7 hr with whole-body exposure to the solvent.
Acute pulmonary edema, coma, and hypotension with a blood pressure of 88/20
mm Hg occurred, although kidney and liver function were reported to be nor-
mal. Other cases of chemical burns resulting from perchloroethylene have been
reported by Weiss (1969), Feldman (1969), and Morgan (1969). Rowe et al.
(1963) have reported skin irritation with exposure in rabbits.
In addition to chemical burns, occupational exposure occasionally produces
signs of narcosis. Factory workers, who were exposed to perchloroethylene va-
pors during degreasing operations, complained of lightheadedness, dizziness,
and a feeling of intoxication with the accompanying hangover. This report
(Coler and Rossmiller, 1953) is discussed in the following section. It should
be noted that the workers reported that their symptoms were aggravated in high
humidity.
A tank car cleaner overcome by perchloroethylene fumes also exhibited
central nervous system depression and transient minimal liver damage (Stewart,
1969). Seventy-five percent of 40 workers exposed to perchloroethylene vapor,
varying from 400 mg/m to 913 mg/m , complained of headaches, fatigue, sleepi-
ness, dizziness, and drunkenness. Urinary metabolites were found to be tri-
chloroacetic acid (maximum 41 mg/liter) and trichloroethanol (maximum 116
mg/liter) (Medek and Kovarik, 1973). Mucous membrane irritation, severe
5-226
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pulmonary edema, depression of the central nervous system, mild hepatic and
renal damage, and coma resulted when a dry cleaning worker was exposed to
high concentrations of perchloroethylene vapor for 7 hr. Despite the length
of his exposure, recovery was complete (Patel et al., 1973).
Gold (1969) also described severe central nervous system disturbances,
indicative of possible cerebral-cortical damage and basal ganglia involvement
in a man who had been chronically occupationally exposed over a 3-year period.
Cardiovascular failure attributable to chronic perchloroethylene exposure
was reported by Trense and Zimmerman (1969) for a dry cleaning establishment
worker who, on autopsy, was found to have liver necrosis and toxic myocardial
fatty degeneration. Analysis of the cerebral tissue revealed quantities of
chlorinated hydrocarbon metabolites.
Stewart et al. (1961b) reported .that perchloroethylene was detectable
for 2 weeks on the breath of a man overcome by fumes. During the second and
third weeks after exposure, this man exhibited liver dysfunction with symptoms
of mild hepatitis. Saland (1967) reported that nine firemen, exposed to per-
chloroethylene vapors for about 3 min, complained of a lightheaded and uncoor-
dinated feeling and disturbances in depth perception which disappeared upon
returning to fresh air. Twelve days after exposure, eight of the nine showed
elevations of SCOT enzyme activity, indicative of liver damage. In seven of
those eight men, the enzyme levels had returned to normal by 22 days.
McConnell et al. (1975) reported the presence of perchloroethylene in
human tissues on autopsy. These values were said to reflect the background
levels of the chemical in the environment. Body fat samples from eight autop-
sies contained perchloroethylene in concentrations which ranged from 0.4 to
29.2 Mg/kg wet tissue. Levels in the liver were measured in six cases, and
values ranged from less than 0.5 to 3.4 ,ug/kg. No correlation of concentration
with age was seen, but in subjects with high liver levels, the body fat con-
tent was also high.
Because of the occupational exposure of workers, attempts have been made
to correlate exposure to perchloroethylene with urinary excretion of the com-
pound and its metabolites (Kundig and Hogger, 1970; Ikeda et al., 1972).
Ikeda et al. (1972) reported that among workers using the compound as a dry
cleaning solvent, excretion of urinary metabolites rose to and remained at a
stable value (a plateau) when workers were exposed to perchloroethylene at
atmospheric concentrations less than 100 ppm. These results were supported
with studies on rats. Kundig and Hogger (1970) also found no direct correla-
tion between urinary metabolite concentration and extent of exposure. The
presence of metabolites in the urine was, however, a reliable indication that
exposure had occurred.
5-227
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An epidemiological study on laundry and dry cleaning workers, sponsored
by the National Cancer Institute, is under way and in the follow-up phase,
according to a communication from Dr. Aaron Blair, NCI.
The cohort consists of 10,000 members belonging to a St. Louis, Missouri
labor union. In addition, a mortality study of 330 deaths from St. Louis and
Kansas City union locals is under way and scheduled for release in late 1979 or
1980. According to preliminary reports, there was a 30% greater-than-expected
rate from cancer deaths in this group when compared to the entire U.S. popu-
lation. Additional statistical work is necessary before interpretation is
possible. The low wage scale for the laundry and dry cleaning workers may
mean that other well-known epidemiologic factors are producing the excess
in cancer in this group when it is compared--not to identical controls--but
to the population of the United States as a whole. Additional caution is
necessary in interpreting the data and ascribing any effects to perchloro-
ethylene. It was noted that in the 10,000-cohort study, there was no distinc-
tion between those shops using perchloroethylene and those with carbon tetra-
chloride, trichloroethylene, or other petroleum solvents. Although multiple
chemical exposures may have occurred, perchloroethylene has been the most
frequently used solvent for 20 to 25 years and is used by approximately 75%
of the present plants according to the study (Canter, 1978; Blair, 1979;
Brown, 1979).
In an attempt to simulate working conditions, Stewart et al. (1970) ex-
posed humans to single doses and repeated doses for 7 hr at 100 ppm perchloro-
ethylene. During repeated exposures, there was a definite acclimation to the
chemical and persons repeatedly exposed exhibited fewer toxic effects. During
a single 7-hr exposure, 25% of the people reported a mild headache, 60% re-
ported eye, nose, and throat irritation which developed in the first few hours,
40% felt sleepy, and 25% had difficulty in speaking. These symptoms are simi-
lar to those reported by occupationally exposed people.
Two reports of gastrointestinal disturbances as the result of chronic ex-
posure of factory workers to perchloroethylene have been made (Coler and
Rossmiller, 1953; Moeschlin, 1959); however, these symptoms have not been re-
produced in a laboratory situation.
5.3.5.2 Other Human Exposure Studies—
No controlled, matched pair, or actuarial studies on perchloroethylene
exposure have been completed. The widespread use of the compound in the dry
cleaning industry means that many people are exposed to this chlorinated
hydrocarbon. Both NIOSH and NCI are carrying out surveys on workers in the
dry cleaning industry. NIOSH is conducting an "industrial hygiene assessment;"
NCI is examining the mortality of persons who were dry cleaning establishment
workers.
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Stanford Research Institute is developing a retrospective cohort study
monitored by NIOSH (Biometry Section, Industry-wide Studies Branch). The
study analyzes the union records of 1,700 dry cleaning workers that had been
employed in the industry for at least 1 year before 1960. Since perchloro-
ethylene came into high use only in the middle 1940's (1943 to 1945), the
"person-years" of exposure avoid to the greatest extent possible the workers
who had employment exposure to carbon tetrachloride and other early dry clean-
ing solvents. The experimental design groups the mortality rate (observed
versus expected) over a 5-year period by 5-year age groups, separated by age,
sex, and race. The data should be completed and published in late 1979 or
1980 (personal communication; Brown, NIOSH, May 1979). A preliminary propor-
tionate mortality report on union-workers in the dry cleaning industry has
been published (Blair, 1979). The complete design of this perchloroethylene
study is not available. It compares the cause of death of perchloroethylene-
exposed workers with the cause of death of a total population group. Thus far,
data have been gathered for 330 workers in the Kansas City and St. Louis,
Missouri, dry cleaning industry.
Animal studies in progress by various groups include a behavioral tera-
tology study and a teratogenicity/mutagenicity assay, both sponsored by the
National Institute for Occupational Safety and Health (NIOSH, 1978a; Toxic
Material News, 1978).
EPA has recently published a review of perchloroethylene as an ambient
air pollutant (Toxic Material News, 1979b). The document reviews the toxicity
of perchloroethylene to animals, the effects on man, perchloroethylene trans-
port and metabolism, and the NCI carcinogenesis bioassay.
Extensive exposure to perchloroethylene, however, is certainly not new.
Hookworm treatment by oral perchloroethylene was popular in the 1920's and
1930's in India and the Pacific Islands. Kendrick (1929) treated 1,500 priso-
ners in the Madras jails and reported one severe case of toxicity, after a 3-
ml oral dose, where the patient became unconscious for 3 hr but recovered.
An average "worming dose" to the human prisoners of 0.15 ml/kg was reported.
Lambert (1933) gave 46,000 hookworm treatments in the South Pacific
Islands with no deaths from oral perchloroethylene and reported fewer toxic
symptoms than from other anthelmintics. A review in the late 1930's stated
that 100,000 treatments for hookworms had been given without a death.
In India, Fernando et al. (1939) gave perchloroethylene to a large group
with confounding pathologies and who ranged from 1 year of age to 70. Tests
were run that would identify severe liver damage, hemolysis or renal pathology
as a result of the perchloroethylene dosage. Six milliliters to adults fre-
quently produced giddiness. Elevated bile pigments were seen in the urine
of some patients, particularly those with malaria and anemia. Children tol-
erated doses of "4 to 5 times their age in minims" which is about 5 drops of
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perchloroethylene orally for every year of age. The Fernando paper reported
effects of 11 subjects who were given 6.0 to 8.0 ml orally:
1 of 11 had a drop in blood pressure from 135/80 to 112/70
1/11 was semiconscious for 4.5 hr
4/11 had considerable depressant effects: sleepy, faint, drowsy
11/11 were giddy
0 of 11 had "appreciable" liver or kidney toxicity.
The only serious narcotic effect, noted above, occurred in a man whose weight
was so low that the oral dose was 0.21 ml/kg body weight. Four milliliters
perchloroethylene was reported to cause no "untoward effect" in any subjects,
and that was the usual dose.
The use of perchloroethylene for worm medication in humans was not dis-
cussed except for rare mention in the U.S. medical literature of the 1920's
and 1930's. It may be inferred that perchloroethylene anthelmintic usage was
not as common in the United States as in India.
It is noted, however, that although the doses were high and the number
of humans exposed was large, the use of perchloroethylene in worm medication
was usually a single, acute exposure.
A case of chronic exposure ranging from 2 to 6 years was experienced by
seven men who worked in degreasing operations with perchloroethylene at 230
to 385 ppm for 2 days a week. Coler and Rossmiller (1953) report that all seven
exhibited memory impairment, staggering gait, and a drunkenlike state. Medical
histories revealed no extensive alcohol consumption by any worker, but one of
the seven had a gastric hemorrhage and cirrhosis of the liver. Three of seven
were found to have liver toxicity as diagnosed by sulfobromophthalein sodium
dye retention; four of seven had positive urobilinogen.
Another study on long-term exposure was reported by Tuttle et al. (1977).
Behavioral effects in 18 exposed workers were measured; these data were dis-
cussed under Central Nervous System Effects earlier in this report.
Yoshida (1977), in a recent Japanese review, summarized published informa-
tion on the human health effects of perchloroethylene. This extensive review
grouped organic solvents into three toxicity categories according to their al-
lowable concentration levels in workplace air; perchloroethylene was in the
group with acetone and methyl ethyl ketone. Toxic tolerances to perchloro-
ethylene by humans were reviewed, as were effects on biological processes and
functions.
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5-243
-------
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Yllner, S. 1961. Urinary metabolites of l^C-tetrachloroethylene in mice.
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5-244
-------
CONTENTS
Page
6. Ecological Effects 6-3
6.1 Environmental Fate 6-3
6.1.1 Modes of release 6-3
6.1.2 Tropospheric reactions 6-4
6.1.2.1 Methyl chloroform 6-4
6.1.2.2 Trichloroethylene and perchloro-
ethylene 6-7
6.1.3 Tropospheric half-lives 6-11
6.1.4 Stratospheric reactions 6-13
6.1.5 Hydrolytic degradation and volatilization . 6-15
6.1.6 Reactions in soil and sediment 6-18
6.1.6.1 Soil 6-18
6.1.6.2 Sediment 6-18
6.1.6.3 Biological degradation 6-18
6.1.7 Sewage treatment 6-19
6.1.8 Greenhouse effect 6-20
6.2 Environmental Effects 6-20
6.2.1 Effects on fish 6-20
6.2.1.1 Toxicity 6-20
6.2.1.2 Uptake and accumulation 6-23
6.2.2 Effects on other aquatic plants and
animals 6-26
6-1
-------
CONTENTS (continued)
Page
6.2.2.1 Effects on aquatic plants 6-26
6.2.2.1.1 Toxic effects 6-26
6.2.2.1.2 Uptake and accumulation . . . 6-26
6.2.2.2 Effects on other aquatic organisms . 6-27
6.2.2.2.1 Toxic effects ... 6-27
6.2.2.2.2 Accumulation 6-28
6.2.3 Effects on birds 6-28
6.2.4 Effects on mammals 6-28
6.2.5 Effects on other terrestrial organisms,
plants and protista 6-28
6.2.5.1 Other terrestrial organisms 6-28
6.2.5.2 Terrestrial plants 6-28
6.2.6 Effects on protista 6-31
6.2.7 Bioaccumulation 6-32
References 6-24
6-2
-------
SECTION 6
ECOLOGICAL EFFECTS
This section of the report is divided into two major subsections. The
first subsection presents information on the modes of environmental release
and transport for trichloroethylene (CHCl=CCl2)» methyl chloroform (CH^CC^),
and perchloroethylene (Cl2G=CCl2) and on the chemical and biological reac-
tions these substances may enter into in the environment. The second subsection
describes the effects these chlorinated hydrocarbons can have on living
species other than humans or laboratory animals and the accumulation and
biomagnification which can occur in these living organisms.
6.1 ENVIRONMENTAL FATE
In this subsection, the areas to be discussed include modes of release,
tropospheric and stratospheric reactions, hydrolytic degradation, reactions
in the soil and sediment, effects on sewage treatment, and potential "green-
house" effects.
6.1.1 Modes of Release
The three compounds under study reportedly do not have a natural ori-
gin; their presence is due to anthropogenic sources (Singh, 1977; Gay et al.,
1976). The modes by which these subject compounds are released into the envi-
ronment and the quantities emitted by each mode have been discussed in detail
earlier in this report (see Section 3). Each of the three compounds are re-
leased primarily through air emissions by user facilities. For methyl chloro-
form and trichloroethylene, these user facilities are the multitude of com-
panies, large and small, that employ a metal cleaning operation, either cold
cleaning or vapor degreasing. For perchloroethylene, the largest user is the
dry cleaning industry which emits over 50% of the total U.S. consumption of
this compound. The scouring operations in the textile industry, vapor degreas-
ing systems, and cold cleaning operations follow, in that order, as emitters
of perchloroethylene to the environment.
6-3
-------
6.1.2 Tropospheric Reactions
The laboratory studies of the decomposition of trichloroethylene, methyl
chloroform, and perchloroethylene can be conveniently divided into two parts:
studies of methyl -chloroform and studies of trichloroethylene and perchloro-
ethylene. The reaction rates, mechanisms, and products are considerably dif-
ferent for methyl chloroform than they are for either trichloroethylene or
perchloroethylene.
6.1.2.1 Methyl Chloroform —
Appleby (1976) studied the gas phase photolysis of methyl chloroform un-
der several conditions, including with added nitric oxide (N02), ozone,
atomic oxygen, free radicals, and simulated sunlight. From the studies, it
could be inferred that methyl chloroform will not decompose in the troposphere,
The nonsensitized photooxidation of methyl chloroform vapor in air was
studied by Christiansen et al. (1972). The only quantitatively important
products detected were hydrogen chloride, phosgene, and the carbon oxides.
Trace quantities of acetic acid (hydrolysis product of acetyl chloride) and
1,1,1,2-tetrachloroethane were also found. The quantum yield of phosgene was
approximately 1.3 and independent of both light intensity and the partial
pressure of methyl chloroform. Neither chloral nor formaldehyde was found.
Chloral might be anticipated through a reaction of oxygen and the CC13CH2
radical, which was postulated as an intermediate in the chlorine sensitized
oxidation. Formaldehyde might result from a decomposition of the CC13CH20
radical, a reaction which is analogous to the formation of phosgene in the
oxidation of trichloroethylene and perchloroethylene.
However, if the peroxy radical (CC^Cl^C^) is formed instead of the
CC13CH20 radical, then cleavage of the C-C bond can occur with the formation
of the CC13 radical, carbon monoxide (CO), and water. The CCl3 radical can
undergo subsequent reaction with oxygen to form an oxy or peroxy radical. De-
composition of this radical would lead to the formation of phosgene (COC12)
and either a Cl radical or CIO.
Christiansen et al. (1972) state that since the C-Cl bond energy is
much lower than the excitation energy, the most probable primary process
should be:
6-4
-------
CH3CC13 —+ CH3CC12* + Cl
The quantum yield of the primary process should be 1, and since the quantity
of acetyl chloride (as acetic acid) was only a small fraction of that for
phosgene (quantum yield — 1), it was concluded that the fate of the primary
radical was not oxidation to acetyl chloride. If the CH3CCl202 and CH3CC120
radicals are formed and the latter decomposes to phosgene and methyl radicals,
as well as to acetyl chloride and chlorine atoms, the authors state that this
would provide an explanation for the quantum yields, light intensity, and the
independence of the methyl chloroform pressure. No detailed reaction mechanism
for the production of the final products was postulated.
Spence and Hanst (1978) irradiated (365 and 310 nm) a mixture of 10 ppm
methyl chloroform and 10 ppm chlorine in one atmosphere of dry air for 6 min.
At the end of the irradiation period, 80% of the methyl chloroform was unre-
acted. The only chlorocarbon product resulting from the irradiation was phos-
gene. Other products included CO, G02, and hydrogen chloride. No evidence of
chloral was found. Of the eight chlorinated ethanes studied, methyl chloro-
form was the least reactive. A reaction mechanism was proposed in which chlo-
rine atoms are generated by the photodissociation of molecular chlorine. The
chlorine atoms abstract a hydrogen atom from the methyl chloroform, thus sim-
ulating hydroxyl attack in the ambient atmosphere. This proposed mechanism will
also account for the reaction products observed by Christiansen et al. (1972).
A quantum yield of < 2 was reported for the oxidation of methyl chloro-
form in the presence of chlorine and oxygen by Bertrand et al. (1971). No
identification of the primary oxidation products was stated. The authors
state that, according to a generalized reaction mechanism, long-chain oxi-
dation can occur only if the quantum yield of the oxidation reaction is »
1. This is not the case for methyl chloroform. Bond energies of the radical
species are used to differentiate which radicals will proceed by long-chain
oxidation.
Dilling et al. (1976) estimated the decomposition rate of methyl chloro-
form, under simulated atmospheric conditions, to be less than 5% after 23.5
hr with 5 ppm of added NO. With 16.8 ppm of N02 added, they found less than
5% decomposition after 8 hr. In a reaction mixture of 50 ppm methyl chloro-
form and 10 ppm N02> less than 5% decomposition was found after irradiation
for 28 days.
The tropospheric destruction of halocarbons containing labile hydrogen
atoms (e.g., methyl chloroform) or carbon-carbon double bonds (e.g., per-
chloroethylene and trichloroethylene) occurs principally by reaction with
hydroxyl radicals (Derwent and Eggleton, 1978; Lovelock, 1977; Crutzen et al.,
1978; Neely and Plonka, 1978).
6-5
-------
General reactions leading to the formation and destruction of the hydroxyl
radical are as follows:
hv
Formation: 03 > 02 + 0»
hv
N0 — > NO + 0«
0- + H20 > 2 HO-
Destruction: H0« + CH^CC^
H0» + CO
H0» + CH4
The reaction of the hydroxyl radical with methyl chloroform is the rate deter-
mining step in the destruction of methyl chloroform in the troposphere (Neely
and Plonka, 1978). Different rate coefficients have been published for the
hydroxyl radical abstraction reaction with methyl chloroform (Crutzen et al«,
1978; Derwent and Eggleton, 1978; Neely and Plonka, 1978). An average rate
coefficient of k = 3.6 x 10~12 exp (-1600/T) has been used in recent cal-
culations of hydroxyl radical concentrations in the troposphere (Neely and
Plonka, 1978).
The obvious importance of the hydroxyl radical reaction with methyl
chloroform is that with increasing tropospheric reaction, less methyl
chloroform is available to migrate to the stratosphere. However, the other
two destructive reactions of hydroxyl radicals could possibly also play a
significant role. As carbon monoxide and methane concentrations increase,
which could happen as the degree of industrialization increases, more
hydroxyl radicals are removed by these two processes and less are available
for reaction with methyl chloroform. Hence, it may be possible that a greater
percentage of the methyl chloroform would be available for transport to the
stratosphere (Crutzen and Fishman, 1977).
Because of the importance of the hydroxyl radical reaction with methyl
chloroform, numerous calculations have been made of the time-averaged hemi-
spheric concentration of this radical. Neely and Plonka (1978) have summarized
11 calculated levels for the northern troposphere. If the four obviously high
values are eliminated, the average of the seven remaining calculated levels
is 4.6 x 1CH molecules per cubic centimeter. The actual hydroxyl radical con-
centration varies diurnally, seasonally, as well as vertically and horizon-
tally. The time-averaged concentration of hydroxyl radical assumed to be
6-6
-------
present in the troposphere becomes very important for modeling purposes to cal-
culate the quantities of methyl chloroform transported to the stratosphere,
Pitts et al. (1977) compiled a tabular reactivity classification of or-
ganic (and selected inorganic) compounds based on their reaction with the hy-
droxyl radical• All reactivities were compiled relative to methane and then
separated into three classes, depending upon the relative reaction rate.
Methyl chloroform was in Class I (very low reactivity) with a reaction rate
only twice that of methane. Trichloroethylene and perchloroethylene were not
included in the tabulation.
6.1.2.2 Trichloroethylene and Perchloroethylene--
Numerous studies have been conducted on the initiation of the photolytic
decomposition, reaction products, and the mechanisms of the photolysis of
trichloroethylene and perchloroethylene. A recent review article (Sanhueza
et al., 1976) summarizes the studies of the oxidation of haloethylenes with
respect to the various methods of initiation or sensitization.
Dahlberg (1969) confirmed that the overall reaction in the nonsensitized
photooxidation of trichloroethylene in air, as shown by earlier studies, was:
2 C2HC1 + 1.5 0 > CHC1 COC1 + COC1 4- HCl 4- CO
dichloroacetyl phosgene
chloride
and that the primary path of the oxidation is directly to dichloroacetyl chlo-
ride not via an epoxide intermediate. The rates of formation of the acetyl
chloride and phosgene are linearly dependent upon the absorbed light intensity,
as in the case of the chlorine-sensitized reaction. For wavelengths below 230
nm, the results indicate that the quantum yield is nearly constant. Initiation
of the reaction was proposed to be as follows:
hv
C2HC13 ^ C2HC13
-------
and that once the chlorine atom has been produced, the reaction proceeds in
the same manner as proposed for the chlorine photosensitized oxidation of
trichloroethylene.
The chlorine-atom-initiated oxidation of trichloroethylene and perchloro-
ethylene proceeds by a long-chain free-radical process (Sanhueza et al., 1976).
The major products for trichloroethylene at high oxygen pressure were found to
be 9070 dichloroacetyl chloride, carbon monoxide, and phosgene; the quantum
yield of oxidation was 200. For perchloroethylene under the same conditions,
the major products were 757o trichloroacetyl chloride and 2570 phosgene; the
quantum yield of oxidation was 300. Reaction products are generally identi-
fied by spectrometric methods and not isolated. These results were obtained
in laboratory studies but would not be expected to occur under actual
tropospheric conditions. Under such conditions, the concentrations would be
in the parts per billion range and the chain reactions would be preempted by
the reaction of the chlorine atom with methane to form hydrogen chloride and
methyl radical. For trichloroethylene and perchloroethylene, oxygen had an
inhibiting effect on the photochlorination reaction. Hydrocarbons also show
an inhibiting effect on the photooxidation of these compounds (Appleby, 1976).
Both trichloroethylene and perchloroethylene are proposed to follow the
same general free radical mechanism in the chlorine-initiated photooxidation
(Sanhueza et al., 1976; Sanhueza et al., 1977). For perchloroethylene, the
mechanism is:
2 Cl-
ci3c-cci2
C13C-CC1202-
2 C13CCC1202 —
2 C13CCC1202
(C13CCC120)2
ci3ccci2o- —
— > 2 C13CCC120- + 02
— *• (ci3ccci2o)2 •*• o2
— > 2 C13CCC120-
— > CljCCOCl + Cl
(trichloroicecyl
chloride)
•coci2
(phosgene)
C13C-
2 C13C02
-------
This review also summarized the effects of ozone and fluorine on the chlorine-
initiated photooxidation, as well as the mercury [Hg 6(3P)] sensitization
(with and without oxygen), the reaction with oxygen atoms (with and without
added oxygen), and the reactions with ozone.
However, as stated previously in the discussion of methyl chloroform, the
principal mode for tropospheric decomposition of trichloroethylene and per-
chloroethylene is attack by the OH radical. Arrhenius rate constant expressions
have been derived for the reaction of the OH radical with trichloroethylene
and perchloroethylene. Chang and Kaufman (1977) calculated 5.3 x 10~*3 exp
(445/T) cm3/sec for trichloroethylene and 9.4 x 1CT12 exp (-1199/T) cm3/sec
for perchloroethylene. Crutzen et al. (1978) calculated 2.8 x 10~H exp
(-1530/T) cm3/sec for perchloroethylene.
From their data, Chang and Kaufman (1977) concluded that reactions of tri-
chloroethylene and perchloroethylene with OH radicals are much faster than
those with other reactive atmospheric species such as 0 (3P) or ( D), 03, H,
or H02 when both the rate constants and the normal atmospheric concentrations
of the species are considered. The authors also conclude that the mechanism
of OH radical attack cannot be ascribed to simultaneous addition and hydrogen
abstraction channels; hydrogen abstraction would be quite slow because of
large C-H bond strength in trichloroethylene. Chang and Kaufman suggest an
attack by the OH radical on the C=C pi bonds, formation of a complex between
the oxygen and the pi bonds, and subsequent rearrangement and decomposition
to the products.
Howard (1976) also stated that the trichloroethylene mechanism is certainly
not a hydrogen atom abstraction and that OH radical attack on the 0=0 pi
bond would lead to an excited ethyl radical complex which would decompose to
stable products.
The atmospheric oxidation of chlorinated ethylenes was reported by Gay
et al. (1976). Trichloroethylene and perchloroethylene were photooxidized in
air with added N02» Analysis of reaction products was by infrared spectroscopy.
Oxidation of trichloroethylene produced spectral evidence for phosgene, formyl
chloride, and dichloroacetyl chloride. The half-life of formyl chloride was
stated to be approximately 20 min at 25°C; it dissociates to give carbon mon-
oxide and hydrogen chloride. Perchloroethylene was found to be the least re-
active of the chlorinated ethylenes. Spectral evidence was found for the
presence of phosgene, formic acid (likely from formyl chloride), carbon
•monoxide, hydrogen chloride, and trichloroacetyl chloride.
Singh et al. (1975) performed experiments which showed that irradia-
tion of perchloroethylene in air for 7 days led to the formation of about
8% (by weight) carbon tetrachloride (CCl^) and 70 to 85% phosgene (COCl2)«
6-9
-------
The authors suggested that trichloroacetyl chloride (C13CCOC1) was the pre-
cursor of the carbon tetrachloride. In addition, Singh et al. (1977a) believe
that trichloroethylene can be photooxidized to form phosgene and chloroform
(CHCl3)» The authors suggested that dichloroacetyl chloride, in a manner
similar to perchloroethylene, was the precursor of the chloroform. However,
the authors also state that the existence of tropospheric sinks precludes
the possibility of any significant stratospheric impact due to phosgene.
Appleby (1976) studied the photolysis of trichloroethylene under several
conditions and found that it is stable towards direct ozone attack. In all sys-
tems, phosgene was found to be the major decomposition product and the rate
of formation varied depending upon the specific system. Chloroform was detected
in all systems where light was employed with the maximum concentration reach-
ing 8 to 15 parts per billion (ppb), depending upon the system. Other products
qualitatively detected were dichloroacetyl chloride and hydrogen chloride. The
photolysis of perchloroethylene was also studied under several conditions.
In "ultra zero" air at 50% relative humidity, 100% of the perchloroethylene
had reacted in 1.5 to 2 hr. With N02 added to this system, the time required
for complete reaction was approximately 8 hr; the addition of hydrocarbons re-
quired 23 to 31 hr for complete reaction. In each system, phosgene was iden-
tified as a decomposition product with the maximum production occurring in the
system of ultra zero air plus added N02« Carbon tetrachloride was observed as
a product during the longer term photolytic runs (5 to 7 days) of perchloro-
ethylene in air plus added N02« The carbon tetrachloride and phosgene were de-
tected by gas chromatography . Dichloroacetyl chloride was tentatively identi-
fied as a product by gas chromatographic analysis of the isopropyl ester.
The formation of phosgene and trichloroacetyl chloride in the nonsensi-
tized ultraviolet photooxidation (213 nm) of perchloroethylene was studied by
Andersson et al • (1975). In this system, the initiating step is a dissocia-
tion of the perchloroethylene molecule to produce the C2C13 radical and the
chlorine radical.
hv
> C2CV + C1
The chlorine may then initiate the chain reaction given earlier for the
chlorine-sensitized oxidation process. This study found a linear relation-
ship between the rates of trichloroacetyl chloride formation, phosgene for-
mation, and absorbed light. Yields were found to be independent of the per-
chloroethylene pressure.
From the results, a chain mechanism was proposed for the formation of
phosgene which parallels the general mechanism given earlier for perchloro-
ethylene. In addition, dichloroacetylene (C2C12) was also detected by gas
chromatography as a decomposition product. It is proposed to arise from the
reaction:
6-10
-------
ci-
This C2C13 radical may also be an alternative route to the production of
phosgene.
C2C13* + 02
G2C13°2* - ^ COC12 + COC1'
COC1- + C2Cl4 - > COC12
Chain termination can occur by the formation of dichloroacetylene or by the
reaction:
C2C13°2 -- >C2C12 + °2 + Cl
Billing et al. (1976) estimated the decomposition rates of trichloro-
ethylene and perchloroethylene under simulated atmospheric conditions. For
trichloroethylene, the half-life was 3.5 hr in a system containing 5 ppm of
added NO and 2.9 hr with 16.8 ppm of added N02» With perchloroethylene, the
extrapolated half-lives were 14.2 hr with 5 ppm of added NO and 8.3 hr
for 16.8 ppm of N02» This study also measured the effect of varying
compound/NO ratios on the half-lives and the effects of varying relative
humidity on the half-life of trichloroethylene.
6.1.3 Tropospheric Half-Lives
The tropospheric half-lives of trichloroethylene, methyl chloroform, and
perchloroethylene are given in Table 6-1. Half-life values for trichloro-
ethylene range from about 2 hr to 6 weeks. Perchloroethylene values are of
about the same order of magnitude as those for trichloroethylene, ranging
from 1 day to a high of 27 weeks. The half-life values for methyl chloroform
are considerably longer than for the other two compounds. These values range
from 23 weeks to 12 years. The different half-life values for each compound
reflect different methods of determination and the different rate constants
utilized.
6-11
-------
TABLE 6-1. TROPOSPHERIC HALF-LIVES
Compound
Half-life
Method
Reference
Perchloroethylene
Trichloroethylene ~ 2 hr
< 2 days
4 days
11 days
2 weeks
6 weeks
1 day
< 4 days
10 days
12 weeks
21 weeks
21 weeks
27 weeks
Methyl chloroform 23 weeks
1.1 years
3 years
7.2 years
8 years
8 years
8 years
5-10 years
6-8 years
4.4 years
3.3 years
5.4 years
6 years
8-il years
12 years
9-12 years
Experimental race
Smog chamber
OH concentration and rate constant
Photochemical-diffusion model
OH concentration
Experimental rate
Estimate based on Gay
Unknown
OH concentration and rate constant
Laboratory rate
Atmospheric budget model
OH concentration
Photochemical-diffusion model
Laboratory rate
OH concentration
OH concentration and rate constant
Atmospheric budget model
OH concentration and rate constant
Unknown
OH concentration and rate constant
Calculated from industrial release
data
Atmospheric budget model
Photochemical-diffusion model
OH concentration
OH concentration
Estimated from experimental data
Estimated from experimental data
Calculated from atmospheric data
Calculated from data by Krasnec
Gay et al. (1976)
Singh (1976); Singh et al. (1977b)
Yung et al. (1975)
Crutzen et al. (1978)
Derwent and Eggleton (1978)
Pearson and McConnell (1975)
Rasmussen (1977)
Singh (1976)
Yung et al. (1975)
Pearson and McConnell (1975)
Singh (1977a)
Derwent and Eggleton (1978)
Crutzen et al. (1978)
Pearson and McConnell (1975)
Cox et al. (1976)
Yung et al. (1975)
Singh (I977a)
McConnell and Schiff (1977)
Rasmussen (1977)
Singh (1977b)
Lovelock (1977)
Crutzen and Fishman (1977)
Crutzen et al. (1978)
Neely and Plonka (1978)
Derwent and Eggleton (1978)
Rowland (1979)
Singh (1979)
Chang; cited by Singh (1979)
Singh (1979)
-------
6.1.4 Stratospheric Reactions
Ozone (03) is a natural minor constituent of the earth's atmosphere found
predominantly in the stratosphere between approximately 15 and 50 km with a
maximum ozone density at about 25 km. The ozone layer acts as a filter to
shield the earth's surface from ultraviolet light. Formation of ozone occurs
by photolysis of oxygen at wavelengths below 242 run.
hv
0 - >2 0.
+ 0 + m - > 0 + m m = third body, usually N or 0
Normal destruction of ozone occurs by two mechanisms: (a) photolysis at wave-
lengths between 240 and 320 nm and (b) a catalytic reaction with naturally
occurring nitric oxide, referred to as the NOX cycle.
hv
0
3
0» + 0 •
1
•a
NO + 0 > NO +
3 -, b
NO + 0 • > NO +
The NOX cycle is considered to be the most important natural control of ozone
in both the troposphere and the stratosphere. For further discussion of the
role of ozone, see Graedel and Farrow (1975).
A chain reaction mechanism resulting in ozone destruction can occur with
chlorine atoms. This mechanism is the basic concern involved in the recent
studies of chlorofluorocarbons. The basic reactions and their involvement in
the NOX cycle are:
Cl. + 0 > CIO + 0
CIO +0- > 0 + Cl'
CIO + NO > Cl- + N02
NO + 0« > NO + 0
6-13
-------
Initially the chlorine cycle was not considered to be important because no sig-
nificant source of chlorine entry into the stratosphere was known. However, in
1974, laboratory experiments combined with stratospheric measurements showed
that chlorofluorocarbons, particularly CFC13 (F-ll) and CF2C12 (F-12), may con-
stitute a major source of chlorine entry into the stratosphere. In fact, the
chlorofluorocarbons could supply enough chlorine for the chlorine cycle to re-
place the NOX cycle as the primary mechanism of ozone destruction. A detailed
discussion of the ozone depletion theory and the ramifications of that hypothe-
sis are well beyond the scope and intent of this report. For further details
of this theory, the reports by the National Academy of Sciences (1976) and by
Letkiewicz (1976) are suggested.
The long tropospheric half-life of methyl chloroform would appear to make
this compound a good candidate for transport into the stratosphere and be a
potential source of chlorine atoms by photolytic dissociation. A laboratory
study under simulated stratospheric conditions has not been attempted to prove
conclusively that methyl chloroform will photolyze to produce chlorine atoms.
However, this compound does absorb in the appropriate wavelength range (< 240
nm) to undergo such a reaction and the resultant absorption curves show the
same unstructured shape as that observed for the chlorofluorocarbons F-ll and
F-12. Hydrogen abstraction by hydroxyl radical attack shows a threshold in the
230 nm range and would be competitive with the photolytic reaction (Rowland,
1977). The photolysis and abstraction reactions are shown below:
hv
CH CC1 > CH CC1 • + Cl»
4- HO* > -CH CC1 + HO
In the overall view, it actually makes little difference whether or not methyl
chloroform is photolyzed to produce chlorine atoms. Upon entry into the
stratosphere, the chlorine in methyl chloroform will enter the HCl-Gl-ClO pool,
regardless of the form in which the chlorine first leaves the methyl chloroform
molecule. In a study by McConnell and Schiff (1977), they state that Crutzen
et al. (1977) have calculated that approximately 12% of the methyl chloroform
released will reach the stratosphere where it will be rapidly photolyzed to
yield Cl* and GlO. These two species can be involved in ozone destruction
processes.
Singh (1977b) estimated that 15% of the methyl chloroform released at
ground level will reach the stratosphere. Derwent and Eggleton (1978) esti-
mated that 9.4% survives to reach the stratosphere. Singh et al. (1977a)
stated that 2.4% of the perchloroethylene and 0.4% of the trichlbroethylene
released into the troposphere are expected to enter the stratosphere.
6-14
-------
The study by McConnell and Schiff was a computer simulation of the im-
pact of releases of methyl chloroform on stratospheric ozone as compared with
the impact of the chlorofluorocarbons, F-ll and F-12. Release rates for methyl
chloroform were based on past and projected production rates until 1982 and
several scenarios were projected for release rates beyond that date.
Calculations were accomplished using a so-called one-dimensional (1-D)
model where the transport is described by a mean, global, vertical eddy-
diffusion coefficient, K , which is assumed to be only a function of alti-
tude.
In these calculations, the chemical reaction products from the reactions
of methyl chloroform are released at all altitudes. A maximum stratospheric
production of C10X from methyl chloroform occurs several kilometers lower
than for the chlorofluorocarbons. Because of this, methyl chloroform is not
as efficient in effecting ozone destruction as the chlorofluorocarbons. How-
ever, the calculations showed that, based on projected release schedules of
methyl chloroform, a steady state ozone depletion about 20% as large as
those for chlorofluorocarbons was obtained.
Crutzen et al. (1978) have performed calculations based on a one-
dimensional photochemical-diffusive model of the atmosphere. Their results
show that methyl chloroform destruction of stratospheric ozone is approxi-
mately 25% of that due to F-ll and F-12. Estimates for 1976 are that past
chlorocarbon emissions may be responsible for a 1.5% reduction in the total
global ozone content (0.8% by F-ll and F-12; 0.5% by CG14; and 0.2% by
methyl chloroform). However, from a figure in the publication by Crutzen
et al., it can be estimated that by about the year 2010, the reduction in
total ozone content due to methyl chloroform will be approximately 7 to 87o as
compared to 0.2% as of 1976. Crutzen et al. concluded that since the use of
methyl chloroform is rapidly growing at the present time, it is important to
consider the possible future atmospheric effects. Similar views have also been
expressed by Singh (1977b).
Neely and Plonka (1978) using a tropospheric residence time of 2 to 4
years stated that if at some future time a problem arises, the troposphere
will cleanse itself of methyl chloroform much more rapidly than for the
chlorofluoromethanes.
6.1.5 Hydrolytic Degradation and Volatilization
The principal mode of environmental degradation of each of the three sub-
ject compounds is via tropospheric reactions. Degradation in the hydrosphere
is very small since transfer reactions from the hydrosphere to the atmosphere
occur rapidly compared to the hydrolytic half-life.
6-15
-------
Evaporation rates for all three compounds have been studied under labora-
tory conditions (Dilling et al., 1975; Dilling, 1977). The rates followed first
order kinetics for the first 2 to 5 half-lives; the average evaporation half-
lives were 20.3 min for methyl chloroform, 19.9 rain for trichloroethylene, and
24.2 min for perchloroethylene (Dilling, 1977).
Only two laboratory studies were found on the hydrolytic half-lives of
these chlorinated hydrocarbons (Dilling et al., 1975; Pearson and McConnell,
1975). The two studies had one significant difference in the method of calcu-
lating the hydrolytic half-life. In each study, an air space was present above
the surface of the aqueous solution. In the study by Dilling et al. (1975),
the fact that some of the chlorinated compound volatilized from the aqueous
solution to the air space was recognized but no correction factor was applied
to their calculations. Pearson and McConnell (1975) recognized that volatili-
zation would occur and, therefore, allowance was made for this by using a pre-
determined partition coefficient. Half-life calculations were extrapolated
back to zero compound volatilization.
Methyl chloroform hydrolyzes at ambient temperature (25°C) to produce
acetic acid and hydrochloric acid; the dehydrochlorination product, vinylidene
chloride (H2C=CCl2)» is normally a minor product (Dilling et al., 1975). How-
ever, Pearson and McConnell (1975) noted that at 10°C and under slightly alka-
line conditions (pH =8), the major end product was vinylidene chloride. The
hydrolytic half-life of methyl chloroform appears to be in the range of 5 to
9 months (see Table 6-2)j the estimated half-life in seawater at pH 8 and
25°C is 39 weeks (Pearson and McConnell, 1975).
Trichloroethylene and perchloroethylene are both reported to be resistant
to hydrolysis, even at temperatures of lOO^C or more. The presence of oxygen
at ISO^C will accelerate the decomposition of perchloroethylene and allow iden-
tification of the hydrolysis products, trichloroacetic acid (Cl^CCC^H) and hy-
drochloric acid (Dilling et al., 1975). In Table 6-2, a wide variation is
shown for the hydrolytic half-lives of trichloroethylene and perchloroethylene.
One possible explanation for the short times would be that a portion of the
trichloroethylene (or perchloroethylene) evaporated into the air space above
the liquid and was photodecomposed. As discussed previously, the photolysis
reaction occurs very rapidly compared to the times shown in Table 6-2.
6-16
-------
TABLE 6-2. HYDROLYTIC HALF-LIFE OF TRICHLOROETHYLENE,
METHYL CHLOROFORM, AND PERCHLOROETHYLENE
Compound
Estimated half-life^'
(months)
References
Trichloroethylene
Methyl chloroform
Perchloroethylene
7.2,^ 10.7£/
30
6.9
9
6.4,£/ 8.8£/
72
Dilling et al. (1975)
Pearson and McConnell (1975)
Dilling et al. (1975)
Referenced in Dilling et al.
(1975)
Pearson and McConnell (1975)
Dilling et al. (1975)
Pearson and McConnell (1975)
al Derived from laboratory experiments.
b_/ In sunlight.
c_/ In darkness.
d_/ Rate was same for sunlight and darkness.
From an evaluation of the evaporation and hydrolysis data, it is evident
that the hydrolysis process will play a small role in the decomposition of
any of the three compounds. Evaporation from the hydrosphere to the atmosphere
will occur much more rapidly than the hydrolysis process.
Dilling et al. (1975), in an attempt to simulate conditions more nearly
like those in the environment, studied the evaporation rates of the three
chlorinated hydrocarbons from water in the presence of 500 ppm of bentonite
clay, dolomitic limestone, Ottawa silica sand and peat moss (Table 6-3). The
addition of 500 ppm of each of these materials had relatively little effect
on the evaporation rate from water.
6-17
-------
TABLE 6-3. EVAPORATION OF CHLORINATED HYDROCARBONS FROM
WATER CONTAINING VARIOUS SOIL TYPES
Condition—'
Ottawa silica sand
Dolomitic limestone
Peat moss
Wet bentonite clay
Time (rain)
CHC1=CC12
27
20
20
20
for 50% disappearance
CH3CC13
27
20
20
20
CC12=CC12
27
20
21
20
£/ 500 ppm
6.1.6 Reactions in Soil and Sediment
6.1.6.1 Soil--
Movement of these selected chlorinated hydrocarbons from the point of
disposal through various soils by leaching, volatilization, uptake or absorp-
tion have not been studied. Trichloroethylene is apparently capable of moving
from disposal sites, such as lagoons or landfills, through the soil to under-
ground aquifers. This conclusion will be discussed further in Section 7.
Monitoring data indicate that these chlorinated compounds are taken up
in the soil. Trichloroethylene and methyl chloroform have been detected in
soils in the low parts-per-billion range (Battelle, 1977). Perchloroethylene
concentrations were not determined.
6.1.6.2 Sediment--
Experimental data are unavailable on the movement of the three chlorine
compounds through sediments, and few reports are available on their uptake by
sediments. A study by Battelle (1977) indicates that trichloroethylene and
methyl chloroform are present in some sediments in the low parts-per-billion
range. Perchloroethylene concentrations were not studied. As mentioned pre-
viously, the presence of various sedimentary materials in water did not ap-
preciably increase or decrease the volatility of the three compounds (see
Table 6-3). The persistence of trichloroethylene, methyl chloroform or per-
chloroethylene in sediments has not been determined.
6.1.6.3 Biological Degradation--
Biological degradation of these three chlorinated hydrocarbons by micro-
organisms is considered to be negligible. McConnell et al. (1975) stated that
microorganisms (either aerobic or anaerobic) apparently do not have the ability
to degrade these compounds.
6-18
-------
6.1.7 Sewage Treatment
Limited data were found on the effect of trichloroethylene on an acti-
vated sludge system. Su and Garin (1972) found that excessively high concen-
trations of trichloroethylene have a potential for disrupting activated sludge
systems; concentrations above 500 ppm of trichloroethylene had a significant
potential for completely repressing bacterial activity and partially inhibiting
the synthesis of enzymes. They concluded that, at concentrations up to 300
ppm, very little, if any, effect would occur.
The literature on the toxic effects of these compounds on anaerobic di-
gestion processes is limited, as was the case with activated sludge systems.
The most toxic of the three compounds to anaerobic digestion is methyl chloro-
form. Trichloroethylene and perchloroethylene are similar in toxicity. These
compounds are all toxic to the methane-producing bacteria in the anaerobic
process which are responsible for degrading short chain aliphatic compounds
into methane and carbon dioxide. These "methane" bacteria are very sensitive
to many chemicals. If the biological system is disturbed and the methane bac-
teria are destroyed, then the digestion fails and offensive sludge results.
The addition of trichloroethylene to anaerobic systems can inhibit di-
gestion (Swanwick and Foulkes, 1971; Barrett, 1972). Camisa reported that the
minimum concentration causing inhibition ranged from 200 to 1,200 rag/kg dry
solids (Camisa, 1975). In a study of the partitioning characteristics of
trichloroethylene-bearing wastes, considerable adsorption of trichloroethylene
onto sludge solids was demonstrated. The maximum quantity of trichloroethylene
that was adsorbed onto sludge solid was 3,030 mg trichloroethylene per kilo-
gram solids (Camisa, 1975), a sufficient concentration to cause difficulties
in the anaerobic digestion system.
Barrett (1972) discovered in laboratory experiments that when a shock dose
of 60 ppm of trichloroethylene was added to the digestor, the gas production
was inhibited up to 50% (depending on the feed time) for a 20-day detention
period.
Swanwick and Foulkes (1971) reported some inhibition of sludge digestion
in the presence of trichloroethylene and perchloroethylene at concentrations
of 60 ppm. At a mass concentration of 1,775 mg of trichloroethylene or per-
chloroethylene per kilogram of dry sludge solids in the digestor, gas produc-
tion was inhibited 26 and 6%, respectively. Methyl chloroform was more toxic
to the methane bacteria in the second stage of anaerobic digestion. Gas pro-
duction was inhibited by 80% at a mass concentration of 60 mg/kg of dry sludge
solids.
6-19
-------
Jackson et al« (1970) reported the toxicity of these organic compounds
to the anaerobic digestion of sewage sludge. All three compounds were found
to be toxic to the methane bacteria in the second stage of anaerobic diges-
tion. The concentrations which are toxic to methane bacteria in sludge are:
> 20 ppm for trichloroethylene and perchloroethylene and 1 ppm for methyl
chloroform. Concentrations above these levels may prevent production of well-
digested, inoffensive sludge.
Methyl chloroform has been shown to have slightly more than an additive
effect with chloroform (Swanwick and Foulkes, 1971). The addition of these
compounds together, in a laboratory study, resulted in a reduction of gas
production. The gas production was reduced to 86.2% by a chloroform concen-
tration of 14.6 mg/kg. After 32.2 rag/kg of methyl chloroform was added alone
to sewage sludge, a reduction to 607., was observed. When these same concentra-
tions were added together a reduction to 41.7% occurred.
6.1.8 Greenhouse Effect
There is some concern that halocarbons may add to the global "greenhouse
effect," i.e., that certain atmospheric constituents can absorb infrared radi-
ation emitted from the earth's surface and prevent it from radiating into
space, thereby warming the atmosphere. Ramanathan (1976) has suggested that
because halocarbons absorb infrared radiation in the wavelength region of 8
to 13 /xm, halocarbons can contribute to this effect.
Wang (1976) also believes that anthropogenic materials, having infrared
absorption bands in the 7 to 14 pm region, would absorb the infrared radiation
transmitted to the earth's surface or lower atmosphere and have climatic sig-
nificance. These chlorinated solvents have infrared absorption in the range
of 7 to 14 /im: trichloroethylene, 10.8 /nm; perchloroethylene, 11.1/im; and
methyl chloroform, 13.9 /^m. Thus, all three chlorinated hydrocarbons may con-
tribute to the greenhouse effects. However, the minimum level or concentration
for these halocarbons needed to produce a significant greenhouse effect has
not been determined.
6.2 ENVIRONMENTAL EFFECTS
In this subsection, the areas to be discussed include effects on fish,
other aquatic plants and animals, birds, mammals, and other terrestrial orga-
nisms, plants and protista.
6.2.1 Effects on Fish
6.2.1.1 Toxicity—
Limited data are available on the toxicity of these selected hydrocarbons
on fish (Table 6-4). All the investigations were concerned with acute and
6-20
-------
TABLE 6-4. TOXICITY OF TRICHLOHDETHYLENE, METHYL CHLOBDPORM, AND PERCHLORDETHYLENE
TO FRESH AND SALTWATER FISH
I
NJ
Compound
Trichloroethylene
Organism
nab
(Limanda
limanda)
Fathead minnow
(Pimephales promelas)
Methyl chloroform
Plnpearch
(Lagodon
Fish
(species
Bluegill
(Lepomis
Dab
rhomebodlus)
not stated)
macrochirus)
Fathead minnow
Perch loroe thy lene
Dab
Fathead minnow
Test
condition
Flow through
Static
Static
Temperature
(°C) Toxic
LC
12 LC
LC
50
50
50
effect
(96
(96
(24
Stupified
10 min
Static
Flow through
Static
Flow through
Static
LC
LC
12 LC
LC
12 LC
50
50
50
50
sn
(96
(96
(96
(96
(96
hr)
hr)
hr)
in
hr)
hr)
hr)
hr)
hr)
Concentration
(ma/JO
16
66.8
75-100
55
44.7
33
105
5
21.4
Reference
McConnel 1
Alexander
et al
et al
. (1975)
. (1978)
Garrett (1957)
McKee and
EFA (1978)
McConnel 1
Alexander
McConnell
Alexander
Wolf
et al
et al
et al
et al
(1963)
. (1975)
. (1978)
. (1975)
. (1978)
-------
subacute toxicity and reported as median lethal concentrations (LC5())» Fish
appear to be sensitive to low concentrations (ppm) of these chlorinated hydro-
carbons*
Aquatic toxicity studies were conducted on adult fathead minnows,
Pimephales promelas* by Alexander et al. (1978) using both static and flow-
through techniques. Perchloroethylene, trichloroethylene, and trichloroethane
were among those tested for 96 hr LDso and LCcg values.
The static bioassay test for aquatic organisms utilizes one initial ex-
posure to an appropriate concentration of a chemical or effluent to determine
toxicity. The flow-through bioassay tests differ from the static tests in that
a fresh solution containing the test chemical is continuously or intermittently
supplied to the aquaria throughout the test period. A problem with the static
tests is that the test concentrations may change rapidly due to volatilization
or degradation of certain test compounds.
Dechlorinated Lake Huron water (pH =7.8 to 8.0) was used and maintained
at a constant temperature of 12°C. Dissolved oxygen concentrations were moni-
tored daily and kept above 5.0 ppm. Carrier solvents (methanol or ethanol)
were used for all three compounds. Concentrations of the methyl or ethyl al-
cohol were always below 0.3 and 0.5 ppm, respectively, for all test solutions.
Levels of the chlorinated compounds in water were analyzed by gas chromatog-
raphy.
A comparison of the static tests with the flow-through tests shows that
the flow-through toxicities were less than the static values (Table 6-5).
Methyl chloroform was the most toxic followed in decreasing order by tri-
chloroethylene and perchloroethylene in both test systems. Toxicity was re-
corded as LC5Q values, with a confidence level of 95%.
TABLE 6-5. COMPARISON OF ACUTE FLOW-THROUGH AND STATIC FISH
TOXICITY LC5Q VALUES
Compound
Methyl chloroform
Hour
96
ppm
Flow-throughi'
52.8
StaticJi/
105
(43.7-77.7)£/ (91-126)
Trichloroethylene 96 40.7 66.8
(31.4-71.3) (59.6-74.7)
Perchloroethylene 96 18.4 21.4
(14.8-21.3) (16.5-26.4)
a/ Calculated using the measured concentration in the water.
b/ Calculated using the nominal water concentration (amount added at start
of the test).
c/ 95% confidence limits.
Source: Alexander et al. (1978).
6-22
-------
Table 6-6 shows a comparison between the effective concentration values
(concentrations which produce loss of equilibrium) and lethal concentration
values for the three subject compounds in flow-through tests. The effects ob-
served were: loss of equilibrium, melanization, narcosis, and swollen,
hemorrhaging gills. Concentrations producing one or more of these effects in
50% of the fish (£059) ranged from 11.1 ppm for methyl chloroform to 23.0 ppm
for trichloroethylene (Alexander et al., 1978),
The acute toxicity for the three halocarbons were found for dabs (a salt
water flat fish) in experimental work by Pearson and McConnell (1975). The 96-
hr LC50's were determined by a method similar to that of Doudoroff et al.
(1951). An all-glass flow-through apparatus was used to house the fish. Since
it was impractical to aerate the water because of the high volatility of the
tests compound, only the oxygen present in the influent seawater was available.
At the inlet of the test tank a metering device supplied the proper amount of
chlorinated hydrocarbon. The LC^Q'S for perchloroethylene, trichloroethylene,
and methyl chloroform were 15, 16, and 33 ppm, respectively.
Static toxicity tests were conducted on pinpearch (Lagodon rhomebodius)
using methyl chloroform. The compound was added to an aquarium containing 30
liters of fresh salt water, and air was constantly admitted through stone
breaker tips. The results showed that the 24-hr LC5Q level for pinpearch was
between 75 to 100 ppm for methyl chloroform.
McKee and Wolf (1963) stated that fish were stupified within 10 min after
adding 55 ppm of trichloroethylene to the water.
6.2.1.2 Uptake and Accumulation--
Data are limited on the uptake and accumulation* of trichloroethylene,
methyl chloroform, and perchloroethylene by fish. Only one field study was
found which quantified the concentrations of these compounds in the flesh and
liver of fish (Table 6-7). This study, which was conducted in England, indi-
cated that fish do take up and accumulate these solvents from an aqueous envi-
ronment. Analysis of the water showed an average concentration of 0.5 ppb for
these chlorinated solvents, whereas concentrations in fish were up to 100 times
the concentrations found in water. However, no evidence was presented to indi-
cate accumulation through food chains.
Accumulation is the increase in the levels of a material in the tissues of
the test organism. Bioaccumulation is the increase in concentration of a
material up a food chain.
6-23
-------
TABLE 6-6. CHLORINATED SOLVENTS FLO¥-THBDUGH FISH TOXLCITY STUDIES
I
N>
•P-
Compound
Metliyl chloroform
Trichloroethylene
Perch loroethylene
Effective
Hr EC10
24 10.5 .
(8.0-11. S)5'
48 10.0
(7.8-10.9)
72 9.0
(6.7-10.0)
96 9.0
(6.7-10.0)
24 15.2
(10.0-18.3)
48 16.9
(11.6-19.6)
72 15.5
(10.0-18.2)
96 13.7
(8.5-16.6)
24
48
72
96
mg/f
concentration (EC) valued'
EC50
12.1
(10.9-U.5)
11.5
(10.4-12.8)
11.1
(10.0-12.6)
11. 1
(10.0-12.6)
23.0
(19.8-27.4)
22.7
(19.7-27.3)
22.2
(18.9-27.3)
21.9
(18.4-28.5)
Plotted TE^,-
14.4
14.4
14.4
14.4
ECoo
14.1
(12.9-18.3)
13.2
(12.1-17.3)
13.8
(12.3-13.8)
13.8
(-)
36.2
(30.3-51.2)
30.6
(26.0-49.2)
31.8
(26.2-55.0)
34.9
(27.3-70.9)
Lethal concentration (LC) value
LC10
34.1
(20.8-41.2)
30.8
(18.8-37.6)
34.7
(24.4-41.4)
27.7
(17.3-35.0)
20.9
(11.9-26.1)
17.4
(9.0-22.9)
15.1
(9.1-18.5)
13.9
(7.8-16.7)
13.2
(7.5-16.0)
13.2
(7.5-16.0)
LC50
55.4
(46.2-82.7)
52.8
(43.7-77.7)
52.4
(44.3-65.7)
53.3
(43.1-75.5)
39.0
(31.8-57.5)
40.7
(31.4-71.8)
23.5
(19.5-28.2)
19.6
(15.9-22.8)
18.9
(15.3-22.1)
18.4
(14.8-21.3)
LCoo
89.9
(67.0-254.7)
90.8
(66.4-245.9)
79.1
(63.7-131.6)
102.6
(73.3-238.0)
72.6
(51.7-109.2)
95.0
(59.0-419.9)
36.6
(30.0-59.1)
27.6
(23.6-42.7)
27.1
(23.1-41.2)
25.6
(22.0-38.0)
Slope
6.09
(2.47-9.70)
5.45
(2.41-8.48)
7.16
(3.79-10.54)
4.51
(2.39-6.63)
4.73
(2.15-7.31)
3.47
(1.60-5.35)
6.65
(3.35-9.94)
8.56
(3.67-13.44)
8.18
(3.69-12.67)
8.90
(3.88-13.91)
a/ The effective concentration Is the concentration producing an adverse effect. In this case, the effect noted was loss of
equilibrium.
bf The 957. confidence limits are shown In parentheses.
£/ TE,,, - median tolerance effect 13 obtained by a logarithmic plot of the data. Insufficient data were available to obtain a com-
puter plot by Flnney's problt analysis.
Source: Alexander et al. (1978).
-------
TABLE 6-7. ACCUMULATION OF CHLORINATED HYDROCARBONS IN FISH
to
Ul
Species
Raja clavata (ray)
Pleuronectes platessa
(placlce)
Platycthys flesus
(flounder)
Limanda limanda
(dab)
Scomber scombrus
(mackerel)
Limanda limanda
Pleuronectes platessa
Solca solea (sole)
Aspltrigla cuculus
(red gurnard)
Trachurus trachurus
(scad)
Trisopterus luscus
(pout)
Squalus acanthias
(spurdog)
Scomber scombrua
(mackerel)
Clupea sprattus
Gadus morrhua
(cod)
Organ
Flesh
Liver
Flesh
Liver
Flesh
Liver
Flesh
Liver
Flesh
Liver
Flesh
Flesh
Flesh
Flesh
Guts
Flesh
Guts
Flesh
Flesh
Flesh
Flesh
Flesh
Flesh
Air bladder
Source^'
Liverpool Bay
Liverpool Bay
Liverpool Bay
Liverpool Bay
Liverpool Bay
Liverpool Bay
Liverpool Bay
Liverpool Bay
Liverpool Bay
Liverpool Bay
Redcar, Yorks
Thames Estuary
Thames Estuary
Thames Estuary
Thames Estuary
Thames Estuary
Thames Estuary
Thames Estuary
Thames Estuary
Thames Estuary
Torbay, Devon
Torbay, Devon
Torbay, Devon
Torbay, Devon
CC12CHC1
0.8-5
5-56
0.8-8
16-20
3
2
3-5
12-21
5
8
4.6
2
3
2
11
11
6
2
2
3
2.1
3.4
0.8
< 0.1
CC1,CC12
0.3-8^
14-41
4-8
11-28
2
1
1.5-11
15-30
1
ND0-/
5.1
3
3
4
1
1
2
4
2
1
ND
1.6
< 0.1
3.6
CH3CCl3 +
2-13
1.5-18
CH,CC1 _ '
4J
3
5
3
4
3
2
26
4
10
1
2
ND
-> 2-47
>/
1.3-8
2-14
9.9
2.4"
5.6
3.3
HA
CC14
CCl,
1}
2b/
0.3
2
ND
0.3
0.9
6
1
0.6
0.3
2
0.3
1
ill The average concentrations found in water were 0.5 ppb,
n
b/ Parts per 10 by mass on wet tissue.
c/ Not detectable.
Source! Pearson and McConnell (1975).
-------
Similar accumulation of residues have been shown to occur under labora-
tory conditions. Neely et al. (1974) found an accumulation factor* of 40 in
rainbow trout for perchloroethylene. This number was based on the ratio of the
concentration of the chemical in trout muscle to the exposure water. The rate
constants for uptake and clearance were found to be 3.323 + 0.45 hr~^ and
0.0823 + 0,030 hr~l, respectively. When the fish were placed in fresh water,
the compound was rapidly dissipated (Farber, 1977).
Pearson and McConnell (1975) detected concentrations of perchloroethylene
in the flesh and liver of dabs after exposure and observed a concentration
factor of 10 times for the flesh and 100 times for the liver. They also noted
that, when the test organisms were returned to clean water, the concentrations
of perchloroethylene within their tissues decreased, indicating it is not per-
sistent in the tissues. No further details were given concerning the recovery
of the test organisms.
6.2.2 Effects on Other Aquatic Plants and Animals
6.2.2.1 Effects on Aquatic Plants—
6.2.2.1.1 Toxic effects—Pearson and McConnell (1975) determined the
toxicity (EC5())» °f trichloroethylene, methyl chloroform, and perchloroethylene
to the unicellular algae, Phaeqdactylum tricornutum. The toxicity was deter-
mined by measuring the changes in the uptake of carbon, from atmospheric car-
bon dioxide, during photosynthesis. Use of carbon-14 labeled carbon dioxide
was used to measure the uptake of carbon dioxide.
All three compounds showed £059"s to the algae in the low parts-per-
million range. Methyl chloroform was the most toxic followed by trichloro-
ethylene and perchloroethylene. The £050*8 were 5, 8, and 10.5 ppm, respec-
tively.
6.2.2.1.2 Uptake and accumulation--0nly one report was located which
was concerned with the uptake and accumulation of the subject compounds in an
aquatic plant (marine algae). This study by Pearson and McConnell (1975) in-
dicated that algae are capable of taking up and accumulating trichloroethylene,
methyl chloroform, and perchloroethylene at concentrations in the low parts-
per-million range (Table 6-8). Algae had an accumulation factor of less than
100.
Accumulation factor is the ratio of the concentration of the material in
the tissue to the concentration of the test medium.
6-26
-------
TABLE 6-8. CHLORINATED HYDROCARBON CONCENTRATIONS FOUND
IN MARINE ALGAE
Species
Enteromorpha compressa
Ulva lactuca
Fucus vesiculosus
Fucus serratus
Fucus spiralis
a/
Source2'
Mersey Estuary
Mersey Estuary
Mersey Estuary
Mersey Estuary
Mersey Estuary
TCE-^7
19-20£7
23
17-18
22
16
PCB^7
14-14.5
22
13-20
15
13
MG= and CCl*
24-27
12
9.4-10.5
35
17
£/ The average concentration found in the water for these chlorinated com-
pounds was 0.5 ppb.
t>/ TCE = trichloroethylene; PCE = perchloroethylene; MC = methyl chloro-
form.
£/ Concentrations expressed as parts per 10' by mass on wet tissue.
Source: Pearson and McConnell (1975).
6.2.2.2 Effects on Other Aquatic Organisms--
6.2.2.2.1 Toxic effects--Again, limited data were available on toxicity.
One laboratory study was conducted on the median lethal concentration of these
compounds to barnacle larvae and one concerned with the concentrations of tri-
chloroethylene resulting in death of daphnia.
Tests were conducted on the toxicity of some halogenated hydrocarbons to
the barnacle larvae, Elminius modestus. The 48-hr LCcQ was determined by en-
closing 20 nauplii (first larval stage) in a glass-stoppered bottle contain-
ing a known concentration of the chlorinated hydrocarbon in clean seawater.
After 48 hr, the larvae were examined and the mortality was determined. Inves-
tigators found that perchloroethylene was the most toxic followed by methyl
chloroform and trichloroethylene. The LC5Q for perchloroethylene was 3.5 ppm,
for methyl chloroform 7.5 ppm, and for trichloroethylene 20 ppm (Pearson and
McConnell, 1975).
McKee and Wolf (1963) stated that trichloroethylene at 660 ppm had a
toxic effect on daphnia (all died within 40 hr). However, a concentration of
99 ppm had no toxic effect.
Using 24-hr-old animals from a clone of Daphnia magna, Bringmann and Kvihn
(1977) found the 24-hr LC5Q for trichloroethylene and methyl chloroform to be
>1,000 and > 1,300 ppm, respectively.
6-27
-------
In other acute tests on the same species, the 48-hr LCcQ (static bioassay)
was determined to be 85 ppm for trichloroethylene (EPA, 1978). A wide variation
in results exists between the Bringmann and EPA studies which may be due to
the differences in test time.
In a chronic study on Daphnia magna, a life cycle value of > 10 ppm was
determined for trichloroethylene (EPA, 1978). No effects were observed in the
test organisms in this study.
6»2.2.2.2 Accumulation--Literature searches located only one study which
was concerned with the accumulation of these compounds in aquatic invertebrates
(Pearson and McConnell, 1975). These marine invertebrates are capable of accumu-
lating trichloroethylene, methyl chloroform, and perchloroethylene in the low
parts-per-million range with accumulation factors of less than 100 (see Table
6-9).
6.2.3 Effects on Birds
No toxicity studies were found concerning birds. Based on limited field
tests these selected halogenated hydrocarbons have the ability to be taken up
and accumulated in the eggs and bodies of fresh and salt water birds in the
low parts-per-billion range (Table 6-10).
6.2.4 Effects on Mammals
Limited toxicity data on mammals other than man or laboratory animals were
found in the literature. From the limited data, it appears that these mammals
(aquatic) are able to take up and accumulate the three subject compounds in
the low parts-per-billion range (Table 6-11).
6.2.5 Effects on Other Terrestrial Organisms, Plants and Protista
6.2.5.1 Other Terrestrial Organisms--
The only information found on the toxic effects of trichloroethylene, per-
chloroethylene, or methyl chloroform on terrestrial organisms other than labora-
tory animals, was a study by Kocher (1954) on adult houseflies. Trichloroethylene
and perchloroethylene were applied topically to adult houseflies; the latter
produced tremors with subsequent recovery, while the former was found to be
comparatively nontoxic. No concentrations were given.
6.2.5.2 Terrestrial Plants-
Few data are available pertaining to the toxicity of the three subject
compounds to plants, and no data are available on their uptake by plants.
6-28
-------
TABLE 6-9. CHLORINATED HYDROCARBONS IN MARINE ORGANISMS
to
Species
Plankton
Plankton
Nereis diversicolor (ragworm)
Mytilus edulis (mussel)
Cerastoderma edule (cockle)
Ostrea edulis (oyster)
Buccinum undatum (whelk)
Crepidula fornicata
(slipper limpet)
Cancer pagurus (crab)
Carcinus maenas (shore crab)
Eupagurus bernhardus
(hermit crab)
Crangon crangon (shrimp)
Asterias rubens (starfish)
Solaster sp. (sunstar)
Echinus esculentus (sea urchin)
Source^'
Liverpool Bay
Torbay
Mersey Estuary
Liverpool Bay
Firth of Forth
Thames Estuary
Liverpool Bay
Thames Estuary
Thames Estuary
Thames Estuary
Tees Bay
Liverpool Bay
Firth of Forth
Firth of Forth
Firth of Forth
Thames Estuary
Firth of Forth
Thames Estuary
Thames Estuary
Thames Estuary
CC12CHC1
0.05-0. A
0.9
ND£/
4-11.9
9
8
6-11
2
ND
9
2.0
10-12
15
12
15
5
16
5
2
1
CC12CC12
1
0.05-0.5-/
2.3
2.9
1.3-6.4
9
1
2-3
0.5
1
2
2.3
8-9
7
6
15
2
3
1
2
1
CH3CC13 +
0. 03-10. 7-/
2
0
2.4-
10
5
0-2
0.9
6
4
8.
5-34
1
14
0.7
2
2
5
3
3
CC14
0.04-0.9-/
.2
.6
5.4
2
0.7
0.4-1
0.1
0.9
0.3
4
3-5
2
3
1
0.2
6
0.8
0.2
0.1
a^l Average concentrations of the chlorinated compounds found in these waters were 0.5 ppbi
bf Concentrations expressed as parts per 10 by mass on wet tissue.
£/ ND = Not detectable.
Source: Pearson and McConnell (1975).
-------
TABLE 6-10. CHLORINATED HYDROCARBON LEVELS IN FRESH
AND SALTWATER BIRDS
Species
Sula bassana
(gannet)
Phalacrocerax
aristotelis (shag)
Alcq torda (razorbill)
Uria aalge (guillemot)
Rissa tridactyla
(kittiwake)
Cygnus olor (swan)
Galllnula chloropus
(moorhen)
Anas platyrhyncos
(mallard)
Site of
uptake
Liver
Eggs
Eggs
Eggs
Eggs
Eggs
Liver
Kidney
Liver
Muse le
Eggs
Eggs
Source
Irish Sea-7
Irish Sea
Irish Sea
Irish Sea
Irish Sea
North Sea
Frodsham March
(Merseyside)
(Merseyside)
(Merseyside)
(Merseyside)
(Merseyside)
TCE^7
4.5-6.S/
9-17
2.4
28-29
• 23-26
33
2.1
14
6
2.5
6.2-7.8
9.8-16
PC^7
1.5-3.2
4.5-26
1.4
32-39
19-29
25
1.9
6.4
3.1
0.7
1.3-2.5
1.9-4.5
a/
1.2-1.9
17-20
4.2
39.4-41
35-43
40
4.7
2.4
1.6
1.1
14.5-21.8
4.2-24
a/ TCE = trichloroethylene; PCE = perchloroethylene; MC = methyl chloroform.
_b/ Average concentrations of the compounds in these waters were 0.5 ppb.
cl Concentrations are expressed as parts per 10^ by mass of wet tissue.
Source: Pearson and McConnell (1975).
TABLE 6-11. CONCENTRATIONS OF CHLORINATED HYDROCARBONS IN MAMMALS
Species
Halichoerus grypus
(grey seal)
Site of
concentration
Blubber
Liver
Source
Farno Island
Farno Island
TCE^7" PCE-7
2. 5-7. 2^ 0.6-19
3-6.2 0-3.2
MC-ttCl^
16-30
0.3-4.6
Sorex araneus
(common shrew)
Frodsham Marsh 2.6-7.8
2.3-7
al TCE = trichloroethylene; PCE = perchloroethylene; MC = methyl chloroform.
b/ Concentrations expressed as parts per 109 mass of wet tissue.
Source: Pearson and McConnell (1975).
6-30
-------
Phytotoxicity studies were conducted by Cast and Early (1956). Methyl
chloroform and trichloroethylene were applied separately to the foliage of
seeding plants at two different concentrations, 0.5 and 570. The test solutions
were applied in the form of water emulsions or solutions. A qualitative evalu-
ation was made of the resultant damage to each plant (see Table 6-12). Tri-
chloroethylene was found to be more phytotoxic than methyl chloroform.
TABLE 6-12. PHYTOTOXICITY OF METHYL CHLOROFORM AND TRICHLOROETHYLENE
Compound
Concentration Test plant
(%) Bean Corn Cotton Cucumber Tomato
Methyl chloroform
Trichloroethylene
5.0
0.5
5.0
0.5
2
0
3.5
0
2.5
0
2.5
0
0.6
0
1.5
1
1
0
1
0
1
0
2
1
Key: 0 = no injury, 1 = slight injury, 2 = moderate injury, 3 = heavy in-
jury, 4 = severe injury or dead plant.
Source: Cast and Early (1956).
Recently, trichloroethylene has been shown to cause mutations in plants
(Sparrow, 1976). Somatic mutation response was observed in a Tra.descan.tia
test system (Clone 4430) following a 6-hr exposure to trichloroethylene.
Exposure levels were made as high as 30 ppm. The maximum response was observed
at 0.5 ppm. Approximately 44,000 stamen hairs were examined indicating a muta-
tion frequency (minus control) of 0.112 + 0.036 per 100 hairs. This response
was significantly above background at the 17o statistical level (p = 0.01).
From an extensive review of the literature, only one study was found per-
taining to phytotoxicity of perchloroethylene. Horsfall and Rick (1955) re-
ported that perchloroethylene, among other compounds, reduced sporulation of
the fungi, Monilinia fructicola. The authors did not report the exact concen-
trations which reduced sporulation. He dispersed two separate concentrations
(100 and 400 ppm) of each compound into melted agar. Each of the chemicals
tested, including perchloroethylene, reduced sporulation at one or the other
of these concentrations.
6.2.6 Effects on Protista
Little data were found on the toxicity of the selected chlorinated hydro-
carbons on protista. Bacteria was the only group of the protista in which in-
formation was available.
6-31
-------
The deleterious effect of 170 selected water pollutants, including tri-
chloroethylene, on bacteria (Pseudomonas putida) and blue green algae
(Microcystis aeruginosa) was investigated. Threshold lethal concentrations for
Microcystis and for Pseudomonas were determined in water at pH = 7. Threshold
lethal concentration was defined as the concentration at which the initial in-
hibiting effect of the toxic chemicals on cell multiplication was observed.
The threshold lethal concentration of trichloroethylene for Microcystis and
Pseudomonas was 63 and 65 ppm, respectively. Certain of the other compounds
tested were highly selective against either the Pseudomonas or the Microcystis;
however, trichloroethylene did not exhibit selectivity and was highly effective
against both species (Bringmann and Kuhn, 1976),
Escherichia coli were exposed to various concentrations of anesthetics
(trichloroethylene, halothane, chloroform, methoxyflurane, and diethyl ether)
by Horton et al. (1970), A single strain of E_. coli bacteria was grown on the
surface of blood agar and exposed to anesthetic vapors for a period of 2 hr«
The experiments were carried out in an atmosphere of air or oxygen at high
relative humidity, A reduction in the viability of the bacteria was seen at
normal anesthetic concentrations. In the case of trichloroethylene, a 1.9%
vapor concentration resulted in a 55% mean surviving rate for IS. coli (p = 0.02)
as compared to controls. The highest concentration tested for trichloroethylene
(3.9%) caused a mortality rate of 100% (p < 0.01).
Luminescent bacteria, Photobacterium phosphoreum (NCMB 844) and Ph.
fischeri (NCMB 1281), were exposed to anesthetic vapors of halothane, me-
thoxyflurane, trichloroethylene, chloroform, and one agent not used in clini-
cal anesthesia, Freon 22. The EDcn values were recorded. Thirteen to sixteen
experiments were conducted for each anesthetic using a different culture each
time. Trichloroethylene had an ED^g value of 0.6% vapor concentration (White
and Dundas, 1970).
6.2.7 Bioaccumulation
Limited information suggests that plants and animals are able to accumu-
late all three of these compounds. Field studies indicate that the concentra-
tions found in plant and animal species are in the high parts-per-billion to
low parts-per-million range. There appears to be little bioaccumulation up the
food chain.
Only one investigation, that of Pearson and McConnell (1975), studied the
concentrations of these compounds in aquatic organisms and plants to determine
if a pattern of bioaccumulation exists. From these studies, estimates of bio-
accumulation in nature were made. The maximum overall increase in concentration,
between seawater and the tissues of animals at the top of food chains (such
as fish liver, sea bird eggs, and sea seal blubber) is less than 100-fold for
the solvents trichloroethylene and perchloroethylene. Since concentrations of
6-32
-------
methyl chloroform and CCl4 were often included together in the data of Pearson
and McConnell (see, for example, Tables 6-9 and 6-10), estimates on bioac-
cumulation for methyl chloroform are not possible. Pearson and McConnell con-
cluded that an overall pattern of extensive bioaccumulation up the marine food
chain does not occur.
6-33
-------
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6-38
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CONTENTS
7. Monitoring Data and Exposure Levels 7-3
7.1 Atmospheric Levels 7-3
7.1.1 Manufacturing sites 7-3
7.1.2 User sites 7-3
7.1.3 Other U.S. sites 7-10
7.1.4 Non-U.S. sites 7-14
7.1.5 Stratospheric levels 7-17
7.2 Water Levels 7-18
7.2.1 Drinking water 7-18
7.2.1.1 Manufacturing sites 7-19
7.2.1.2 User sites 7-19
7.2.1.3 Other U.S. sites 7-19
7.2.2 Nondrinking water 7-21
7.2.2.1 Manufacturing sites 7-21
7.2.2.2 User sites 7-23
7.2.2.3 Other U.S. sites 7-23
7.2.2.4 Marine environment 7-26
7.2.3 Wastewater 7-27
7.2.4 Case histories 7-29
7.3 Soil and Sediment 7-33
7.3.1 Soil 7-34
7.3.2 Sediment 7-34
7.4 Food 7-35
7.5 Exposure Levels 7-35
7-1
-------
CONTENTS (continued)
7.5.1 Human exposure 7-35
7.5.1.1 Exposure from air 7-38
7.5.1.2 Exposure from water 7-41
7.5.2 Total human exposure 7-43
7.5.2.1 Trichloroethylene 7.45
7.5.2.2 Methyl chloroform 7.45
7.5.2.3 Perchloroethylene 7-46
7.5.2.4 Other assessments of perchloro-
ethylene 7_46
7.5.3 Aquatic species 7-46
7.5.3.1 Trichloroethylene ... 7-47
7.5.3.2 Methyl chloroform .. 7-47
7.5.3.3 Perchloroethylene 7-43
7.5.4 Plants 7-49
References 7-50
7-2
-------
SECTION 7
MONITORING DATA AND EXPOSURE LEVELS
In this section, data will be presented for the concentration levels of
trichloroethylene (TGE), methyl chloroform (MC), and perchloroethylene (PCE)
which have been reported for the various compartments of the environment. This
information has been compiled from reports in scientific journals, government
reports, progress reports on existing governmental contracts, and unpublished
data* Within this section, data will be reported for ambient air concentrations,
upper atmospheric levels, concentrations in drinking and nondrinking water,
and soil and sediment levels* The levels of each of the three subject compounds
in various foods will also be presented*
Wherever monitoring information permits, data will be derived for the ex-
tent of human exposure to each of these compounds. The effects of current en-
vironmental levels of these compounds on nonlaboratory fish and mammals will
also be presented*
In many environmental areas, there exists a definite lack of data with
respect to current concentration levels* This paucity of data results because
concern over the environmental levels of these compounds has been a very recent
development* Therefore, data in several areas are nonexistent at this point*
7.1 ATMOSPHERIC LEVELS
In this section, monitoring data will be presented for manufacturing fa-
cilities, user sites, other sites within the United States, and non-U.S. sites
(including average world figures).
7.1.1 Manufacturing Sites
Only one study (Battelle, 1977) has been published concerning ambient air
concentrations at the specific manufacturing sites of trichloroethylene and
methyl chloroform. The preliminary results of this study are summarized in
Table 7-1. For methyl chloroform and perchloroethylene, the detection limit
was 0.3 ppb, while for trichloroethylene, the limit was 1 ppb.
7-3
-------
TABLE 7-1. AMBIENT AIR MEASUREMENTS AT MANUFACTURING SITES
Concentration (ppb)
Site and products
PPG Industries, Inc.
Lake Charles , LA
(MC production)
Ethyl Corporation
Baton Rouge, LA
(MC production)
Dow Chemical Company
Freeport, TX
(MC production)
Dow Chemical Company
Freeport, TX
(TCE production)
Hooker Chemical Company
Hahnville, LA
(PCE and TCE production)
Vulcan Materials Company
Geismar, LA
(MC production)
High
Low
a/
Average-
High
Low
Average
High
Low
Average
High
Low
Average
High
Low
Average
High
Low
Average
MC
8.5
< 0.3
— r /
1.3 (47 )-'
3.9
< 0.3
0.6 (48)
11.5
< 0.3
1.7 (85)
4.6
< 0.3
0.5 (51)
/all \
I values]
y< 0.3/ (55)
155
< 0.3
15.0 (66)
TCE
15.0
< 1.0
~~~
2.4 (47)
7.2
< 1.0
1.4 (49)
/all\
[values I
\< 1 /(86)
11.5
1
1.8 (50)
270
< 1
13.9 (55)
/.u\
lvalues]
\< 1 / (66)
PCE
5.0
< 0.3
0.7 (47)
37
< 0.3
1.6 (49)
ND^
ND
ND (86)
3.4
< 0.3
0.5 (51)
47
< 0.3
4.5 (55)
23
< 0.3
2.2 (65)
a/ For the calculation of average values, all individual values of < 0.3 or
< 1 were assumed to be 0.3 and 1, respectively. This procedure may lead
to an average value slightly higher than actually present.
b/ ND = Not determined.
c_/ Numbers in parentheses indicate the number of samples averaged.
Detection limits: MC = 0.3!ppb; TCE =1.0 ppb; PCE =0.3 ppb.
Source: Battelle (1977).
7-4
-------
In general, the results show that average ambient air concentrations of
methyl chloroform are below 2 ppb except for one manufacturing site which
showed an average value of 15 ppb (see Table 7-1). All sample values for this
compound were below 12 ppb except for one value of 155 ppb. For trichloro-
ethylene, the average ambient air concentrations were all below 2.5 ppb except
for one manufacturing site with an average level of approximately 14 ppb. In
terms of the highest single sample values for trichloroethylene, all values
except one were 15 ppb or less. The production facility that showed the high-
est average value also had a single sample level of 270 ppb. For all produc-
tion sites monitored, the average ambient air concentrations of perchloro-
ethylene were all below 5 ppb. The highest single sample value observed was
47 ppb.
7.1.2 User Sites
Very little information is currently available concerning ambient air
concentrations from the facilities of users of each of these three compounds.
Battelle (1977) presented results for one methyl chloroform and one trichloro-
ethylene user. The Boeing Corporation uses methyl chloroform for metal clean-
ing operations at the Auburn, Washington, facility; at their Seattle,
Washington, site, they use trichloroethylene for metal cleaning. The data pre-
sented for the Seattle site were rather limited with respect to the number of
samples obtained. A different analytical method was used at these two sites
compared to the manufacturing sites. Measurements at Dow, Hooker, Ethyl Cor-
poration, PPG, and St. Francis National Forest (rural background) were per-
formed with a Varian 1200 EC/GC system. A system using the more sensitive
Analog Technology Corporation, Model 140A, EC detector was used for measure-
ments at the Boeing Company plants. In this case, the detection limits for
methyl chloroform, perchloroethylene, and trichloroethylene were 0.02, 0.02,
and 0.03 ppb, respectively. The results of their analyses are shown in Table
7-2. At the Seattle facility, the highest trichloroethylene value occurred at
a sample site 0.3 mile (0.5 km) south-southeast (140 degrees) of the facility
in a residential area. At the time of sampling, the wind was from the west
(270 degrees) at a speed of approximately 2 mph (0.9 m/sec).
In general, the average ambient air concentration at the methyl chloro-
form user site is higher than at the methyl chloroform manufacturing sites
(excluding Vulcan Materials Company). Based on very limited sampling data, the
average air concentrations at the trichloroethylene user site is higher than
those values obtained for the manufacturing facilities (see Table 7-1).
The International Fabricare Institute (IFI, 1975) has gathered solvent
emission data on 39 perchloroethylene dry cleaning plants under actual operat-
ing conditions. The determinations of perchloroethylene vapor emissions to the
atmosphere were based on the final source in the solvent recovery process in
the plants surveyed. Of the 39 perchloroethylene plants visited, the final
source in 20 plants was the solvent recovery tumbler. In the remaining 19
plants, the final source was the activated carbon vapor adsorber.
7-5
-------
TABLE 7-2. AMBIENT AIR MEASUREMENTS AT
BOEING CORPORATION
Concentration (ppb)
Site MC TCE PCE
Auburn, WA
(38 samples)
Seattle, WA
(7 samples)
High
Low
Average
High
Low
Average
10.0
0.4
4.4
1.0
0.20
0.45
1.8
0.14
0.64
44.0
0.1
19.8
1.4
0.06
0.59
1.1
0.12
0.66
Source: Battelle (1977).
For those plants with vapor adsorbers, total vapor emissions in the ex-
haust were measured using a GasTech Halide Meter. In those plants without vapor
adsorbers, the emissions were either calculated based on measurements of the
efficiency of the tumbler in recovering the solvent present in a typical load
or based on actual measurements of the vapor concentrations in the tumbler
exhaust*
The solvent losses to the atmosphere from 50 perchloroethylene dry clean-
ing plants are listed in Table 7-3• The data show a wide variation in amount
of perchloroethylene lost to the atmosphere even among plants which operate
at the same capacity.
A properly operated and desorbed carbon bed vapor adsorber should have
no higher than 30 ppm of perchloroethylene in the exhaust air (IFI, 1975). Of
the 19 plants with adsorbers, exhaust measurements were not available in four;
of the remaining 15 plants, 10 had exhaust concentrations of 70 ppm or higher.
Table 7-4 contains the data obtained on the plant operation of the absorber
and measurements of the vapor concentrations in the adsorber exhaust as ob-
tained with the GasTech Halide Meter. The base reading (in parts per million)
sums up the proper or improper operation of the vapor adsorber. As an example,
a "standard" perchloroethylene vapor adsorber has an exhaust air capacity of
600 cfm; at this capacity, a steady 500-ppm breakthrough of vapors into the
exhaust is the equivalent of 72 liquid ounces of solvent lost per hour (IFI,
1975).
7-6
-------
TABLE 7-3. SOLVENT LOSSES TO THE ATMOSPHERE
FROM PERCHLOEOETHYLENE DRY
CLEANING PLANTS
Plant
No.
1
2
4
5
6
7
10
11
12
13
14
19
20
21
22
23
24
25
27
29
30
31
32
34
35
36
37
38
39
40
41
42
43
44
45
47
Cleaning
volume
(Ib/week)
3,300
1,000
5,000
6,115
2,300
1,300
2,500
519
NA
900
7,900
1,000
2,500
2,700
2,800
2,230
2,000
1,100
10,135
1,200
1,750
1,500
3,231
2,000
2,000
1,076
3,000
1,700
1,100
800
603
1,500
9,000
1,500
6,500
1,350
Loss to
Calculation
based
on
VA
TE
RE
VA
RE
RE
VA
RE
VA
VA
VA
RE
VA
RE
VA
RE
VA
RE
VA
VA
VA
VA
RE
VA
VA
RE
RE
RE
RE
TE
RE
RE
VA
VA
VA
RE
atmosphere
Gal/week
26.8
6.9
232.5
13.5
49.6
82.3
20.7
*/
NA
19.8
37.5
21.6
1.0
y
T.3
41.8
3.7
23.9
0.6
0.7
0.7
0.7
67.0
15.8
1.7
a/
37.2
17.3
37.7
7.3
a/
a/
NA
4.0
38.1
NA
(continued)
7-7
-------
TABLE 7-3. (continued)
Plant
No.
48
49
50
Cleaning
volume
(Ib/week)
2,800
3,175
2,000
Loss to
Calculation
based
on
VA
TE
RE
atmosphere
Gal/week
NA
10.5
12.7
aV In several plants, the weight of the solvent and water re-
covered from the tumbler condenser was greater than the dif-
ference between wet and dry load weights. This implies
greater than 1007o recovery efficiency, which is an impossi-
bility. Therefore, these data were dropped.
Note: VA - atmospheric loss calculations based on vapor adsorber
exhaust concentrations.
TE - atmospheric loss calculations based on tumbler ex-
haust concentrations.
RE - atmospheric loss calculations based on recovery effi-
ciency measurements.
NA - not available.
Source: Adapted from IFI (1975).
7-8
-------
TABLE 7-4. PLANTS EQUIPPED WITH CARBON ADSORBER
Plant
No.
1
5
10
12
13
14
20
22
24
27
29
30
31
34
35
43
44
45
48
Period of
daily use
6 hr
8 hr
8 hr
10 hr
8 hr
8 hr
8 hr
Every aerate cycle
of cleaner
8 hr
8 hr
8 hr
8 hr
8 hr
Only when cleaning
8 hr
8 hr
Only when cleaning
8 hr
8 hr
Frequency
of stripping
Daily
1 bed/day
Every 3 days
Weekly
3-1/2 days
-
1 bed/day
Each load
Daily
Daily
Daily
Daily
1 bed/load
Daily
Daily
Daily
Daily
1 bed/day
1 bed/day
No. loads /week
75
109
65
NA
50
211
(70/machine)
85
60
35
270
30
80
35
40
45
110
40
145
75
Concentration
in exhaust -
base reading
(ppm)
500
200
> 1,000
NA
900
500
20
NA
240
70
10
10
10
700
30
NA
220
700
NA
Note: NA = not available.
Source: Adapted from IFI (1975)
7-9
-------
Several other studies have been conducted on the levels of perchloro-
ethylene emitted from dry cleaning establishments. One of the studies was at
Texas Industrial Services, San Antonio, Texas (MRI, 1976a), a large industrial
dry cleaning facility. This plant employed a 250-Ib transfer system equipped
with a single carbon adsorption bed. The carbon bed was used for only part of
each cleaning cycle: dryer deodorizing (1 min 40 sec), dryer unloading (vari-
able time), and the transfer of material from the washer to the dryer (~ 1
min). During other segments of the operation, the system is operated either
sealed or vented directly to the atmosphere. Perchloroethylene concentrations
measured in the outlet air vent to the roof averaged 3.0 ppm for the first 2
days of testing and 1.0 ppm for the last day of testing.
Another study was conducted at Westwood Gleaners, Kalamazoo, Michigan
(MRI, 1976b), a neighborhood "Mom and Pop" type of operation. This facility
employed a 40-lb dry-to-dry system with dual carbon adsorption beds. Each sam-
pling run covered one complete cycle of the dry cleaning machine. Sampling was
conducted in the outlet air vent pipe. The average results of this study are
as follows:- 76 and 73 ppm for Run No. 1; 138 and 120 ppm for Run No. 2j and
98 and 94 ppm for Run No. 3. The emission rate appeared to depend heavily upon
the type and size of load, as well as other factors, i.e., bed overloading or
control valve leakage.
A perchloroethylene emission study was conducted at the Hershey Dry Glean-
ing and Laundry Plant, a commercial dry cleaning establishment at Hershey,
Pennsylvania (Scott Environmental Technology, 1976). This facility employs one
washer (110-lb capacity) and two dryers. Since two dryers are required to han-
dle one washer load, all machines run continuously throughout most of the day.
Emissions were monitored at the inlet and outlet of a dual carbon adsorption
bed. The carbon adsorption unit reclaims solvent from three areas: the washer,
dryer, and floor vents around the units. Hourly average concentrations of per-
chloroethylene in the outlet air vent pipe were measured over a 3-day period.
The average perchloroethylene level in the outlet vent for the sampling period
was 22.8 ppm; the maximum emission level was 72 ppm and the minimum was 5 ppm.
7.1.3 Other U.S. Sites
The vast majority of the available data for other sites in the United
States is concerned with concentrations near metropolitan areas, primarily the
New York, New Jersey, and Delaware areas, California, and the Houston area.
Very little ambient air concentration data have been published for large in-
dustrialized cities such as Detroit, Chicago, Pittsburgh, and others. In cit-
ies for which data are available, the levels appear to be well distributed
with atmospheric concentrations in the parts per billion to parts per trillion
range. The data compiled from various literature sources are shown in Table
7-5.
7-10
-------
TABLE 7-5. AMBIENT AIR CONCENTRATIONS IN SELECTED U.S. CITIES
Concentration (ppb)
Site
Seagirt, NJ
N«w York, NY
Sandy Hook, NJ
Delaware City, DE
Baltimore, HD
Wilmington, Oil
Bayonne , NJ
White Face Mountains, NY
Houston, TX
Deer Park, TX
Freeport, TX
Ln Parte, TX
Pasadena, TX
Mt. Diablo CA
Pompanio Beach, CA
Mammoth Lakes, CA
Los Angeles Basin, CA
^»n ft*" a H4nrt Mmtn*- 1 c PA
St. Francis Natl. Forest, AR
Rural Pullman, WA
Urban Los Angeles, CA
Urban Los Angeles, CA
Palm Springs, CA
Palm Springs, CA
Yosemite Natl. Park, CA
Yosemite Natl. Park, CA
Stanford Hills, CA
Stanford Hills, CA
Point Reyes, CA
Point Reyes, CA
Max
0.20
1.6
0.33
0.30
0.21
0.35
14.4
0.13
0.17
0.18
3.05
5.09
T
< o.oio
~< 0.010
< 0.010
0 27
2.30
< 0.3
-
7.66
7.66
0.45
0.45
0.13
0.13
0.57
0.57
0.23
0.23
MC
Mln
0.044
0.10
0.03
0.03
0.044
0.03
0.075
0.032
0.10
ND
2.79
T
ND
-
-
0.01
< 0.3
-
0.10
0.10
0.08
0.08
0.07
0.07
0.07
0.07
0.06
0.06
Mean
0.10
0.61
0.15
0.10
0.12
0.097
1.59
0.067
0.09
0.05
2.92
1.93
-
_
-
0.37
0.100
1.54
1.54
0.16
0.16
0.10
0.10
0.14
0.14
0.11
0.11
Max
2.8
I. I
0.80
0.56
< 0.05
0.63
8.8
0.35
0.01
0.47
0.037
< 0.01
n.945
Not
< 1.0
-
1.77
1.77
0.83
0.83
0.022
0.02
5.49
5.49
0.06
0.06
TCE
Mln
< 0.05
O.I I
< 0.05
< 0.05
< 0.05
< 0.05
< 0.05
< 0.05
Nl>2' <
ND
0.02
ND <
0.014
determined -
determined -
H«» f-oi-ml n*»H
determined -
A t- 1 H
< 1.0
<
0.03
0.03
0.13
0.01
0.014
0.01
0.01
0.01
0.013
0.01
Mean
0.26
0.71
0.14
0.35
-
0.19
0.92
0.10
0.01
0.08
0.029
0.01
0.48
_
0.005
0.31
0.31
0.040
0.04
0.016
0.02
0.11
0.11
0.03
0.02
Max
0.88
9.75
1.4
0.51
0.29
0.69
8.2
0.19
0.004
0.30
0.23
0.012
0.003
Not
0 12
4.2
< 0.3
-
2.27
2.27
1.15
1.15
-
0.09
Not
2.49
Not
3.70
PCE
Mln
0.10
1.0
0.15
< 0.02
< 0.02
< 0.02
0.30
< 0.02
fb/
ND
0.014
T
0.003
determined
determined
< 0.01
< 0.3
-
0.061
0.06
0.017
0.02
-
0.02
determined
0.02
determined
0.02
Mean
0.32
4.5
0.39
0.24
0.18
0.15
1.63
0.07
-
0.05
-
-
0.003
1.24
0 09
0.020
0.67
0.67
0.28
0.28
0.031
0.03
— —
0.20
0.21
Reference
Lillian et al. (1975)
Lillian et al. (1975)
Lillian et al. (1975)
Lillian et al. (1975)
Lillian et al. (1975)
Lillian et al. (1975)
Lillian et al. (1975)
Lillian et al. (1975)
Pellizzari (1977)
Pelllzzarl (1977)
Pelllzrari (1977)
Pellizzari (1977)
Pellizzari (1977)
Tyson (1975)
Tyson (1975)
Tyson (1975)
Lillian and Singh (19
7i1
Simraonds et al. (1974)
•>
Battelle (1977)
Grimsrud and Rasmussen (1975)
Singh (1976a); Singh
Singh et al. (1977a)
Singh (1976a); Singh
Singh et al. (1977a)
Singh (1976a); Singh
Singh et al. (1977a)
Singh (1976b)
Singh et al. (1977a)
Singh (1976b)
Singh et al. (1977a)
(1976b)
(1976b)
(1976b)
ND = Not detected.
T = Trace quantity.
-------
In the study of Lillian et al. (1975), methyl chloroform was ubiquitous
and generally present in sub-parts per billion concentrations. It was further
stated that atmospheric methyl chloroform is clearly anthropogenic, Perchloro-
ethylene was measured at least 50% of the time at all sampling sites at con-
centrations in excess of 0,06 ppb. Its nonubiquitous nature was attributed to
its reactivity in the troposphere, Trichloroethylene, a nonubiquitous halo-
genated hydrocarbon, was observed over 90% of the time at all urban locations
(except Baltimore) at concentrations over 0,05 ppb.
In these studies, the minimum detectable levels of perchloroethylene and
trichloroethylene were 0,02 and 0,05 ppb, respectively. While a minimum level
was not stated for methyl chloroform, other studies have shown that it is gen-
erally the same level as for perchloroethylene. The data for Bayonne, New
Jersey, were obtained during a 3-day inversion in that city, and showed that,
at times, meteorological conditions are probably more significant than local
emission patterns. Under extended periods of inversion, the ambient levels of
ubiquitous materials may attain values as high as 100 to 500 times their mini-
mum concentrations. In addition to the data shown in Table 7-5, representative
levels that one can expect for urban and rural areas were also given for methyl
chloroform, trichloroethylene, and perchloroethylene. Data were also given to
indicate the increase in the concentration of these three compounds as an in-
version layer was entered from aloft. These figures are shown in Table 7-6,
TABLE 7-6. TYPICAL LEVELS OF HALOGENATED HYDROCARBONS UNDER
INVERSION CONDITIONS
Location MCS./ TCE£/ PCES/
Urban New York, NY
White Face Mountains, NY
Seagirt, NJ
Sandy Hook, NJ (3 miles offshore)
Wilmington, OH (above inversion)
Wilmington, OH (inversion layer)
0.28
0.083
0.072
0.18
0.025
0.065
0.11
<0.05
<0.05
0.18
<0.05
0.075
1.2
0.09
0.25
0.73
<0.02
0.73
&l Concentrations in parts per billion; MC — methyl chloroform, TCE
trichloroethylene, PCE = perchloroethylene.
Source: Lillian et al. (1975).
7-12
-------
The study by Tyson (1975) (Table 7-5) was basically directed towards the
measurement of selected chlorofluorocarbons by mass spectrometric identifica-
tion at the parts per trillion level* Methyl chloroform was identified by the
characteristic isotope peaks in the mass spectrum even though no flame ioniza-
tion detector response was recorded from the gas chromatograph.
Simmonds et al. (1974) determined the concentration levels and distribu-
tion of various halogenated compounds which accumulated in the Los Angeles air*
Data were collected in the Pasadena area, along a line from the west San Gabriel
Valley to Manhattan Beach, a large geographical area of the Los Angeles Basin,
and in the San Bernardino Mountains* No information was given regarding the
detection limits of the analytical methods. Methyl chloroform and perchloro-
ethylene were two of the four principal components observed in all analyses,
Trichloroethylene was a minor component observed infrequently at different
locations throughout the Los Angeles area, but the levels were not quantified.
The highest concentrations of perchloroethylene were observed in the Pasadena
area, but methyl chloroform levels peaked in Orange County. The results of a
vertical profile study showed that levels of both compounds decreased with
increasing altitude, even through an inversion layer at 1,700 m» Simmonds et
al* stated that the levels of both methyl chloroform and perchloroethylene
represent emissions only from stationary sources in the Los Angeles Basin.
Grimsrud and Rasmussen (1975) studied the ambient air levels of a large
number of chlorocarbons and chlorofluorocarbons in rural air samples from
southeastern Washington in an attempt to more fully define the types and
amounts of organic carriers present in background air. This study employed gas
chromatographic/mass spectrometric analytical methods which allowed a detection
limit of 0.005 ppb for each of the three subject compounds. The carrier gas
used in the gas chromatograph was contaminated with perchloroethylene so that
the accuracy of the determination of this component was limited.
Singh (1976b) measured ambient air levels of phosgene (13 to 61 ppb) at
urban and nonurban locations in California. Since perchloroethylene and tri-
chloroethylene will photolytically decompose to give phosgene and other prod-
ucts, the levels of these two compounds (see Table 7-5) were also studied
(Singh et al., 1977a; 1977b).
In an evaluation of the use of gas-phase coulometry, Lillian and Singh
(1974) reported ambient air levels of methyl chloroform and perchloroethylene
in New Brunswick, New Jersey (see Table 7-5). Trichloroethylene was not amen-
able to this type of analysis.
Bunn et al. (1975) studied the applicability of computerized gas
chromatography/mass spectrometry techniques to the analysis of organic com-
pounds in the air at a National Air Surveillance Network Station in Kansas
City, Kansas* Methyl chloroform and trichloroethylene were detected in the
air samples, but no data were given regarding quantitative values or detection
limits of this technique.
7-13
-------
Fuller (1976) summarized the air pollution problems of trichloroethylene
and perchloroethylene. According to the report, about 60% (600,000 tons) of
the total world production of trichloroethylene is released to the atmosphere
each year* However, due to its low solubility in water, high vapor pressure,
and high atmospheric photodegradation rate, trichloroethylene is not expected
to persist in the environment* Ambient concentrations in the atmosphere of
industrial areas are about 11 ng/m^ or 20 ppt.
7.1.4 Non-U.S. Sites
There is very limited information in the literature regarding non-U.S.
and worldwide ambient air concentration data.
Pearson and McConnell (1975) measured the concentration of six chlorinated
hydrocarbons, including trichloroethylene, methyl chloroform, and perchloro-
ethylene, in the atmosphere over various areas of England. A summary of their
results is presented in Table 7-7. The high ambient air levels at the Runcorn
Works perimeter are because this facility is an organochlorine manufacturing
site. Similar results were presented earlier for U.S. manufacturing sites.
TABLE 7-7. AMBIENT AIR LEVELS IN ENGLAND
Concentration (ppb)
Location MC TCE PCE
Runcorn Works perimeter
Runcorn Heath
Liverpool/Manchester surburban area
Moel Famau, Flintshire
Rannock Moor, Argyllshire
Forest of Dean, Monmouthshire—
16
6.2-11
< 0.1-6
2-4
1-1.5
2.8
40-64
12-42
1-20
1-9
2.5-8
5
15-40
0.2-5
< 0.1-10
< 0.1-2.5
0.3-1
3
al Single sample.
Source: Pearson and McConnell (1975).
Ambient air concentrations of trichloroethylene and perchloroethylene were
measured by Murray and Riley (1973) in rural areas of the British Isles (cen-
tral Exmoor and the moorlands of North Wales) and over the northeast Atlantic
along a line between Cap Blanc (Spanish Sahara) and Lands End. The concentration
varied significantly from one site to another and no attempt was made to inter-
pret the distribution pattern due to the small number of samples available. In
7-14
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general, the concentration ranges of these compounds in air over the ocean were
quite similar to those measured over land away from urban areas*
Lovelock (1974) measured the air levels of selected chlorofluorocarbons
and chlorinated hydrocarbons at Adrigole, Ireland, and in mid-Atlantic aboard
a research vessel during its cruise from Hamburg to Santo Domingo. At Adrigole,
methyl chloroform, trichloroethylene, and perchloroethylene concentrations were
found to be 0,065, 0.015, and 0.028 ppb, respectively. In the north Atlantic,
the air levels for methyl chloroform, trichloroethylene, and perchloroethylene
were measured at 0.075, < 0.005, and 0.021 ppb.
Ambient air levels were measured on a monthly basis at 26 different sites
in Tokyo from May 1974 to April 1975 by Ohta et al. (1976). The average air
levels for methyl chloroform, trichloroethylene, and perchloroethylene were
found to be 0.8, 1.2, and 1.2 ppb, respectively. These levels are comparable
to those found over the Los Angeles Basin by Simmonds et al. (1974).
Ohta et al. (1977) measured the levels of trichloroethylene and methyl
chloroform in ambient air over a 7-week period in Tokyo to determine the dif-
ference in concentrations on clear, cloudy, and rainy days. The average con-
centrations, depending on sky conditions, are:
Methyl chloroform: Clear 1.6 ppb
Cloudy 1.8 ppb
Rainy 1.1 ppb
Trichloroethylene: Clear 3.0 ppb
Cloudy 3.4 ppb
Rainy 2.6 ppb
Perchloroethylene was measured, but, due to activity of dry cleaning shops
within 500 m of the sampling station, no further evaluation was made.
Louw et al. (1977) measured the levels of perchloroethylene in the cen-
tral areas of three major cities in South Africa. The levels were found to be
2.2 ppb in Pretoria, 2.1 ppb in Johannesburg, and 0.6 ppb in Durban.
Methyl chloroform levels in the air at Cape Grim, Tasmania, were estimated
to be 40 to 60 ppt during a 6-month sampling period (Fraser and Pearman, 1978).
Correia et al. (1977) studied the levels of trichloroethylene, methyl
chloroform, and perchloroethylene in a number of western European countries.
The results of these measurements are shown in Table 7-8.
7-15
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TABLE 7-8. AMBIENT AIR LEVELS IN SELECTED WESTERN EUROPEAN COUNTRIES
Concentration (oob)
Location Country
Liverpool (Childwall) U.K.
Widnes (Pex Hill)
Delamere
Frodsham
Moel Famau (N. Wales)
Rannock Moor (Scotland)
Forest of Dean
Hengelo (Open Country) NL
Hengelo (Centre)
Weiwerd
Munich (Centre) D
Munich 1 km f.c.
Munich 5 km f.c.
Munich 10 km f.c.
Munich 20 km f.c.
Uberackern
Ranzel
Langel
Unkendorf
Bruxelles Nord B
Uccle
Uccle
Namur
Saint Auban F
Lyon (Centre)
Lyon 20 km f.c.
Monte Tauro (Sicily) I
Floridia (Sicily)
Melilli (Sicily)
TCE
0.34-1.19
1.53
0.51-1.36
0.68-3.40
0.17-1.53
0.42-1.36
0.85
< 0.02-0. 17
< 0.02-0 .09
<0.09
0.85-3.92
0.17-3.59
0.17-5.45
0.17-3.06
ND
1.36-8.5
0.68-1.02
0.68-1.36
ND
0.17-1.36
0.17-8.15
< 0.83-4.23
< 0.83-2.54
PCE
0.07-0.68
0.03
0.03-0.14
< 0.01-1 .35
< 0.01-0.34
0.04-0.14
0.4
0.03-0.08
0.01-0.13
0.03-0.08
0.27-0.81
0.14-3.38
0.14-1.49
ND-2.30
0.14
0.13-2.30
0.81-2.02
1.62-3.24
< 0.41
0.27-0.41
0.14-0.41
0.14
0.14-1.22
0.07-4.7
2.84-5.0
2.16-4.72
0.27-0.41
0.27
0.68-1.35
MC
0.17
0.34
0.03-0.20
0.05-1.01
0.34-0.68
0.17-0.25
0.47
0.02-0.05
< 0.02-0. 13
<0.02
ND3/
0.17-0.67
ND-0.50
ND-0.34
ND
1.51-1.68
1.51-6.55
<0.50
0.17-0.39
<0.17
ND
ND-0.34
< 0.84-2 .01
< 0.84-0 .84
a/ ND = Not detected.
Source: Correia et al. (1977).
7-16
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Cox et al. (1976) measured ambient air levels in the Northern and South-
ern Hemispheres. The Southern Hemisphere data were compiled at Blouberg Sea-
shore, near Cape Town, South Africa. Methyl chloroform and trichloroethylene
concentrations were 0.024 and 0.002 ppb, respectively. Perchloroethylene was
not measured at this site. Northern Hemisphere data were obtained at Adrigole,
Ireland. The ambient air levels at this site for methyl chloroform, trichloro-
ethylene, and perchloroethylene are the same as those stated previously for
Lovelock (1974).
Northern Hemisphere background concentrations of the three subject com-
pounds were stated by Singh et al. (1977b) and Singh (1977c) to be 0.099,
0.016, and 0.031 ppb, respectively, for methyl chloroform, trichloroethylene,
and perchloroethylene. These measurements were made at a clean air continental
site at Badger Pass in Yosemite National Park, California. Singh concluded
that the ambient air levels of these three compounds are primarily anthropo-
genic in nature.
Methyl chloroform concentrations have been measured by Lovelock (1977)
over a 5-year period at sites in rural regions of the Northern Hemisphere
(British Isles) and Southern Hemisphere (Cape Providence, South Africa, and
Antarctica). Average levels in the Southern Hemisphere ranged from approxi-
mately 12 ppt in 1972 to about 50 ppt in 1977. In the Northern Hemisphere,
levels ranged from approximately 32 ppt in 1972 to about 97 ppt in 1977.
Singh et al. (1978) measured methyl chloroform levels during a trip from
New Zealand to the United States and in selected cities throughout the world.
Their analysis of the results showed that up to about 30°N (latitude) the
Northern Hemisphere concentration appears to be well mixed with an average
concentration of about 120 ppt. A fairly sharp decline occurs between 20°N and
20°S; the levels of methyl chloroform level off at about 70 ppt below 20°S.
This decline is explained by an increase in hydroxyl radical concentration
around the equator due to higher water vapor levels and intense sunlight. The
authors state that an average uniformly mixed concentration of about 113 ppt
in the Northern Hemisphere and 75 ppt in the Southern Hemisphere best describes
the methyl chloroform burden.
7.1.5 Stratospheric Levels
Cronn et al. (1977) conducted the first study on the distribution of halo-
carbons in the stratosphere. Air samples were taken over the Pacific Northwest
at different altitudes using a Lear jet. A total of 80 samples were collected
in March 1976 on seven flights at altitudes ranging from 4.6 (15,088 ft) to
14.6 km (48,000 ft) with an average height of 10.8 km (35,424 ft). Samples were
analyzed for several halogenated compounds, including trichloroethylene, methyl
chloroform, and perchloroethylene. The detection limits were less than 3 ppt
for all species measured*
7-17
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The stratosphere is characterized by a temperature inversion—a region in
which the temperature remains constant or increases with altitude. Temperature
profiles for the atmosphere vary with latitude so that the bottom of the strato-
sphere is at a considerably higher altitude at the equator than it is, for ex-
ample, at 70 degrees latitude. The base of the stratosphere is known as the
tropopause, which varies in altitude from about 8 km or less at high latitudes
to about 16 km over the equator. The area from sea level to the tropopause is
known as the troposphere.
The average tropospheric background concentrations for methyl chloroform
was 94.5 + 8.2 ppt. Trichloroethylene had an average concentration of 20 ppt
with a standard deviation of 3.9 ppt. An average perchloroethylene level of
16 + 4.6 ppt was found in the troposphere.
In the lower stratosphere, methyl chloroform and perchloroethylene were
detected but no trichloroethylene. The concentration of methyl chloroform above
the tropopause varied from 60 to 95 ppt with an average of 79 ppt. Concentra-
tion levels of perchloroethylene in the stratosphere ranged from 0 to 18 ppt
with an average of 6.5 ppt.
The authors state that this study demonstrated that selected chlorinated
hydrocarbons, especially methyl chloroform, can and do reach the stratosphere.
They tend to remain for long time periods, since the nearly constant tempera-
ture distribution (throughout the stratosphere) results in a stable atmosphere.
In general, three conclusions were derived from the sampling data. First,
the altitude profiles indicated a wider variety of halocarbons exists in the
lower stratosphere than had previously been measured, indicating that signifi-
cant transport of these species occurs. Secondly, the concentrations found in
the lower stratosphere for a given compound were smaller than the tropospheric
concentrations. Finally, greater day-to-day variability and different concen-
tration gradients between successive layers in the lower stratosphere were ob-
served for the chlorinated hydrocarbon concentrations.
7.2 WATER LEVELS
In this subsection, data will be presented on levels of trichloroethylene,
methyl chloroform, and perchloroethylene in drinking water, nondrinking water,
and wastewater in the vicinity of manufacturing facilities, user sites, sites
within the United States, and in the marine environment. Case histories of
drinking water contamination will also be included.
7.2.1 Drinking Water
The occurrence of halogenated hydrocarbons in drinking water has been de-
tected in a number of cities. All three of the subject compounds have been
found in drinking water throughout the United States. Trichloroethylene was
7-18
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found in concentrations as high as 32 ppb; the highest reported occurrence of
methyl chloroform was 17 ppb; and for perchloroethylene, 2 ppb. A summary of
the levels found in drinking water is presented in Table 7-9.
TABLE 7-9. CONCENTRATIONS IN DRINKING WATER
Concentration (ppb)
Location
TCES/
MC
PCE
Reference
E vans vi lie, OH
Cincinnati, OH
Hun ting ton, OH
Pittsburgh, PA
Beaver Fall, PA
Chicago, IL
Chicago, IL
New Orleans, LA
Miami, FL
Seattle, WA
Ottumwa, IA
Philadelphia, PA
Cincinnati, OH
Tucson, AZ
New York, NY
Lawrence, MA
Grand Forks, ND
Terrebonne Parish, LA
Freeport, TX
Baton Rouge, LA
Helena, AR
Lake Charles, LA
Des Moines, IA
5
ND£/
ND
ND
ND
ND
2
Detected
0.2
0.1
0.2
0.5
0.1
ND
ND
Detected
ND
ND
19
0.4
22
0.1
32.0
<1
< 1
<1
<1
<1
ND
1
Detected
ND
ND
Detected
Detected
Detected
ND
ND
ND
ND
ND
17
0.05
0.4
0.3
ND
<1
ND
ND
<1
<1
2
1
Detected
0.1
ND
0.2
0.4
0.3
0.1
0.4
0.07
0.2
ND
ND
ND
ND
ND
ND
Chian and Ewing (1975)
Chian and Ewing (1975)
Chian and Ewing (1975)
Chian and Ewing (1975)
Chian and Ewing (1975)
Chian and Ewing (1975)
Chian and Ewing (1975)
Dowty et al. (1975a)
EPA (1975)
EPA (1975)
EPA (1975)
EPA (1975)
EPA (1975)
EPA (1975)
EPA (1975)
EPA (1975)
EPA (1975)
EPA (1975)
Battelle (1977)
Battelle (1977)
Battelle (1977)
Battelle (1977)
Battelle (1977)
a/ TCE = trichloroethylene; MC = methyl chloroform; PCE = perchloroethylene.
b/ ND = Not determined.
7.2.1.1 Manufacturing Sites--
Only one study briefly mentioned the levels of these compounds in drink-
ing water. When Battelle (1977) monitored surface waters in the vicinity of
producers, they also tested drinking water levels at Freeport, Texas, and at
Baton Rouge and Lake Charles, Louisiana. The same detection equipment and lim-
its used for monitoring surface waters were employed to monitor drinking water.
7-19
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The lowest concentrations were found in Lake Charles, Louisiana, while the
highest concentrations were at Freeport, Texas (see Table 7-9).
7.2,1.2 User Sites-
No studies of drinking water levels at user sites have been found in the
literature.
7.2.1.3 Other U.S. Sites—
The recent study by the University of Illinois (Ghian and Ewing, 1977) sam-
pled tap water in different areas of the United States. During the investigation,
they also detected chlorinated hydrocarbons in the finished water (water which
has been processed by a water treatment plant (WTP)). The highest concentrations
were 5 ppt trichloroethylene (at the OTP in Evansville, Ohio) and 2 ppt per-
chloroethylene (at the WTP in Chicago, Illinois). Samples were taken of the
water before entering the WTP (raw water) and again after processing was com-
plete (finished water). No significant changes in concentrations were noted be-
tween the raw water and finished water found at 10 water treatment plants moni-
tored in this study, except for the facility in Evansville, Ohio. At this WTP,
the concentration of trichloroethylene increased from "not detected" in the raw
water outside the plant to 5 ppb trichloroethylene in the finished water.
Battelle (1977) reported levels of 22 ppb for trichloroethylene and 0.4
ppb for methyl chloroform in the drinking water (tap water) at Helena, Arkansas.
Dowty et al• (1975a; 1975b) presented their findings on the New Orleans
drinking water analyses. However, they reported relative concentrations thereby
not permitting comparisons with concentrations detected in other cities' water
supplies. The investigation did detect trichloroethylene, perchloroethylene,
and methyl chloroform in the tap water. Dowty et al. (1975a) did indicate that
many of the halogenated organics such as trichloroethylene pass through the
municipal treatment plant unaltered. They also examined the halogenated organ-
ics found in commercially bottled artesian water, but they did not detect the
presence of trichloroethylene, perchloroethylene, or methyl chloroform.
Trichloroethylene was present at a concentration of 32 ppb in finished
drinking water at Des Moines, Iowa (Battelle, 1977). EPA, Region VII, partici-
pated in a sampling and analysis effort to determine the source of the tri-
chloroethylene. Although it was determined that the compound was entering the
treatment plant through the 3-mile-long gallery infiltration system (one
source of raw water for this treatment plant), no exact source was located.
The source of the contamination was later determined to be a general manufac-
turing plant which uses trichloroethylene as part of a metal cleaning opera-
tion (Johnson, 1978). This plant disposes its cleaning tank sludges in an ad-
jacent landfill. The recent sampling tests indicate that trichloroethylene was
seeping into the ground water at the manufacturing plant and entering the gal-
lery infiltration system (about 1/2 mile away).
7-20
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Trichloroethylene and perchloroethylene were identified in the drinking
water supplies of communities on the Ohio, Potomac, and Mississippi rivers
(Abrams et al», 1975)• The researchers, in evaluating the two compounds for
their biodegradability and persistence, rated them both "four." Only five rat-
ings were listed with No. 5 being "refractory." No. 4 refers to "very diffi-
cult to degrade."
In response to the Safe Drinking Water Act (P.L. 93-523), EPA has moni-
tored the drinking water in a number of cities and compiled the data in the
National Organics Reconnaissance Survey (NORS) and in other reports. The 1975
report to Congress (EPA, 1975) contains these EPA articles. In all, 129 com-
pounds were detected. All three of the compounds (trichloroethylene, perchloro-
ethylene, and methyl chloroform) were detected in the drinking water of at
least three of the 10 cities tested. Perchloroethylene was detected in eight
of the cities while trichloroethylene was found in five and methyl chloroform
in three (Table 7-9). The highest concentration of trichloroethylene found was
0.5 jig/liter (5 ppb), and perchloroethylene was 0.4 /zg/liter (4 ppb)j methyl
chloroform was detected but not quantified.
7.2.2 Nondrinking Water
Levels of each of the subject compounds were compiled for manufacturing
sites, user sites, other U.S. sites, and the marine environment.
7.2.2.1 Manufacturing Sites-
Only one published study was concerned with the surface water levels
at specific manufacturing sites of trichloroethylene and methyl chloroform.
Battelle (1977) monitored sites upstream and downstream from the manufacturers'
outfall pipes and at the outfall pipes. Samples were normally taken at a depth
of 2 to 5 cm below the surface. At one site, Dow Chemical Company, bottom sam-
ples were also taken. The preliminary results of this study are summarized in
Table 7-10. All samples were taken within 1 km upstream or downstream of the
producers' outfalls. The detection limits were 50 ppt.
In general, the results show that the average concentration found in sur-
face waters above the producer sites was below 2 ppb for methyl chloroform and
below 5 ppb for trichloroethylene, except for one manufacturing site with an
average level of 132 ppb for methyl chloroform and 353 ppb for trichloroethylene.
(These values occurred 50 m upstream of the plants' outfall.) Perchloroethylene
levels were not measured at any of the sites. Downstream of the plants, concen-
trations of methyl chloroform and trichloroethylene were higher than the up-
stream levels in all cases (see Table 7-10). The average methyl chloroform con-
centrations found downstream of the plants' outfalls ranged from a low of 0.8
ppb at Dow to a high value of 169 ppb at the Vulcan Plant. The lowest average
value for trichloroethylene was 5 ppb at Dow, and the high was 403 ppb which
occurred at PPG.
7-21
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TABLE 7-10. NONDRINKING WATER LEVELS AT PRODUCER SITES
Sample site
Dow Chemical Company
Upstream (800 m)
Outfall No. 1
Outfall No. 2
Downstream (400 m)
Hooker Chemical
Upstream (50 m)
Outfall
Downstream (1 km)
Ethyl Corporation
Upstream (200 m)
Outfall
Downstream (300 m)
PPG Industries, Inc.
Upstream (50 m)
Outfall No. 1
Outfall No. 2
Downstream (50 m)
Vulcan Materials Company
Upstream (30 m)
Outfall
Downstream (75 m)
Concentration
TCE
0.9
-
172
197
126
122
5
13
1.0
535.0
22.0
0.4
128
37
353
447
179
403
5
74
24
(ppb)
MC
0.1
-
20
23
117
119
0.8
1
0.5
5.0
4.0
0.4
74
20
132
181
58
151
2
344
169
Source
Surface
Bottom
Surface
Bottom
Surface
Bottom
Surface
Bottom
Surface
Surface
Surface
Surface
Surface
Surface
Surface
Surface
Surface
Surface
Surface
Surface
Surface
Note: TCE = trichloroethylene; MC = methyl chloroform,
Source: Battelle (1977).
7-22
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7.2.2.2 User Sites--
Few data are available concerning concentrations of the subject compounds
in the vicinity of users. Battelle (1977) monitored surface water in the vi-
cinity of Boeing Corporation, which uses methyl chloroform for metal cleaning
operations at their Auburn, Washington, plant. The limit of detection was 50
ppt. The average methyl chloroform and trichloroethylene levels 30 m upstream
from the users* outfall were 6 and 5 ppb, respectively. Downstream (100 m) con-
centrations were the same for methyl chloroform and only slightly higher for
trichloroethylene (8 ppb). During the study, a site in a residential area 1.5
km downstream of the plant was sampled. The concentrations detected at this
point were higher for both compounds than either of the two previous sites.
Trichloroethylene levels were an average value of 26 ppb; average methyl
chloroform levels were 18 ppb.
Three dry cleaning operations were monitored for perchloroethylene emis-
sions in effluent water. These studies indicate that perchloroethylene is found
in the effluent water in the parts per million range. One study was conducted
by MRI (1976a) at Texas Industrial Services. At this facility, the wastewater
containing perchloroethylene is flushed into the sewer system. During a 4-day
study in March 1976, MRI detected perchloroethylene in the wastewater at con-
centrations ranging from 38 to 113 ppm.
Another site monitored was Westwood Cleaners in Kalamazoo, Michigan. MRI
(1976b) measured perchloroethylene levels in wastewater derived from steam
stripping operations at the site. In all three samples, perchloroethylene was
found in the parts per million range. The average results are as follows: 102
ppm for Sample No. 1, 100 ppm for Sample No. 2, and 71 ppm for Sample No. 3.
The third site studied was at the Hershey Dry Cleaning and Laundry Plant
in Hershey, Pennsylvania (Scott Environmental Technology, 1976). Several water
samples were collected from the decanter outlet of the carbon bed steam purge.
This wastewater is discharged into the sewer system. Three samples were ob-
tained, one representing the start of the desorption cycle, another, the middle,
and a third at the end of the cycle. The respective concentrations were 1,010,
62.2, and 5.6 ppm. The results suggest that perchloroethylene concentrations
in this wastewater are highly dependent upon the stage of the desorption cycle.
7.2.2.3 Other U.S. Sites—
A study is being conducted by the University of Illinois for the detection
of previously unrecognized pollutants in surface water at different sites in
the United States (Chian and Ewing, 1977). Detection limits were not given. In
this study, methyl chloroform, trichloroethylene, and perchloroethylene are
three of the many pollutants which have been identified and in most cases quan-
tified. Of the 204 sites sampled, only 11 (5%) of these sites showed concentra-
tions of methyl chloroform, trichloroethylene, and perchloroethylene greater
than 6 ppb by weight. In general, approximately 75% of the sites sampled de-
tected these three halocarbons at < 1 ppb. The maximum level detected for
7-23
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methyl chloroform was 8 ppb in Cook County, Illinois,* For perchloroethylene,
the highest level was 45 ppb which was observed in Ashtabula, Ohio, The highest
level of trichloroethylene was 188 ppb in Ashtabula, Ohio. The areas sampled
during this study are shown in Figure 7-1. The study indicates that these halo-
genated hydrocarbons can be found in surface waters in the low parts per bil-
lion range throughout the United States,
In the Hudson River, only three of 16 sampling sites showed concentrations
of trichloroethylene above 1 ppb. Levels of methyl chloroform and perchloro-
ethylene were all < 1 ppb. The highest trichloroethylene level was 6 ppb at a
site upstream from the mouth of the river; further upstream, a level of 2 ppb
was found, and, at a site above the confluence of the Mohawk River, a level of
4 ppb was measured. However, in the Upper Bay-Lower Bay-Raritan Bay area around
New York City, Staten Island, and New Jersey, somewhat higher levels of all
three compounds were found. Of the 13 sample sites, 10 showed levels of each
compound in excess of 1 ppb. The highest concentration of trichloroethylene was
7 ppb near the mouth of Newark Bay.
The Delaware River and two tributaries, the Lehigh and Schuylkill rivers,
contained 1 ppb or less of all three compounds except at three sites. In the
vicinity of Philadelphia, a level of 18 ppb of trichloroethylene, 2 ppb of
methyl chloroform, and 3 ppb of perchloroethylene was found.
Levels of all three compounds were 1 ppb or less (or not detected) along
the Ohio River Basin and at the confluence of its tributaries (Tennessee,
Wabash, Miami, Scioto, Kanawha, Beaver, Allegheny, and Monongahela rivers).
As with the Ohio River Basin, all sites sampled in the Great Lakes either
had no detectable levels of these compounds or they were found at 1 ppb or
less, except at one specific point; at Ashtabula (south edge of Lake Erie),
trichloroethylene levels were 188 ppb, perchloroethylene levels were 45 ppb,
and methyl chloroform levels were < 1 ppb.
The Tennessee River was found to contain < 1 ppb of all three compounds
at each of six sampling sites except for Chattanooga. At this site, perchloro-
ethylene levels were 13 ppb, while methyl chloroform and trichloroethylene
levels were 4 and 3 ppb, respectively.
Sites along the Black Warrior and Tombigbee rivers and in the Mobile Bay
area of Alabama were sampled, and all were found to contain 1 ppb or less of
all three chlorinated hydrocarbons.
Several sites were sampled in the greater Chicago area. The highest level
of trichloroethylene, 10 ppb, was found in Lake Michigan near the central water
filtration plant. All other sites showed levels of trichloroethylene of 6 ppb
or less. For perchloroethylene and methyl chloroform, the highest levels found
were 5 and 8 ppb, respectively.
7-24
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I
rO
Cn
Production Sites
O Trichloroethylene
D Methyl Chloroform
A Tetrachloroethylene
Source: Derived from data in Chian and Ewlng (1977).
.1) Hudson River - Rariatan Bay
(T) Delaware - Schuylkill Rivers
(3) Ohio River and Tributaries
(4) Great Lakes
(7)Ashtabula, Ohio
[6) Tennessee River Basin
L 7) Black Warrior - Tombigbee Rivers
(5) Chicago
(?) Illinois River
(lO) Upper Mississippi River and
Tributaries
QJ) Lower Mississippi River
M2) Houston Ship Channel -
Galveston Bay
M3) Los Angeles
Q4) San Francisco
(l|) Port land - Willamette River
(\6) Seattle - Puget Sound
Figure 7-1. Sites of surface water sampling,
-------
From the origin of the Illinois River in Chicago to a point about 50 miles
downstream from Joliet, five specific sites were sampled for these chlorinated
hydrocarbons. The highest concentration, 7 ppb, was found south of Joliet. Five
other sites, four downstream and one 50 miles upstream of Peoria, were sampled
and all found to contain 1 ppb or less of these compounds*
The Upper and Middle Mississippi River (upstream from St* Louis) and three
tributaries (St. Groix, Wisconsin, and Illinois rivers) were also studied* The
three tributaries, sampled no further than a few miles upstream from the con-
fluence, were found to contain 1 ppb or less of all three compounds* At one
site south of Minneapolis, a level of 13 ppb of trichloroethylene was found;
at St. Louis, 5 ppb of trichloroethylene was found* All other sample sites were
1 ppb or less*
On the Lower Mississippi River, all three compounds were 1 ppb or less
at eight of 11 sampling sites. Only at Vicksburg (20 ppb trichloroethylene)
and the most southern sites around Pilottown (13 ppb trichloroethylene) were
the levels significantly greater than 1 ppb*
High concentrations of trichloroethylene (29 ppb) and perchloroethylene
(15 ppb) were found in the Houston Ship Channel, but only 1 ppb or less of all
three compounds were found in the Galveston Bay area prior to convergence with
the channel*
In all samples taken in the western states of California, Oregon, and
Washington, these compounds were either not detected or found at < 1 ppb* Six
sampling sites were monitored in the vicinity of the Los Angeles Harbor and
Santa Monica Bay* Specific creeks, channels, or rivers that were sampled in-
cluded: Ballona Creek, Dominquez Channel, and the Los Angeles and Burbank
Western Wash* Four sites were sampled in the San Francisco Bay* In Oregon,
three sites were monitored along the Willamette River from Salem to Portland*
Finally, two of the sampling sites were taken in the Puget Sound area*
7*2*2*4 Marine Environment--
Pearson and McConnell (1975) reported the concentration of trichloro-
ethylene, perchloroethylene, and methyl chloroform in marine water near the
Runcorn Works, a major producer of chlorinated hydrocarbons, in England. The
normal limit of detection for each compound, the average concentration, and
the maximum concentrations found are reported in Table 7-11* There was no con-
sistent pattern of correlation between the concentration of a compound and the
location of water containing it* There was, however, a tendency for higher con-
centrations to be found in the estuary near the production site and over the
disposal grounds used for dumping sewage sludge*
7-26
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TABLE 7-11. CONCENTRATIONS OF CHLORINATED HYDROCARBONS
IN LIVERPOOL BAY SEAWATER
Compound
Normal
limit of
detection^
Average
concentration^
Maximum
concentration
found3'
Trichloroethylene
Perchloroethylene
Methyl chloroform
0.01
0.01
0.2
0.3
0.12
0.25
3.6
2.6
3.3
a^l Parts per 10' by mass (ppb).
Source: Pearson and McConnell (1975).
Murray and Riley (1973) reported concentrations of chlorinated hydrocarbons
in northeast Atlantic surface water during August 1972. Trichloroethylene con-
centrations ranged from 0 to 11 ppb and perchloroethylene ranged from 0.2 to
0.8 ppb« The average concentrations found for trichloroethylene and perchloro-
ethylene were 7 and 0.5 ppb, respectively. These results indicate the presence
of significant amounts of the same chlorinated hydrocarbons that were detected
in the air samples. With the exception of perchloroethylene, these were present
in ratios which were roughly similar to those in air.
7.2.3 Wastewater
Organochlorine compounds have been found in effluents of waste treatment
plants. All three subject compounds have been detected in the final effluent
of wastewater treatment plants in the parts per billion range (Table 7-12).
The study by Chian and Ewing (1977) included data for compounds in waste-
water treatment plant effluents. In general, the concentrations detected in
final effluent water from the sewage treatment plants monitored in Illinois
were 4 to 10 ppb trichloroethylene and 1 to 8 ppb for methyl chloroform. No
detection limits were given for the analytical procedures.
Camisa (1975) reported that trichloroethylene wastes from a decaffeina-
tion process were discharged into a treatment plant in the San Francisco Bay
community of San Lorenzo, California. The average concentration of trichloro-
ethylene in the 13 million gallon per day (mgd) wastewater flow was 1.2 mg/
liter (ppm), which was equivalent to a mass discharge rate of 120 Ib/day.
7-27
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TABLE 7-12. AVERAGE LEVELS OF SOME CHLORINATED HYDROCARBONS
IN WASTEWATER
i
to
oo
Site
Dalton, GA
Rome, GA
Cook County, IL .
(West Southwest WTP^ )
Cook County, IL
(North Side WTP)
Cook County, IL
(West Side WTP)
Cook County, IL
(Calumet WTP)
Cincinnati, OH
(unknown)
England
(unknown)
Concentrations (ppb )
TCE PCE MC Reference
5 - Battelle (1977)
5 - - Battelle (1977)
5 5 Chian and Ewing
(1977)
10 4 8 Chian and Ewing
(1977)
5 44 Chian and Ewing
(1977)
4 46 Chian and Ewing
(1977)
9.8 4.2 8.5 Bellar et al. (1974)
2-300 - 0-10 Montgomery and
Conlon (1967)
_a/ Waste treatment plant.
Note: TCE = trichloroethylene; PCE = perchloroethylene; MC = methyl chloroform.
Source: Chian and Ewing (1977).
-------
Bellar, Lichtenberg, and Kroner (1974) reported the concentration of tri-
chloroethylene, methyl chloroform, and perchloroethylene in the influent and
effluent of a municipal sewage treatment plant in Cincinnati, Ohio. Their re-
sults showed influent levels of trichloroethylene to be 40.4 jug/liter (ppb),
a methyl chloroform level of 16.5 ppb, and perchloroethylene at 6.2 ppb. Treat-
ment of the influent decreased the levels of trichloroethylene, methyl chloro-
form, and perchloroethylene to 8.6, 9.0, and 3.9 ppb, respectively. Subsequent
chlorination of the effluent resulted in little change in the concentrations
of the three compounds.
Several EPA regional offices have analyzed various waters for trichloro-
ethylene (Battelle, 1977). The Surveillance and Analysis Division of Region IV
has detected trichloroethylene at three locations in the following estimated
concentrations:
Dalton, Georgia, Wastewater Treatment Plant < 5 ppb
Rome, Georgia, Treatment Plant < 0.5 ppb
Rome, Georgia, Wastewater Treatment Plant < 5 ppb
The concentrations of trichloroethylene and methyl chloroform in sewage
sludge were reported by several workers from England. Montgomery and Gonlon
(1967) reported trichloroethylene (0.02 to 0.3 mg/liter) and methyl chloroform
(0 to 0.01 mg/liter) in samples of sewage sludge. The detection limit for tri-
chloroethylene was 0,01 mg/liter, but the limit for methyl chloroform was not
given.
7.2.4 Case Histories
Recently there have been reports of trichloroethylene contamination of
well water. This compound appears to be capable of entering underground aqui-
fers, where it may be transported to wells used for drinking water.
Trichloroethylene has been detected in the water of at least 20 wells in
Pittsylvania County in the vicinity of Danville, Virginia (Haley, 1977). It
was first detected by the State Health Department of Richmond, Virginia, after
several complaints were filed concerning strange tasting well water in March
1977. The State Health Department tested the well water and found trichloro-
ethylene present in the supply at levels up to 10 ppm. The agency recommended
that alternate sources of drinking water be supplied and consumption from the
contaminated wells ceases. During subsequent investigations, it was discovered
that a large local tool manufacturer, Disston, Inc., has two lagoons for the
disposal of their wastes (of which trichloroethylene is a contaminant). Both
lagoons are in close proximity to the contaminated wells. It is not known ex-
actly how long the company has been using trichloroethylene (perhaps 20 years)
or how much trichloroethylene has been discharged into the lagoon. Apparently
the trichloroethylene has migrated from the lagoon into an underground aquifer
and is then carried through the aquifer to the wells.
7-29
-------
The nearest well to the manufacturing company was 160 ft deep and was
found to contain the highest concentration (10 ppm). In total, 20 wells were
contaminated. As expected, the further the wells were from the lagoons, the
lower the levels of trichloroethylene. The closest noncontaminated well was
several hundred feet from the lagoons* Due to possible litigation, no state-
ments regarding toxicity have been reported for the people who drank the con-
taminated well water.
A death was reported which may be attributable to release of trichloro-
ethylene and methyl chloroform from the Disston plant into a sewer line. About
1 month prior to the well water contamination, a man died suddenly while clean-
ing a wet well at the Greenwood sewage pumping station in Danville (North,
1977). An accidental cross-connection at the Disston plant allowed the two
chemicals to enter the sanitary sewer. Disston normally discharges some indus-
trial waste into this line; however, the company did not have a permit to dis-
charge trichloroethylene or methyl chloroform at the time of the incident.
Not only was trichloroethylene found in the well waters of residents in
the proximity of the manufacturing company outside of Danville, Virginia, but
it also was found in two small lakes downstream from the plant. Some of the
waste was discharged into the receiving stream and carried downstream. The two
small lakes, which received water from the contaminated river, were found to
contain 127 ppb of trichloroethylene in the upper lake and 34 ppb in the lower
one.
An incidence of well water contamination with trichloroethylene has also
been reported in southeast Pennsylvania (Kraybill, 1977). Residents of West
Ormrod community in the North Whitehall Township of Lehigh County, Pennsylvania,
complained of taste and odor problems in their drinking water supply in August
1976. The water supply source was analyzed and found to contain up to 38 ppm
of trichloroethylene. The water supply for the community association was taken
from a single drilled well and piped to the distribution system.
The West Ormrod Water Association currently has a permanent interconnec-
tion with another public water supply in the area. Legal proceedings are pend-
ing against the Heleva Landfill, the suspected source of the contamination.
Trichloroethylene and other chemicals were being dumped directly into the
ground at this sanitary landfill. The Pennsylvania Department of Environmen-
tal Resources is evaluating the possibility of cleanup of the groundwater
through an air stripping technique (Boob, 1978).
Groundwater studies have been conducted in the West Ormrod area to define
the extent of contamination and determine appropriate methods for recovery and
treatment. Other domestic wells sampled in the area indicate concentrations of
1 ppm or less of trichloroethylene. Observation wells drilled in the suspect
area contain concentrations of trichloroethylene up to 260 ppm.
7-30
-------
Several other cases involving trichloroethylene contamination of ground-
water have occurred in the southeastern section of Pennsylvania (Boob, 1978).
The Uniform Tube Company, Collegeville, Montgomery County, Pennsylvania,
used trichloroethylene as a degreaser and cleaner in their manufacturing pro-
cess* They stored the solvent in three, 500-gal. underground tanks. Trichloro-
ethylene was not to be stored in the tanks for longer than 2 years. During an
investigation in 1978 of complaints of odors coming from groundwater sources
in the area, the Pennsylvania Department of Environmental Resources discovered
concentrations as high as 330 ppm trichloroethylene in Uniform Tube's private
well. Further investigation led to the discovery of contamination through leak-
age of one of Uniform Tube's underground storage tanks. A survey of the area
has identified at least 25 private wells and two public water supply wells af-
fected. Uniform Tube has been treating their well by spray irrigating for a
year now. This process involves spraying the contaminated groundwater into the
air causing trichloroethylene removal by evaporation. This treatment process
does reduce the trichloroethylene concentrations after spraying; however, the
groundwater concentrations have not been significantly reduced. It is felt by
the company's consultant that the leachate through the spray field is rinsing
the soil of the trichloroethylene adhering to it. Soil analysis under the spray
field indicates levels of 5,000 to 7,000 ppb trichloroethylene. The groundwater
concentration will not be significantly reduced until the soil is adequately
flushed. It is unknown when this will occur and the spray operation is continu-
ing.
Around November 1975, the Pennsylvania Department of Environmental Re-
sources traced a private well to a groundwater discharge from Superior Tube
Company, Upper Providence Township, Montgomery County. The well had concentra-
tions as high as 17 ppm trichloroethylene. Superior Tube Company is using a
vertical pack air stripping technique for reduction of trichloroethylene. The
contaminated well is used for cooling water only. The air stripping technique
appears to be doing a good job. The Pennsylvania Department of Environmental
Resources does not have sufficient data at this time to determine the treat-
ment technique's impact on groundwater quality in the immediate area. Ground-
water quality in this area will be monitored in the future.
As a result of poor handling procedures, trichloroethylene used by the
Reading Door Closer Corporation contaminated their own well and a public water
supply well owned by the East Cocalico Township Water Authority, Lancaster
County. The public water supply was required to shut down Well No. 1 where con-
centrations of 40 ppb trichloroethylene were found. As a result of shutting
down Well No. 1, Well No. 3A (which is on the same aquifer as Well No. 1 and
Reading Door Closer's well but farther away) began to show concentrations of
the solvent. To slow this migration to Well No. 3A, the well was cut back to
one-fourth its production rate and Well No. 1 was pumped to a nearby stream.
7-31
-------
The discharge from Well No. 1 is being monitored and the instream concentra-
tion at the nearest downstream water supply intake is less than the detectable
limit. This action appears to have slowed the trichloroethylene migration to
Well No. 3A« The water supplier made an interconnection with Denver Borough
using Civil Defense pipe and pump. The water supplier is also developing an-
other well on a different aquifer. The industry has improved their handling
procedure and has employed a consultant to assist the water supplier and de-
velop a scheme for renovation of the contaminated groundwater.
In Middletown Township, Delaware County, an investigation into a taste
and odor complaint has led to the discovery of groundwater contamination of
a private well with levels of 200 to 300 ppb trichloroethylene. This residence
is located in a rural area with no industrial use of this solvent in proximity
to the well. An investigation indicates that the source of contamination was
the result of a neighbor treating his sewage system with a chemical product
designed to unclog drain fields. Laboratory analysis of this product and of
the contaminated well both show concentrations of trichloroethylene and simi-
lar chemical constituents. Investigations in this case are continuing at the
time of this report.
Currently, 18 community drinking water supply wells have been closed in
Nassau County, New York, by the New York State Health Department. Sixteen of
these wells are closed due to contamination by methyl chloroform, trichloro-
ethylene, perchloroethylene, or any combination of two or more compounds.
[Note: detection of 50 ppb (in two consecutive tests) of any organic chemical
is necessary before a well is closed.] There is a total of 440 water supply
wells in this county, and all drinking water in the county comes from these
wells (Fleisher, 1978).
Some of the present contamination is due to the use of halogenated hydro-
carbon cesspool cleaners (and drain openers). Until recently, about 75,000 gal.
of cesspool cleaner (from 11 formulators) were used each year in Nassau County.
These high volumes are consumed because much of the county is not connected to
a municipal sewer system.
The major product contained 30% methyl chloroform (in addition to 20%
methylene chloride and 50% petroleum distillates). The cesspool cleaners are
sold in 5-gal. cans; 1 can per month is generally used. Nine of 11 formulators
have agreed to stop selling in Nassau County; one formulator is conducting
biodegradation tests on its product, the other is under litigation by the New
York State Attorney General's office to stop selling. Halogenated hydrocarbon
cesspool cleaners are currently being used in Nassau County, although it is
not known to what extent.
7-32
-------
The maximum detected levels of the subject compounds in the contaminated
drinking water wells are:
Trichloroethylene 300 ppb
Perchloroethylene (tetrachloroethylene) 375 ppb
Methyl chloroform (1,1,1-trichloroethane) 310 ppb
However, in observation wells (drilled for contaminant monitoring purposes),
methyl chloroform has been detected as high as 5,000 ppb.
Trichloroethylene and perchloroethylene are generally not used as cess-
pool cleaning agents or drain cleaners in this county. Their presence is most
likely due to past industrial dumping. (Dumping is currently outlawed.) Most
of the methyl chloroform contamination is occurring in the unsewered area and
is not currently a county-wide problem.
Trichloroethylene and methyl chloroform (and other organic solvents) have
been detected (at levels greater than 300 ppb) in well water of residents liv-
ing in Gray, Maine (Toxic Materials News, 1978). The solvents were seeping into
the soil from an industrial waste contractor operating on a 1-1/2-acre site,
which resulted in localized contamination of nearby (up to 3/4 mile from the
site) wells on that aquifer. In addition, samples taken from the Gray Water
District supply (treated water also from a groundwater source, although on a
different aquifer) contained traces (1 to 2 ppb). No health effects were re-
ported by either the residents served by Gray Water District or those with
wells. A waterline from Gray Water District now serves the residents in the
problem area (Healy, 1978). Residents living near the industrial waste con-
tractor first became aware of the contamination because of taste and odor
problems due to dimethyl sulfoxide in the well water.
Trichloroethylene, perchloroethylene, and methyl chloroform have been de-
tected in the soil in the Love Canal area of Niagara Falls, New York (Huffaker,
1978). Heavy rains in that area have caused pools of toxic liquid waste to form
in basements and yards. Residents of the Love Canal area have relocated. The
source of the contamination has been traced to the dumping of industrial waste
into the canal over the years.
7.3 SOIL AND SEDIMENT
In this subsection, data will be presented for concentrations of the sub-
ject compounds detected in soil and sediment near manufacturing plants, user
sites, other sites within the United States, and non-U.S. sites. Due to the
small amount of information, all available data will be combined under the
subheadings of either soil or sediment.
7-33
-------
7.3.1 Soil
The only study concerned with the concentrations of the three subject
compounds in soil was conducted recently by Battelle (1977). They studied the
levels of trichloroethylene and methyl chloroform in soil in the vicinity of
producers and users. The concentrations of trichloroethylene and methyl chloro-
form were found generally in the parts per trillion level and occasionally in
the low parts per billion range. The range of concentrations detected varied
from "not detected" for both trichloroethylene and methyl chloroform to a high
of 3.4 ppb of methyl chloroform at the Dow Chemical facility in Freeport,
Texas, and 5.6 ppb of trichloroethylene at the Hooker Chemical plant in Taft,
Louisiana. The detection limits were 6 pg for methyl chloroform and 10 pg for
trichloroethylene.
7.3.2 Sediment
Methyl chloroform and trichloroethylene levels in fresh water sediment
were measured by Battelle (1977) in the vicinity of producers and users. Methyl
chloroform was generally detected in the parts per trillion range and in the
low parts per billion range. The levels varied from "not detected" to a high
of 6.1 ppb at the Dow facility in Freeport, Texas.
Trichloroethylene levels varied widely from "not detected" to a high of
300 ppb at the Hooker Chemical facility at Taft, Louisiana. Of the samples
taken, only four showed levels greater than approximately 3 ppb. These were
300 ppb in the black ooze of an open canal 100 m from a highway near the Hooker
Chemical facility, 146 ppb in the black ooze 50 m upstream from the PPG facil-
ity outlet at Lake Charles, 116 ppb at a point 300 m upstream of the Ethyl Cor-
poration outfall, and 15 ppb at the confluence of the PPG southern effluent
canal and the bayou. With the latter exception, none of the high values were
at the outfalls or downstream of the outfalls. Two were upstream and the third,
the highest, was at a point on the opposite side of the plant from the outfall.
The high levels in the roadside canal could result from transport trucks leak-
ing trichloroethylene and rainfall washing the compound into the canal. At the
Ethyl facility, the level of 116 ppb of trichloroethylene was found 300 m up-
stream of the outfall, but a sample taken 200 m upstream of the outfall did
not show any detectable levels of trichloroethylene.
Marine sediments in the Liverpool Bay near a major producer of chlori-
nated hydrocarbons were analyzed and reported by Pearson and McConnell (1975).
These concentrations range from a few parts per trillion to a maxima of about
10 ppb for trichloroethylene, 4.8 ppb for perchloroethylene, and 5.5 ppb for
combined methyl chloroform and carbon tetrachloride. These concentrations are
very similar to those found in the water samples from Liverpool Bay. However,
there was no direct correlation between the concentration in sediment and that
of the water which was above it at the time of sampling, nor was there any ap-
parent correlation between high concentrations and geographical features.
7-34
-------
7.4 FOOD
The Food and Drug Administration (FDA) is currently sampling freshwater
fish (species unidentified) and shellfish (unidentified) for levels of tri-
chloroethylene and perchloroethylene (Entz, 1978). This agency is also working
on a methodology for sampling foodstuffs, but no decision has been made to in-
clude these compounds in the FDA "Market Basket Survey." For the freshwater
fish, perchloroethylene has been detected at levels of less than 10 ppb, but
this may have been due to contamination in the storage procedure. Trichloro-
ethylene has not been detected in any freshwater fish samples. Thus far, very
little sampling has been done with shellfish.
Only one study conducted in England by McGonnell et al. (1975) reported
the concentrations of trichloroethylene, methyl chloroform, and perchloro-
ethylene found in foodstuffs. This study analyzed a wide variety of food of
both animal and vegetable origin (Table 7-13). They found levels ranging from
0.01 to 60 ppb. Tea (packet) contained the highest level of these compounds
(60 ppb). No trade name for the tea was given. Olive oil (Spanish) contained
the highest concentration of methyl chloroform (10 ppb), while English butter
contained the highest concentration of perchloroethylene (13 ppb).
7.5 EXPOSURE LEVELS
7.5.1 Human Exposure
Trichloroethylene, methyl chloroform, and perchloroethylene can be assim-
ilated by inhalation, ingestion (food or water), and absorption through the
skin. All three compounds are used in a variety of commercial products; the
vast majority of these products being pesticides and cleaner-type products
(see Appendix A). The number of individual products containing these compounds
is rather small and the total quantity of material employed in these products
is very small compared to the other use areas. While this source of exposure
cannot be disregarded as a potential source of exposure to elevated concentra-
tions, data related to the frequency and duration of use, concentration levels
during use, and the number of individuals affected are not available. For
these reasons, exposure due to commercial products will not be considered in
this discussion.
Absorption through the skin can occur during bathing or swimming in wa-
ter containing these compounds. In view of the short exposure time associated
with these activities, the relatively low levels found in water supplies, and
the relatively long time required for absorption, the amount of absorption
through the skin during bathing and swimming is considered negligible compared
to the amounts which would be assimilated.
7-35
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TABLE 7-13. CHLORINATED HYDROCARBONS IN ENGLISH FOODSTUFFS
Methyl
Foodstuff chloroform
Dairy produce
Fresh milk
Cheshire cheese
English butter
Hen eggs
Meat
English beef (steak) 3
English beef (fat) 6
Pig liver 4
Oils and fats
Margarine
Olive oil (Spanish) 10
Cod liver oil 5
Vegetable cooking oil
Castor oil 6
Beverages
Canned fruit drink
Light ale
Canned orange juice
Instant coffee
Tea (packet) 7
Wine (Yugoslav)
Fruit and vegetables
Potatoes (S. Wales) 4
Potatoes (N.W. England) 1
Apples 3
Pears . 2
Tomatoes^ .
Black grapes (imported)-
Fresh bread 2
Trichloroethvlene
0.3
3
10
0.8
16
12
22
6
9
19
7
ND
5
0.7
ND
4
60
0.02
ND
3
5
4
1.7
2.9
7
Perchloroethvlene
0.3
2
13c/
ND^'
0.9
1.0
5
7
7
2
0.01
3
2
ND
ND
3
3
ND
ND
0.7
2
2
1.2
ND
1
a/ Tomato plants were grown on a reclaimed lagoon at Runcorn Works of ICI.
bi HCBD is still used in some countries as an insecticide for vineyards.
_c/ ND = not detected.
Note: Concentrations in micrograms per kilogram (ppb).
Source: McConnell et al. (1975).
7-36
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For perchloroethylene, the only major use different from the other two
compounds is in the dry cleaning industry. Most dry cleaning establishments,
in which consumers operate the machines, employ the dry-to-dry method of clean-
ing so that the potential for contact with liquid perchloroethylene would be
very minor compared to the potential for inhalation. Thus, absorption through
the skin is considered to be negligible for all three compounds.
Levels of each of these three compounds in foodstuffs have not been de-
termined except in England. The FDA is developing the methodology for analysis
of the levels of trichloroethylene, methyl chloroform, and perchloroethylene
in foodstuffs in the United States, but no decision has been made to include
these compounds in the "market basket survey" (Entz, 1978).
On the basis of the above information, the two sources of introduction
of these compounds into the body considered in this subsection are inhalation
and ingestion of contaminated water.
In preceding subsections, data were presented for ambient air concentra-
tions and drinking water levels for each of the three subject compounds in
various cities and areas within the United States. As evidenced from that com-
pilation, a relatively limited amount of data exists for either ambient air or
drinking water levels and in only very few cities or areas, primarily the man-
ufacturing sites, are data available for both air and water levels. Because
of the lack of data, it is very difficult to calculate or assess total exposure
values for any large geographical areas.
There are additional factors that must also be considered concerning the
available data. For air data, the sample site in geographical relation to the
highly industrialized areas of the city and the prevailing wind direction would
be significant factors in the observed levels. As an example, New York City
lies to the northeast of the highly industrialized sector of New Jersey. With
a southwesterly prevailing wind, ambient air levels could be subject to consid-
erable variation depending upon the location of the air sampling sites within
the city. This same type of rationale would also be true for any sample sites
in other highly industrialized cities such as Chicago, Cleveland, Detroit,
Pittsburgh, and others.
Drinking water levels may also be affected by the source of the water
and the particular site of the raw water intake system. If river or lake water
is utilized by large metropolitan cities, multiple intake systems may be em-
ployed. The site of these systems, in relation to the effluents from highly
industrialized areas, may have a pronounced effect on the levels of certain
constituents in the finished drinking water.
7-37
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Few studies have been conducted on the effects on humans from chronic ex-
posure to trichloroethylene, methyl chloroform, or perchloroethylene. Without
these data, there is no substantial basis for determining the minimum daily
intake necessary to produce an onset of toxic symptoms, and the effects of long
term, low level exposure to these compounds can only be estimated. In certain
instances, data from laboratory animals can be utilized to provide a tentative
guideline as to potential chronic effects in humans*
Data for total inhalation levels of each of the three compounds (presented
in the next subsection) are based on an average body weight for an adult of
70 kg and an average daily inhalation volume of 20 np of air per day (Gember,
1969). An average adult will ingest approximately 2.2 liters/day of water from
foods and fluids. If drinking water used for personal hygiene and other miscel-
laneous routes of ingestion are included, the estimated, average daily intake
volume is 3 liters.
Values appear in the literature for the calculated retention of these com-
pounds but, due to the nature of the studies, i.e., long time measurement of
exhaled quantities and the wide variation in the values, none are completely
suitable for the required calculations. One study, Morgan et al. (1970), in-
volved the inhalation of a single dose of isotopically labeled compound. Ex-
haled air was trapped for a period of 1 rain following inhalation and the quan-
tity of exhaled compound measured. The estimated total dose inhaled was 5 mg
for each compound. For trichloroethylene, methyl chloroform, and perchloro-
ethylene, percentages of each compound exhaled were found to be 15, 44, and
10%, respectively, over the 1-min time period. Although it is recognized that
this study is not directly applicable, retention values of 56% for methyl
chloroform, 8570 for trichloroethylene, and 90% for perchloroethylene will be
assumed for these calculations.
7.5.1.1 Exposure From Air~
The calculated levels of human exposure to trichloroethylene, methyl
chloroform, and perchloroethylene for various cities and areas in the United
States are summarized in Table 7-14. These calculated levels are based on mon-
itoring data presented earlier in this section. For trichloroethylene, the
calculations show that only five cities have bodily retentions of greater than
1.5 /ug/kg body weight per day (/^g/kg/day). Seattle, site of a trichloroethylene
user facility, ,had the highest level (25.8 /ag/kg/day). The other four cities,
Hahnville (18.08), Lake Charles (3.12), Freeport (2.31), and Baton Rouge (1.82)
are all sites of manufacturing plants. All of the samples were taken at sites
near the production facilities. A second set of data taken in Freeport showed
a value of < 1.29 jug/kg/day. Sampling data from large cities with a high popu-
lation density, e.g., New York, Los Angeles, and Houston, all showed values
of about 1 /ng/kg/day or less. Data for two areas isolated from the production
or use of trichloroethylene, White Face Mountains and St. Francis National
Forest, showed values of 0.14 and < 1.29 /zg/kg/day, respectively.
7-38
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TABLE 7-14. CALCULATED LEVELS OF HUMAN EXPOSURE BASED UPON
AIR CONCENTRATION DATA
Trichloroethvlene
Site
New York, NY
Seagirt, NJ
Sandy Hook, NJ
Bayonne , NJ
tfhiteface Mountains, NY
Delaware City, DE
Baltimore, HD
Wilmington, OH
St. Francis National Forest, AR
Geisraar, LA
Hahnvllle, LA
Baton Rouge, LA
Lake Charles, LA
Freeport, TX
Freeport, TX
Houston, TX
Pasadena, TX
Deer Park, TX
La Porte, TX
Los Angeles, CA
Los Angeles Basin, CA
Pa la Springs, CA
San Bernardino, CA
Santa Clara Valley, CA
Pomponio Beach, CA
Mt. Diablo, CA
Stanford Hills, CA
Point Reyes, CA
Maumoth Lakes, CA
Yoaemite, CA
Pullman, WA
Seattle, WA
Cone.
in air
(ppb)
0.71
0.26
0.34
0.92
0.1
0.35
ND*/
0.19
< 1
< 1
13.9
1.40
2.4
< 1
1.8
<0.01
0.48
0.08
<0.01
0.31
NS
0.04
NS
ND
ND
ND
0.11
0.03
ND
0.016
< 0.005
19.8
Exposure
(ng/kg/day)
0.92
0.34
0.45
1.20
0.14
0.46
-
0.26
< 1.29
<1.29
18.08
1.82
3.12
<1.29
2.31
<0.02
0.62
0.10
<0.02
0.41
-
0.05
-
-
-
.
0.14
0.03
-
0.02
<0.01
25.80
Methyl
chloroform
Cone.
in air
(ppb)
0.61
0.10
0.15
1.59
0.067
0.10
0.12
0.097
< 0.3
15.0
<0.3
0.60
1.3
1.7
0.5
0.09
(T)£/
0.05
1.93
1.54
0.37
0.16
0.05
0.01
0.01
0.01
0.14
0.11
0.01
0.1
0.1
0.45
Exposure
(f.g/kg/day)
0.52
0.09
0.14
1.39
0.07
0.09
0.10
0.09
<0.26
12.86
< 0.26
0.53
1.11
1.46
0.43
0.09
<0.02
1.68
1.34
0.33
0.14
0.05
0.02
0.02
0.02
0.12
0.10
0.02
0.09
0.09
0.39
Perchloroethylene
Cone.
in air
(ppb)
4.5
0.32
0.39
1.63
0.07
0.24
0.18
0.15
<0.3
2.2
4.5
1.60
0.7
NS^
0.5
NS
0.003
°-05 H/
0.012^
0.67
1.25
0.28
0.09
ND
ND
ND
NS
NS
ND
NS
0.02
0.66
Exposure
(jig/kg/day)
7.80
0.55
0.69
2.83
0.12
0.41
0.31
0.26
<0.51
~3.86
7.80
2.78
1.20
-
0.86
<0.01
~0.09
0.02
1.17
2.18
0.50
0.15
-
-
-
-
-
-
-
0.03
1.15
Population
9,597,000
3,607
Unknown
68,900
Unknown
2,204
2,148,700
10,300
Unknown
100
2,522
419,400
151,600
10,600
2,364,794
73,000
7,000
4,512
6,987,200
6,755,000
27,000
107,000
86,800
Unknown
Unknown
Unknown
300
900
900
21,906
1,385,198
Calculation parameters: Trlchloroethylene - 1 ppb = 5.36 ug/m3
857. retention In lungs, 15% immediately exhaled
(Morgan et al., 1970).
Methyl chloroform - 1 ppb =5.44 ug/m3
56% retention in lungs, 44% immediately exhaled
(Morgan et al., 1970)
Perchloroethylene - 1 ppb =6.75 ug/m3
907. retention in lungs, 107. immediately exhaled
(Morgan et al., 1970).
a/ ND « not detected.
j>/ NS - not sampled.
£/ (T) » trace quantity.
d/ Maximum perchloroethylene level.
Source: Exposure values calculated by reported air concentration data.
7-39
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Ambient air level data for trichloroethylene from the manufacturing facil-
ities and the one user site were average values. If the maximum concentration
level recorded for any single sample were used, then considerably higher values
would be obtained* Using these maximum levels, body retention values for tri-
chloroethylene from manufacturers are all above 9 /^g/kg/day with Hahnville be-
ing the highest at a value of about 350 /jg/kg/day; all other manufacturers were
less than 20 /ug/kg/day. For the trichloroethylene user facility at Seattle, the
body retention value was about 57 /^g/kg/day.
For methyl chloroform, only one city showed a bodily retention value in
excess of 2 |Ug/kg/day. The city was Geismar, a manufacturing facility for methyl
chloroform, and the value near the facility was 12*86 /ig/kg/day. All other val-
ues ranged from a high of 1,68 at La Porte to a low of < 0»02 at Deer Park.
Sampling data from large cities with a high population density, e.g., New York,
Los Angeles, Baltimore, and Houston, ranged from a high of 1.34 in the general
Los Angeles area to a low of 0.09 in Houston and 0.10 in Baltimore. An average
of a number of samples taken at various sites in the Los Angeles Basin gave a
body retention value of 0.33 /ig/kg/day. Calculated values for the two areas
isolated from the production or use of methyl chloroform, White Face Mountains
and St. Francis National Forest, were 0.07 and < 0.26, respectively. Ambient
air level data for the manufacturing facilities and the one user site were av-
erage values. If the maximum concentration level of any single sample were used,
then significantly higher body retention values would be obtained. Using these
maximum air levels, calculated retention values for methyl chloroform from man-
ufacturers are all above 3 /xg/kg/day with Geismar being the highest at a value
of approximately 135; other values are 10.0 and 7.4 //g/kg/day. (Ethyl Corpora-
tion at Baton Rouge has discontinued production of methyl chloroform.) For the
methyl chloroform user site in Seattle, Washington, the maximum calculated body
retention value was 8.7 ^g/kg/day.
In Table 7-14, calculated bodily retention values for perchloroethylene
are less than 1.2 ^8/kg/day in all cities and areas except for New York City,
Bayonne, Geismar, Hahnville, Baton Rouge, and the Los Angeles Basin. New York
City and Hahnville showed the highest values at 7.8, followed by Geismar (3.86),
Bayonne (2.83), Baton Rouge (2.78), and the Los Angeles Basin (2.18). Of these
cities, Hahnville, Geismar, and Baton Rouge are production sites. New York City
and the Los Angeles Basin represent areas in which a high population density
is exposed to perchloroethylene, with the level of the New York area being
approximately 3.5 times that of Los Angeles. The greatest percentage of the
emissions probably results from dry cleaning establishments, so that it might
be anticipated that levels in other large cities may also be in this range.
However, calculated body retention levels for Baltimore and Seattle, the only
other cities with populations over 1 million that were sampled, are both less
than 1.2 />g/kg/day.
7-40
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Using the maximum air levels recorded for single samples at manufacturing
sites, calculated body retention values are all above 5 /zg/kg/day, with
Hahnville being the highest at 81.6, Baton Rouge at 64.2, and Geismar at 39,9.
In general, the data presented in Table 7-14 show that, for the cities
and areas sampled, a relatively small segment of the general population is ex-
posed to trichloroethylene or methyl chloroform ambient air concentrations that
would result in the bodily retention of greater than 1,5 jug/kg body weight per
day. However, it should also be noted that the one user site showed the high-
est level for trichloroethylene. Highly industrialized cities with many metal
cleaning facilities may also show high values. Obviously, additional data are
required for such cities before any conclusions can be drawn regarding user
sites. For perchloroethylene, it would seem that dry cleaning establishments
are a major source of ambient air levels. However, the data presented earlier
in this section for the dry cleaning establishments in California and the other
three establishments in Michigan, Texas, and Pennsylvania were for intermittent
emissions. While these emissions were often over 100 ppm, it is very difficult
to establish any type of exposure data because of the nature of the emissions.
These sources will have an effect on the ambient air levels in the vicinity of
these establishments, but the overall exposure due to the ambient air levels
cannot be readily obtained from these data.
7.5.1.2 Exposure From Water--
The presence of trichloroethylene, methyl chloroform, or perchloroethylene
in water occurs primarily due to discharge of these chemicals by manufacturers
or users. Since the use of these chemicals is much more geographically diversi-
fied than the manufacture, the primary source of widespread aqueous contamina-
tion is due to the discharge of waste material by users rather than by manu-
facturers. Principal sources of these chemicals result from metal cleaning
operations and from discharge into sewer systems by dry cleaning establishments.
Ghlorination of raw water supplies in water purification plants may be a
potential source of these chlorinated materials. Evansville, Ohio, was cited
as one instance in which the level of trichloroethylene increased from unde-
tectable in the raw water supply to 5 ppb in the finished water. However, at
eight other sampling sites, no difference was found between the concentrations
in the raw water supply and the finished water. Differences in water quality
and the specific impurities in the raw water supply could have an effect on
the products resulting from the chlorination process.
Drinking water data have been compiled from the literature for samples
taken in 20 cities in the United States. Of these cities, two (Terre Bonne
Parish, Louisiana, and Seattle, Washington) were found to contain no detect-
able levels of trichloroethylene, methyl chloroform, or perchloroethylene.
Table 7-15 presents the calculated exposures to trichloroethylene.
7-41
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TABLE 7-15.
CALCULATED EXPOSURE TO TRICHLOROETHYLENE
FROM DRINKING WATER
Site
Philadelphia, PA
Miami, FL
Evansville, OH
Cincinnati, OH
Chicago, IL
Des Moines, IA
Ottumwa, I A
Helena, AR
Baton Rouge, LA
Lake Charles, LA
Freeport, TX
Cone, in
drinking
water
(/^g/&)
0.5
0.2
5.0
0.1
2.0
32. O^/
0.1
22.0
0.4
0.1
19.0
Calculated
exposure
(/ig/kg/day)—
0.03
0.01
0.25
< 0.01
0.10
1.60
< 0.01
1.10
0.02
< 0.01
0.95
Population
4,782,100
2,345,000
350
1,422,000
7,655,000
310,000
28,200
9,700
419,400
151,600
10,600
a_l Based on an average intake of 3 £/day.
b/ Contaminated water supply (see subsection on monitoring
data).
Source: Midwest Research Institute; from concentration data
presented earlier in Section 7.
In addition to those sites listed in the table, trichloroethylene was not de-
tected in samples taken from the following cities: Lawrence, Massachusetts;
New York, New York; Beaver Falls, Pennsylvania; Pittsburgh, Pennsylvania;
Huntington, Ohio; Cincinnati, Ohio (one study); Grand Forks, North Dakota; and
Tucson, Arizona* Two cities, Des Moines (1*60) and Helena (1.10), were found
to have body intake values for drinking water in excess of 1 /ug/kg body weight
per day. Freeport showed a calculated value of 0.95 /ug/kg/day, and all other
cities had values of 0.25 or less. No data are available for raw water levels
at Helena, Arkansas. The only available data are for samples from the
Mississippi River at Memphis, Tennessee, upstream from Helena. Those samples
were found to contain 1 jug or less of trichloroethylene. Freeport is the site
of a large manufacturer of trichloroethylene.
The data for methyl chloroform is more difficult to assess than that for
trichloroethylene because of the lack of precise quantitative data. Des Moines,
Iowa, samples were not analyzed for methyl chloroform. Samples of drinking wa-
ter were found to contain no detectable quantities of methyl chloroform in the
7-42
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following cities: Lawrence, Massachusetts; New York, New York; Philadelphia,
Pennsylvania; Miami, Florida; Ottumwa, Iowa; Grand Forks, North Dakota; and
Tucson, Arizona* Quantities of methyl chloroform were detected but quantified
only as less than 1 |Ug/liter in the following cities: Beaver Falls,
Pennsylvania; Pittsburgh, Pennsylvania; Huntington, Ohio; Evansville, Ohio;
and Cincinnati, Ohio (one study). A second study of the drinking water at
Cincinnati showed trace quantities of methyl chloroform to be present. Data
for the remaining five cities were calculated to be as follows:
Cone, in
drinking Calculated
water exposure
City (tfg/1) (Mft/kg/day)
Chicago, IL 1.0 0.05
Baton Rouge, LA 0.05 0.01
Lake Charles, LA 0.3 0.02
Freeport, TX 17.0 0.85
Helena, AR 0.4 0.02
The only city with significant calculated bodily intake quantities is Freeport,
which was also among the three highest for trichloroethylene. Dow Chemical Com-
pany produces methyl chloroform in Freeport. Large metropolitan areas, with
high population densities, generally show little, if any, methyl chloroform
in the drinking water.
A summary of the exposure data calculated for perchloroethylene is shown
in Table 7-16. Drinking water samples were not analyzed for perchloroethylene
in Des Moines, Helena, Baton Rouge, Lake Charles, and Freeport. Cities in which
perchloroethylene was not detected were Huntington and Cincinnati (one study).
In Beaver Falls, Pittsburgh, and Evansville, perchloroethylene was detected in
the samples, but it was only stated that the levels were less than 1 ^g/liter.
Of the cities shown in the table, only Chicago had calculated body intake lev-
els above 0.02 /^g/kg/day for drinking water.
7.5.2 Total Human Exposure
For a few cities, both ambient air concentrations and drinking water lev-
els have been determined. The summary presented in Table 7-17 shows the esti-
mated quantities of trichloroethylene, methyl chloroform, and perchloroethylene
introduced into the body from both ambient air and drinking water concentrations.
There are few cities for which both sets of data (air and water) are available.
Because of this, it is very difficult to estimate the total intake of these
compounds for any sizable geographical area. While extrapolations based solely
on the population of a given city to other cities of similar size might be at-
tempted, the air and water levels show a significant variation among cities of
7-43
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TABLE 7-16.
CALCULATED EXPOSURE TO PERCHLORO-
ETHYLENE FROM DRINKING WATER
Site
Lawrence, MA
New York, NY
Philadelphia, PA
Miami, FL
Cincinnati, OH
Chicago, IL
Ottumwa, I A
Grand Forks, ND
Tucson, AZ
Cone . in
drinking
water
(Mg/JO
0.07
0.46
0.4
0.1
0.3
2.0
0.2
0.2
0.01
Calculated
exposure
(/.g/kg/day^7
< 0.01
0.02
0.02
< 0.01
0.02
0.10
0.01
0.01
< 0.01
Population
272,600
9,597,000
4,782,100
2,345,000
1,422,000
7,655,000
23,200
4;;, 100
465,900
j./ Based on an average intake of 3 i/day.
Source: Midwest Research Institute; from concentration data
presented earlier in Section 7.
TABLE 7-17.
CALCULATED EXPOSURE FROM AIR AND
DRINKING WATER
Location
Trichloroethylene
New York, NY
Baton Rouge, LA
Lake Charles, LA
Freeport, TX
Seattle, WA
Methyl chloroform
New York, NY
Baton Rouge, LA
Lake Charles, LA
Freeport, TX
Seattle, WA
Perchloroethvlene
New York, NY
Seattle, WA
Ambient air
(ng/kg/day)
0.92
1.82
3-12a/
2.31-
25.80
0.52
0.53
1.11 ,
1.46*'
0.39
7.80
1.15
Drinking water
(ng/kg/day)
0
0.02
< 0.01
0.95
0
0
< 0.01
0.02
0.85
0
0.02
0
Population
9,597,000
419,400
151,600
10,600
1,385,198
9,597,000
419,400
151,600
10,600
1,385,198
9,597,000
. 1,385,198
£/ The highest ambient air levels in Table 7-14 were used to obtain a
"worst case" total level.
Source: Midwest Research Institute; from data presented earlier in Section 7.
7-44
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approximately the same population (e.g., New York City, Los Angeles, and
Chicago or Cincinnati and Seattle). For this reason, no attempt will be made
to generalize on these data, since such generalizations would necessarily be
very broad and could lead to misinterpretation*
7.5.2.1 Trichloroethylene--
New York and Seattle are the only two nonmanufacturing cities for which
data are available, and these two show a strikingly wide variation* While nei-
ther city showed detectable levels of trichloroethylene in the drinking water,
the calculated bodily intake levels from inhalation represented the highest
and lowest of the five cities. New York has a calculated total body intake of
0*92 /ng/kg/day, all due to ambient air concentrations. In contrast, Seattle
has a calculated total intake of 25 »8 /^tg/kg/day, the highest of the five cit-
ies. As with New York, this level is due solely to inhalation. Seattle was the
only identified trichloroethylene user site for which data were available.
For Baton Rouge, a total daily intake of 1.84 /ig/kg/day is calculated. In Lake
Charles, the total of the ambient air data and the drinking water data is ap-
proximately 3.12 //g/kg/day. In both of these cities, the principal source of
the total daily intake is the ambient air, with the values for water playing
a minor role. Freeport represents the only city in which the water levels of
trichloroethylene constitutes a significant part of the calculated total daily
body intake. The body levels due to inhalation is 2.31 /ig/kg/day; combining
that value with the one for drinking water (0.95) gives a total daily body in-
take of 3.26 M8/kg/day.
In terms of widespread population exposure to trichloroethylene, there is
insufficient data to attempt any type of accurate representation of the extent
of total human exposure to the compound. However, some generalizations can be
made with regard to those cities having production facilities for trichloro-
ethylene. Geismar showed an air value of < 1.29 /ng/kg/day so that if the water
value is assumed to be in the range of those calculated for Baton Rouge and
Lake Charles (~ 0.02 jzg/kg/day), the total calculated body intake would be ap-
proximately 1.3 |ig/kg/day. Hahnville presents a situation in which the value
calculated from the air concentrations (18.08) is considerably higher than the
values for the other production sites. If, as for the other production sites
in Louisiana, the calculated daily intake values for water are minor compared
to the air levels, then the total intake values might be expected to be of the
order of 18 /^g/kg/day.
7.5.2.2 Methyl Chloroform—
For this compound, data are available for the same five cities as for
trichloroethylene. New York and Seattle, both nonproduction sites, show total
daily intake values of 0.52 and 0.39 /ug/kg/day, respectively, which are at-
tributable solely to air levels. No detectable levels of methyl chloroform
were found in the drinking water of either city. Baton Rouge, a former pro-
duction site, has a calculated total intake value approximately the same as
for New York. The remaining two cities are active production sites and show
7-45
-------
total values higher than the previous three cities. Lake Charles shows a total
intake value of 1.13 /ig/kg/day. As in the case with trichloroethylene, the in-
take from water is minor compared to the intake from air* The total intake for
Freeport is 2.31 jxg/kg/day. The intake from drinking water was approximately
50% of the intake from air. This ratio is different from the other four cities
in which the water intake was a small fraction of the total intake. As with
trichloroethylene, there is insufficient data to assess the overall human ex-
posure for large population access.
7.5.2.3 Perchloroethylene--
The data base for total exposure to this compound is very small with val-
ues for only two cities, New York and Seattle. These cities, however, show con-
trasting levels. New York has a calculated total daily intake of 7.82 of which
7.80 is due to inhalation. In contrast, Seattle showed a total intake of 1.15,
all of which was due to inhalation. No generalizations with regard to overall
population exposure to perchloroethylene seem appropriate, except to note that
the exposure in New York represents a very large population base.
7.5.2.4 Other Assessments of Perchloroethylene--
A study has been conducted to estimate the environmental exposure of the
U.S. population to atmospheric perchloroethylene emissions (SRI, 1979). The
three principal sources of atmospheric perchloroethylene considered in the
study were facilities in which the chemical was produced or used as an inter-
mediate, dry cleaning operations, and metal cleaning operations. Average an-
nual concentrations in the vicinity of manufacturing facilities were esti-
mated by dispersion modeling for populations exposed to average annual levels
greater than 0.01 ppb; for urban dry cleaning and metal cleaning operations,
average annual concentrations were estimated for populations exposed to av-
erage annual levels greater than 0.05 ppb.
The two largest sources of exposures are commercial dry cleaners and metal
cleaning operations, each of which affect 30 million people. Metal cleaning op-
erations are also the source of the largest number of exposures at concentrations
greater than 1.0 ppb. Weighted exposures were calculated by multiplying the popu-
lation exposed by the annual average concentration in each range to produce es-
timates expressed in ppb-persons-years. Those results show that the highest ex-
posures result from metal cleaning operations (8.0 x 10° ppb-persons-years), fol-
lowed by commercial dry cleaners (7.8 x 10"), industrial dry cleaners (1.2 x
10^), coin-operated dry cleaning (0.6 x 10^), and production facilities (0.01 x
10"). These preliminary estimates indicate that the total exposed population
is substantial and that further monitoring and sampling data are required for
a more thorough assessment.
7.5.3 Aquatic Species
The toxic effects of each of the subject compounds were summarized in
Section 6. In this subsection, an assessment will be made of the known toxic
effects with relation to the levels observed in sampling studies.
7-46
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7.5.3.1 Trichloroethylene--
Unicellular algae with an LC50 level (96 hr) of 8 ppm are the most sensi-
tive species to trichloroethylene. In 96-hr tests, the fathead minnow showed
an EC^Q level of about 14 ppm and an LC-^g level of about 17 ppm. The LC^g
level (96 hr) for the dab is 16 ppm, while for the barnacle, the 48-hr LCcg
is 20 ppm.
Sampling studies of surface water at sites, other than manufacturing and
user sites, showed that of the 204 sites only 11 had trichloroethylene levels
in excess of 5 ppb. Of those 11, four were at levels of 6 and 7 ppb. The high-
est level was about 188 ppb in Lake Erie at Ashtabula, Ohio. This level is ap-
proximately 43 times less than the LG5g level for algae, the most sensitive
species. The next highest level was 29 ppb in the Houston Ship Channel, a fac-
tor of about 275 less than the lethal level for algae. All of the remaining
levels were between 10 and 20 ppb. These levels are a factor of 400 to 800
less than the LG5g level for unicellular algae.
For manufacturing facilities, the highest trichloroethylene level measured
was 535 ppb at the outfall of the Hooker Chemical facility in Hahnville,
Louisiana. Other levels at the outfalls were 447, 179, 172, 128, 126, and 74
ppb. The facility which showed outfall levels of 447 and 179 ppb had a level
of 353 ppb of trichloroethylene at a site 50 m upstream from the outfalls. The
high outfall level is a factor of about 15 less than the LC5g level for algae
and approximately a factor of 30 less than the lowest reported lethal concen-
trations for dabs and fathead minnows. Other outfall levels range from a fac-
tor of 18 to 108 less than the LCgg level for unicellular algae.
Downstream levels greater than 5 ppb were reported to be 403, 37, 24, and
22 ppb. The 403 ppb was at the same facility (Lake Charles, Louisiana) that
showed a level of 353 ppb upstream of the plant outfall. This represents a
level about 20 times below the LCcg level for the unicellular algae. The other
downstream levels represent factors of about 220 to 360 less than the reported
toxic level of the algae.
In general, the data show no sites to exceed the reported toxicity level
for any species. For sites not in the vicinity of manufacturing or user facil-
ities, the trichloroethylene levels are generally a factor of 275 or more less
than the reported toxic limit for the most sensitive species. The lone excep-
tion is a site in Lake Erie. Areas in the vicinity of manufacturing facilities,
however, have trichloroethylene concentrations which range from a factor of
about 15 to 108 less than the IC$Q level for unicellular algae, the most sen-
sitive species.
7.5.3.2 Methyl Chloroform—
The lowest cited toxic effect is for unicellular algae (Phaeodoctylum
tricornutum) for which the LC^g concentration (96 hr) is 5 ppm. Barnacle
nauplii (Elmmius modestus) showed the next lowest LC^g concentration (48 hr)
7-47
-------
of 7*5 ppm* Lethal concentration levels (96 hr) for the other species were all
above 30 ppm* For fathead minnows (Pimephales promelas), an EC^g level of 9.0
ppm was found after 96-hr exposure*
Sampling studies of surface water at sites, other than manufacturing and
user sites, showed no levels of methyl chloroform in excess of 5 ppb* This
level is approximately 1,000 times lower than the LC^g level for the unicellu-
lar algae, the most sensitive species*
Data for the one user facility showed water levels of methyl chloroform
at 6 and 18 ppb; the higher level being a factor of about 275 less than the
lethal concentration for the unicellular algae, and a factor of 500 less than
the level at which toxic effects are seen in 10% of the fathead minnows*
At manufacturing facilities, the aqueous levels of methyl chloroform are.
generally higher* The highest level was 344 ppb at the outfall of the facility
in Geismar, Louisiana. This is only approximately a factor of 15 less than the
LCcQ level of the unicellular algae, a factor of 26 less than the ECiQ level
and about 90 less than the LCiQ level of fathead minnows, and a factor of about
96 less than the LC50 level of the dab. Other outfall levels were 181, 117, 74,
and 58 ppb* These concentrations are 30 to about 85 less than the LG5Q value
of the most sensitive species. At sites downstream from the outfalls, the con-
centrations of methyl chloroform range from less than 5 to 169 ppb. These
levels are about 30 to about 1,000 less than the lethal concentration for the
unicellular algae. The downstream values are dependent upon the initial out-
fall levels and the distance measured downstream. In addition, the levels at
a downstream site are dependent on other factors as well, such as stream flow
volume, turbulence, seasonal variations in flow volume, mixing characteristics,
and outfall volume*
In general, the data show that at no reported site do the methyl chloro-
form levels exceed any reported toxicity level* For nonmanufacturing or user
sites, the methyl chloroform levels are generally about 1,000 or more below
the toxic limit for the most sensitive species* At manufacturing site out-
falls, however, these factors range from about 15 to 85 below the toxicity
levels* Downstream values are between 30 and 1,000 times less than the toxic
limits for the algae, the most sensitive species*
7*5*3*3 Perchloroethylene—
As with methyl chloroform, the barnacle nauplii is the most sensitive
species cited with a 48-hr LGcQ concentration of 3*5 ppm of perchloroethylene*
The dab had a 96-hr LC5Q level of 5.0 ppm. All other reported species have
either 24- to 96-hr LC^g, LG^Q, or EC^g levels greater than 10 ppm (see Table
6-6).
The only sampling studies reported for surface waters are those for sites
not directly associated with the manufacture or use of perchloroethylene* In
7-48
-------
these studies, only four sites showed levels greater than 5 ppb. As with tri-
chloroethylene, the highest level (45 ppb) was found in Lake Erie near
Ashtabula, Ohio. This is a factor of 78 less than the toxic level for the
barnacle* Other sampling sites showed levels of 15, 13, and 6 ppb, which cor-
respond to levels of 233 to 583 less than the LC^g level for the most sensi-
tive species*
For all three subject compounds, no sampling sites were found at which
the toxic levels for the most sensitive species were exceeded* At sites not in
the vicinity of manufacturing or user facilities, the levels generally were a
factor of approximately 250 or more less than the toxic level of the most sen-
sitive species* A concentration factor of 200 less than the toxic limits is
generally accepted to be very desirable to prevent environmental insults which
could result from inadvertent surges in the concentration levels of toxic sub-
stances* For manufacturing sites, outfall levels generally had factors 10 to
200 less than the toxic concentration of the most sensitive species* These
values are in excess of the desired "safety factor" of 200,
7.5,4 Plants
Only one study (Cast and Early, 1956) was found concerning the potential
toxic effects of any of the three subject compounds on plants* In this study,
beans, corn, cotton, cucumbers, and tomatoes were exposed to water containing
0,5 and 5*0% concentrations of methyl chloroform and trichloroethylene* No
major toxic effects were seen on any of the plants at the lower concentration
level* At the higher level, moderate to heavy damage was observed for all of
the plants* At the normal levels found in the environment, no toxic effects
would be anticipated for these plants, except in the instances of an unusually
high concentration such as spills, accidental discharge, leakage of waste con-
tainers, or other similar incidents.
7-49
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REFERENCES
Abrams, E. F., K. M. Slimak, D. L. Derkies, D. K. Guinar, and C. C. V. Fong.
1975. Identification of organic compounds in effluents from industrial
sources. EPA Contract No. 68-01-2926. April 1975.
Battelle. 1977. Determination and evaluation of environmental levels of methyl
chloroform and trichloroethylene. Battelle Columbus Laboratories. March 1977.
Bellar, T. A., J. J. Lichtenberg, and R. C. Kroner. 1974. The occurrence of or-
ganohalides in chlorinated drinking waters, J» Am. Water Works Assoc. 66:703»
Boob, D. R. 1978. Pennsylvania Department of Environmental Resources,
Harrisburg, Pennsylvania. Personal communication. October 20, 1978.
Bunn, W. W., E. R. Deane, D. W. Klein, and R. D. Kleopfer. 1975. Sampling and
characterization of air for organic compounds. Water, Air and Soil Poll.
4:367.
Camisa, A. G. 1975. Analysis and characteristics of trichloroethylene wastes.
J. Water Pollution Control Fed. 47:1021.
Cember, H. 1969. Introduction to health physics, Appendix III: The standard
man. Pergamon Press, New York. p. 408.
Chian, E. S. K., and B. B. Ewing. 1975. Monitoring data to detect previously
unrecognized pollutants. EPA Contract No. 68-01-3234. Institute for Environ-
mental Studies, University of Illinois at Urbana-Champaign.
Correia, Y., G. J. Martens, F. H. Van Mensch, and B. P. Whim. 1977. The occur-
rence of trichloroethylene, tetrachloroethylene, and 1,1,1-trichloroethane
in western Europe in air and water. Atmos. Environ. 11:1113.
Cox, R. A., R. G. Derwent, A. E. J. Eggleton, and J. E. Lovelock. 1976. Photo-
chemical oxidation of halocarbons in the troposphere. Atmos. Environ. 10:305.
Cronn, D. R., R. A. Rasmussen, E. Robinson, and D. E. Harsch. 1977. Halogenated
compound identification and measurement in the troposphere and lower strato-
sphere. J. Geophys. Res. 82:5935.
Dowty, B. J., D. R. Carlisle, and J. L. Laseter. 1975a. New Orleans drinking
water sources tested by gas chromatography-mass spectrometry. Environ. Sci.
Technol. 9:762.
Dowty, B» J., D» R» Carlisle, and J. L. Laseter. 1975b. Halogenated hydrocar-
bons in New Orleans drinking water and blood plasma. Science 187:75.
Entz, R. 1978. Food and Drug Administration, Washington, D.G., telephone com-
munication, November 1978. 7-50
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Environmental Protection Agency. 1975. Preliminary assessment of suspected car-
cinogens in drinking water: report to Congress. Report No. 560/4-75-005.
Washington, D.C.
Fleisher, M. 1978. State of New York, Department of Health, Long Island, New
York. Personal communication. October 1978.
Eraser, P. J. B., and G. I. Pearman. 1978. Atmospheric halocarbons in the
southern hemisphere. Atmos. Environ. 12:839.
Fuller, B. B. 1976. Air pollution assessment of trichloroethylene. EPA Contract
No. 68-02-1495. February 1976.
Cast, R., and J. Early. 1956. Phytotoxicity of solvents and emulsifiers used
in insecticide formulations. Agr. Chem. 11:42.
Grimsrud, E. P., and R. A. Rasmussen. 1975. Survey and analysis of halocarbons
in the atmosphere by gas chromatography-mass spectrometry. Atm. Environ. 9:
1014.
Haley, M. J. 1977. State Department of Health, Richmond, Virginia. Personal
communication. June 1977.
Healy, J. 1978. U.S. Environmental Protection Agency, Region I, Boston,
Massachusetts. Personal communication. September 1, 1978.
Huffaker. 1978. State of New York, Department of Health, Division of Labora-
tories and Research, Albany, New York. Personal communication. December 12,
1978.
IFI. 1975. International Fabricare Institute - Research Center. Experimental
study on solvent discharge from dry cleaning establishments to the environ-
ment (field study of selected California dry cleaning plants). Silver
Springs, Maryland. May 21, 1975.
Johnson, D. 1978. Des Moines Water Works, City of Des Moines, Des Moines, Iowa.
Personal communication. October 1978.
Kraybill. 1977. Department of Environmental Resources, Harrisburg, Pennsylvania.
Personal communication. June 1977.
Lillian, D., and H. B. Singh. 1974. Absolute determination of atmospheric halo-
carbons by gas phase coulometry. Anal. Chem. 46:1060.
7-51
-------
Lillian, D., H. B. Singh, A. Appleby, L. Lobban, R. Arnts, R. Gumpert, R.
Hague, J. Tooney, J. Kazazis, M. Antell, D. Hansen, and B. Scott. 1975.
Atmospheric fates of halogenated compounds. Environ. Sci. Technol. 9:1042.
Louw, C. W., J. F. Richards, and P. K. Faure. 1977. The determination of vola-
tile organic compounds in city air by gas chromatography combined with stan-
dard addition, selective subtraction, infrared spectroscopy, and mass spec-
trometry. Atmos. Environ. 11:703.
Lovelock, J. E. 1974. Atmospheric halocarbons and stratospheric ozone. Nature
252:292.
Lovelock, J. E. 1977. Methyl chloroform in the troposphere as an indicator of
OH radical abundance. Nature 267:32.
Lyne, F. A., and T. McLachlan. 1949. Contamination of water by trichloro-
ethylene. Analyst 74:513.
McConnell, G., D. M. Ferguson, and C. R. Pearson. 1975. Chlorinated hydrocar-
bons and the environment. Endeavor 34:13.
McConnell, G. 1976. Halo organics in water supplies. J. Inst. Water Eng. Sci.
30:431.
Midwest Research Institute. 1976a. Test of industrial dry cleaning operations.
Draft final report, EPA Contract No. 68-02-1403, Task 21. April 1976.
Midwest Research Institute. 1976b. Source test of dry cleaner. Draft final re-
port, EPA Contract No. 68-02-1403, Task 23. May 1976.
Montgomery, H. A. C., and M. Conlon. 1967. The detection of chlorinated sol-
vents in sewage sludge. Water Pollution Control 66:190.
Morgan, A., A. Black, and D. R. Belcher. 1970. The excretion in breath of some
aliphatic halogenated hydrocarbons following administration by inhalation.
Ann. Occup. Hyg. 13:219.
Murray, A. J., and J. P. Riley. 1973. Occurrence of some chlorinated aliphatic
hydrocarbons in the environment. Nature 242:37.
North, J. 1977. Water board plans heavy metal contamination probe. The Danville
Register. Danville, Virginia. March 23, 1977.
Ohta, T., M. Morita, and I. Mizoguchi. 1976. Local distribution of chlorinated
hydrocarbons in the ambient air over Tokyo. Atm. Environ. 10:557.
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Ohta, T., M. Morita, I. Mizoguchi, and T. Tada. 1977. Washout effect and di-
urnal variation for chlorinated hydrocarbons in ambient air. Atm. Environ.
11:985.
Pearson, C. R., and G. McConnell. 1975. Chlorinated C^ and ^2 hydrocarbons
in the marine environment. Proc. R. Soc. London. B. 189:305.
Pellizzari, E. D., J. E. Bunch, R. E. Berkley, and J. McRae. 1976. Determina-
tion of trace hazardous organic vapor pollutants in ambient atmospheres by
gas chromatography/mass spectrometry/computer. Anal. Chem. 48:803.
Scott Environmental Technology, Inc. 1976. A survey of perchloroethylene emis-
sions from a dry cleaning plant. EPA Report No. 76-DRY-l. Research Triangle
Park, North Carolina. March 1976.
Simmonds, P. G., S. L. Kerrin, J. E. Lovelock, and F. H. Shair. 1974. Distri-
bution of atmospheric halocarbons in the air over the Los Angeles basin. Atm.
Environ. 8:209.
Singh, H. B. 1976a. Atmospheric fates of halogenated compounds. EPA Grant No.
R-80380201. September 1976.
Singh, H. B. 1976b. Phosgene in the ambient air. Nature 264:428.
Singh, H. B., L. Salas, H. Shigeishi, and A. Crawford. 1977a. Urban-nonurban
relationships of halocarbons, SF^, ^0, and other atmospheric trace constitu-
ents. Atm. Environ. 11:819,
Singh, H. B., L. Salas, and L. A. Cavanagh. 1977b. Distribution, sources, and
sinks of atmospheric halogenated compounds. J. Air Pollut. Control Assoc.
27:332.
Singh, H. B. 1977c. Atmospheric halocarbons: evidence in favor of reduced av-
erage hydroxyl radical concentrations in the troposphere. Geophys. Res. Lett.
4:101.
Singh, H. B., L. J. Salas, H. Shigeishi, and E. Scribner. 1978. Global distri-
bution of selected halocarbons, hydrocarbons, SF^, and N?0. Phase II Interim
Report, Environmental Sciences Research Laboratory, EPA, Research Triangle
Park, North Carolina, Grant No. 8038020. May 1978.
Stanford Research Institute (SRI). 1979. Assessment of human exposures to
atmospheric perchloroethylene. Draft final report, Contract No. 68-02-2835.
Office of Air Quality Planning and Standards, Environmental Protection
Agency, Research Triangle Park, North Carolina, January.
Toxic Materials News. 1978. L. A. Eiserer, Publisher. Washington, D.C. 5(3):17.
Tyson, B. J. 1975. Chlorinated hydrocarbons in the atmosphere - analysis at
the parts-per-trillion level by GC-MS. Anal. Lett. 8:807.
7-53
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CONTENTS
Page
8. Regulations and Standards 8-3
8.1 Federal, State, Local, and Other Regulations . . . 8-3
8.1.1 Environmental Protection Agency 8-3
8.1.1.1 Office of Drinking Water 8-3
8.1.1.2 Office of Hazardous Spills 8-3
8.1.1.3 Office of Water and Waste
Management 8-5
8.1.1.4 Office of Air Quality Planning and
Standards (OAQPS) 8-5
8.1.1.5 Office of Pesticide Programs .... 8-7
8.1.1.6 Office of Solid Waste 8-7
8.1.2 Food and Drug Administration 8-8
8.1.3 Consumer Product Safety Commission 8-9
8.1.4 Department of Defense 8-9
8.1.5 General Services Administration 8-9
8.1.6 State regulations 8-9
8.1.7 Local regulations 8-14
8.1.8 Foreign countries 8-15
8.2 Standards and Recommendations 8-15
8.2.1 Federal standards/recommendations 8-15
8.2.1.1 Occupational Safety and Health
Administration 8-15
8.2.1.2 National Institute for Occupational
Safety and Health 8-17
8.2.2 Other standards/recommendations 8-18
8-1
-------
CONTENTS (continued)
Page
8.2.2.1 American Conference of Governmental
Industrial Hygienists 8-18
8.2.2.2 American National Standards
Institute, Inc 8-18
8.2.2.3 Workplace quality standards in use
outside the United States 8-20
8.3 Shipping and Transportation Practices 8-21
References 8-28
8-2
-------
SECTION 8
REGULATIONS AND STANDARDS
This section describes the current regulatory restrictions and transporta-
tion practices on trichloroethylene, perchloroethylene, and methyl chloroform.
The three compounds are currently regulated by a number of federal agencies and
state and local governments. In addition, several agencies are anticipating
future actions on these compounds.
Workplace standards are in effect for the three compounds; in addition,
threshold limit values (TLVs) and recommended standards for occupational expo-
sure have been reported. The occupational standards apply to airborn concentra-
tions of the three compounds. These standards do not take into account the re-
cently publicized reports on the carcinogenic potential of trichloroethylene
and perchloroethylene.
Information on regulations and standards was obtained through: the
Federal Register, telephone interviews with representatives of federal agencies
and state and municipal governments, and mail inquiries to state and municipal
governments.
8.1 FEDERAL, STATE, LOCAL, AND OTHER REGULATIONS
8.1.1 Environmental Protection Agency
8.1.1.1 Office of Drinking Water—
The proposed amendment to the National Interim Primary Drinking Water
Regulations (EPA, 1978a) is intended to protect the public health from or-
ganic chemical contaminants in drinking water. The EPA is concerned with the
potential contribution to elevated cancer risks by synthetic organic chemical
contaminants (including trichloroethylene, methyl chloroform, and perchloro-
ethylene). The amendment includes a treatment technique regulation which re-
quires community water systems with populations greater than 75,000 people to
use granular activated carbon (GAG) in their treatment systems. The GAG treat-
ment system must be in operation no later than 3-1/2 years after the effective
date of this amendment (the effective date is 18 months after promulgation).
8-3
-------
The treatment technique was prescribed based on the judgment that it
would not be feasible to monitor for the presence of all the synthetic organic
chemicals in drinking water which may have an adverse effect on human health.
Because of the multitude of organic contaminants that may be present, no maxi-
mum limit has been proposed for any of the three chemicals. The amendment does
specify that the concentration in the effluent of volatile halogenated organic
compounds must not exceed 0.5 /ig/liter. The presence of the volatile compounds
is indicative of the presence of other hazardous substances which would be more
difficult to detect.
8.1.1.2 Office of Hazardous Spills-
Final rules on approximately 271 hazardous substances and related spills
became effective in June 1978 (EPA, 1978b). Although none of the subject com-
pounds are included, Part 116.4 (amended) designates 28 compounds, including
trichloroethylene, as hazardous for which rules are being proposed. Amendments
to the final rule concerning definitions of "the Act" and "discharge" and the
addition of a definition of jurisdiction were published in February 1979 (EPA,
1979a).
This regulation designates hazardous substances, other than oil, under
Section 311 of the Federal Water Pollution Control Act. The 271 hazardous sub-
stances and the 28 compounds for which rules are being proposed will be devel-
oped by the Marine Activities Branch of the Office of Water and Waste Manage-
ment and regulated under the Oil and Special Materials Control Division of
Water Program Operations, whenever final rulemaking is complete.
This regulation was issued concurrently with three additional final rules
on the discharge of hazardous substances. The other three final rules (Sections
117, 118, and 119 of the same part of the Federal Register) determine their
removability, harmful quantities when discharged into the water, and rates of
penalty. However, an injunction was granted in New Orleans at the time the reg-
ulations were published which voided the three rules. The final modified rules
were again passed by Congress on October 15, 1978, and are expected to be pub-
lished soon. The new rules will retain the categories for classification of
harmful quantities in hazardous wastes. Information on the other modifications
in the final rules is not available.
Under the "harmful quantities" section, trichloroethylene has been tenta-
tively identified as a Class "C" waste with a toxicity range of 10 mg < LC5Q <
100 mg/liter and a corresponding reportable quantity of 1,000 Ib. Table 8-1
shows the harmful quantity system for comparison purposes.
8-4
-------
TABLE 8-1. HAZAEDOUS WASTE CLASSIFICATIONS
Category
X
A
B
C
D
Toxicity range
LC50 < 0.1 mg/4
0.1 mg < LC50 < 1 mg/£
1.0 mg < LC50 < 10 mg/4
10 mg < LC50 < 100 mg/4
100 mg < LC5Q < 500 mg/4
Harmful
quantity
(lb)
1.0
10
100
1,000
5,000
Source: Environmental Protection Agency (1978a; 1979a).
8.1.1.3 Office of Water and Waste Management--
Trichloroethylene, methyl chloroform, and perchloroethylene are included
in the publication of the Toxic Pollutants List (EPA, 1978c). The list identi-
fies toxic pollutants to be regulated under Section 307(a)(l) of the Federal
Water Pollution Control Act (as amended by Clean Water Act of 1977). Inclusion
of a compound on this list imposes no direct economic burden. The list does,
however, form a basis for the development of effluent limitations of point
sources.
Estimates of the levels of toxic pollutants in water that will not harm
aquatic life were proposed as water quality criteria. For freshwater aquatic
life, the 24-hr average was 1,500 /xg/liter for trichloroethylene and 310 ^g/
liter for perchloroethylene; ceiling levels were 3,400 and 700 /ixg/liter, re-
spectively. For saltwater aquatic life, levels were given only for perchloro-
ethylene. Those were 79 /ig/liter for the 24-hr average and 180 jxg/liter for
the ceiling levels (EPA, 1979b).
8.1.1.4 Office of Air Quality Planning and Standards (OAQPS)—
The current procedure for establishing ambient air quality with regard to
photochemical oxidants lies with the individual State Implementation Plan (SIP).
Under this procedure, each state agency assembles an air pollution abatement
plan for their particular state and submits this plan to EPA for approval. Most
state plans are derived from, or are a modification of, "Rule 66" (now Rule 442)
which was developed by the Los Angeles County Air Pollution Control District.
Each state plan is tailored to the specific needs or requirements of the indi-
vidual state. Once the plan is submitted to EPA, it is reviewed and either ac-
cepted or rejected. To date, approximately 20 states have EPA-approved SIPs.
8-5
-------
Current EPA policy (EPA, 1977) with respect to photochemical reactivity
of volatile organic confounds (VOCs) is that only a few VOCs have negligible
photochemical reactivity (see Table 8-2) and only five (including methyl chloro-
form) are recommended for exclusion from control under SIP regulations. Ten (10)
other compounds (see Table 8-2) are more reactive than the first five, but do
not contribute large quantities of oxidant under most atmospheric conditions.
Priority should be given to controlling those VOCs more reactive than these 10.
Solvent substitution, except for the five with negligible reactivity, has not
provided sufficient oxidant reduction.
Perchloroethylene was originally included in this table, but has been re-
moved because of reported adverse health effects which are currently under in-
vestigation.
TABLE 8-2. PHOTOCHEMICAL REACTIVITY OF VOLATILE ORGANIC COMPOUNDS
Volatile organic compounds of negligible
photochemical reactivity
Methane
Ethane
1, 1,1-Trichloroethane (methyl chloroform)
Trichlorotrifluoroethane (Freon 113)
Volatile organic compounds of low
photochemical reactivity
Propane
Acetone
Methyl ethyl ketone
Methanol
Isopropanol
Methyl benzoate
Tertiary alkyl alcohols
Methyl acetate
Phenyl acetate
Ethyl amines
Acetylene
N.N-Dimethyl cormamide
Source: Environmental Protection Agency (1977).
In general terms, Rule 442 states that emission of photochemically reac-
tive solvents is limited to approximately 8 Ib/hr or approximately 40 Ib/day.
Nonphotochemically reactive solvents are limited to emissions of approximately
400 Ib/hr or approximately 3,000 Ib/day. Disposal of photochemically reactive
materials is limited to 1.3 gal/day.
8-6
-------
For dry cleaning establishments, most states generally require a reduc-
tion in uncontrolled emissions of organic materials of at least 85%. This re-
duction includes trichloroethylene but excludes methyl chloroform and per-
chloroethylene.
This office has recently issued a report setting forth guidelines for the
control of VOGs, specifically perchloroethylene, from all dry cleaning systems
which use this solvent (EPA, 1978e). The prescribed methodology represents the
presumptive norm or reasonably available control technology (RACT) that can be
applied to existing perchloroethylene dry cleaning systems.
8.1.1.5 Office of Pesticide Programs—
The three compounds under study have registered pesticide uses. Two of
the compounds, trichloroethylene and perchloroethylene, are currently under-
going a preliminary investigation by the Office of Pesticide Programs. The pur-
pose of this investigation is to collect and review the existing toxicological
and environmental health information and determine whether or not the compounds
should be considered for restriction by issuing a rebuttal presumption against
registration (RPAR) review for each compound. The current investigation is re-
ferred to as pre-RPAR. Currently this office considers it likely that RPAR re-
views will be issued on the two compounds; however, they currently have a low
priority and no results are anticipated in the near future. Methyl chloroform
is not being considered for an RPAR review at this time.
8.1.1.6 Office of Solid Waste-
Currently this office has no regulations concerning any of the three com-
pounds. However, it is expected that the three compounds will be regulated
under the "Resource Conservation and Recovery Act of 1976" (RCRA), Public Law
94-580, whenever the "Identification and Listing of Hazardous Substances" sec-
tion of RCRA is complete. Under RCRA, the term solid waste includes discarded
materials including liquids from industrial and municipal sources. The iden-
tification and listing of hazardous wastes, when complete, is expected to in-
clude all of the substances mentioned in the Toxic Pollutants List (those reg-
ulated under Section 307 of the Federal Water Pollution Control Act) whenever
these substances are considered as wastes.
Proposed standards applicable to transporters of hazardous wastes were
published in the Federal Register (EPA, 1978d). These standards are issued
under Section 3003 of RCRA to create a management control system for hazard-
ous wastes which includes appropriate monitoring, recordkeeping, and reporting
within this system. These standards will most likely be applicable to all three
compounds, whenever the identification of hazardous wastes under RCRA is com-
plete.
8-7
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8.1.2 Food and Drug Administration
The Food and Drug Administration (FDA) published final rules on aero-
solized drug products which contain 1,1,1-trichloroethane (methyl chloroform)
(FDA, 1977a). The rule states that "any aerosol drug product containing tri-
chloroethane and labeled, represented, or advertised for use by inhalation is
a new drug and subject to regulatory proceedings unless it is the subject of
a new drug application . . ." This action was taken by FDA because there is
no evidence to establish that methyl chloroform is safe and effective for its
intended use in such products. Effective January 1978, all such products will
require new drug applications as a condition for marketing.
With regard to usage in the food industry, the following limits are cur-
rently in effect:
Tolerance for Residues of Trichloroethylene
30 ppm in spice oleoresins
25 ppm in decaffeinated ground coffee
10 ppm in decaffeinated instant coffee
FDA believes, however, that the food industry stopped using trichloroethylene
in these products at the time of the proposed rule (FDA, 1977b) to prohibit
the usage*
A proposed rule (FDA, 1977b) would amend the food additive regulations
by prohibiting trichloroethylene in human food because "it may pose a risk of
cancer in man." This proposed rule would revoke the provisions for tolerances
for residues of trichloroethylene resulting from its use in the manufacture
of decaffeinated ground coffee, decaffeinated instant coffee, and spice oleo-
resins. This rule would also revoke provisions for use as: a component of
food-packaging adhesives and vinyl chloride-hexene-1 copolymers and as a sol-
vent in the manufacture of modified hop extracts.
In addition the FDA (1977b) is proposing: (a) to declare that any human
food or animal feed containing trichloroethylene is deemed adulterated and in
violation of this act; (b) to declare that any cosmetic product containing the
compound is deemed to be adulterated; (c) to declare that any human or animal
drug product containing trichloroethylene is classified as new drug and thus
misbranded; and (d) to amend the color additive regulations to delete provi-
sions for the use of the compound in the manufacture of color additives.
The FDA believes that the proposed rules will be published unchanged as
final rules sometime late in 1978.
8-8
-------
8,1.3 Consumer Product Safety Commission
A federal court in Lake Charles, Louisiana, issued a temporary injunction
in September 1978 restraining the Consumer Product Safety Commission (CPSC)
from enforcing any regulations under its cancer policy because the agency did
not follow proper procedures in its carcinogen classification system (Environ-
mental Health Letter, 1978). Originally, the temporary order applied only to
perchloroethylene, but was later expanded to include CPSC's entire classifi-
cation system.
Under the proposed CPSC carcinogen policy, carcinogens or potential car-
cinogens were classified into categories A, B, or C, based on toxicological
data. Category "A" contains the most hazardous substances under this classifi-
cation system. Perchloroethylene was classified under category A. Consumer
products containing compounds listed under the above categories would have
been regulated at a later date under regulations not yet announced. As a re-
sult of the court ruling, the CPSC has been enjoined from using this classifi-
cation system; however, an appeal is being considered (Jacobsen, 1978). CPSC
is conducting an in-house investigation to determine the number and types of
products containing perchloroethylene, concentrations in consumer products,
and additional toxicity data (Toxic Materials News, 1979). Trichloroethylene
and methyl chloroform are not on the CPSC carcinogen policy list.
8.1.4 Department of Defense
The Occupational Safety and Health Program of the Department of Defense
(DOD) requires the use of OSHA standards, including OSHA Emergency Temporary
Standards, when issued, in workplaces within DOD. Any branch of DOD may use
other more stringent national concensus standards, such as the ACGIH TLVs, in
place of the OSHA standards (Siebert, 1978).
8.1.5 General Services Administration
Federal specifications for methyl chloroform, trichloroethylene, and per-
chloroethylene are shown in Tables 8-3 through 8-5, respectively.
8.1.6 State Regulations
Twenty-one states were contacted to obtain information regarding standards
for the subject compounds. Seventeen states responded to the inquiries. Offi-
cials from Texas reported that there were no standards involving the subject
compounds in that state. Kentucky and Illinois require that consumer products
containing the subject compounds be marked with appropriate cautionary labels.
If any of the subject compounds appear in Kentucky as hazardous waste, they
are governed by hazardous waste regulations.
8-9
-------
TABLE 8-3. FEDERAL SPECIFICATIONS FOR METHYL CHLOROFORM
U.S. Federal specification on O-T-6200, 1,1,1-trichloroethane, technical,
inhibited
Appearance: Clear; free of sediment and suspended matter
Water content, max: 100 ppm
Distillation range: 760 mm Hg IBP-DP; 72-88°C
Specific gravity at 25°/25°C: 1.320-1.324
Nonvolatile residue, max: 10 ppm
Purity:
1,1,1-Trichloroethane content
Minimum by weight: 94.5%
Minimum by volume: 90.0%
Individual halogenated impurities: 0.5%
Total halogenated impurities: 1.0%
Acidity (as HC1), max: 5 ppm
Color, APHA, max: 10
Free halogens: None
Acid acceptance (as NaOH), min: 0.20%
Source: Franklin Institute Research Laboratories (1975).
8-10
-------
TABLE 8-4. FEDERAL SPECIFICATIONS FOR TRICHLOROETHYLENE
U.S. Federal specification on 0-T-634a, technical grade dated
Appearance: Clear and free of suspended matter or sediment
Specific gravity 20°/20°C: 1.450-1.475
Acidity as HCl: 0.01% max
Alkalinity as NaOH: 0.01% max
Water content: No cloud at 0°C
Copper corrosion and free chlorine: Must pass government test
Color: Shall not be darker than a solution containing 0.0045 g potassium
dichromate in 1 liter distilled water
Source: Waters et al. (1976).
TABLE 8-5. FEDERAL SPECIFICATIONS FOR TECHNICAL GRADE
PERCHLOROETHYLENE
Chemical or physical property
Color, Pt-Co scale
Residual odor
Cloud point, °C
Acidity (as HCl), %
Alkalinity (as NaOH), %
Specific gravity, 20fl/20°C
Nonvolatile residue, %
Distillation range, °F
Initial boiling point
End point
Stability with copper
Flask loss, mg/30 cm
Soxhlet loss, mg/30 cm^
Condenser loss, mg/30 cm
Acidity, ml of 0.01 N NaOH
Minimum Maximum
20
None
0
0.0005
0.020
1.620 1.630
0.01
120
122
10
20
20
15
Source: General Services Administration, Federal Specifica-
tion 0-T-236b (February 28, 1967) for tetrachloro-
ethylene (perchloroethylene), technical grade.
8-11
-------
The majority of the states regulate the subject compounds via hazardous
waste regulations or Toxic Substances Regulations. Those states are West
Virginia, California, New York, Massachusetts, Delaware, Florida, South
Carolina, Washington, Indiana, New Jersey, Maryland, and Washington, D.C.
West Virginia does not have specific regulations for the subject com-
pounds but considers them to be toxic substances and regulates their discharge
into waters of the state (West Virginia Administrative Regulations, State Wa-
ter Resources Board, Chapter 20-5 and 20-5A Series I (1965)). Toxic substances
are not to exceed 1/10 of the 96-hr median tolerance limit.
California regulates trichloroethylene and perchloroethylene as hazardous
waste. Perchloroethylene is considered toxic and an irritant, while trichloro-
ethylene is toxic and flammable (Division 4, Chapter 2, Title 22, California
Administrative Code, "Minimum Standards for Management of Hazardous and Ex-
tremely Hazardous Wastes").
The Department of Environmental Conservation for the State of New York
currently has controls only over the transportation, treatment, and disposal
of waste chemicals. The New York legislature has recently passed a bill which
will provide the additional regulatory authorities to carry out the provisions
of subtitle C of RCRA. This bill is expected to be signed into law in the near
future. The New York State Department of Health has pending regulations which
would limit the concentrations of halogenated solvents (as well as other toxic
compounds) in drinking water.
The State of Massachusetts regulates halogenated solvents as hazardous
wastes.
The State of Delaware has regulations controlling the generation, trans-
portation, and disposal of hazardous waste materials pending, but no current
standards*
The State of Florida has no standards controlling the manufacture, formu-
lation, distribution, or use of halogenated solvents. Disposal of hazardous
waste falls under the purview of the Florida Department of Environmental Regu-
lation. Such materials must be "rendered safe and sanitary prior to disposal"
(Chapter 17-7.04(3) F.A.C.)* Wastes not amenable to land disposal (trichloro-
ethylene, perchloroethylene) must be returned for recovery, or shipped out of
state to an approved hazardous waste treatment/disposal site. The Department
is currently proposing enabling legislation in order to effect a more compre-
hensive waste management program.
Disposal of chlorinated solvents in the State of South Carolina is cur-
rently governed by the Industrial Solid Waste Disposal Regulation for Minimum
Standards and Permit Application Guidelines. In May 1978, the South Carolina
Hazardous Waste Management Act was passed and signed into law. When the
8-12
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regulations are promulgated (they will be referenced to Section 3 of the Haz-
ardous Waste Management Act and to the Resource Conservation and Recovery Act),
a significant effect on the transport, treatment, and disposal of hazardous
waste can be expected.
The State of Washington governs the disposal of hazardous waste (Chapter
70.105 Revised Code of Washington, Hazardous Waste Disposal of 1976). Washington
Administrative Code (WAG) 173-302 provides specific regulations for identifica-
tion of extremely hazardous waste and is applicable to all generators, treaters,
and transporters of extremely hazardous wastes. The development and implementa-
tion of WAG 173-302 was the responsibility of the Department of Ecology. Sec-
tions 110, 120, and 130 of WAG 173-302 delineate extremely hazardous wastes
based on criteria concerning specific toxicity, environmental persistence, and
quantity of the waste.
The State of Indiana regulates these compounds as hazardous and/or toxic
wastes and has four state laws which can be utilized in the control effort.
These four are: (a) Indiana Stream Pollution Control Law (IC-13-1-3); (b)
Refuse Disposal Act (IC-19-2-1); (c) Environmental Management Act (IC-13-7);
and (d) Air Pollution Control Law (IC-13-1-1).
Control of accidental and intentional discharges of hazardous substances
(halogenated hydrocarbons) in New Jersey are regulated by the Spill Composi-
tion and Control Act (1977), the Water Pollution Control Act (1977), and/or
the Solid Waste Act. Companies handling such substances must have permits re-
garding the discharge to air and water.
Maryland legislation relevant to the disposal of subject chemicals would
be Section 8-1413-2 of the Annotated Code of Maryland, Department of Natural
Resource Article. Regulations promulgated pursuant to this Act are 08.05.05 -
Control of the Disposal of Designated Hazardous Substances.
The District of Columbia passed a Hazardous Waste Management Act (Bill
2-163) which empowers the Administration to establish procedures and require-
ments for transporting, storing, and disposing of hazardous and toxic mate-
rials.
The State of Michigan licenses the operation of commercial and self-
service dry cleaning plants which use perchloroethylene (Act 327, P.A. 1947).
This statute has been revised and incorporated in the new Public Health Code
with provisions for promulgating licensing rules. These rules are expected to
deal with the operation of the plant and the disposal of waste materials.
Michigan also plans to include trichloroethylene and perchloroethylene in the
1978 Michigan Critical Materials Register (MCMR). The inclusion of these mate-
rials requires Michigan industry to report use and discharge of these materi-
als. The data submitted on annual reports will be compiled and analyzed to
identify potential environmental and human health problems.
8-13
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The State of Virginia passed the Toxic Substances Information Act of 1976
(modified in 1977) which requires all companies in Virginia to file, with the
State Health Department, an inventory of chemicals manufactured or used in man-
ufacturing. Additionally, the State Board of Health will propose Glass I sub-
stances, which on the basis of substantial evidence it believes pose the great-
est threat to human health and the environment. Class I reports covering Class
I substances will be required of those using or manufacturing such substances.
Currently there are no Class I designations. A tentative initial list (list
has had no formal consideration) includes halogenated solvents.
8.1.7 Local Regulations
The following metropolitan cities were contacted in order to determine
whether or not they had drinking water, wastewater, or air quality standards
for trichloroethylene, perchloroethylene, or methyl chloroform.
Municipality Drinking water Wastewater Ambient air
Philadelphia No No No
Pittsburgh No No No
New York No No No
Cleveland No No No
Chicago - No
Detroit No No No
New Orleans No No No
Houston No No
Los Angeles No Yes3-'
Orange County No Yes^
Seattle^' No No No
_a/ Classified as hazardous chemical waste in Los Angeles
Municipal Code 64-30.
b/ Orange County and Los Angeles are two of four counties
in the South Coast Air Quality Management District, the
remaining ones being San Bernadino (excluding the South-
east Desert Air Region) and Riverside.
£/ Regulated by general category as chlorinated hydrocarbons.
Limit of 0.02 mg/liter.
_d/ Classified as hazardous chemicals; requires fire depart-
ment permits for use and storage (Article 19 of City Or-
dinance).
8-14
-------
According to information obtained through personal contact with city and/
or county officials, no municipal drinking water or ambient air guidelines or
standards were identified. Insofar as drinking water quality is concerned, con-
tacts indicated that they intend to follow either: (a) the proposed federal
drinking water guidelines, when adopted, or (b) state guidelines drafted so
as to be comparable with federal recommendations.
8.1.8 Foreign Countries
The International Register of Potentially Toxic Chemicals of the United
Nations (IRPTC) was unable to provide any specific information.
Canada has no regulations on halogenated solvents.
New Zealand has no regulations on perchloroethylene or methyl chloroform.
Trichloroethylene is listed as a "poisonous substance" under the Poisons Regu-
lations of 1964, which requires labeling of the product and licensing of formu-
lators and/or packagers.
Germany is currently working on comprehensive legislation dealing with
environmental chemicals.
8.2 STANDARDS AND RECOMMENDATIONS
8.2.1 Federal Standards/Recommendations
In order to control occupational exposures to airborne concentrations of
chemicals (and other agents), standards for workplace quality have been devel-
oped. Certain standards exist only as reconmendations or for guidance; others
are legally binding. In addition to U.S. standards, several foreign countries
have developed their own workplace standards or have adopted the U.S. stan-
dards. In the United States, the standards issued by OSHA are legally enforce-
able, not the TLVs recommended by ACGIH.
8.2.1.1 Occupational Safety and Health Administration--
Standards for occupational exposure to airborne concentrations of tri-
chloroethylene, perchloroethylene, and methyl chloroform are contained in the
General Industry Safety and Health Standards (OSHA, 1977), as part of 29 CFR,
Part 1910. These standards represent occupational exposure limits for workplace
concentrations of the subject compounds, which, by law, cannot be exceeded.
The current employee standards for the subject compounds are listed as part
of Table 8-6.
The OSHA standards on trichloroethylene, perchloroethylene, and methyl
chloroform are not based on the recent findings of their carcinogenicity or
potential carcinogenicity (see section on NIOSH). At present, OSHA has no plans
to change the current time weighted average (TWA) or short-term exposure limit
(STEL) for any of the three compounds.
8-15
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TABLE 8-6. SUMMARY OF NIOSH RECOMMENDATIONS FOR OCCUPATIONAL HEALTH STANDARDS
00
I
Substance
1,1,1 , -Trich lor oe thane
(Methyl chloroform)
Trichloroethylene
Tetrachloroethylene
(Perch lor oe thy lene )
Current OSHA
Transmitted to environmental
OSHA standard
July 2, 1976 350 ppm, 8-hr TOA
July 23, 1973 100 ppm, 8-hr TWA;
200 ppm acceptable
ceiling; 300-ppm max-
imum ceiling; (5 rain
in any 2 hr)
July 2, 1976 100 ppm, 8-hr TWA;
200 ppm acceptable
maximum ceiling;
300 ppm maximum ceiling
(5 min in 3 hr)
NIOSH recommendation
for environmental
exposure limit
350 ppra ceiling
(1,910 mg/cu m)
(15 min)
100 ppm TWA
(537 mg/cu m) ;
150 ppm ceiling
(806 mg/cu m)
(10 min)
50 ppm TWA
(339 mg/cu m) ;
100 ppm ceiling
(678 mg/cu m)
(15 min)
Health effect
considered
Nervous system,
liver, and heart
effects
Central nervous
system depressant
Nervous system,
heart, respiratory,
liver effects
Comments
Action level set at
200 ppm TWA; medical
warning of possible
congenital abnormal-
ities required.
NIOSH reevaluating
environmental limit.
Medical warning of
possible congenital
abnormalities required
Note: NIOSH TWA recommendations are based on up to a 10-hr exposure unless otherwise noted.
Source: NIOSH (1978b).
-------
However, OSHA issued a tentative list of Category I chemicals (which in-
cludes trichloroethylene) which may be regulated under its proposed generic
carcinogen policy. The policy (OSHA, 1977b) would classify chemicals into one
of four categories based upon the substances known or suspected carcinogenic-
ity. Classification into either Category I or II would subject a chemical com-
pound to regulatory action based on model standards in the proposal.
The potential implications of a Category I classification include an
issuance of emergency temporary standards and, within 6 months, permanent
standards which would reduce employee exposure to the lowest feasible level.
8.2.1.2 National Institute for Occupational Safety and Health-
One of the functions of this agency is to make recommendations and pro-
vide valid criteria for the determination of occupational standards. Table 8-6
contains a summary of the major recommendations found in the Criteria Documents
on occupational exposure to trichloroethylene, perchloroethylene, and methyl
chloroform. Also included is the current Federal Standard and the date of
transmittal to the Department of Labor. In addition, the major health effects
that were considered in the derivation of the recommendations are listed.
NIOSH has issued bulletins on the three subject compounds in light of re-
cent data on carcinogenicity or potential carcinogenicity. Although no new
formal recommendations have been issued by NIOSH, this agency has cautioned
against relying upon the existing standards and recommendations for worker pro-
tection*
NIOSH notes that both the OSHA standard (100 ppm) and the NIOSH recommen-
dation (50 ppm) for occupational exposure to perchloroethylene are not based
on findings of the compound's carcinogenic potential. Consequently, neither of
these levels may provide adequate worker protection from cancer (NIOSH, 1978a)«
In addition, NIOSH notes that the OSHA exposure limit of 100 ppm for trichloro-
ethylene, which is not based on findings of the compound's carcinogenic po-
tential, is inadequate for worker protection and should be reevaluated (NIOSH,
1978b). Although methyl chloroform has not been shown to be carcinogenic, NIOSH
recommends that this compound should be treated in the workplace with caution
because of its structural similarity to other chloroethanes shown to be carcin-
ogenic in NCI bioassay tests (NIOSH, 1978d).
As stated previously, no new formal exposure limit recommendations have
been issued on any of the three compounds; however, an occupational hazard
review on trichloroethylene was published (NIOSH, 1978d) which contains some
occupational control recommendations. NIOSH recommends that the permissible
limit for occupational exposure to trichloroethylene be reduced and that tri-
chloroethylene be controlled as an occupational carcinogen. Current informa-
tion on engineering feasibility indicates that personnel exposures of 25 ppm
as TWA can be readily attained. (Note that this is not a recommended standard.)
NIOSH indicates that the 25 ppm value should not serve as the final goal and
8-17
-------
that industry should pursue further reductions in worker exposure as advance-
ments in technology research develop (NIOSH, 1978d). A major manufacturer of
solvent vapor degreasing equipment in the United States does not agree that
personnel exposures of 25 ppm as TWA can be readily attained (Schlossberg,
1979).
At present, NIOSH is soliciting information (including information on safe
levels) which would be helpful in updating the existing criteria document on
methyl chloroform (OHS, 1978). In addition, NIOSH is planning to revise the
criteria documents on trichloroethylene and perchloroethylene.
The NIOSH recommended standard for workplace air exposures to halogenated
anesthetic agents, including trichloroethylene as waste anesthetic gases, is
2 ppm (10.75 mg/m^). Waste inhalation of anesthetic gases and vapors are those
which are released into work areas associated with the administration of a gas
for anesthetic purposes in locations including operating rooms, delivery rooms,
labor rooms, recovery rooms, and dental operatories (NIOSH, 1977). Trichloro-
ethylene is not a commonly used anesthetic agent in hospitals.
8.2.2 Other Standards/Recommendations
8.2.2.1 American Conference of Governmental Industrial Hygienists--
One of the functions of the Conference is to promote standards and tech-
niques in industrial health. Each year ACGIH publishes a list of TLVs for Chem-
ical Substances and Physical Agents in the Workroom Environment (1977). ACGIH
is not a federal agency and consequently the current TLVs do not represent
federal standards. However, the TLVs for 1968 were adopted as the official
federal standards for industrial air by OSHA in 1971. The TLVs for the subject
compounds are summarized in Table 8-7.
8.2.2.2 American National Standards Institute, Inc.—
The American National Standards Institute, Inc. (ANSI), has developed work-
place quality standards on methyl chloroform (ANSI, 1970), trichloroethylene
(ANSI, 1967a), and perchloroethylene (ANSI, 1967b). The purpose of the ANSI
standards is to provide information and guidance for the control of occupa-
tional exposures and to aid in the design and operation of equipment in order
to protect the health of workers. The standards specify acceptable concentra-
tions of the subject compounds including a TWA, a ceiling concentration, and
a maximum peak concentration.
The ANSI TWA standards are essentially the same as the time-weighted 8-hr
average of the TLV proposed by ACGIH. The acceptable ceiling concentration is
the maximum level allowable during the period of exposure, assuming that the
TWA is not exceeded. However, excursions above this ceiling limit may be ex-
ceeded under certain conditions up to a level specified in the acceptable
maximum concentration, assuming that the TWA is not exceeded. The ANSI A-37
workplace quality standards are summarized as follows:
8-18
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TABLE 8-7. THRESHOLD LIMIT VALUES
Adopted values Tentative values
TWA STEL
Substance ppn^ mg/m — ppnt^ mg/m — '
1,1,1-Trichloroethane 350 1,900 440 2,380
(methyl chloroform)
Trichloroethylene 100 535 150 800
Tetrachloroethylene 100 670 150 1,000
(perch loroe thy lene)
_a/ Parts of vapor or gas per million parts of contaminated air
by volume at 25°C and 760 mm Hg pressure.
b/ Approximate milligrams of substance per cubic meter of air.
Note: TLVs refer to airborne concentrations and represent con-
ditions under which it is believed that nearly all workers
may be repeatedly exposed day after day without adverse
effect. TWA (time weighted average) concentration for a
normal 8-hr workday or 40-hr workweek to which workers may
be repeatedly exposed, day after day, without adverse ef-
fect.
TLV-STEL, TLV-short term exposure limit—the maximum con-
centration to which workers can be exposed for a period
up to 15 min continuously without suffering intolerable
irritation, chronic tissue change, or narcosis. The
STEL should be considered maximal allowable concentra-
tion, or absolute ceiling, not to be exceeded at any
time during the 15-min excursion period.
Source: American Conference of Governmental Industrial Hygienists
(1977).
8-19
-------
Maximum acceptable
Acceptable Acceptable ceiling peak concentrations
Substance TWA (ppm) concentration (ppm) (ppm)
Methyl 400 500 800
chloroform
Trichloro- 100 200 300
ethylene
Perchloro- 100 200 300
ethylene
8.2.2.3 Workplace Quality Standards in Use Outside the United States-
In addition to the United States, the following countries have hygienic
standards for chemicals in the workplace, including standards on methyl chloro-
form, trichloroethylene, and perchloroethylene; the Soviet Union (USSR); the
Federal Republic of Germany (BRD); the German Democratic Republic (DDR); Sweden;
and Czechoslovakia (CSSR). In other countries, such as Argentina, Great Britain,
Norway, and Peru, the U.S. standards are applied (winell, 1975).
Table 8-8 shows the differences which exist between the hygienic standards
for the subject compounds in different countries.
TABLE 8-8. WORKPLACE QUALITY STANDARDS IN USE
IN DIFFERENT COUNTRIES
TCE
USA (OSHA 1974)
BDR 1974
DDR 1973
Sweden 1975
CSSR 1964
USSR 1972 (C)
ppm
100
49
47
30
47
2
mg/nr5
535
260
250
160
250
10
PCE
ppm
100
100
45
30
37
2
mg/nr5
670
670
300
200
250
10
MC
ppm
350
199
92
99
92
4
mg/nr*
1,900
1,080
500
540
500
20
Note: TCE = trichloroethylene; PCE = perchloroethylene; MC
methyl chloroform.
(C) = ceiling value.
Source: Adapted from Winell (1975).
8-20
-------
In general, the standards decrease from the top to the bottom of the column,
the United States showing the highest values and the USSR the lowest. There
are great differences between U.S. and Soviet standards for substances affect-
ing the central nervous system, e.g., halogenated hydrocarbons. Only the USA,
Federal Republic of Germany (BRD), and Czechoslovakia (CSSR) have published
the underlying documentation on which their standards are based. In the ab-
sence of documentation from other countries listed in Table 8-8, a comparison
of standards must be limited to a comparison of figures (Winell, 1975).
8.3 SHIPPING AND TRANSPORTATION PRACTICES
In domestic practice, the three compounds are shipped to consumers in tank
cars, tank trucks, and metal drums (e.g., 208-liter or 55-gal.). Single and
multiple compartment tank cars are used to ship bulk quantities in amounts
up to about 20,000 gal. per car.
The National Tank Truck Carriers, Inc., have set forth certain recommen-
dations for truck transportation regarding tank types, metals to be used in
tank construction, precautions for handling, and procedures to follow in case
of accidental spills. These recommendations and data are given in Tables 8-9
through 8-11.
For trichloroethylene, methyl chloroform, and perchloroethylene, the
Department of Transportation (DOT) requires that all shipping containers be
tagged with a label marked ORMA (other regulated materials) along with the
name and quantity of the solvent being shipped.
Data from DOT (1976) on rules and regulations for the three compounds show
that the maximum quantity of any of these solvents in one container that may be
shipped in a passenger-carrying aircraft is 37.85 liters (10 gal.) and that the
corresponding quantity for cargo aircraft is 208 liters (55 gal.). When offered
for transportation on a passenger carrying aircraft, the container must be pack-
aged as follows (DOT, 1976):
* Wooden box with inside earthenware, glass, metal, or plastic packagings
of not more than 2 gal. capacity each, with sufficient cushioning and
absorbent material to prevent breakage and leakage.
* Fiberboard box with similar packaging of not more than 3.785 liters
(1 gal.) capacity each.
* Metal drum of not more than 37.85 liters (10 gal.) capacity.
8-21
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TABLE 8-9. HANDLING AND SHIPPING DATA FOR TRICHLOROETHYLENE
Weight per gallon at 60°F
12.3 Ib
Nonflammable, nondangerous liquid
Characteristics
(a) Type commodity
(b) If flammable liquid, flash
point open cup test
(c) If compressed gas, vapor pres-
sure at 115°F
(d) Temperature at which trans-
ported
(e) Concentrations usually shipped
(f) Freezing point -124.2°F
Recommended type tanks MC-300, 301, 302, 303, 304, 305,
306, 307
Type DOT marking required on tanks None
Recommended metals to be used in
tanks
Recommended lining
Recommended insulation
Steel (black iron); steel (high-
tensile); aluminum alloys 5052,
5054; stainless 302, 304, and 316
None
None
Recommended pump types
Recommended hose types
How unloaded
Method used to clean tank
Centrifugal, black iron, Teflon
packing
Polyethylene, Viton, flexible steel
or polyvinyl alcohol solvent hose
Gravity, pump or air pressure
Will usually dry-clean on emptying.
Steam to remove fumes, wire brush,
water rinse, clean and dry to re-
move deposits. Air out by opening
top and bottom openings. Rinse
with cold water
Corrosion problems
None, except that degreased steel
will rust on exposure to moist air
(continued)
8-22
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TABLE 8-9. (continued)
Materials or accessories NOT satis'
factory
(a) Tank material
(b) Linings or paints
(c) Hoses
(d) Pumps
Problems in handling
Special precautions in handling
All linings, except baked phenolic
Rubber, all types
Avoid water and color pickup in
cleaning and by careless handling.
Difficult to clean stains. Will
leak through slightest crack in
fittings, seals, etc.
Avoid breathing fumes and contact
with skin and eyes. Wear protec-
tive clothing. Heavy weight and
low viscosity increase surge prob-
lem.
What to do in case of spill
Flush thoroughly with water.
evaporate rapidly.
Will
Source: National Tank Truck Carriers, Inc. (1969a).
8-23
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TABLE 8-10. HANDLING AND SHIPPING DATA FOR METHYL CHLOROFORM
Weight per gallon at 60°F
11.08 Ib
Characteristics
(a) Type commodity Solvent
(b) If flammable liquid, flash None
point open cup test
(c) If compressed gas, vapor pres-
sure at 115°F
(d) Temperature at which trans- Atmospheric
ported
(e) Concentrations usually shipped Full strength
(f) Freezing point
Recommended type tanks
Recommended metals to be used in
tanks
-26.5°F
MC-300, 301, 303, 304, 306, 307
Type DOT marking required on tanks None
Stainless steel; carbon steel
(clean, dry and free from odor
or scale)
Recommended lining
Recommended insulation
Recommended pump types
Recommended hose types
Stainless or carbon steel; air
pressure
Polyethylene, Viton, seamless stain-
less steel, Teflon, seamless
bronze
How unloaded
Method used to clean tank
Corrosion problems
Materials or accessories NOT satis-
factory
(a) Tank material
(b) Linings or paints
(c) Hoses
(d) Pumps
Pump or air
Rinse with water, steam, rinse and
dry
None
Aluminum
Rubber
Aluminum
(continued)
8-24
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TABLE 8-10. (continued)
Problems in handling
Special precautions in handling
Provide adequate ventilation; use
leather gaskets (one time only)
Wear protective safety equipment.
Gloves and goggles. No contact
allowable with rubber, plastic or
aluminum
What to do in case of spill
Flush off area with water. If
spilled on personnel, flush with
water. See doctor. If spill is
in enclosed area evacuate until
ventilated. Use air or gas masks
while decontaminating
Source: National Tank Truck Carriers, Inc. (1969b).
8-25
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TABLE 8-11. HANDLING AND SHIPPING DATA FOR PERCHLORDETHYLENE
Weight per gallon at 60°F
13.50 Ib
Characteristics
(a) Type commodity Solvent
(b) If flammable liquid, flash None
point open cup test
(c) If compressed gas, vapor pres- Nil
sure at 115°F
(d) Temperature at which trans- Atmospheric
ported
(e) Concentrations usually shipped Full strength
(f) Freezing point -22°F
Recommended type tanks MC-300, 305, 306, 307
Type DOT marking required on tanks None
Recommended metals to be used in
tanks
Recommended lining
Recommended insulation
Recommended pump types
Recommended hose types
How unloaded
Method used to clean tank
Corrosion problems
Stainless steel, aluminum, carbon
steel
If required, Heresite Lining
None required
Stainless steel, cast iron or steel,
monel or bronze
Polyethylene, Viton, seamless stain-
less steel, Teflon, seamless bronze,
Neoprene with rubber gaskets
Pump or air pressure
Flush with water, steam, rinse and
dry
None; all commercial perchloroethyl-
enes contain inhibitors
(continued)
8-26
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TABLE 8-11. (continued)
Materials or accessories NOT satis-
factory
(a) Tank material
(b) Linings or paints
(c) Hoses
(d) Pumps
Problems in handling
Special precautions in handling
What to do in case of spill
Plastics
Rubber
Rubber (Rubber gaskets have proved
satisfactory)
Aluminum not recommended
Provide adequate ventilation; avoid
contact with rubber and plastic
Use protective goggles; avoid con-
tact with skin and avoid breath-
ing heavy fume concentrations
Flush thoroughly with water; venti-
late area
Source: National Tank Truck Carriers, Inc. (1969c)«
8-27
-------
REFERENCES
American Conference of Governmental Industrial Hygienists (ACGIH). 1977.
Threshold limit values for chemical substances and physical agents in the
workroom environment. Cincinnati, Ohio.
American National Standards Institute (ANSI). 1967a. USA standard acceptable
concentrations of trichloroethylene. USAS Z37.19-1967.
American National Standards Institute (ANSI). 1967b. USA standard acceptable
concentrations of tetrachloroethylene. USAS Z37.22-1967.
American National Standards Institute (ANSI). 1970. American national stan-
dard acceptable concentrations of methyl chloroform (1,1,1-trichloroethane).
ANSI Z37.26-1970.
Department of Transportation (DOT). 1976. Hazardous materials regulations.
Federal Register. 41(188):42399.
Environmental Health Letter. 1978. G. W. Fishbein, Publisher. Washington, D.C.,
Vol. 17, No. 19.
Environmental Protection Agency (EPA). 1977. Air quality. Federal Register.
42(131):35314.
Environmental Protection Agency (EPA). 1978a. Interim primary drinking water
regulations. Control of organic chemical contaminants in drinking water.
Federal Register. 43(28):5756.
Environmental Protection Agency (EPA). 1978b. Water programs. Designation of
hazardous substances. Federal Register. 43(49):10474.
Environmental Protection Agency (EPA). 1978c. Publication of toxic pollutant
list. Federal Register. 43(21):4108.
Environmental Protection Agency (EPA). 1978d. Standards applicable to trans-
porters of hazardous wastes. Federal Register. 43(83):18506.
Environmental Protection Agency (EPA). 1978e. Guideline series: control of
volatile organic emissions from perchloroethylene dry cleaning systems.
Report No. EPA-450/2-78-050. Office of Air Quality Planning and Standards,
Environmental Protection Agency, Research Triangle Park, North Carolina.
December 1978.
Environmental Protection Agency (EPA). 1979a« Designation of hazardous sub-
stances. Federal Register, 44(34):10266.
8-28
-------
Environmental Protection Agency (EPA)» 1979b. Water quality criteria. Federal
Register. 44(52):15926.
Food and Drug Administration (FDA). 1977a. Trichloroethane: status of a new
drug in aerosolized drug products intended for inhalation. Federal Register.
42(242):63386.
Food and Drug Administration (FDA). 1977b. Trichloroethylene. Federal Register,
42(187):49465.
Franklin Institute Research Laboratories. 1975. Preliminary study of selected
potential environmental contaminants. Report No. EPA-560/2-75-002. Environ-
mental Protection Agency, Washington, D.C. July 1975.
General Services Administration (GSA). 1967. Federal specifications 0-T-236b
for technical grade perchloroethylene. Washington, D.C.
Jacobsen, C. 1978. Consumer Product Safety Commission, Washington, D.C., Per-
sonal Communication. October 7, 1978.
National Institute for Occupational Safety and Health (NIOSH). 1977. Criteria
for a recommended standard . . . occupational exposure to waste anesthetic
gases and vapors. U.S. Department of Health, Education, and Welfare,
Washington, D.C., Publication No. 77-140.
National Institute for Occupational Safety and Health (NIOSH). 1978a. Current
intelligence bulletin 20, tetrachloroethylene (perchloroethylene). U.S. De-
partment of Health, Education, and Welfare, Washington, D.C., Publication
No. 78-112.
National Institute for Occupational Safety and Health (NIOSH). 1978b. Summary
of NIOSH recommendations for occupational health standards. U.S. Department
of Health, Education, and Welfare, Washington, D.C., March 1978.
National Institute for Occupational Safety and Health (NIOSH). 1978c. Special
occupational hazard review with control recommendations, trichloroethylene.
U.S. Department of Health, Education, and Welfare, Washington, D.C., Publi-
cation No. 78-130.
National Institute for Occupational Safety and Health (NIOSH). 1978d. Current
intelligence bulletin 27, chloroethanes: review of toxicity. U.S. Depart-
ment of Health, Education, and Welfare, Washington, D.C., Publication No.
78-181.
National Tank Truck Carriers, Inc. 1969a. Commodity and equipment data sheet -
CED-34. Washington, D.C., Reissued May 1969.
8-29
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National Tank Truck Carriers, Inc. 1969b. Commodity and equipment data sheet -
CED-63. Washington, B.C., Reissued May 1969.
National Tank Truck Carriers, Inc. 1969c. Commodity and equipment data sheet -
CED-78. Washington, D.C., Reissued May 1969.
Occupational Health and Safety Letter (OHS). 1978. G. W. Fishbein, Publisher.
Washington, D.C., Vol. 8, No. 14.
Occupational Safety and Health Administration (OSHA). 1977a. Selected general
industry safety and health standards. Federal Register, Part IV, 29 CFR
1910.1000, December 13, p. 62868.
Occupational Safety and Health Administration (OSHA). 1977b. Identification,
classification and regulation of toxic substances posing a potential occupa-
tional carcinogenic risk. Federal Register. 42(192):54148.
Schlossberg, L. 1979. Detrex Chemical Industries, Detroit, Michigan, Letter to
Dr. Stanley C. Mazaleski, Environmental Protection Agency, Washington, D.C.,
April 6.
Siebert, G. 1978. Department of Defense, Energy Environment and Safety Office,
Pentagon, Washington, D.G., Personal Communication. October 1978.
Toxic Materials News. 1978. NIOSH urges mandatory lowering of worker exposure
to TCE. L. A. Eiserer, Publisher, Washington, D.C., March 15, p. 67.
Toxic Materials News. 1979. CPSC staff to conduct in-house investigation of
tetrachloroethylene. L. A. Eiserer, Publisher, Washington, D.C., March 21,
p. 92.
Waters, E. M., H. B. Gerstner, and J. E. Huff. 1976. Trichloroethylene - I.
An impact overview. Oak Ridge National Laboratory, Report No. ORNL/TIRC-76/2,
Contract No. W.7405-eng-26, Oak Ridge, Tennessee, May 1976.
Winell, M. A. 1975. An international comparison of hygiene standards for chem-
icals in the work environment. Ambio. 4(1):34.
8-30
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CONTENTS
Page
9. Solvent Emissions: Control, Recovery, and Disposal .... 9-3
9.1 Metal Cleaning Industry 9-3
9.1.1 Sources of solvent emission ........ 9-3
9.1.2 Cold cleaning control systems 9-5
9.1.3 Open top vapor degreasing control systems . 9-6
9.1.4 Conveyorized degreasing control systems . . 9-9
9.2 Dry Cleaning Industry 9-12
9.2.1 Perchloroethylene losses in dry cleaning . 9-14
9.2.1.1 Previous studies of solvent loss . . 9-14
9.2.1.1.1 Retail dry cleaning plant . . 9-14
9.2.1.1.2 Industrial cleaning plant . . 9-15
9.2.1.1.3 California study 9-15
9.2.1.2 Information from present survey . . 9-18
9.2.1.2.1 Current experience with per-
chloroethylene mileage . . 9-18
9.2.1.2.2 Data from 1978 Street
survey 9-21
9.2.2 Perchloroethylene emission reduction . . . 9-26
9.2.2.1 Recovery via mechanical engineer-
ing 9-27
9.2.2.2 Equipment based on F-113 designs . . 9-28
9.3 Solvent Recovery or Disposal 9-28
9-1
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CONTENTS (continued)
9.3.1 Distillation 9-29
9.3.2 Incineration 9-30
9.3.2.1
9.3.2.2
9.3.2.3
9.3.2.4
9.3.2.5
9.3.2.6
Multiple hearth incineration ....
Liquid injection incineration ...
9-31
9-31
9-32
9-32
9-33
9-33
9.3.3 Landfill disposal 9-33
9.4 Container Labels 9-34
References 9-39
9-2
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SECTION 9
SOLVENT EMISSIONS: CONTROL, RECOVERY, AND DISPOSAL
In this section, an analysis will be made of the various solvent emission
control technologies available to the metal cleaning industry, emissions and
control potential for the dry cleaning industry, solvent recovery by distil-
lation, incineration of waste solvent, and current container labeling prac-
tices.
9.1 METAL CLEANING INDUSTRY
This subsection describes operating procedures and available control
devices which may be applied to control emissions from the three basic types
of solvent metal cleaners: cold cleaners, open top vapor degreasers, and
conveyorized degreasers. Information is provided on nominal control efficien-
cies (i.e., percent emission reduction) for some control devices. Also, the
potential cost savings from use of the controls are indicated to the extent
that such information is available. Solvent metal cleaners and the emission
control techniques that may be applied to them have been the subject of in-
tensive study. Three major reports have dealt with this topic so that a
lengthy, in-depth discussion would be redundant and inappropriate. The three
reports are Dow Chemical Company (1976), Environmental Protection Agency
(1977), and Mitre Corporation, Metrek Division (1978); information presented
in this discussion was summarized from these reports. The American Society
for Testing Materials (ASTM) has also published a booklet on the recommended
procedures and practices for vapor degreasing (ASTM, 1976).
9.1.1 Sources of Solvent Emission
Control procedures and devices are designed to match the requirements of
various emission sources. A brief review and discussion of emission sources
is presented herein for each type of solvent metal cleaner.
The major cold cleaner emission sources are: bath evaporation, solvent
carryout, bath agitation, spray evaporation, and waste solvent evaporation.
Failure by the operator to cover the solvent bath whenever parts are not
being handled in the cold cleaner results in solvent emissions. Excessive
drafts in the work area can also significantly increase solvent bath
9-3
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evaporation. Inadequate freeboard* height above the solvent level in the
bath contributes to emissions. The extent of carryout emissions depends on
the orientation of the work part for proper drainage and on the existence
and use of proper facilities (i.e., racks or shelves) to allow drainage of
excess solvent off cleaned parts prior to removal from the cleaner. Bath
agitation promotes cleaning but also tends to increase solvent emissions;
the emission rate also depends on the extent of use of the tank cover, agi-
tation system adjustments, and the solvent volatility. Emissions from solvent
spraying of parts increase with the pressure of the spray, the fineness of
the spray, an increase in volatility of the solvent used, and the tendency
to splash and overspray out of the tank. The greatest source of emissions
from cold cleaning is waste solvent evaporation; this emission depends not
only on the amount of waste solvents but also upon the method of disposal.
Solvent volatility at the operating temperature is the most important single
variable affecting the emission rate from a cold cleaner.
In contrast to cold cleaners, open top vapor degreasers lose a rela-
tively small proportion of their solvent in waste material and as liquid
carryout. The quantity of vapor emissions depends to a large extent on the
operator.
Most vapor degreaser emissions consist of diffusion losses, i.e., the
escape of solvent vapors from the vapor zone of the degreaser. The mixing
of solvent vapors with air at the top of the vapor zone increases with drafts
and with disturbances from cleaned parts being moved in and out of the vapor
zone, and solvent vapors thus diffuse into the room air. These emissions in-
clude the convection of warm solvent-laden air upwards out of the degreaser.
Carryout emissions are the liquid and vaporous solvent entrained on the
cleaned parts as they are removed from the degreaser. Exhaust systems known
as lip or lateral exhausts are frequently used on larger than average open
top vapor degreasers; these systems draw in solvent-laden air around the top
perimeter of the degreaser. This exhaust system, although a collector of
emissions, can increase evaporation from the solvent bath, especially if the
exhaust ventilation rate is excessive. Emissions may also result from im-
proper disposal of waste solvent sludge, i.e., in ways where the solvent can
evaporate into the atmosphere.
There are seven principal types of conveyorized degreasers: monorail,
cross-rod, vibra, ferris wheel, belt, strip, and circuit board cleaners.
Most of these types may be used with cold or vaporized solvent; the first
The freeboard serves primarily to reduce drafts near the air/solvent inter-
face. Freeboard is the distance from the top of the tank to this interface.
All cold cleaners should have a minimum freeboard ratio of 0.5, where this
ratio is defined as the height of the tank above the solvent level divided
by the tank width.
9-4
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four are almost always vapor degreasers. About 85% of the units are vapor
types and 15% are nonboiling degreasers.
Conveyorized degreasers are usually enclosed except for a small entrance
and exit. The diffusion and convection losses of solvent vapors from the sol-
vent bath are, therefore, considerably less for conveyorized degreaser than
for open top degreasers.
Since conveyorized degreasers are usually automated, operating practice
is a minor factor while design and adjustment are major factors affecting
emissions. Adjustment of the degreasing system primarily influences bath evap-
oration and exhaust emissions, while operation and equipment design affect
carryout and waste solvent evaporation. The principal adjustment affecting
the batch evaporation rate is the heating and cooling balance. Cooling provided
by the primary condensing coils should be adequate to condense all vaporized
solvent. Emissions of solvent vapors occur at the open entrance and exit areas
of the degreaser. The spray system can cause excessive turbulence at the air/
vapor interface and result in solvent emissions. In some instances, solvent
emissions can be high because of an excessive ventilation rate.
The major emission from conveyorized degreasers is usually the carry-
out of vapor and liquid solvent as parts are moved out of the unit. Factors
affecting these emissions are the drainage of cleaned parts and their drying
time. The smallest emission source is the evaporation from waste solvent dis-
posal. In most conveyorized degreaser systems, an external still is connected
to the degreaser so that solvent can be constantly pumped out, distilled, and
returned. Therefore, the wastes usually consist only of still bottoms. The
method of disposal of the waste determines the amount of solvent that evapo-
rates into the atmosphere.
9.1.2 Cold Cleaning Control Systems
The most important emission control factor for cold cleaners is the proper
control of waste solvent. Waste solvent should be either reclaimed or disposed
of in such a manner that a minimum is introduced into the environment. The
principal control equipment for these cleaners includes a cover, a facility
for draining cleaned parts, an adequate freeboard, a visible fill line, and a
permanent label which summarized operating requirements.
All cold cleaners should be equipped with well-designed covers. Covers
which make a good seal and which are mechanically assisted, and, therefore,
easily operated provide the best deterrent to evaporation of solvent from.
the bath, if properly used. The efficiency of control for covers is reported
to be 92% for bath evaporation.
The principal control device for carryout emissions is a simple drain-
age facility consisting of external or internal drainage racks or shelves.
The internal drainage facility which is located beneath the cover may be a
9-5
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basket suspended over the bath or a shelf to permit solvent drainage. When
external racks are used, they are fastened to the side of the cold cleaner
near the top; liquid solvent from cleaned parts drains into a trough and is
returned to the bath. Proper drainage time for drain racks or baskets is a
minimum of 15 sec or until dripping of solvent from the cleaned part ceases.
This procedure minimizes solvent carryout losses. The efficiency of control
with drain racks or baskets is reported to be 50% for solvent carryout losses.
Each cold cleaner unit should have a permanent, conspicuous label attached
which summarizes the operating requirements. The operator has an important role
in control of emissions.
The control devices and operating practices for two systems (A and B) are
shown in Table 9-1. There is not a great difference in effect between the two
systems since most of the emissions are controlled in System A. If all opera-
tors strictly adhered to the requirements of System A, there would be little
need for System B requirements. However, operators may often become lax in
following procedures. Even though the effectiveness of the control systems
depends greatly on the quality of operation, System A could reduce cold clean-
ing emissions by 50 (+ 20) percent and System B by 53 (+ 20) percent for low
volatility solvents (EPA, 1977). The lower values represent emission reduction
resulting from poor compliance and the upper values represent excellent com-
pliance. However, methyl chloroform and trichloroethylene have moderate to
high evaporation rates and perchloroethylene has a moderate to low rate (see
evaporate rate, Table 4-1). For cold cleaners with high volatility solvents,
bath evaporation may contribute approximately 50% of the total emission. In
this case, System B may achieve 69 (+ 20) percent control efficiency and Sys-
tem A only 55 (+20) percent control (EPA, 1977).
9.1.3 Open Top Vapor Degreasing Control Systems
The principal components of a control system for open top vapor degreasers
are good operational practices and the use of control equipment. Control equip-
ment includes a cover, safety switches, and a major control device (either high
freeboard, refrigerated chiller, enclosed design, or carbon adsorption).
The recommended type of cover opens and closes in a horizontal motion, so
that the air/vapor interface disturbance is minimized. These types include
roll-type plastic covers, canvas curtains, and guillotine covers. For the ^-'
larger vapor degreasers (cover weight of over 30 Ib or > 1 m open surface
area), it is generally advantageous to employ a power-assisted cover. The ef-
ficiency of control for bath evaporation emissions by proper use of a cover is
reported to range from 30 to 5070.
Safety switches are used to prevent solvent emissions in the event of ab-
normal operating conditions of open top vapor degreasers. The five principal
types of switches are: (a)'vapor level control thermostat; (b) condenser wa-
ter flow switch and thermostat; (c) sump thermostat; (d) solvent level control;
9-6
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TABLE 9-1. COLD CLEANING CONTROL SYSTEMS
Control Sysjiem A
Control Equipment:
1. Cover.
2. Facility for draining cleaned parts.
J. Permanent, conspicuous label, summarizing the operating requirements.
Operating Requirements:
1. Do not dispose of waste solvent or transfer it to another party, such chat greater
than 20% of the waste (by weight) can evaporate into the atmosphere.—' Store waste solvent
only in covered containers,
2. Close degreaser cover whenever not handling parts in the cleaner.
3. Drain cleaned parts for at least 15 sec or until dripping ceases.
Control System B
Control Equipment:
1, Cover: Same as in System A, except if (a) solvent volatility is greater than 2 kPa
(15 mm Hg or U.'i psi) measured at 38°C (100°F),- (b) solvent is agitated, or (c) solvent is
heated, then the cover must be designed so that it can be easily operated with one hand.
(Covers for larger degreasers may require mechanical assistance, by spring loading, counter-
weighting or powered systems.)
2. Drainage facility: Same as in System A, except that if solvent volatility is
greater than about 4.3 kPa (32 mm Hg or 0.6 psi) measured at 38°C (100°F), then the drainage
facility must be internal, so that parts are enclosed under the cover while draining. The
drainage facility may be external for applications where an internal type cannot fit into
the cleaning system.
3. Label: Same as in System A.
4. If used, the solvent spray must be a solid, fluid stream (not a fine, atomized or
shower type spray) and at a pressure which does not cause excessive splashing *
5. Major control device for highly volatile solvents: If the solvent volatility is
> 4.3 kPa (33 mm Hg or 0.6 psi) measured at 38°C (100°F), or if solvent is heated above
50°C (120&F), then one of the following control devices must be used.
a. Freeboard that gives a freeboard ratio^' > 0.7.
b. Water cover (solvent must be insoluble in and heavier than water).
c. Other systems of equivalent control, such as a refrigerated chiller or carbon
adsorption.
Operating Requirements:
Same as in System A.
a/ Water and solid waste regulations must also be complied with.
b/ Generally solvents consisting primarily of mineral spirits (Stoddard) have volatilities
< 2 kPa.
c/ Freeboard ratio is defined as the freeboard height divided by the width of the degreaser.
Source: Taken from Environmental Protection Agency (1977).
9-7
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and (e) spray safety switch. The first four switches turn off sump heat, while
the fifth turns off the spray.
The vapor level control thermostat is activated when the solvent vapor
zone rises above the designated operating level. This condition can occur if
the coolant flow to the condenser is interrupted.
The condenser water flow switch and thermostat is activated when either
the condenser water stops circulating or the condenser water becomes warmer
than acceptable. When properly adjusted, this device serves as a back-up for
the vapor thermostat.
The buildup of oils, greases, and other contaminants in the solvent can
result in an increase in the boiling point of the solvent bath. The sump ther-
mostat turns off the heat when the sump temperature rises significantly above
the solvent's boiling point. The solvent level control turns off the heat when
the liquid level of the sump is reduced to the height of the sump heater coils.
Without these safety devices, excessive heat could decompose the solvent.
The spray safety switch helps prevent spraying above the vapor level which
causes excessive emissions. If the vapor level drops below a specified level,
the switch turns off the pump for the spray application.
Freeboard for an open top vapor degreaser is defined as the distance from
the top of the vapor zone to the top of the degreaser. Freeboard ratio is this
height divided by the width at the open top of the degreaser. A high freeboard
reduces the potential effects of drafts or other disturbances affecting the
air-vapor interface. Normally, the freeboard ratio is 0.5 to 0.6, except for
very volatile solvents (e.g., CH2Cl2> F-113, etc.) where a minimum freeboard
ratio of 0.75 is used. ASTM has recommended that a minimum freeboard ratio of
0.75 or a maximum of 4 ft be an alternative control for open top vapor degreas-
ers using all solvents. It has been reported that the use of the 0.75 freeboard
ratio with all solvents has an efficiency of control for bath evaporation emis-
sions of 20 to 30%.
In open top vapor degreasers, solvent vapors created within the unit are
prevented from overflowing the equipment by means of condenser coils and a wa-
ter jacket below the freeboard. Addition of a refrigerated freeboard chiller
adds a second set of condenser coils located slightly above the primary con-
denser coils. The chiller unit impedes the diffusion of solvent vapors from
the vapor zone into the room atmosphere by creating a cold air blanket imme-
diately above the vapor zone. A third type of refrigerated chiller, known as
the refrigerated condenser coil, is available. The condenser coil units do not
provide an extra set of chilling coils; the primary condenser coils are re-
frigerated. The application of refrigerated freeboard chillers to open top va-
por degreasers is reported to reduce bath evaporation emissions of solvent by
30 to 40%.
9-8
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One enclosure design for open top vapor degreasers is an automated cover-
conveyor system which closes the cover of the degreaser when parts are being
cleaned and dried. The cover is open only for the short periods of time when
dry parts are actually entering or exiting. When a part is conveyed by a hoist,
the cover is designed to close horizontally and be split into two parts so that
it closes at the center where the cable is located. If parts are conveyed by a
shelf which automatically lowers and rises, then the vapor degreaser can be
covered by a permanent enclosure with a vertical door. Emissions occur only
when parts enter or exit the degreaser.
Carbon adsorption units are used in conjunction with ventilation apparatus
to capture solvent emissions from metal cleaning operations. Recovered solvent,
obtained in the regeneration cycle by stripping the carbon with steam, is rarely
identical to that used in the cleaning system. Thus, in some cases, fresh sol-
vent, stabilizers and/or co-solvents must be added to the recovered solvent be-
fore it is reused. Carbon adsorption units are reported to have a control effi-
ciency of 40 to 657o for ventilation emissions (EPA, 1977).
The control devices and operating requirements for two systems (A and B)
are shown in Table 9-2. With respect to the safety switches discussed earlier,
the vapor level thermostat is required by OSHA on open surface vapor degreasing
tanks so it was not included in these systems. In addition, the solvent level
control and sump thermostat are used primarily for the prevention of solvent
degradation and for the protection of equipment; they are not included in the
systems shown in Table 9-2.
System A employs only a cover as control equipment; this system may reduce
open top vapor degreasing emissions by 45 (+ 15) percent. System B employs a
cover, safety switches, and one major control device; this system may reduce
emissions by 60 (+ 15) percent.
9.1.4 Conveyorized Degreasing Control Systems
Emission controls are specified according to the type of conveyorized de-
greaser in use: (a) conveyorized vapor degreaser or (b) conveyorized cold
cleaner.
The two major emission control devices for the conveyorized vapor de-
greaser are carbon adsorption and refrigerated freeboard chillers. In the ad-
sorption system, an exhaust fan draws the solvent-air mixture from the de-
greaser and passes it through a bed of activated carbon. When the carbon has
adsorbed a maximum quantity of solvent (based on a time cycle), the carbon bed
is desorbed; the steam condensate passed through a separator; and the recov-
ered solvent is returned to the degreaser. The control efficiency of a carbon
adsorber used in the exhaust system of conveyorized degreasers is reported to
be 50 to 70%, depending upon the configuration of the degreaser (Mitre Corpora-
tion, 1978).
9-9
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TABLE 9-2. OPEN TOP VAPOR DECREASING CONTROL SYSTEMS
Control System A
Control Equipment:
1. Cover that can bt opened and closed easily without disturbing the vapor zone.
Operating Requirements:
1. Keep cover closed at all times except when processing work loads through the de-
greaser.
2. Minimize solvent carry-out by the following measures:
a. Rack parts to allow full drainage.
b. Move parts in and out of the degreaser at less than 3.3 m/sec (11 ft/min).
c. Degrease the work load in the vapor zone at least 30 sec or until condensation
ceases.
d. Tip out any pools of solvent on the cleaned parts before removal.
e. Allow parts to dry within the degreaser for at least 15 sec or until visually
dry.
3. Do not degrease porous or absorbent materials, such as cloth, leather, wood or rope.
4. Work loads should not occupy more than half of the degreaser's open top area.
5. The vapor level should not drop more than 10 cm (4 in.) when the work load enters
the vapor zone.
6. Never spray above the vapor level.
7. Repair solvent leaks immediately or shut down the degreaser.
8. Do not dispose of waste solvent or transfer it to another party such that greater
than 207. of the waste (by weight) will evaporate into the atmosphere. Store waste solvent
only in closed containers.
9. Exhaust ventilation should not exceed 20 m /min/m (65 cfm/ft ) of degreaser open
area, unless necessary to meet OSHA requirements* Ventilation fans should not be used near
the degreaser opening.
10. Water should not be visually detectable in solvent exiting the water separator.
Control System B
Control Equipment:
1. Cover (same as in System A).
2. Safety switches.
a. Condenser flow switch and thermostat (shuts off sump heat if condenser coolant
is either not circulating or too warm).
b. Spray safety switch (shuts off spray pump if the vapor level drops excess-
ively, about 10 cm (4 in.).
3. Major control device:
Either: a. Freeboard ratio greater than or equal to 0.75, and if the degreaser opening
is > 1 m^ (10 ft ), the cover must be powered.
b. Refrigerated chiller.
• c. Enclosed design (cover or door opens only when the dry part is actually
entering or exiting the degreaser).
(continued)
9-10
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TABLE 9-2. (continued)
d. Carbon adsorption system, with ventilation > 15 m /mln/m*" (50 cfm/ft ) of
air/vapor area (when cover is open), and exhausting < 25 ppm solvent averaged over one com-
plete adsorption cycle.
e. Control system, demonstrated to have control efficiency equivalent to or
better than any of the above.
C. Permanent, conspicuous label, summarizing operating procedures No. 1 to No. 6.
Operating Requirements:
Same as in System A,
Source: Taken from Environmental Protection Agency (1977).
9-11
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The freeboard chiller for a conveyorized vapor degreaser functions in the
same manner as for an open top vapor degreaser.
Carryout losses may be reduced by using a drying tunnel with a monorail
degreaser or a downdraft tunnel with a cross-rod degreaser. In both cases, a
carbon adsorber is used to remove the solvent from the air stream and recycle
it back into the degreaser.
Emissions of solvent vapor by convection or diffusion from the entry and
exit ports of a monorail degreaser can be reduced by decreasing the port area
using silhouette cutouts of hanging plastic flaps. The average clearance be-
tween parts and the edge of the degreaser opening should be either < 10 cm (4
in.) or < 10% of the width of the opening. The use of downtime covers, closing
off the entrance and exit, minimizes vaporization losses during cooling, warmup,
and shutdown periods. These covers also reduce solvent losses from conveyorized
cold cleaners.
Some of the same safety switches recommended for open top vapor degreasers
are also useful equipment for conveyorized units. These include condenser flow
switch and thermostat, spray safety switch, and vapor level control thermostat.
Since conveyorized degreasers are essentially enclosed systems, control
devices tend to work more effectively on these units. A refrigerated chiller
will likely have a high control efficiency because room drafts generally do
not disturb the cold air blanket. Carbon absorbers also tend to produce a high
efficiency due to a more effective vapor collection system and inlet air streams
with higher solvent concentrations.
Two emission control systems for conveyorized degreasers (vapor and cold)
are described in Table 9-3. System A requires only proper operating procedures
which can, in most cases, be implemented with only a small capital expenditure.
Control efficiency for System A is estimated at 25 (+5) percent. System B re-
quires the installation or utilization of a major control device and three
other control devices of nominal cost with respect to their potential solvent
savings. The estimated control efficiency for System B is 60 (+ 10) percent
(EPA, 1977).
9.2 DRY CLEANING INDUSTRY
This subsection deals with the losses of perchloroethylene currently ex-
perienced in the dry cleaning industry of the United States. By surveying a
number of industry contacts, an attempt has been made to compile the best cur-
rent data concerning the quantity of perchloroethylene vapors discharged by
various types of dry cleaning plants and the loss rate of solvent per unit of
fabric processed.
In the past, there has been considerable uncertainty and lack of agreement
among various estimates of the extent and rate of solvent loss by the industry
9-12
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TABLE 9-3. CONVEYORIZED DEGREASER CONTROL SYSTEMS
Control Svstem A
Control Equipment: None.
Operating Requirements:
I. Exhaust ventilation should not exceed 20 m-Vmiti/m (65 cftn/ft ) of degreaser open-
ing, unless necessary to meet OSHA requirements. Work place fans should not be used near
the degreaser opening.
2. Minimize carry-out emissions by:
a* Racking parts for best drainage.
b. Maintaining verticle conveyor speed at < 3.3 m/min (11 ft/min).
3. Do not dispose of waste solvent or transfer it to another party such that greater
than 207, o£ the waste (by weight) can evaporate into the atmosphere. Store waste solvent
only in covered containers.
4. Repair solvent leaks immediately, or shut down the degreaser.
5. Water should not be visibly detectable in the solvent exiting the water separator.
Control Svstem B
Control Equipment:
1. Major control devices; the degreaser must be controlled by either:
a. Refrigerated chiller.
b. Carbon adsorption system, with ventilation > 15 m /min/m2 (50 cfm/ft^) of air/
vapor area (when downtime covers are open), and exhausting < 25 ppm of solvent by volume av-
eraged over a coroplete adsorption cycle•
c. System demonstrated to have control efficiency equivalent to or better than
either of the above.
2. Either a drying tunnel or another means such as rotating (tumbling) basket suffi-
cient to prevent cleaned parts from carrying out solvent liquid or vapor.
3. Safety switches.
a. Condenser flow switch and thermostat (shuts off sump heat if coolant is either
not circulating or too warm).
b. Spray safety switch (shuts off spray pump or conveyor if the vapor level drops
excessively, e.g., > 10 cm (4 in.)).
c. Vapor level control thermostat (shuts off sump heat when vapor level rises too
high).
4. Minimized openings: Entrances and exits should silhouette work loads to that the
average clearance (between parts and the edge of the degreaser opening) is either < 10 cm
(4 in.) or < 107. of the width of the opening.
5. Downtime covers: Covers should be provided for closing off the entrance and exit
during shutdown hours.
Operating Requirements:
1. - 5. Same as for System A.
6. Downtime cover must be placed over entrances and exits of conveyorized degreasers
immediately after the conveyor and exhaust are shut down and removed just before they are
started up*
Source: Taken from Environmental Protection Agency (1977).
9-13
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as a whole, and more particularly the range of solvent losses experienced by
plants of differing types using various kinds of dry cleaning equipment. It is
anticipated that more detailed information on the atmospheric emissions of per-
chloroethylene from various types of dry cleaning plants may be considered in
the development of new standards and regulations for the reduction of atmo-
spheric emissions.
In subsequent parts of this subsection, the following topics are covered:
* The present situation regarding perchloroethylene losses in dry cleaning.
* Factors associated with the wide range of variation observed in solvent
losses.
* Engineering changes or other developments that are being explored to
reduce solvent losses.
* The range of improvement that seems realistically attainable.
A general overview of the perchloroethylene segment of the dry cleaning industry
was presented in Section 3.
9.2.1 Perchloroethylene Losses in Dry Cleaning
Substantially all of the perchloroethylene consumed in dry cleaning opera-
tions is ultimately discharged as atmospheric emissions. Relatively small quan-
tities of perchloroethylene may be discharged as waterborne emissions from the
solvent separation system. Solvent contained in discarded filter media or dis-
tillation sludge is usually placed in containers and sent to landfills. Recent
estimates of total dry cleaning consumption of perchloroethylene were presented
in Section 3. As of 1978, approximately 350 to 385 million pounds of perchloro-
ethylene is consumed annually in dry cleaning. There is much less general agree-
ment regarding the rate of loss of perchloroethylene in dry cleaning a given
quantity of fabric. Perchloroethylene loss rate or "mileage" figures are most
commonly expressed in the trade in terms of pounds of clothing cleaned per 700-
Ib drum of solvent. More recently, solvent loss rates have been expressed as
pounds of solvent consumed per 100 Ib of fabric processed.
9.2.1.1 Previous Studies of Solvent Loss—
Air pollution emission tests have been conducted on modern dry cleaning
units equipped with carbon adsorption beds to reduce perchloroethylene emis-
sions to the atmosphere. The results show that low solvent loss rates can be
achieved, at least over short test periods, on correctly maintained and prop-
erly operated dry cleaning units. The results from two such tests are discussed
in the following paragraphs. These studies were summarized in Section 7.
9.2.1.1.1 Retail dry cleaning plant—A typical size, commercial dry-to-
dry perchloroethylene dry cleaning unit at Kalamazoo, Michigan, was tested in
9-14
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1976 to determine the effectiveness of the dual carbon adsorption beds in re-
ducing solvent emissions to the atmosphere (MRI, 1976a). The results indicate
that perchloroethylene concentrations at the outlet ranged from 5 to 11 ppm
when the unit was empty or not discharging vapors through the adsorption unit
to as high as 371 ppm near the end of a heavy load (rugs). Over typical clean-
ing cycles, the integrated emissions averaged 102 ppm for a calculated total
solvent vapor discharge averaging 0.226 lb/30-lb cycle. The implied solvent
loss rate is exceptionally low; approximately 0.75 Ib perchloroethylene per
100 Ib of fabric. Discharge of dissolved perchloroethylene from the water sep-
arator to the sewer averaged 0.029 lb/100 Ib of fabric cleaned. The carbon ad-
sorbers showed better than 95% effectiveness in reducing perchloroethylene
emissions.
9.2.1.1.2 Industrial cleaning plant—A large size industrial perchloro-
ethylene transfer dry cleaning machine in San Antonio, Texas, was tested in
1976 (MRI, 1976b). This unit was equipped with a single carbon adsorption bed
to reduce solvent emissions. From 13 to 16 loads of work clothing were cleaned
each day; pants at 300 Ib/load, shirts at 200 Ib/load. Integrated gas sampling
results show outlet stream concentrations of less than 5 ppm perchloroethylene.
Total solvent emissions through the adsorber for 1 day average 0.136 Ib, equiv-
alent to a consumption rate of 0.03 Ib of perchloroethylene per 100 Ib of
fabric.
Solvent losses during loading of this transfer machine ranged from 1,800
to 8,700 ppm; these levels reflect the vapors picked up by the vent system
around the door during the 3- to 4-min loading period. Other losses include
emissions from the still vent and the discharge to the sewer of perchloro-
ethylene in water from the carbon bed regeneration. Such solvent losses typi-
cally increase solvent consumption by 1.0 to 3.0 Ib of solvent per 300-Ib load.
9.2.1.1.3 California study—The California State Board of Fabricare in
1974 and 1975 commissioned a detailed statewide study of solvent emissions
from dry cleaning plants (IFI, 1975). From a listing of 3,214 dry cleaning
plants in the State of California, 150 plants were drawn at random. Members
of the State Board of Fabricare then selected the 50 plants to be included in
the study from the random sample of 150 plants. Of the 50 plants studied, 39
(78%) were perchloroethylene plants and 11 (22%) used petroleum solvent. This
distribution is fairly close to the national average for all dry cleaning
plants (74 and 26%).
Among the perchloroethylene plants studied, 23% used dry-to-dry machines
(versus 16% nationally), while 77% employed transfer units. Slightly more than
51% of all plants studied employed carbon adsorbers, almost identical to the
national average of 49%. Thus, the plants studied are fairly representative
of the types of equipment used across the nation, and the findings regarding
solvent losses should be indicative of current experience.
9-15
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The operator of each plant reported the weekly pounds of fabric cleaned
and the solvent mileage in pounds per 52-gal. drum of solvent. From these re-
ports, the expected solvent losses could be compared with those estimated from
actual in-plant measurements.
Data were recorded for the weight of garment loads before cleaning, after
extraction (for transfer units), and after drying. The quantity of perchloro-
ethylene recovered from the condenser was measured, so that recovery efficiency
could be determined. Atmospheric emissions were measured at the vapor adsorber
exhaust or the tumbler exhaust. Losses of solvent from the still, muck cooker,
and cartridge filters were measured, so that total solvent losses per week
could be derived. A summary of the losses from the 39 perchloroethylene plants
surveyed is presented in Table 9-4. Data from the same study pertaining to sol-
vent loss to the atmosphere were presented in Section 7.
The reported weekly losses, some of which reflect the operators experience
(or expectation) often differ markedly from the weekly losses calculated on the
basis of in-plant tests conducted during this survey. While some plants (e.g.,
Nos. 1, 2, 10, 13, 34, 40, 44, 45, 49, and 50) showed good agreement between
reported and calculated solvent losses, other plants showed test losses that
ranged from one-tenth the reported levels (Nos. 20, 22, 27, 29, and 35), up to
factors of 5 or 10 times the reported losses (Nos. 4, 7, 23, and 39). One pos-
sible conclusion may be that the solvent losses obtained in any particular test
often bear little relationship to environmental emissions over the longer term.
Several comments were noted during plant tests which partially account
for some of the erratic solvent losses observed.
* In several plants, visible leakage of perchloroethylene was observed.
* One machine went into deodorize cycle much too early due to possible
faulty controls.
* Measured recovery efficiency in numerous plants was low (ranged from
14.2% to 74.6%).
* Draperies were air dried outside after cleaning; residual solvent
losses not known.
* In one case, three recovery tumblers were ducted into a single vapor
adsorber.
The primary factors leading to adsorber breakthrough are said to be:
* Inadequately sized carbon adsorbers.
* Too many loads dried between desorptions.
9-16
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TABLE 9-4. PERCHLOROETHYLENE SOLVENT MILEAGE AND LOSSES
Reported data
Plant
No.
1
2
4
5
6
7
10
11
12
13
14
19
20
21
22
23
24
25
27
29
30
31
32
34
35
36
37
38
39
40
41
42
43
44
45
47
48
49
50
Cleaning
volume
(Ib/week)
3,300
1,000
5,000
6,115
2,300
1,300
2,500
519
NA
900
7,900
1,000
2,500
2,700
2,800
2,230
2, -000
1,100
10,135
1,200
1,750
1,500
3,231
2,000
2,000
1,076
3,000
1,700
1,100
800
603
1,500
9,000
1,500
6,500
1,350
2,800
3,175
2,000
Solvent
mi leage
(Ib/drum)
4,700
6,400
6,870
14,008
3,417
9,500
6,100
5,240
NA
2,810
5,300
4,033
6,000
7,500
7,500
12,567
11,266
6,000
10,135
2,400
10,710
4,440
6,619
4,880
3,440
5,900
15,600
2,600
7,150
3,605
14,000
6,200
10,140
11,500
7,323
5,070
8,000
11,000
9,013
Weekly
Reported
(Sal/week)
36.5
8.1
37.8
22.7
65.7
7.1
21.3
5.2
NA
16.7
77.5
12.9
21.7
18.7
19.4
9.2
9.2
9.5
52.0
26.0
7.3
17.6
25.4
21.3
66.2
9.5
10.0
34.0
8.0
11.5
2.2
12.6
46.2
6.8
46.2
13.8
18.2
15.0
11.5
losses
Calculated
(gal/week)
27.0
7.0
233.5
13.5
49.5
82.5
22.0
b/
NA
21.5
40.0
23.0
2.5
b/
2.5
42.0
6.5
24.0
6.5
1.5
2.0
1.0
NA
16.5
4.5
b/
40.0
19.5
38.0
7.5
b/
12.6
b/
4.0
40.5
b/
_b/
10.5
15.5
Loss in residues
(Rol/week)
Cartridge
Still Cooker filter
0.2
0.3
1.2
NA '
0.1
0.1
1.2
0.3
NA NA
0.3 - 1.2
2.6
NA - 1.3
0.8 0.7
0.9 0.5
1.3
0.1
2.7
0.1
6.0
0.7
1.5
0.2
NA
0.9
2.7
1.4
3.0
2.3
0.5
0.3
0.4
0.2
0.4
NA
2.2
1.8
1.5
NA
2.7
Loss to atmosphere
Calcul.
based
on
VA
TE
RE
VA
RE
RE
VA
RE
VA
VA
VA
RE
VA
RE
VA
RE
VA
RE
VA
VA
VA
VA
RE
VA
VA
RE
RE
RE
RE
TE
RE
RE
VA
VA
VA
RE
VA
TE
RE
Gal /week
26.8
6.9
232.5
13.5
49.6
82.3
20.7
b/
NA
19.8
37.5
21.6
1.0
b/
1.3
41.8
3.7
23.9
0.6
0.7
0.7
0.7
67.0
15.8
1.7
b/
37.2
17.3
37.7
7.3
b/
b/
NA
4.0
38.1
NA
NA
10.5
12.7
Total
losses^
(gal/week)
27.0
7.0
233.5
13.5
49.5
82.5
22.0
(0.5)
NA
21.5
40.0
23.0
2.5
(1.5)
2.5
42.0
6.5
24.0
6.5
1.5
2.0
1.0
NA
16.5
4.5
(1.5)
40.0
19.5
38.0
7.5
(0.5)
(0.0)
(0.5)
4.0
40.5
(2.0)
(1.5)
10.5
15.5
Legend:
a/ Figures rounded to nearest 0.5.
b/ In several plants, the weight of the solvent and water recovered from the tumbler condenser was greater than the dif-
ference between wet and dry load weights. This implies greater than 100% recovery efficiency, which is an impossibility.
Therefore, these data were dropped.
( ) - Where atmospheric solvent losses could not be calculated, brackets in the "Total Losses" column indicate that the figures
inside the brackets pertain to losses in residues only.
VA - Atmospheric loss calculations based on vapor adsorber exhaust ppm.
TE - Atmospheric loss calculations based on tumbler exhaust ppm.
RE - Atmospheric loss calculations based on recovery efficiency measurements.
NA - Not available.
Source: IF1 (1975).
9-17
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* Insufficient drying of the carbon bed after desorption.
* Pickup of petroleum solvent vapors by the carbon bed.
9.2.1.2 Information From Present Survey--
To augment and update the information developed in previous studies, a
number of specialists in the cleaning industry were contacted for data on the
present situation regarding perchloroethylene losses in dry cleaning and the
major factors affecting solvent consumption.
9.2.1.2.1 Current experience with perchloroethylene mileage—The experi-
ence of dry cleaning industry personnel will be summarized in brief form, along
with specific comments relating to solvent consumption. Although several
sources willingly provided information, they requested not to be specifically
identified with their views. Detailed data on solvent consumption recently col-
lected by R. R. Street and Company are presented separately.
Data and comments provided by sources from various sectors of the dry
cleaning industry are provided in the following paragraphs.
Equipment manufacturer
Current solvent mileage for perchloroethylene
National average 6,000 Ib/drum
Modern transfer units with 8,000-10,000 Ib/drum
carbon adsorbers
A few plants with careful 15,000-18,000 Ib/drum
operators
Comments related to these solvent mileage figures are as follows
'* Almost any plant can get 5070 higher than normal mileage over
a short test period.
* The type of material cleaned is important. Woolens and cottons
do not show high mileage; synthetics and synthetic blends give
much better solvent mileage; heavy industrial cleaning of tow-
els and gloves often falls to about 4,000 Ib/drum.
* Within recent years quite a number of the larger commercial
and industry dry-to-dry or "hot" machines have been converted
back to "cold" or transfer operation. This was done to obtain
greater productivity, not to save solvent.
9-18
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* For most transfer machines, the addition of carbon adsorbers
of the proper size could pay back in 1 to 3 years. Dry-to-
dry units take significantly longer to justify carbon ad-
sorption beds strictly from solvent savings.
Equipment sales and service manager
Current solvent mileage for perchloroethylene
Average transfer machine 6,000-8,000 Ib/drum
Well maintained transfer unit 10,000 Ib/drum
with meticulous operator
Largest, size (330 lb/30-min cycle) 13,000-19,760 Ib/drum
dry-to-dry machines
Latest model commercial dry-to-dry Up to 20,800 Ib/drum
machines using chiller pebble
bed resolver
"Handful" of very best installa- 26,000-36,000 Ib/drum
tions having good documentation
Comments related to these solvent mileage figures are as
follows
* Frequent checking of recovery unit efficiency and regular
cleaning of condenser coils will generally yield up to one-
third greater perchloroethylene mileage.
* Good steam supply helps both in the dryer heater and in strip-
ping of the carbon beds. Plants that have been achieving 5,000
Ib/drum with low pressure steam and air entering the dryer at
52° C are now obtaining 10,000 Ib/drum with air entering the
dryer at 63°C.
* Cooling water temperature at the condenser coils is critical
and must be held in the 16 to 21°C range or lower for effi-
cient solvent recovery. Poor efficiency often results from
summertime operation with a water supply above the best tem-
perature range.
* Proper operation and maintenance of manual, single bed carbon
adsorbers usually requires at least 1 hr of the operators
time each day. Although automatic units are expensive, they
reduce the chances of operator oversight.
9-19
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Technical director and sales manager, cleaning, and solvent recovery
equipment
Current solvent mileage for perchloroethylene
Average dry-to-dry plant 7,500-9,000 Ib/drum
Most advanced series dry- 29,000 Ib/drura
to-dry machines with
dual automatic carbon
adsorption beds
Comments relating to the solvent mileage figures are as follows
* In recent years, a substantial percentage of new units have
been machines made by European producers. The best U.S. ma-
chines give equal or better performance with regard to sol-
vent mileage.
* Carbon adsorbers are most attractive for use with transfer
machines.
* Only a small percentage of operators will select double car-
bon beds with automatic timers to optimize the efficiency
of solvent recovery due to the higher cost ($5,100 versus
$3,100) and the need for increased horsepower.
* Recovery of solvent from cartridge filters can improve mile-
age significantly. The wider use of drying cabinets vented
through solvent recovery units is a logical step.
Chief engineer, equipment manufacturer
Current solvent mileage for perchloroethylene
IFI and DuPont studies 4,000-7,000 Ib/drum
Transfer machines with >6,000 Ib/drum
diatomaceous filter
cake and distillation
residues of 15%
Dry-to-dry machine, well main- 14,000 Ib/drum
tained by a careful operator
Comments regarding the solvent mileage figures are as follows
* New installations using clay center cartridge filters and
semiautomatic carbon bed adsorbers are initially capable of
a perchloroethylene mileage of 14,000 Ib/drum.
9-20
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* Carbon adsorption solvent recovery units are cost effective
for most transfer plants. It is unlikely that most modern
dry-to-dry plants can justify installation of adsorption units
on the basis of solvent recovery. These units collect solvent
primarily from the last minute of each cycle and typically
return about 1 pint of perchloroethylene per day.
* Carbon adsorption units typically require $6,000 to $7,000/
installation, plus 10 sq ft of floor space, good quality
steam for 10 hr/day of operation, and cold water for the
condensers.
* If necessary, the manufacturer could certify new installa-
tions to operate at 16,000 Ib/drum of perchloroethylene.
* There is no feasible way that manufacturers could develop
and offer retrofit kits to upgrade the performance of older
and substandard machines.
9.2.1.2.2 Data from 1978 Street survey--Two major surveys of perchloro-
ethylene mileage among dry cleaning plants were compiled in the summer of 1978
by the field representatives of R. R. Street and Company, Inc. (Mayberry et
al., 1978). Specialists who regularly visit nearly 11,000 dry cleaning plants
over a period of 2 months were requested to collect operating records on machine
and plant characteristics and solvent consumption per unit of output.
One survey covered transfer machines that were equipped with carbon bed
adsorption units. The second survey covered dry-to-dry machines with and with-
out solvent recovery units (approximately 34% of these dry-to-dry machines had
adsorbers, but individual installations are not identified).
Two factors concerning the sample of plants should be mentioned. First,
the geographic areas surveyed represent primarily the heavily populated states
with heaviest concentration in major cities; the mountain states, northern
plains, and some south central states are not adequately covered in the survey.
However, specialists familiar with the dry cleaning industry believe that the
solvent losses experienced by operators in the under-represented regions prob-
ably do not differ from those of operators within the area surveyed (Street,
1978).
The second factor may, however, introduce some degree of bias into the
surveys. Solvent mileage data were collected only from those plants that kept
adequate and systematic records of perchloroethylene consumption and clothing
poundage cleaned. Only 262 plants of the total population of over 10,000 loca-
tions maintained readily available and complete records. It is strongly sus-
pected that those operators who keep solvent mileage records are more conscious
9-21
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of solvent losses and may also be more meticulous in such areas as equipment
maintenance. Hence this survey data may represent the results obtained by a
more technically oriented fraction of all dry cleaners. The fact that the av-
erage perchloroethylene mileages are slightly above the national averages lends
credence to this possibility.
Perchloroethylene mileage data for 69 dry-to-dry machines ranged from a
low of 2,119 Ib/drum of perchloroethylene to a maximum of 26,156 Ib/drum. A
plot of mileage as a function of the cumulative fraction of the total number
of plants showed that mileage increases steadily for about 75% of the plants
with considerably higher mileage obtained by the remaining 25% of the plants.
In these data, five brands of machines were represented. An analysis of vari-
ance was performed to determine whether machine type had a systematic effect
on solvent mileage; no machine effect was found.
Corresponding data for 193 transfer machines equipped with carbon adsorp-
tion systems were analyzed. Solvent mileage for transfer units ranged from
2,740 Ib/drum up to 22,000 Ib/drum. A plot of solvent mileage versus cumulative
fraction of the number of plants showed the data to be nonlinear with respect
to solvent efficiency. Approximately 10% of the plants obtained a mileage less
than 4,550 Ib/drum and about 15% showed mileages in excess of 10,000 Ib/drum.
Many different types and makes of machines were represented in the data base
so that a complete analysis of machine effect on solvent consumption was not
feasible. No significant machine effect was found for the four makes of ma-
chines most frequently represented in the data base.
Statistical analysis of the Street data comprised the following steps:
1. Obtain the descriptive statistics for each data set to determine
whether the data are "normally" distributed.
2. Find a probability distribution that adequately fits each data set.
3. Describe in conventional terms the theoretical populations of ma-
chines from which the samples were drawn.
4. Determine the differences (if any) between the data for dry-to-dry
and transfer machines.
5. Estimate the proportion of machines in each population that currently
meet a level of 14,000 Ib/drum.
The statistics for the 69 dry-to-dry machines surveyed are presented in
Table 9-5 together with estimated statistics for the theoretical population
of all similar machines from which the sample was taken. The basis for these
population estimates is explained in the following discussion.
9-22
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TABLE 9-5. PERCHLOROETHYLENE MILEAGE
DRY-TO-DRY PLANTS
(mileages in Ib/drum)
S amp 1 e of
69 plants
Mean 10,119
Median 8,268
Mode
Std. dev. 6,186
95% C.I. median
Total
population
10,965
8,441
5,740
7,244
7,261-9,791
Note: An estimated 21.2% of all dry-to-dry machines
currently meet a level of 14,000 Ib/drum. Not
less than 11.6%, and not more than 30.8%, cur-
rently show this level of solvent losses (con-
fidence level 97.5%).
Source: MRI analysis of data supplied by Street
(1978).
As would be expected, those cleaning plants that have greater than average
solvent loss rates are responsible for a disproportionate share of the emissions.
A plot of the cumulative percentage of emissions versus the cumulative percentage
of dry-to-dry plants showed that 50% of the total perchloroethylene emissions re-
sulted from 28% of the plants. The most efficient 20% of these plants were re-
sponsible for only 7% of the emissions.
Examination of the statistics for the data and a distribution histogram
of the solvent loss rates show that the data cannot be considered to be "nor-
mally" distributed. A majority of plants are clustered in the high solvent loss
ranges with units showing low solvent loss rates straggling (skewed) along the
upper tail of the distribution. This nonnormal distribution is also shown by
the fact that the midpoint (median) of the sample is 8,268 Ib/drum, signifi-
cantly lower than the mean for all 69 plants.
The data distribution was tested against several appropriate probability
distributions including the log-normal and Weibull functions. The log-normal
distribution provided a highly satisfactory fit to the data and proved superior
to a Weibull distribution. In other words, the logarithms of solvent mileage
are themselves distributed in a normal, symmetrical, Gaussian fashion. Accept-
ing this hypothesis that the total population of dry-to-dry plants from which
9-23
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the sample of 69 machines was drawn exhibits mileages that are normal in their
logarithms permits the total population performance to be estimated. The sta-
tistics for the total population are also given in Table 9-5.
In terms of a level of performance of 5 Ib of perchloroethylene emitted
per 100 Ib of fabric cleaned (14,000 Ib/drum), the results indicate that an
estimated 21.2% of all dry-to-dry machines may meet this level. The 97.5% con-
fidence level shows that not less than 11.6% nor more than 30.8% of current
machines now meet this level of performance.
The 193 transfer plants utilized 26 different makes of washer-extractor
machines. A total of 214 carbon reclaimers were used, representing 10 differ-
ent manufacturers. Due to the varied mixture of machines employed, it was not
possible to test the data to determine if the make of machine affected the mean
of solvent mileage. For three makes of dry cleaning systems that were repre-
sented most frequently in the sample, no machine effect could be detected.
Load size ranged from 20 to 145 Ib with an average load size of 45.5 Ib.
Recovery cycles in the reclaimers averaged 19 min but ranged from 8 min up to
30 min. Maximum air temperatures during recovery ranged from a low of 52°C up
to 74°C with an average temperature of 65°C.
Carbon adsorbers were stripped with varying frequency by different opera-
tors. The most commonly reported practice was to strip the adsorbers once each
working day. Some operators scrupulously stripped the adsorbers after every
three loads and a few only once per week.
One plant that maintained complete records illustrates the variance of
solvent mileage observed using the same equipment:
Perchloroethylene
mileage
Year (Ib/drum)
1973 7,712
1974 10,426
1975 11,461
1976 11,253
1977 9,292
The results of a statistical analysis of the 193 transfer machines
equipped with activated carbon adsorption systems are shown in Table 9-6. Al-
though the mean mileage for the 69 dry-to-dry units is slightly greater than
that for the 193 transfer machines (10,119 versus 8,456), the difference is
not significant (Barrons-Fisher "t" (87) = 0.92 not sig. ). A distribution
histogram of the solvent loss rates showed the data cannot be considered to
9-24
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be "normally" distributed. The data were found to best fit a log-normal distri-
bution so that estimates could be made for the total population of transfer
plants using carbon adsorption. The histogram showed the most frequently re-
ported loss rate was 7 Ib of perchloroethylene per 100 Ib of clothing (10,000
Ib/drum).
TABLE 9-6. PERCHLOROETHYLENE MILEAGE—TRANSFER
MACHINES WITH ADSORBERS
(mileages in Ib/drum)
Sample of
193 plants
Mean 8,456
Median 7,914
Mode
Std. dev. 3,327
95% C.I. median
Total
population
9,682
7,848
6,733
3,439
7,150-8,558
Note: An estimated 6.8% of all transfer machines
equipped with adsorbers currently meet a possible
standard of 14,000 Ib/drum. Not less than 3.2%
and not more than 10.47,, currently show this level
of solvent losses (confidence level 97.5%).
Source: MRI analysis of data supplied by Street (1978).
From a plot of cumulative percent emissions versus cumulative percent of
plants, it was shown that those transfer plants exhibiting high perchloro-
ethylene losses are not responsible for as large a fraction of the total emis-
sions as observed for the dry-to-dry plants. In the case of transfer machines,
50% of the total perchloroethylene emissions resulted from 34% of the plants
(compared to 28% for dry-to-dry). The most efficient 20% of the plants were
responsible for 10% of the total emissions (compared to 7% for dry-to-dry).
There is a highly significant difference between the two types of machines
with respect to the variance of mileage. Somewhat surprisingly, dry-to-dry units
show a standard deviation twice as large as the larger sample of transfer ma-
chines. The variance of solvent losses is reliably different for the two sam-
ples (F (68,190) = 2.62 p < 0.001).
9-25
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Only an estimated 6.8% of all transfer machines using carbon adsorbers
currently achieve solvent mileages of 14,000 Ib/drum or greater. It is highly
probable (p = 0.025) that not less than 3.2% and not more than 10.4% of such
units currently provide this level of performance.
It is widely acknowledged that operation of a dry cleaning plant so that
solvent loss is at an absolute minimum requires frequent and systematic atten-
tion to a host of machine characteristics and procedures. Not so generally rec-
ognized is the frequency with which plants that have been operating consistently
with low perchloroethylene losses may unexpectedly go "out of control" and ex-
hibit high solvent loss rates. Even in dry cleaning plants of the most advanced
and modern design, where solvent losses have been reduced to very low levels,
unforeseen problems can suddenly result in dramatically increased solvent losses.
Sometimes the malfunction can be found and promptly corrected; however, all too
often, a prolonged period of troubleshooting and experimentation with the equip-
ment may be required to locate the cause and bring the plant back to its former
level of efficiency.
9.2.2 Perchloroethylene Emission Reduction
Reduction of solvent loss was one of the primary reasons for the introduc-
tion of combination washer-extractors to replace separate units. The development
of "kissing" transfer machines (units designed such that the doors of the clean-
ing machine and the dryer can be brought into close proximity for transfer of
the load) resulted in solvent savings for the larger industrial cleaning plants.
The evolution of modern dry-to-dry machines has had solvent conservation as one
of its main driving forces.
According to surveys conducted by members of the Laundry and Cleaners Al-
lied Trade Association (LCATA), the conservation of perchloroethylene has been
improved about 100% since 1965 (Knite, 1978; Kennedy, 1978). A portion of this
improvement was due to the processing of more man-made fiber and less cotton
and wool. There also has been slow but steady improvement on solvent mileage
as newer systems replaced the older equipment.
Some of the advances and innovations that contributed to the reduction
of solvent losses include:
* Better centrifugal extraction in washer (Kennedy, 1978).
* Improved filtration systems (Kennedy, 1978; Mayberry et al., 1978).
Clay core and carbon.
Pleated paper/carbon core.
Cartridge units.
* Better stills and residue recovery (Landon, 1978).
9-26
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* Automatic controls and interlocks (Landon, 1978).
* Improved shaft seals and gaskets (Pappas, 1978).
* Solvent recovery systems (McMonagle and Barber, 1978; Pappas, 1978).
Activated carbon adsorption.
Refrigeration recovery.
* Filter drying cabinets (Kennedy, 1978).
* Expansion chambers used on Valclene® machines (McMonagle and Barber,
1978; Kennedy, 1978).
* Door and floor pickups with automatic fan activation (Landon, 1978).
* Integrated cleaning machines (dry-to-dry operation) (McMonagle and
Barber, 1978; Bryson, 1978).
Virtually all of these improvements have been incorporated on dry clean-
ing equipment sold over the past 15 years. Several sources stated that since
the introduction of dry-to-dry machines, the design and operation of cleaning
equipment has changed very little.
9.2.2.1 Recovery Via Mechanical Engineering--
Possibly the only development currently being tried to reduce solvent
emissions is a renewed analysis of refrigerated condensation systems. These
solvent strippers are intended to perform the same function as carbon adsorp-
tion systems in reducing emissions to the atmosphere.
At least two manufacturers (Spencer and Kleenrite) have introduced commer-
cial units called "resolvers" for use by the dry cleaning industry. The key
element is a bed of carefully sized stone pebbles in contact with refrigerated
coils. Solvent laden air passes downward through the pebble bed (which is held
at ~ 0°C), resulting in condensation of the perchloroethylene vapor on the
large surface area of the pebbles. The considerable thermal mass of the stone
bed also provides "storage" of the heat capacity needed, thereby minimizing
the size of refrigeration unit required (Pappas, 1978).
The major advantage of such a system is that there is no outlet or vent
from the machine to the atmosphere. All air is cycled through the bed and back
to the tumbler; hence, there is no breakthrough or overloading of the solvent
recovery system. Little attention is required compared to a carbon adsorption
system. It is claimed that solvent recovery efficiency is at least equivalent
to a well maintained carbon adsorption system (Pappas, 1978). The Kleenrite
design is apparently still in the prototype stage; no operating units were
9-27
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found. According to an industry source, Kleenrite intends to use chevron-
shaped "A" coils similar to the evaporation coils in air conditioning units
rather than a chilled pebble bed (Kennedy, 1978).
The overall solvent mileage achieved is comparable to the better dry-to-
dry machines using dual automatic carbon adsorption beds. Several plants have
records showing several months of operation with perchloroethylene mileages
ranging from 19,000 to 32,000 Ib cleaned per drum (Pappas, 1978).
This development is relatively new in the United States, and no laboratory
studies of vapor concentrations associated with condensing recovery plants
could be found. It may be possible that British or European studies have been
performed. It would appear appropriate to consider undertaking careful sampling,
analysis, and mass balance determinations in some of the plants now operating
in the United States to determine the technological potential of no-vent, re-
frigerated systems to reduce solvent emissions. The relative cost, energy con-
sumption, reliability and longer term maintenance requirements of such units
also needs to be established.
9.2.2.2 Equipment Based on F-113 Designs—
According to several equipment makers, one of the next logical steps that
might be taken to further reduce perchloroethylene losses would be the use of
chambers similar to those used on Valclene® (F-113) machines (McMonagle and
Barber, 1978; Kennedy, 1978; Bryson, 1978). No test data could be found to de-
termine whether such steps would be practical or cost-effective. Some engineers
questioned whether an expansion chamber would work with a perchloroethylene
system. It was stated that the widespread belief that losses using Valclene®
are substantially lower than for perchloroethylene units may not be substan-
tiated. One group cited the long term results from tests conducted at the
International Fabricare Institute model plant in Joliet, Illinois, that show
perchloroethylene mileage equal or better than Valclene® consumption. Over a
64-week period, the perchloroethylene machine cleaned 164,492 Ib of fabric
consuming 962 gal. of perchloroethylene. Solvent loss rate was 7.87 lb/100
Ib of fabric for a mileage of 8,891 Ib cleaned per drum. In a 47-week test
using Valclene®, 12,154 Ib of clothing was cleaned consuming 85 gal. of sol-
vent. Solvent loss rate was 9.20 Ib of Valclene® per 100 Ib of fabric for a
mileage of 7,435 Ib cleaned per drum (Mayberry et al., 1978).
9.3 SOLVENT RECOVERY OR DISPOSAL
This subsection will present a brief discussion of the available methods
of solvent recovery or disposal. In the metal cleaning subsection, techniques
were discussed by which the quantity of the three compounds reaching the en-
vironment could be reduced. It is inherent that as the quantity of solvent re-
leased to the environment decreases the amount of waste or used solvent in-
creases. A discussion will be presented of the techniques for recycling the
waste solvent or for disposal with minimum insult to the environment.
9-28
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9.3.1 Distillation
Chlorinated solvent reclamation by distillation is the most environmen-
tally acceptable method for treating waste solvent from vapor degreasing and
cold cleaning operations. Waste solvent from vapor degreasing may contain from
10 to 3070 oil and other contaminants removed from the metal surface. For cold
cleaning, the percentage of oil and other contaminants is usually lower than
for vapor degreasing so that solvent recovery would be more advantageous in
terms of waste control.
Reclamation can occur by basically two processes: (a) a contract service
and (b) in-house distillation. With the contract reclamation service, the con-
tractor collects the waste solvent, distills it, and returns the reclaimed por-
tion to the solvent user. If the percentage of solvent in the original waste
is low, a service charge may be added to the cost. However, the price of the
returned solvent is usually equal to 50% of the market value of the solvent.
In industrial areas where large quantities of waste trichloroethylene, methyl
chloroform, or perchloroethylene are being generated, contract solvent reclama-
tion is being practiced. In other areas where the volume of waste is considerably
lower, collection and transportation can be a factor. It may be possible for
these users to store the waste solvent in sealed containers until sufficient
volume is acquired to make the process economical (EPA, 1977).
Many users generating large volumes of waste solvent utilize in-house dis-
tillation. In vapor degreasing operations, the use of stills for solvent recov-
ery is fairly common. Nearly all large open top vapor degreasers and conveyor-
ized vapor degreasing or cold cleaning units utilizing methyl chloroform,
trichloroethylene, or perchloroethylene are equipped with external stills. These
stills are customarily employed because they reduce the maintenance cost of
cleaning the equipment, enable the system to remove collected soils without in-
terruption of the cleaning process, and to recover quantities of the solvent.
Users employing multiple open top vapor degreasers can use a centralized still
to recover solvent from all of the degreasers. It has been estimated that the
total annual cost of in-house reclamation (60-gal/hr still) of trichloro-
ethylene can be recovered from the first 350 gal. distilled per year (Dow,
1976).
Bottoms from all distillation equipment contain metals, sludges, residual
solvent, oils, and other material that must be properly disposed of by con-
trolled high temperature incineration or chemical landfill. These two areas
will be briefly discussed in subsequent subsections.
Reclamation by distillation does, however, present some potential problem
areas for the three chlorinated hydrocarbons. Stabilizers present in each of
the solvents may be partially or completely removed from the distilled solvent
during reclamation. Prior to reuse, the distillate must be analyzed to determine
the level of stabilizers present and additional stabilizers added as needed to
9-29
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prevent decomposition during use. Unfortunately, the composition of stabilizer
packages employed by most solvent manufacturers or distributors is considered
proprietary information. Thus, reconstruction of the distilled solvent to its
original composition is not a simple task. Other potential problem areas in-
clude the formation of azeotropic mixtures between the solvent to be recovered
and a contaminant present in the waste solution. This situation may require
further treatment of the distilled solvent by chemical or physical means. Ad-
verse chemical reactions could potentially occur under the conditions of dis-
tillation with the resultant formation of an explosive mixture, a hazardous
product, or other potentially harmful situations.
In general, a company employing in-house distillation is not seriously
impeded by the latter two problem areas since the solvents and contaminants
are known and the situation can be closely controlled. For reclamation ser-
vices, however, waste solvent is obtained from numerous sources so that anal-
ysis of the waste material is normally performed to avoid these potential prob-
lem areas.
In terms of overall reduction of waste solvent volume, reclamation by the
use of distillation can generally result in the recovery of 80 to 85?0 or more
of the solvent contained in the initial waste solution (EPA, 1977). Certain
potential problems must be recognized but the method can be very effective as
an emission control method.
9.3.2 Incineration
Aside from solvent recovery, the complete and controlled high temperature
oxidation in air or oxygen (with supplemental fuel) combined with adequate
scrubbing and ash disposal facilities offers the greatest immediate potential
for the safe disposal of trichloroethylene, methyl chloroform, or perchloro-
ethylene (Powers, 1976). Incineration is commonly used for the disposal of
many toxic industrial wastes; however, specific incinerator design and opera-
tion requirements for trichloroethylene, perchloroethylene, and methyl chloro-
form are not standardized. Effective temperature/residence time relationships
must be empirically established for any given waste material; however, most
toxic organic chemicals can be completely destroyed at 1000°C with an incin-
erator residence time of 2 sec by a combination of pyrolysis and oxidation
reactions (Shen et al., 1978).
As with most combustion processes, consideration must be given to the en-
vironmental impact of the products emitted from the process. Products resulting
from the combustion of trichloroethylene, methyl chloroform, or perchloro-
ethylene at various temperatures and under selected conditions were discussed
earlier in Section 3. In addition to mixtures of carbon monoxide, carbon di-
oxide, and water vapor, products from the combustion will include hydrogen
chloride and, possibly, phosgene. Levels of phosgene will become significant
if the combustion of any of- the three chlorinated compounds is incomplete.
9-30
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Scrubbers are employed to remove hydrogen chloride and phosgene formed during
the incineration so that these potentially detrimental environmental contami-
nants are eliminated at the source in one disposal step.
There are four general types of incinerators commercially available for
the destruction of liquid toxic organic wastes from industrial operations.
Multiple hearth, rotary kiln, fluidized bed, and liquid injection incinerators
represent proven technology in liquid waste disposal techniques (Wilkinson et
al«, 1978). The first three types are versatile units which are capable of in-
cinerating a wide variety of solid, liquid, and gaseous organic wastes. The
liquid injection incinerator is limited to pumpable liquids and slurries.
There are approximately 25 to 50 facilities in the United States capable
of the incineration of these three chlorinated solvents (EPA, 1977). Chem-Trol
Pollution Services, Inc., Model City, New York, is one of the larger and more
complex central disposal operations currently in operation. Chem-Trol claims
capabilities to handle and treat virtually any liquid industrial waste which
is not radioactive or explosive (Scurlock et al., 1975).
Each of the four types of incinerators that can be used to dispose of
chlorinated hydrocarbon solvents is described briefly below. Examples of the
types of incinerators are included (Scurlock et al., 1975).
9.3.2.1 Multiple Hearth Incineration--
Process principle; Solid feed slowly moves through vertically stacked
hearths, gases, and liquids fed through side ports and nozzles. Current appli-
cations largely in sewage sludge incineration.
Application; Most organic wastes; well suited for solids and sludges;
also handled liquids and gases.
Combustion temperatures; 760 to 980°C.
Residence times; Up to several hours for solids.
9.3.2.2 Rotary Kiln Incinerator—
Process principle; Slowly rotating cylinder mounted at slight incline
to horizontal. Tumbling action improves efficiency of solid waste destruction.
Application; Most organic wastes; well suited for solids and sludges;
liquids and gases fired through auxiliary nozzles.
Combustion temperatures; 810 to 1650°C.
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Residence times; Several seconds for liquids and gases to several hours
for solids.
Examples;
1. Thumbleburner - manufactured by Bartlett-Snow
Commercially available
Capacity - 45 kg-1.8 MT/hr (100 Ib - 2 tons/hr)
2. Dow Chemical - Midland, Michigan
Industrial chemical waste unit
Temperatures - 810°C
9.3.2.3 Fluidized Bed Incinerator—
Process principle; Wastes are injected into a hot agitated bed of inert
granular particles; heat is transferred between the bed material (often sand)
and the waste during combustion.
Application; Most organic wastes; ideal for liquids; also handles solids
and gases.
Combustion temperatures; 750 to 870°C.
Residence times; Seconds for gases, liquids; longer for solids.
Examples;
1. LSW Disposal System, Combustion Power Company, Menlo Park,
California
Recently commercially available
Temperatures - 810°C
2. Franklin, Ohio Resource Recovery Plant
EPA demonstration grant - municipal refuse 7.6 m (25-ft) I.D.
reactor - burns organic nonrecoverables
Temperatures - 750 to 810°C
9.3.2.4 Liquid Injection Incineration--
Process principle; Vertical or horizontal vessel; wastes atomized through
nozzles to increase rate of vaporization.
Application; Limited to pumpable liquids and slurries.
Combustion temperatures; 650 to 1650°C.
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Residence times; 0.1 to 1 sec.
Examples;
1. Pickands Mather and Company (Prenco Division)
Commercially available
Temperatures - 870 to 1650°C
2. Vortex Combustor
Commercially available
Temperatures - 650 to 870°C
3. Thermal Oxidizer - Chem-Trol Pollution Services, Inc., Model City,
New York
Central industrial waste facility
Temperatures - 1650°C maximum
4. General Electric Corporation, Pittsfield, Massachusetts (designed
by John Zink Company)
Industrial chemical waste incinerator
Capacity - 8 to 15 liters (2 to 4 gal.) per minute
Temperatures - 980 to 1310°C
Residence time - 1 to 12 sec
9.3.2.5 Molten Salt Combustion—
A promising new technology for destroying toxic halogenated organic wastes
is the use of molten salt combustion technology. In this process, wastes are
injected into a bed of molten salt (usually sodium carbonate) where combustion
occurs. The salts react with and neutralize the acidic off gases so that halo-
genated organics are completely destroyed and the halogen acid gases are effec-
tively controlled (Shen et al., 1978).
9.3.2.6 Cement Kilns —
In addition to the incineration methods previously mentioned, cement kilns
have been used for burning toxic chemical industrial wastes. Various chlori-
nated hydrocarbons can be completely destroyed during normal cement kiln opera-
tions. The hydrochloric acid gases generated from thermal incineration in the
kiln are neutralized by the excess alkali in the cement products. Cement kilns
reach temperatures of about 1400°C and have residence times of 15 sec or more.
9.3.3 Landfill Disposal
At the present time, disposal of waste solvent from metal cleaning opera-
tions ranges from discarding on the back lot to removal by a contract hauler
of hazardous waste. There are hazardous waste landfills approved for the dis-
posal of materials such as the three compounds of interest in this report; how-
ever, disposal by this method presents the potential for atmospheric and
groundwater contamination at some future date.
9-33
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One method for the disposal of wastes containing these chlorinated hydro-
carbons has been to seal the waste solvent in lined drums and surround the
drums with 4 to 20 ft of packed clay. No testing has been performed, however,
to evaluate the effectiveness of this method for the control of organic dis-
charges (EPA, 1977).
According to another source (Powers, 1976), landfill disposal is accept-
able only when the site is totally isolated from ground and surface waters
and meets the standards for a California Class I hazardous waste disposal site.
The California site criteria are shown in Table 9-7.
Overall, most hazardous waste landfills are not adequate for the disposal
of wastes containing trichloroethylene, methyl chloroform, or perchloroethylene
(EPA, 1977).
9.4 CONTAINER LABELS
Proper labeling of containers of trichloroethylene, methyl chloroform,
and perchloroethylene according to the Department of Transportation regula-
tions were summarized in the previous section on regulations and standards.
In addition to those labeling requirements, an ASTM subcommittee (D-26, Sub V)
has recommended labels for containers of each of the three compounds. These
labels have generally been accepted by the compound manufacturers and dis-
tributors (Schlossberg, 1978).
The basic label, as recommended by the ASTM subcommittee, found on con-
tainers of each of the three compounds is as follows:
Identification
Company name
Company address
Company logo
Lot number
Ne t we i ght
Solvent -- (name of chemical)
Grade
Health and Safety Information
WARNING! Harmful if inhaled--high concentrations may cause unconscious-
ness or death.
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TABLE 9-7. CALIFORNIA CLASS 1 SITE CRITERIA
Geological conditions are naturally capable of preventing hydrau-
lic continuity between liquids and gases emanating from the waste
in the site and usable surface or groundwaters.
Geological conditions are naturally capable of preventing lateral
hydraulic continuity between liquids and gases emanating from
wastes in the site and usable surface or groundwaters, or the dis-
posal area has been modified to achieve such capability.
Underlying geological formations which contain rock fractures or
fissures of questionable permeability must be permanently sealed
to provide a competent barrier to the movement of liquids or gases
from the disposal site to usable water.
Inundation of disposal areas shall not occur until the site is
closed in accordance with requirements of the regional board.
Disposal areas shall not be subject to washout.
Leachate and subsurface flow into the disposal area shall be con-
tained within the site unless other disposition is made in accor-
dance with requirements of the regional board.
Sites shall not be located over zones of active faulting or where
other forms of geological change would impair the competence of
natural features or artificial barriers which prevent continuity
with usable waters.
Sites made suitable for use by man-made physical barriers shall
not be located where improper operation or maintenance of such
structures could permit the waste, leachate, or gases to contact
usable ground or surface water.
Sites which comply with 1, 2, 3, 5, 6, 7, and 8 but would be sub-
ject to inundation by a tide or a flood of greater than 100-year
frequency may be considered by the regional board as a limited
Class 1 disposal site.
Source: Taken from Powers (1976), p. 148.
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Precautions
AVOID PROLONGED OR REPEATED BREATHING OF VAPOR.
High vapor concentrations can cause unconsciousness--or death.
USE ONLY WITH ADEQUATE VENTILATION.
Eye irritation and dizziness are indications of overexposure.
DO NOT TAKE INTERNALLY.
Swallowing may cause injury, illness--or death.
AVOID PROLONGED OR REPEATED CONTACT WITH SKIN.
Contact may cause skin irritation and dermatitis.
DO NOT GET IN EYES.
Will cause discomfort and irritation.
SEE MCA CHEMICAL SAFETY DATA SHEET SD24 AND CURRENT OSHA REGULATIONS.
First Aid
INHALATION OVEREXPOSURE—Remove patient to fresh air. If breathing stops,
give artificial respiration, preferably mouth to mouth. If breathing is
difficult, give oxygen. Call a physician.
NOTE TO PHYSICIAN—Avoid use of adrenaline in any case where a person has
been overcome by (name of solvent).
SWALLOWING--Induce vomiting by giving 1 or 2 glasses of water and touching
back of throat with finger or blunt object. Call a physician. Never induce
vomiting or give anything by mouth to an unconscious person.
EYE CONTACT—Flush eyes thoroughly with large amounts of water. If irrita-
tion persists, see a physician.
SKIN CONTACT--Remove contaminated clothing and shoes. Wash skin with warm
water and soap. Wash clothes and air out shoes.
Handling and Storage
IMPORTANT NOTE: Request information from supplier on safe procedures be-
fore blending with other solvents. Under certain conditions solvent decom-
position may occur, followed by the release of toxic and corrosive vapors.
Vapors are heavier than air and will collect in low areas, such as pits,
degreasers, storage tanks, and other confined areas. Enter these areas
only while wearing an airline mask or oxygen supplied equipment and an
observer is present for assistance.
9-36
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Keep drum tightly closed when not in use.
Spills should be cleaned up immediately under maximum ventilation by per-
sonnel wearing an airline mask or oxygen supply equipment. Unprotected
persons should leave area of spill immediately.
This material or its vapors in contact with flames, hot glowing surfaces,
or electric arcs may form toxic and corrosive acid fume.
Store in a cool, dry, well ventilated area.
Do not store in open or unlabeled or mislabeled containers.
Do not store degreaser clean out sludge in tightly sealed containers.
Store containers out-of-doors away from combustible materials.
Do not use cutting or welding torches, open flames, electric arcs, or
glowing surfaces on empty or full drums that contain (solvent name)
KEEP OUT OF REACH OF CHILDREN
Containers of perchloroethylene contain only the above labeling informa-
tion. For trichlordethylene, the proposed container label provides the basic
information plus the following additions:
1. Under Handling and Storage, Important Note: The following sentence
is added "Contact with caustic alkali may cause hazardous and explosive
vapors."
2. Under Handling and Storage, the following warning is added: "DO NOT
USE IN POORLY VENTILATED OR CONFINED SPACES."
3. The phrase "Store in a cool, dry, well-ventilated area" is modified
to read as follows: "Store in a cool, dry, well-ventilated area separate
from caustic soda and caustic potash."
The methyl chloroform label is the same as for trichloroethylene except that
the following sentence has been added. "Liquid oxygen or other strong oxidants
may form explosive mixtures with 1,1,1-trichloroethane solvent when mixed in
confined spaces."
In review comments sent to Dr. Stanley C. Mazaleski (EPA, Office of Toxic
Substances), Dow Chemical stated that the proposed labels for methyl chloro-
form and trichloroethylene have been modified but not adopted by the committee
as follows:
9-37
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1. The warning for trichloroethylene and methyl chloroform regarding con-
tact with caustic alkali was reworded to warn against both explosive vapors
and residues.
2. The warning on liquid oxygen was extended to trichloroethylene and
the wording about confined spaces was deleted.
9-38
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REFERENCES
American Society for Testing Materials (ASTM). 1976. Handbook of vapor
degreasing, Special Technical Publication 310A (04-310010-15). Philadelphia,
PA.
Bryson, J. M. 1978. Columbia Laundry Machinery Company, Kansas City, MO.
Personal communication to Midwest Research Institute.
Dow Chemical Company. 1976. Study to support new source performance standards
for solvent metal cleaning operations. Final Report. Emission Standard
and Engineering Division, Office of Air Quality Planning and Standards,
Environmental Protection Agency, Research Triangle Park, NC.
Environmental Protection Agency (EPA). 1977. Control of volatile organic
emissions from solvent metal cleaning. EPA Report No. 450/2-77-022.
Office of Air Quality Planning and Standards, Research Triangle Park,
NC.
Fisher, W. E. 1978. International Fabricare Institute (IFI) Research Divi-
sion, IFI, Silver Spring, MD. Presentation: Drycleaning: Processes-
Emissions-Controls, EPA Hydrocarbon Control Workshop, Chicago, IL, 1978.
Personal communication to Midwest Research Institute, 1978.
International Fabricare Institute (IFI). 1975. Experimental study of solvent
discharge from dry cleaning establishments to the environment - field
study of selected California dry cleaning plants. Report to California
State Board of Fabric Care, Sacramento, CA.
International Fabricare Institute (IFI). 1978. Fabricare News. Vol. 7.
No. 11. Published by IFI, Silver Spring, MD.
Kennedy, B. 1978. Dextrex Chemical Industries, Detroit, MI. Personal commu-
nication to Midwest Research Institute.
Knite, R. 1978. Laundry and Cleaners Allied Trades Association, Montclair,
NJ. Personal communication to Midwest Research Institute.
Landon, S. 1978. Washex Corporation, Wichita Falls, TX. Personal communica-
tion to Midwest Research Institute.
Mayberry, J. L., S. D. Mathews, J. F. Stucker, and J. A. Limb. 1978. R. R.
Street and Company, Inc., Oak Brook, IL. Technical conference with Midwest
Research Institute. Data supplied: (a) survey of perchloroethylene
plants using transfer units and carbon vapor adsorption, 1978; (b) data
sheets for dry-to-dry cleaning plants.
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McMonagle, R., and J. Barber. 1978. Vic Manufacturing Company, Minneapolis,
MN. Technical bulletins and personal communication to Midwest Research
Institute.
Midwest Research Institute (MRI). 1976a. Air pollution emission test -
Westwood Cleaners, Kalamazoo, Michigan. EPA Project Report No. 76-DRY-
3. Environmental Protection Agency, Research Triangle Park, NC.
Midwest Research Institute (MRI). 1976b. Air pollution emission test -
Texas Industrial Services, San Antonio, Texas. EPA Project Report No.
76-DRY-2. Environmental Protection Agency, Research Triangle Park, NC.
Mitre Corporation (Metrek Division). 1978. Development of standards of
performance for solvent metal cleaning (degreasing). Draft report, August
1978. Office of Air Quality Planning and Standards, Environmental Protec-
tion Agency, Research Triangle Park, NC.
Pappas, A. A. 1978. Spencer America, Inc., St. Louis, MO. Personal communi-
cation to Midwest Research Institute.
Powers, P. W. 1976. How to dispose of toxic substances and industrial
wastes. Noyes Data Corporation, Park Ridge, NJ.
Schlossberg, L. 1978. Detrex Chemical Industries, Detroit, MI. Information
supplied to Midwest Research Institute.
Scurlock, A. C., A. W. Lindsey, x. Fields, Jr., and D. R. Huber. 1975.
Incineration in hazardous waste management. Publication No. SW-141.
Office of Solid Waste Management Programs, Environmental Protection
Agency, Washington, D.C.
Shen, T. T., M. Chen, and J. Lauber. 1978. Incineration of toxic chemical
wastes. Pollution Engineering, 10(10):45, October.
TRW, Inc. 1976. Study to support new source performance standards for
the dry cleaning industry. Task Order No. 4, May 1976. Office of Air
Quality Planning and Standards, Environmental Protection Agency,
Research Triangle Park, NC.
Wilkinson, R. R., G. L. Kelso, and F. C. Hopkins. 1978. State-of-the-art
report: pesticide disposal research. EPA Report No. 600/2-78-183.
Municipal Environmental Research Laboratory, Environmental Protection
Agency, Cincinnati, OH.
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CONTENTS
10. Summary 10-3
10.1 Market Input/Output Analyses 10-3
10.1.1 Physical and chemical data 10-3
10.1.2 Current status and future outlook 10-3
10.1.3 Manufacturing process technology 10-4
10.1.4 Consumption and losses to the environment . 10-5
10.1.5 Use alternative analyses 10-5
10.2 Health Effects 10-6
10.2.1 Trichloroethylene 10-6
10.2.2 Methyl chloroform (1,1,1-trichloroethane) . 10-9
10.2.3 Perchloroethylene 10-13
10.3 Ecological Effects 10-16
10.3.1 Environmental fate 10-16
10.3.2 Environmental effects 10-17
10.4 Monitoring Data and Exposure Levels 10-18
10.4.1 Monitoring data 10-18
10.4.2 Exposure levels 10-20
10.5 Regulations and Standards 10-21
10.5.1 Regulations 10-21
10.5.2 Standards 10-23
10.5.3 Shipping and transportation practices . . . 10-23
10-1
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CONTENTS (continued)
10.6 Solvent Emissions 10-23
10.6.1 Metal cleaning industry 10-23
10.6.2 Dry cleaning industry 10-24
10.6.3 Solvent recovery or disposal 10-24
10.6.4 Container labels 10-25
10-2
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SECTION 10
SUMMARY
A summary of the results obtained in this study are presented for tri-
chloroethylene, methyl chloroform, and perchloroethylene. Topics included
in this section are: market input/output analyses, health effects, ecologi-
cal effects, and monitoring and exposure potential data.
10.1 MARKET INPUT/OUTPUT ANALYSES
In this phase of the study information and data were compiled on physi-
cal and chemical properties, current status and future outlook, manufacturing
process technology, consumers and consumption processes, losses to the envi-
ronment, and other topics.
10.1.1 Physical and Chemical Data
A review was made of the existing information on the chemical and physi-
cal properties of each of the three subject compounds. All are nonflammable,
volatile, slightly soluble in water, and good solvents for oils and greases.
The pure chemicals decompose upon sufficient exposure to light, open flames,
metals, oxygen, or reactive chemicals to form toxic products, such as phosgene
and carbon monoxide. Small quantities of stabilizers are incorporated into
the commercial products to improve stability in industrial uses.
10.1.2 Current Status and Future Outlook
For the period 1965 to 1977, the annual production of trichloroethylene
ranged from a high of about 277,000 metric tons (MT)/year in 1970 to a low of
about 133,000 MT/year in 1977. In 1977, the utilization of total production
capacity was approximately 48%. Domestic end-uses for this compound in 1977
were 86% solvent metal cleaning, 12% exports, and 2% miscellaneous uses. Im-
ports in 1976 were about 7,056 MT.
The annual production of methyl chloroform increased steadily from 1966
to 1974. From 1974 to 1975 the economic recession caused a 22% decrease in
annual production, i.e., from about 268,000 MT to about 208,000 MT. Produc-
tion in 1977 (270 MT) represented approximately 86% of the domestic capacity.
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In 1976, consumption was 75% solvent metal cleaning, 5% exports, and 20%
miscellaneous uses. Imports of methyl chloroform in 1976 were negligible.
For perchloroethylene, production quantities ranged from 195,000 MT in
1965 to about 333,000 MT in 1974. In the 1975 recession, production decreased
slightly to approximately 307,000 MT and have continued to decrease to a level
of 299 MT in 1977. End-uses for perchloroethylene in 1975 were 63% textile
industry, 16% solvent metal cleaning, 11% chemical intermediates, 7% exports,
and 3% miscellaneous uses. Imports of perchloroethylene in 1976 were approxi-
mately 28,000 MT. For all three compounds, the production decreases from 1974
to 1975 were due to economic and not environmental factors.
Future projections of market demands are difficult to assess because of
basic interchangeability of trichloroethylene and methyl chloroform in the
solvent metal cleaning field and the effects of unpredictable potential future
regulations on use of these solvents. By 1982, production of trichloroethylene
is estimated to be 100,000 MT/year, methyl chloroform 375,000 to 395,000 MT/
year, and perchloroethylene 357,000 MT/year. By 1988, domestic production of
trichloroethylene is estimated to decrease to about 90,000 MT and perchloro-
ethylene is estimated to increase to approximately 437,000 MT. Because of the
very large production capacity for methyl chloroform, no realistic predictions
could be made for future production levels.
10.1.3 Manufacturing Process Technology
Trichloroethylene is manufactured by four companies at sites in Texas and
Louisiana. The total production capacity in 1978 was 238,000 MT. PPG Industries,
Inc., and Dow Chemical Company are the leading manufacturers; they represent
about 82% of the domestic production capacity. Other producers are Diamond
Shamrock Corporation and Ethyl Corporation. Two production processes are cur-
rently in use: (a) oxychlorination of ethylene dichloride (90% of total pro-
duction); and (b) chlorination of acetylene (10% of production). In the oxy-
chlorination process, perchloroethylene is formed as a co-product and water
as a by-product.
Methyl chloroform is currently manufactured by three domestic companies
at three sites in Texas and Louisiana. These three producers have a total ca-
pacity of about 313,000 MT. Dow Chemical Company (65%) and PPG Industries, Inc.
(25%) combine to represent 90% of the total domestic production capacity. T,he
other producer is Vulcan Materials Company. Methyl chloroform is currently .pro-
duced by three processes: (a) hydrochlorination of vinyl chloride (6070); (b)
hydrochlorination of vinylidene chloride (30%); and (c) chlorination of. ethane
(10%).
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Seven companies currently produce perchloroethylene at 11 production
sites, primarily in Texas and Louisiana, with a total capacity of approxi-
mately 540,000 MT. Three companies, Dow Chemical Company (24%), PPG Industries,
Inc. (17%), and Vulcan Materials Company (18%), represent about 59% of the
production capacity. Other producers are Diamond Shamrock, DuPont, Ethyl, and
Stauffer. In addition to the oxychlorination of ethylene dichloride process
(34%), perchloroethylene is also manufactured by the chlorination and pyroly-
sis of hydrocarbons (63%) and by chlorination of acetylene (3%). In the
acetylene process, 1,1,2,2-tetrachloroethane is the intermediate.
Current environmental management practices are discussed for specific
plant sites manufacturing trichloroethylene, methyl chloroform, or perchloro-
ethylene.
Waste material disposal practices include incineration at Dow Chemical
Company, PPG Industries, and Vulcan (Wichita), landfills at Stauffer and Vulcan
(Geismar), and deep well injection at Ethyl Corporation. Diamond Shamrock re-
cycles the chlorinated heavy ends as raw material for vinyl chloride monomer
production. Levels of each of the three compounds found in the .air and water
in the vicinity of these manufacturing sites are discussed in subsection 10.4.1.
10.1.4 Consumption and Losses to the Environment
Aside from exports and those quantities used as chemical intermediates,
trichloroethylene and methyl chloroform are used almost exclusively in metal
cleaning applications, either in cold cleaning (room temperature) or vapor
degreasing operations. The number of companies employing these solvents is
well into the thousands so that a compilation of specific companies was not
feasible. Quantities consumed by selected companies and the U.S. government
are presented. Most perchloroethylene is consumed in the textile industry,
primarily in dry cleaning applications. Aside from its use as a chemical
intermediate, its only other major use is in metal cleaning applications.
The primary entry of each of the three compounds to the environment is
by atmospheric emissions from user applications, particularly in dry cleaning
or in metal cleaning. In 1976, it is estimated that approximately 129,000 MT
of trichloroethylene were emitted into the environment from vapor degreasing
and cold cleaning applications. For the same year, methyl chloroform and per-
chloroethylene emissions were about 214,000 and 52,000 MT, respectively, for
vapor degreasing and cold cleaning applications. In addition, approximately
207,000 MT of perchloroethylene were emitted by the textile industry. Estimates
of the geographical distribution of these emissions are that the Northeast,
Midwest, and Far West regions are the primary sources.
10.1.5 Ujse Alternative Analyses
A study was made of other chemicals or systems which could be employed as
alternatives to the current use areas of these compounds. Trichloroethylene
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was chosen as the standard and all comparisons, either for interchangeability
between the three solvents or other methods, were made with respect to this
compound. The advantages and disadvantages of interchanging methyl chloroform
and perchloroethylene with trichloroethylene are discussed. Either of the two
may, within certain limitations, be interchanged for trichloroethylene.
Methylene chloride, Fluorocarbon 113 (F-113), alkaline cleaning agents, and
numerous common solvents were evaluated as potential alternative chemicals in
metal cleaning applications. Methylene chloride can also be used in place of
trichloroethylene in certain situations with minor equipment modification.
Alkaline cleaning solutions are generally less interchangeable with the chlori-
nated hydrocarbons under study. Because of its mild solvent power and other
factors, F-113 would be a suitable alternative only in certain applications.
10.2 HEALTH EFFECTS
Health effects data were compiled for each of the three subject compounds.
Topics reviewed include absorption, excretion, transport, metabolism, toxicity,
sensitization, carcinogenicity, mutagenicity, and several others.
10.2.1 Trichloroethylene
Trichloroethylene is absorbed by humans after inhalation, prolonged skin
contact, and oral ingestion. It is absorbed well after injection by all routes
in experimental animals. Human exposure to 40 ppm trichloroethylene for 4 hr
resulted in an immediate blood level of 0.26 Mg/ml, which then decreased with
time. Human subjects exposed to 500 to 850 ppm trichloroethylene vapor for 5 hr
absorbed 64% of the dose, but volunteers exposed at a higher level (1,042 ppm)
for the same amount of time absorbed only 58% of the inhaled quantity. Animal
experiments also demonstrated a proportionally lower percent absorption as the
breathing concentration increased.
In the first hour, humans exhale 15% of an administered trichloroethylene
dose. Pulmonary excretion rates for methyl chloroform were 44% and for per-
chloroethylene, 10%. The excretion is inversely proportional to the lipid
solubility of the compound. Trichloroethylene is excreted unchanged in ex-
haled breath following all dosage routes in animals and man, but its high
lipid solubility produces widespread distribution in the body. Trichloro-
ethylene is metabolized to a greater extent in man and experimental animals
than are methyl chloroform and perchloroethylene. This finding is of impor-
tance in consideration of the effects of actual and proposed metabolites of
trichloroethylene.
The primary metabolites of trichloroethylene are trichloroethanol and
trichloroacetic acid. Trichloroethanol is usually excreted in a more water-
soluble form (a glucuronide conjugate). One of the intermediate products of
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the metabolism of trichloroethylene is the potent sedative, chloral hydrate.
The major metabolites of trichloroethylene in man are detectable in urine for
390 hr after acute exposure. Exposure to trichloroethylene has been most com-
monly quantitated by measuring urinary trichloroacetic acid or the unmetabolized
solvent in exhaled breath. Both measures reflect the extent of the subject's
exposure to trichloroethylene.
The central question in the toxicology of trichloroethylene, however, is
not the extent of exposure. The narcotic effects are reversible, and good venti-
lation or controlled use reduces the toxic hazard to man's central nervous sys-
tem (CNS). The principal question is one of irreversible toxicity due to the
metabolism of trichloroethylene to compounds with the potential to react with
vital cellular constituents. Theories of action at the level of the cell are
presented and discussed after the summary of trichloroethylene effects at the
whole animal or whole organ level.
The predominant responses to trichloroethylene in man are central nervous
system effects. A single, 2- to 4-hr exposure to trichloroethylene leads to
dizziness, headache, and incoordination at an air level of about 150 ppm in
some persons. The nervous system effects are alleviated when the subject is
removed from the source of exposure or contact, and as such, the effects could
be classified as physiological rather than toxicological. The CNS effects of
trichloroethylene appear to be totally reversible when exposure ceases.
The three subject chlorinated solvents are known from extensive studies
to have effects on the heart of dogs and other animals. In case reports of
trichloroethylene effects on humans, several incidents of sudden death have
occurred which were attributed to irregular, uncontrolled heartbeat (ventricu-
lar fibrillation). Epinephrine, a hormone released normally in the body in
cases of excitement or stress, affects the rate and rhythm of the heart. When
trichloroethylene is inhaled at high levels, these effects are apparently mag-
nified. Trichloroethylene is not, however, as reactive as methyl chloroform
in heart/epinephrine effects.
In cases of death due to abuse or accidental overexposure to trichloro-
ethylene, both liver and kidney damage have been reported. In one death, the
liver damage was described as fatty degeneration. The liver damage appears to
have been more severe in exposed workers who were also heavy drinkers, an
expected effect since alcohol has liver effects of its own. Normal kidney
function tests (measurements of liver-produced enzyme levels such as glutamic
oxalacetic transaminase (SCOT), or glutamic pyruvic transaminase (SGPT)) have
been reported in subjects who were excreting very high levels of trichloro-
acetic acid in the urine, indicating overexposure to trichloroethylene. In-
creased formation of metabolites after long-term exposure to trichloroethylene
has been reported in man and experimental animals, a phenomenon suggested to
be caused by stimulated production of enzymes (enzyme induction). Early reports
indicated a different profile of liver/kidney toxicity due to trichloroethylene
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than did later experiments. The pure commercial trichloroethylene in use now
apparently presents little liver toxicity problem at present industrial expo-
sure levels. Four studies were performed on trichloroethylene carcinogenicity,
all with negative results, before a National Cancer Institute study reported
an apparent tumorigenic effect of trichloroethylene in mice.
A rat strain (Osborne-Mendel), susceptible to liver tumors, was dosed at
1,097 and 549 rag/kg, five times a week for 78 weeks. Survivors were exhaustively
examined for tumors, and more hepatocellular cancers were found in the controls
than in the trichloroethylene-dosed animals. These results in rats may be due
to the toxicity of the very high doses used; the rats died before sufficient
time had elapsed for liver tumors to develop.
The mouse strain which showed hepatocellular tumors was the B6C3F1 strain.
They received trichloroethylene by gastric intubation in oil at doses of 2,339
and 1,169 mg/kg for males and 1,739 and 869 mg/kg for females five times a week
for 78 weeks. Over half the male mice at both dose levels showed hepatocellular
carcinoma, but only 23 and 8% of the females on high and low dose, respectively,
had tumors. One of 20 matched control males and 0/20 female mice showed hepato-
cellular carcinoma.
Many points of contention arose from these tests and the tests are being
repeated. Disagreement arose concerning the animal strains being used; the rats
were of a strain shown to develop liver malignancies after exposure to compounds
that produce only cirrhosis in other strains and the mice were a C^H cross, an
inbred line carrying a murine tumor virus that produces spontaneous tumors.
The trichloroethylene used for the bioassay was stabilized or contaminated at
low levels with at least three compounds shown to be either carcinogenic by
bioassay trials or a potential carcinogen by in vitro tests. Dosage levels of
the animals was designed for a "minimum lethal dose" which has been redefined
by most federal testing agencies and is at a lower dose level based on weight
gain rather than mortality. The dosage levels were not as significant with
trichloroethylene as with methyl chloroform. Sex differences in metabolism
and excretion of these compounds were not adequately incorporated into the
original test design. Additional testing, with experimental modifications
that address most of these points, are being conducted for all three subject
compounds.
Exposure of rats and mice to trichloroethylene caused no significant
maternal, embryonal or fetal toxicity, and no teratogenesis. Experiments on
both man and animals show that trichloroethylene is transported across the
placenta and enters the fetal blood system indicating potential fetal con-
tact but no toxic effects.
A vitally important concept is the mutagenic potential of trichloro-
ethylene. It has been suggested that since trichloroethylene is similar in
chemical structure to other industrial chemicals that are mutagenic and
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carcinogenic, it is particularly suspect. Following incubation with metaboliz-
ing enzymes from rat liver, some metabolites of trichloroethylene were shown
to cause mutations in bacteria. This finding, coupled with suggestions that
trichloroethylene forms a metabolic intermediate which is highly reactive (an
oxirane, or an alpha-chloroether or -onium ion), is the basis for most of the
continuing work on the toxicology of this solvent.
Following many decades of industrial exposure to trichloroethylene, there
has been no increase in tumor occurrence in the liver (or other site) in work-
ers. No reports of fetal mortality in wives of workers or reports of white
blood cell changes in workers exist. (White blood cell chromosomal aberrations
are early signs of mutations.) The absence of these toxic signs are noted here
because they have occurred in workers exposed to vinyl chloride. The toxicity
of vinyl chloride has been ascribed to the same reactive metabolic intermediate
that is proposed for trichloroethylene. The obvious difference in the toxicity
to man and animals of the two compounds indicates that the proposed metabolic
pathway (and its effects) need further investigation before decisions on the
risk of trichloroethylene's cellular reactivity are made.
From the data, it appears that the risk to man of exposure to trichloro-
ethylene is primarily that of exposure to an anesthetic agent, with the ac-
companying risk of loss of consciousness and even death from abuse or over-
dosage, but otherwise the effects are reversible, as they generally are with
anesthetic agents. The excellent fat-solvent properties of the compound cause
liver and kidney effects when an unusually large dose overburdens the detoxifi-
cation or clearance mechanisms of these organs. While these effects produce
cellular change, it is either a temporary effect, dose-related, or, the lesions
heal on cessation of exposure. The potential for a permanent cellular change,
based on the formation of a highly reactive metabolite that interacts with
cellular constituents to produce mutations or cancer, has been suggested for
trichloroethylene based on its structural similarity to more toxic solvents.
There is still considerable debate, however, whether trichloroethylene is in
fact metabolized to a reactive form in man or experimental animals.
10.2.2 Methyl Chloroform (1,1,1-trichloroethane)
The same physical properties that make methyl chloroform a desirable sol-
vent (high fat solvency, volatility) also contribute to the degree of exposure
through inhalation and skin contact. Methyl chloroform readily passes through
intact skin, and is found unchanged in the breath after inhalation or skin
contact in man and animals and after all routes of administration in animals.
The unmetabolized compound is also rapidly excreted in the breath after expo-
sure. In the first hour after human inhalation of a single breath of 5 mg
labeled methyl chloroform, 44% of the dose was excreted on the breath. Rats
excreted 98.7% of an injected dose. Therefore, little remains in the body to
be metabolized or to exert effects on organ systems.
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The health hazard of exposure to anesthetic levels of methyl chloroform
is first the narcotic effect on the central nervous system (CNS). These an-
esthetic effects have been reported to affect brain waves (alpha pattern on
the EEC) at 15 ppm. Behavioral changes, which are measured-by efficiency on
skills tests or questionnaires, have been reported at levels of 250 ppm.
Inebriated-like behavior and complaints of CNS effects occur in most humans
after several hours exposure to 350 to 500 ppm or 20 min at 900 to 1,000 ppm.
An immediate anesthetic effect was reported recently after an accidental ex-
posure to methyl chloroform fumes at an estimated concentration of 7,000 ppm.
Serious impairment of consciousness has occurred in humans experimentally ex-
posed to methyl chloroform concentrations which were increased from 0 to
2,650 ppm over a 15-min period. The lowest level used for producing light
surgical anesthesia was reported to be 10,000 ppm. Human fatalities have oc-
curred at an estimated level of 12,000 ppm. Even with these estimated levels,
it is apparent that methyl chloroform is a potentially dangerous anesthetic '
agent to a certain segment of the population.
Man is the most responsive species in demonstrating CNS effects of methyl
chloroform. Most studies on experimental animals showed behavioral or narcotic
changes (which indicate CNS effects) at much higher levels of exposure than
reported for man. The effects of methyl chloroform on the CNS are those of a
normal anesthetic agent; they are functional changes which, according to
available reports, are reversible in their entirety. In this context, these
effects should not be classified as toxicological changes. Because methyl
chloroform is an effective anesthetic agent, however, it has depressant ef-
fects on all levels of the CNS, including the central control of the breath-
ing centers. Inhalation of high concentrations for extended time periods could
be fatal without the occurrence of any organic or toxicological symptoms to
other organs. Nausea and prolonged listlessness have been observed as side ef-
fects in humans receiving anesthetic doses, but consciousness returns'within
minutes after breathing air free of the compound.
Not all the effects of methyl chloroform on man or experimental animals
can be adequately explained as manifestations of brain or nervous system re-
sponse to an anesthetic-type agent. Heart and liver changes have .been diagnosed
in man following exposure and seen in animals experimentally exposed to methyl
chloroform.
Methyl chloroform has a direct effect on the cardiovascular system as
shown by a decrease in blood pressure within seconds of inhaling high concen-
trations. When it was used to anesthetize humans, most patients experienced
a drop in blood pressure and had electrocardiogram (EGG) changes that could
be interpreted as a more "irritable" heart. ' !
Instances of sudden death have been reported over the last few years fol-
lowing inhalation of products containing methyl chloroform. Although the cause
of death has not been established in these cases, it is generally believed that
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high concentrations of the chlorinated hydrocarbons can sensitize the heart
of some individuals and thereby make the heart abnormally responsive to epi-
nephrine. One of the effects of epinephrine in man and animals is cardiac
arrhythmia. Since methyl chloroform either has arrhythmic effects of its own
or makes epinephrine effects more pronounced, there is a potential for seri-
ous cardiac effects resulting from exposure during excitement or stress when
the body normally releases high levels of epinephrine. If an additional fac-
tor of an old cardiac scar or other cardiovascular problem is added, there
is a physiological potential for serious cardiac effect from high levels of
exposure.
Epinephrine is broken down in the body (after its release during excite-
ment or stress) by two liver enzymes. Biochemical effects on the liver also
occur with methyl chloroform exposure. Persons who chronically abuse this sol-
vent are likely to have liver damage; therefore, high level, acute exposure
is more likely to damage the mechanisms by which epinephrine is broken down
in the body. On the other hand, long-term, low-level exposure to methyl
chloroform should not have the same effects as high exposure on the liver
and its detoxification mechanisms.
The liver changes occurring in man and experimental animals after expo-
sure are not secondary to either central nervous system or cardiac effects of
this solvent. Liver effects occur at rather high levels in man and experimental
animals compared to the behavioral, central nervous system effects. These
changes, however, consist of actual cellular or biochemical damage, while the
central nervous system effects, like those of most anesthetic agents, are
reversible.
Human liver effects have been assessed in some reports by measuring uri-
nary urobilinogen (a bile pigment processed by liver cells and released only
in small amounts by a healthy liver). Serum is frequently analyzed for enzymes
(SGPT and SCOT) which increase in liver disease. The exposure level resulting
in liver change has been delineated in humans and experimental animals. One-
time exposure of human subjects to methyl chloroform, 450 min at ~ 500 ppm or
75 min at ~ 1,000 ppm, failed to produce signs of liver toxicity. Five days
(7 hr/day at ~ 500 ppm) did not produce liver toxicity to experimentally ex-
posed humans. No effects on the liver were seen with methyl chloroform inhala-
tion, 7 hr/day, 5 days/week for 6 months at 500 ppm in rats, rabbits, dogs,
and guinea pigs. Animal toxicity data have shown that the guinea pig is the
most sensitive species to the liver effects of methyl chloroform. Fatty
changes in rodent livers were reported after chronic exposure at 1,000 ppm
in four studies. It was suggested that 2-hr methyl chloroform anesthesia
(10,000-26,000 ppm) in humans would not be hepatotoxic, since trials at this
exposure level produced no change in liver enzyme levels. Other workers,
however, have reported a death at an estimated inhalation level of 12,000
ppm. Even if this death was due to an individual hypersensitivity, it is prob-
able that hepatotoxicity and the more serious cardiotoxicity occur at different
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levels of exposure. One study, with estimates based on mouse and dog data,
suggested that for a single exposure, liver dysfunction occurs at the LD^g
level.
Repeated exposure to methyl chloroform has been shown to increase the ex-
cretion of metabolites in both animals and man, probably by the mechanism of
enzyme induction. The importance of this induction is twofold. First, it is
a mechanism by which the body rids itself of methyl chloroform more rapidly
on chronic exposure; because of this apparent capability, fewer chronic ef-
fects would be expected to occur with methyl chloroform compared with com-
pounds that deposit in tissues. Second, stimulation or induction of some of
these liver enzymes changes the action of many prescription and nonprescrip-
tion drugs since the same enzymes that are induced by methyl chloroform are
responsible for the metabolism of many types of drugs (i.e., sedative hyp-
notics and antipsychotics). Thus, some drugs may have reduced or increased
effects in persons chronically exposed to methyl chloroform.
The toxicity of methyl chloroform to the kidneys has been widely studied
in animals. The kidneys appear to be less vulnerable to this compound than
is the liver.
Human effects of different levels of methyl chloroform exposure are sum-
marized. The effects are tabulated by organ and graduated in intensity. Toxi-
cological parameters by species susceptibility are also summarized.
The NCI has published a bioassay of methyl chloroform for cancer-
producing properties. Rats of the Osborne-Mendel strain and mice (B6C3F1
line) were orally dosed with technical grade methyl chloroform (containing
95% 1,1,1-trichloroethane, 3% £-dioxane, and 2% other stabilizers and
minor impurities). The doses were 1,500 and 750 mg/kg for rats and 5,615 to
2,807 mg/kg average for mice, daily for 78 weeks (5 days/week). The doses
administered to both rats and mice were so sufficiently high that the ex-
perimental groups had early death losses. There was, however, no apparent
relationship of type or incidence of tumor to the chemical treatment in the
survivors. The B6C3F1 strain of mouse used in the study was susceptible to
cancer production by many chlorinated hydrocarbons, as shown by the statis-
tically significant incidence of liver cancer produced by perchloroethylene,
for example, which also was administered at levels producing early deaths in
the animals. The Osborne-Mendel rat strain is more resistant than other common
strains to the acute toxic liver effects of chlorinated hydrocarbons. Thus,
with high doses, they are more likely to survive and develop liver cancers.
In addition to using strains of animals susceptible to liver tumors, the
methyl chloroform was dosed by stomach tube. Oral dosage allows rapid ab-
sorption by the intestine into the portal circulation, and the methyl
chloroform would, therefore, reach the liver at higher levels than it would
after inhalation. A situation was thus apparently produced where liver cancer
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could readily develop, but liver cancer was not seen. The early death losses
in methyl chloroform-dosed rats made the experimental and control groups too
divergent in numbers to allow reliable statistical statements to be made on
the data. Even in view of the early death losses, available data indicate, how-
ever, that methyl chloroform is noncarcinogenic. The carcinogen bioassays are
being repeated using dosages at nonlethal levels to give unequivocal conclu-
sions on this high-use compound.
The state-of-the-art trial, considered necessary to evaluate the mutagen-
icity of a chemical, encompasses a profile of eight tests: three tests detect
gene mutations; three detect chromosomal aberrations; and two detect primary
DNA damage. One of the three gene mutation tests may use the Ames bacterial
assay, nonactivated and activated with metabolizing enzymes. Methyl chloroform
(also trichloroethylene and perchloroethylene) has been found to produce rever-
sions in at least one bacterial mutant strain (Ames test) in at least one
laboratory. The other seven tests have generally not been applied to these
three compounds because the addition of volatile solvents to sterile tissue
culture and bacterial plates presents technical problems. The methods employed
to overcome these problems vary with each laboratory so that quality control
data becomes as important as bacterial colony count in assessing the tests.
An hypothesis resulting from chemical structure studies has suggested that
methyl chloroform (and related, symmetrically chlorinated compounds) does not
follow a metabolic pathway to form reactive epoxides, a pathway implicated in
the mechanisms of mutagenicity.
In the carcinogenesis studies by the National Cancer Institute and in
some toxicity tests, commercial methyl chloroform was specified; these prod-
ucts always contain 3 to 10% stabilizing substances with 5 to 8% being a nor-
mal range. £-Dioxane is nearly always used in the methyl chloroform stabilizer
formulation at levels of 1.8 to 3% by volume. £-Dioxane is more toxic to ex-
perimental animals than methyl chloroform by all routes of administration.
The occurrence of stabilizers and their toxicity is important because not all
studies state whether or not the product used to dose animals was the commer-
cial (stabilized) product or the purified chemical. Both the single teratogen-
icity study and the NCI carcinogenesis study were performed with stabilized
methyl chloroform.
10.2.3 Perchloroethylene
Perchloroethylene is the slowest absorbed and the slowest excreted of the
three subject compounds. This property is the basis for many of the differences
in health effects. Perchloroethylene is only 10% excreted 1 hr after exposure
(44% of a dose of methyl chloroform and 15% of a trichloroethylene dose are
excreted in the same time span). When injected into experimental animals, per-
chloroethylene is nearly twice as toxic as when dosed orally, a fact that is
consistent with its rather poor absorption and slow excretion once it is
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absorbed. The oral LD^Q of perchloroethylene to mice is 8.1 g/kg of body
weight. When injected, the LD5Q is only 4.7 g/kg.
In man, the usual route of exposure is by inhalation. The toxicity of per-
chloroethylene by inhalation has been reported for experimental animals; the
minimum fatal dose was reported to be 2,600 ppm. Three thousand parts per mil-
lion (ppm) for 6 hr killed 3 of 10 rats, and 6,000 ppm for 5 hr killed 12 of
15 rats. In general, concentrations up to 9,000 ppm were not fatal until after
several hours' exposure for all animals (including man); 19,000 ppm quickly
anesthetized all the animals (death occurred unless removed from exposure),
and 31,000 ppm was rapidly lethal.
The dose level at which no effects were reported after multiple inhala-
tion exposures (7 hr/day, 5 days/week for 1 to 3 months) were as follows: 400
ppm for rats, monkeys and rabbits, and 100 ppm for guinea pigs.
Exposure to high levels of perchloroethylene has caused symptoms of acute
effects on the central nervous system. There are reports of loss of conscious-
ness, dizziness, lightheadedness, drunken behavior, and difficulty in walking.
These effects, in humans exposed to the compound, may persist for 2 weeks after
removal from exposure, as might be expected with a solvent deposited in fatty
tissue and then slowly released. With prolonged exposures, symptoms have been
reported of chronic effects on the nervous system. These symptoms include con-
fusion, impaired memory, numbness of extremities, and poor nerve transmission
due to some form of nerve damage, commonly called peripheral neuropathy. In
at least one human case of long-term, high-level exposure, effects remained
1 year after removal from perchloroethylene exposure. There is no indication
whether this "long term" effect was due to the individual being over-sensitive
or whether the exposure produced a permanent nerve change that would occur in
most persons exposed under similar conditions.
Perchloroethylene is an excellent fat (lipid) solvent and is slow to
leave the body once absorbed. The sheath around the larger nerves (myelin)
contains mostly lipid. The possibility of effects of this solvent at this
important site have not been adequately studied in either man or animals;
thus conclusions about permanent central nervous system changes after chronic
perchloroethylene exposure are somewhat premature. Acute effects (behavior
effects and anesthetic effects) are those of normal anesthetic agents, which,
when metabolized or excreted, leave no medically-detectable aftereffects.
Extensive oral dosage of perchloroethylene to man as a worm medication in
Asia during the 1920's and 1930's has shown that narcotic doses occur with
0.21 ml/kg of body weight, but that 0.15 ml/kg is not a narcotic dose. The
effects of the higher dosage, even on very young children, was reversible.
Perchloroethylene may even be less toxic as a narcotic agent than is
methyl chloroform, based on two reports in the literature. Workers have re-
covered from incidents of laying unconscious in the liquid for several hours.
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In contrast, exposure to liquid methyl chloroform in the same quantities has
resulted in fatalities. Differences in absorption rates could contribute to
the above results.
The report also discusses effects due to inhalation of perchloroethylene,
retention and excretion of the solvent by man and other animals, and dose-effect
data for various species. Effects on eyes and respiratory tract encompass sub-
jective reports of irritation or objective reports of redness; effects on the
central nervous system (CNS) are narcosis, dizziness, or other effects expected
of an anesthetic agent; effects on liver were diagnosed by liver function tests,
and heart effects were sought by examination of electrocardiographs.
The principal organic effect which follows exposure occurs in the liver.
The liver effects of perchloroethylene are reported to be nearly 10 times as
severe as those of trichloroethylene. Liver toxicity in man and animals follow-
ing exposure consists of liver enlargement, fatty changes at the cellular level,
and changes in liver enzyme levels. These liver changes have been shown to be
reversible following cessation of exposure in both animals and man.
The guinea pig liver is particularly sensitive to the effects of perchloro-
ethylene. Guinea pig toxicity data, therefore, provide a model with a better
safety factor when used to calculate exposure levels required to produce human
liver toxicity. Guinea pigs exhibit toxicity after inhalation exposure to 400
ppm perchloroethylene for 169 7-hr periods. If lower levels over a more pro-
longed time would cause the same effect, a human might show similar liver tox-
icity after 3 years at 150 ppm.
As an approximation for animals, acute inhalation exposure to 2,000 to
2,500 ppm perchloroethylene is the serious toxic endpoint for effects. At that
exposure level, all rabbit enzymes show damage, rats become unconscious, and
rabbits have significantly reduced kidney excretion (glomerular filtration
rate). Man and other animals exhibit narcosis--the beginning of unconscious-
ness--after only 7-1/2 min at that level.
National Cancer Institute (NCI) tests on the incidence of cancer induced
by perchloroethylene has indicated that liver cancer is produced in mice at a
statistically significant incidence when compared to control mice. Rats used
in the test did not show an increased incidence of malignancies. The charac-
teristics of the test animals with respect to these carcinogenicity studies
were discussed in the previous subsection on methyl chloroform. As with the
other two compounds, perchloroethylene was dosed orally in the cancer stud-
ies, rather than by inhalation. Oral dosage, when absorbed from the intestine,
goes directly to the liver circulation which means a large dose to the liver.
Inhalation-dosed chemicals, on the other hand, are absorbed across the lung
membrane into the general body circulation and affect the liver detoxification
mechanisms more gradually. It may be relevant that the one site of tumors was
the liver. This positive carcinogenesis bioassay is also being repeated by
NCI with results expected in the early 1980's,
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10.3 ECOLOGICAL EFFECTS
Ecological effects data are divided into two major areas of interest:
environmental fate and ecological effects. Environmental fate is concerned
with the tropospheric and stratospheric reactions, hydrolytic stability, modes
of degradation, and reactions in soil and sediment. Ecological effects are
concerned with the effects of these compounds on fish, birds, mammals, other
aquatic and terrestrial animals, and plants.
10.3.1 Environmental Fate
All three compounds enter the environment primarily through atmospheric
emissions. In the lower atmosphere (troposphere), trichloroethylene and per-
chloroethylene are thought to undergo photooxidation to produce the correspond-
ing acetyl chlorides, phosgene, and hydrogen chloride. The tropospheric life-
time of trichloroethylene has been reported to range from ~ 0.1 day to 6 weeks
whereas that for perchloroethylene was reported to be from 1 day to 21 weeks.
The range of tropospheric lifetimes results from the differences in methodology
and rate constants used in the calculations. Regardless of the method, both of
these compounds undergo relatively rapid photooxidation and do not persist in
the atmosphere for extended periods of time. It was estimated that only 2.4%
of the total quantity of perchloroethylene in the atmosphere and 0.4% of the
trichloroethylene would eventually reach the stratosphere.
Methyl chloroform, in contrast, undergoes very slow tropospheric photo-
oxidation (t^/2 — 0.5 to 8 years) to yield phosgene, carbon oxides, and hydro-
gen chloride. Because of its very slow tropospheric decomposition, methyl
chloroform is subject to transport into the stratosphere. Once in the strato-
sphere, methyl chloroform is thought to undergo photodissociation, in much
the same manner as currently hypothesized for the chlorofluorocarbons, to
yield chlorine atoms and chlorine oxide radicals. These atoms and radicals
can participate in ozone depletion reactions. Using a tropospheric residence
time (8 years), it has been calculated that approximately 12 to 15% of the
current tropospheric methyl chloroform levels will reach the lower stratosphere
and result in a steady state depletion of ozone to the extent of about 20% of
that calculated for the chlorofluorocarbons.
In aqueous media, the primary dissipative process is evaporation rather
than hydrolysis. The time required for 90% evaporation has been shown to be
about 1 hr for methyl chloroform and trichloroethylene and 1.5 hr for per-
chloroethylene. Of the quantity hydrolyzed, the relative decomposition rates
are: methyl chloroform > perchloroethylene > trichloroethylene. Trichloro-
ethylene is generally considered to be resistant to hydrolysis under normal
conditions. The principal products resulting from hydrolysis of methyl chloro-
form are acetic acid, hydrochloric acid, and vinylidene chloride, while those
for perchloroethylene are trichloroacetic acid and hydrochloric acid. If
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oxygen is added to the hydrolysis system, the rate of reaction of trichloro-
ethylene is accelerated; dichloroacetic acid and hydrochloric acid are the
major products•
No studies were found relating to the reaction rates, decomposition prod-
ucts or persistence of these compounds in soils or sediments. One study proposed
that the products probably would be the same as for aqueous hydrolysis but no
confirmation was provided.
Biological degradation of the three compounds by aerobic or anaerobic
microorganisms is considered negligible and, for concentrations expected in
municipal waste due to normal usage, these compounds are not toxic to aerobic
or anaerobic digestion processes. At concentrations above 500 ppm, disruption
of aerobic systems may occur. In anaerobic systems, all three compounds are
capable of destroying the methane bacteria in the second stage of digestion.
Of the three compounds, methyl chloroform is the most toxic.
10.3.2 Environmental Effects
Few data are available concerning the acute or chronic toxicities of the
three subject compounds to environmental species. Fish appear to be suscepti-
ble to low parts per million (ppm) concentrations of the three compounds. The
lowest LC^Q values reported were 5 ppm for perchloroethylene, 16 ppm for tri-
chloroethylene, and 33 ppm for methyl chloroform. In general, fish appear to
be capable of bioconcentrating these solvents to levels of approximately 100
times the aqueous concentrations.
Studies have also been conducted on a few other aquatic plants and animals
and, as with fish, these species show similar sensitivity to each of the three
compounds. In general, they are also capable of bioconcentrating these com-
pounds to levels of about 100 times the aqueous concentrations.
No studies were found concerning the toxicity of these compounds to birds.
All three compounds accumulate in the low parts per million range in the liver,
kidney, muscle, and eggs of birds. Perchloroethylene produces tremors (with
subsequent recovery) in adult houseflies but trichloroethylene showed no ef-
fect.
In terrestrial plants, trichloroethylene causes mutations in Wandering
Jews following a 6-hr exposure to less than 30 ppm. Perchloroethylene interferes
with the sporulation of a fruit fungus at concentrations of 400 ppm. In a phyto-
toxicity study on selected common vegetables, such as beans, tomatoes, and corn,
methyl chloroform showed effects only at a 5% concentration level while tri-
chloroethylene showed slight effects at a 0.5% level and slight to heavy injury
at the 5% level.
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In comparison to the previous studies, bacteria are the most resistant
to trichloroethylene. Concentrations required to produce a 50% reduction in
the bacteria levels range from 6,000 to 19,000 ppm. No data were found for
methyl chloroform or perchloroethylene.
Concentrations of all three compounds have been found in numerous plants
and animals. The concentrations vary depending upon the species but are gen-
erally in the low parts per billion range (< 60 ppb). Studies show, however,
that although accumulation occurs, the compounds are rapidly dissipated if
the species are placed in fresh water. This is especially true for fish. The
maximum overall increase in concentration between seawater and the tissues
of animals at the top of the food chain is less than 100-fold for trichloro-
ethylene and perchloroethylene. Bioconcentration factors for methyl chloro-
form have not been determined.
10.4 MONITORING DATA AND EXPOSURE LEVELS
Data were compiled for the levels of each of the three compounds in vari-
ous compartments of the environment, such as air, drinking water, nondrinking
water, soil, and sediment. Using the data from selected compartments and as-
suming average daily intake levels for humans, total daily exposure levels
were calculated for each of the three compounds.
10.4.1 Monitoring Data
Ambient air levels were reported for selected manufacturing and user
sites, other U.S. cities, and non-U.S. sampling sites. For manufacturing sites,
the ambient air levels were generally less than 2 ppb for methyl chloroform,
2.5 ppb for trichloroethylene, and 5 ppb for perchloroethylene. The highest
average levels for any one site were 15 ppb for methyl chloroform and 14 ppb
for trichloroethylene. Concentrations at all perchloroethylene sites were less
than 5 ppb. Levels in single samples often showed concentrations considerably
above the average levels.
Data for only one trichloroethylene and methyl chloroform user site were
reported. At the methyl chloroform user site, the average air levels were ap-
proximately 4.4 ppb or twice the average of the manufacturing sites. At the
trichloroethylene facility, the average levels were about 19.8 ppb or nine
times the average of the manufacturing sites. Air emissions from dry cleaning
establishments using perchloroethylene have been reported. The levels in the
outlet air vents ranged from 1 to > 1,000 ppm, depending upon the sampling
time and the particular establishment.
Ambient air levels have been reported for 27 other cities or areas in
the United States. The mean air levels for trichloroethylene ranged from un-
detectable to a high of 0.92 ppb, while those for methyl chloroform ranged
from undetectable to a high of 2.92 ppb. With perchloroethylene, the mean air
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levels reached a high of 4.5 ppb. At all of the sampling sites for which mean
levels of trichloroethylene were compiled, 79% showed levels above 0.01 ppb.
For methyl chloroform, 77% of the sampling sites showed mean levels greater
than 0.01 ppb while perchloroethylene had mean values above this level at 75%
of the sampling sites. Limited information was available concerning non-U.S.
sampling sites. Data were reported for sites in England and Japan as well as
for northern and southern hemispheric levels.
One study was recently reported in which the stratospheric levels of
methyl chloroform and perchloroethylene were measured. In the lower strato-
sphere, methyl chloroform was found to have an average air concentration of
79 parts per trillion (ppt) while perchloroethylene was found at an average
level of 6.5 ppt.
Twenty-two cities or areas in the United States were sampled for the
presence of one or more of the three compounds in tap water. Trichloroethylene
was detected in 14 of the cities; one city had a level of 32 ppb while 10
cities or areas had levels of 2 ppb or less. The highest concentration of
methyl chloroform was 17 ppb; all other 13 cities were found to have levels
of 1 ppb or less. For perchloroethylene, the highest level was 2 ppb; the
remaining 12 cities had concentrations of 0.4 ppb or less.
Non-tap water concentrations were measured at six manufacturing sites,
one trichloroethylene and methyl chloroform user site, three dry cleaning es-
tanlishments, and 204 other sites in the United States. At the manufacturing
sites, the levels upstream from the plant outlets ranged from 0.4 to 353 ppb
for trichloroethylene and from 0.1 to 132 ppb for methyl chloroform. At the
plant outlets, the levels ranged from 74 to 535 ppb for trichloroethylene and
from 5 to 344 ppb for methyl chloroform. No levels were reported for perchloro-
ethylene at manufacturing sites. For the one user site, the upstream levels
were 5 and 6 ppb, respectively, for trichloroethylene and methyl chloroform.
Downstream of the plant outlet, the levels ranged from 8 to 26 ppb for tri-
chloroethylene and 6 to 18 ppb for methyl chloroform.
At three dry cleaning establishments, wastewater from the carbon bed ad-
sorption system is discarded into the sewer system. Perchloroethylene levels
in the wastewater ranged from approximately 6 to 1,000 ppm, depending upon the
site sampled and the time during the desorption cycle that the sample was
obtained.
Of the 204 other sites sampled in the United States, 95% of the sites
showed levels of trichloroethylene, methyl chloroform, and perchloroethylene
to be less than 6 ppb. Approximately 75% of all sites showed the levels of
these three compounds to be < 1 ppb. The maximum level detected for methyl
chloroform was 8 ppb, while that for perchloroethylene was 45 ppb. Levels for
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trichloroethylene were the highest of the three compounds with a maximum con-
centration of 188 ppb.
Only one study was found in which levels of trichloroethylene and methyl
chloroform were measured in soil; perchloroethylene levels were not deter-
mined. The levels were measured only in the vicinity of manufacturing sitest
At these sites, the concentrations ranged from nondetectable to highs of 5.6
ppb for trichloroethylene and 3.4 ppb for methyl chloroform. In the United
States, sediment levels have been measured only at manufacturing and user
sites. Methyl chloroform levels ranged up to a maximum of approximately
6 ppb. Trichloroethylene levels showed a wide variation in concentration,
ranging from undetectable to a maximum concentration of 300 ppb. As with the
soil samples, no perchloroethylene levels were determined.
10.4.2 Exposure Levels
Trichloroethylene, methyl chloroform, and perchloroethylene can be assimi-
lated by inhalation, ingestion (food and water), and dermal absorption. The
routes of entry into the body chosen for the calculations were inhalation and
water ingestion. For calculated quantities resulting from inhalation, an
average inhalation volume of 20 cu m/day was chosen. Furthermore, for drink-
ing water, an average adult consumption of 3 liters/day was assumed. No data
are currently available for food products in the United States so this route
of intake was not considered. Quantities of each of the three compounds in-
troduced into the body by dermal absorption were considered negligible com-
pared to those quantities from inhalation and water ingestion.
Levels due to inhalation were calculated for each city or area. From the
data for trichloroethylene, only five cities showed levels of exposure greater
than 1.5 /xg/kg body weight per day (/ug/kg/day ). The highest level of those
five was about 26; other levels were approximately 18, 3, and 2 /ug/kg/day.
Calculated levels for all large cities with a high population density were
about 1 ,ug/kg/day or less. For methyl chloroform, only one city (a manufactur-
ing site) showed a calculated level in excess of 2 ug/kg/day. Data for large
cities ranged from a high of 1.3 to a low of 0.1 ,ug/kg/day. Six cities had
calculated levels due to inhalation of perchloroethylene greater than 1.2
#g/kg/day. Of these cities, New York was one of two with the highest cal-
culated level (—7.8,ug/kg/day); the other was a small city with a production
facility. Los Angeles showed a level slightly greater than 2 ,ug/kg/day. In
general, the available data show that a relatively small segment of the
general population is exposed to trichloroethylene or methyl chloroform air
levels that would result in the bodily retention of greater than 1.5 ^g/kg/day.
The same statement is not necessarily true for perchloroethylene.
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Drinking water data for trichloroethylene indicate that only two cities
were found to have calculated exposure levels in excess of 1 ^g/kg/day with
the highest level at 1.6. One other city had a level of 0.95 and all others
were less than 0.25 Mg/kg/day. The data for methyl chloroform were difficult
to assess due to the lack of quantitative values. Only one city, a manufactur-
ing site, showed a calculated level appreciably above 0.05 ^g/kg/day. In gen-
eral, large metropolitan areas showed little, if any, methyl chloroform in
the drinking water. For perchloroethylene, only one city showed a calculated
level for drinking water greater than 0.02 jug/kg/day.
Calculated exposure levels from both ambient air concentrations and drink-
ing water levels were available for only a few cities. One of five cities showed
a total calculated level of trichloroethylene in excess of 4 /xg/kg/day. For
methyl chloroform, one of five cities showed a calculated level greater than
2 Mg/kg/day. All other cities had levels of less than 1.2 ,ug/kg/day. Data for
perchloroethylene were confined to two cities, both of which represent metro-
politan areas with populations in excess of 1 million persons. The highest
level was -~7.8 ^g/kg/day while the other level was •— 1.2 ^g/kg/day.
For aquatic species, no water levels were found to be in excess of the
lowest reported toxic concentration. At nonmanufacturing or user sites, the
levels generally were a factor of about 250 or more below the toxic level of
the most sensitive species. For manufacturing or user sites, the outlet levels
generally ranged from a factor of about 10 to 100 below the toxic concentra-
tion of the most sensitive species.
10.5 REGULATIONS AND STANDARDS
The three compounds are currently regulated (or proposed to be regulated)
by a number of federal agencies and state or local governments. Other agencies
anticipate some future regulatory action.
Workplace standards are in effect for the three compounds; in addition,
threshold limit values and recommended standards for occupational exposure
have been reported. The occupational standards apply to airborne concentra-
tions.
10.5.1 Regulations
The EPA has several offices with current or proposed regulations for the
three subject compounds. These offices include drinking water, hazardous
spills, water and waste management, and air quality planning and standards.
The Office of Drinking Water has a proposed amendment to the National
Interim Primary Drinking Water Regulation to require communities with popula-
tions over 75,000 to use granular activated carbon (GAG) in water treatment
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systems. None of the three compounds are specifically identified; however, the
amendment specifies that the concentration of volatile halogenated organic
compounds in the effluent must not exceed 0.5 /ug/liter.
Trichloroethylene is one of 28 compounds designated as hazardous in an
amendment proposed by the Office of Hazardous Spills. Another proposed final
rule classified the various hazardous wastes by toxicity range and stated the
limits of harmful quantities that may be discharged into water. Trichloro-
ethylene was identified as a Class C waste with a corresponding harmful quan-
tity of 1,000 Ib.
All three chlorinated compounds are included on the Toxic Pollutants List
published by the Office of Water and Waste Management. This list forms a basis
for the development of effluent limitations from point sources; however, no
current regulations are in force for any of the three compounds.
The policy of the Office of Air Quality Planning and Standards (OAQPS)
with respect to photochemical reactivity of volatile organic compounds is that
only a few compounds have negligible reactivity and only five (including
methyl chloroform) are recommended for exclusion from control. Perchloroethylene
was originally listed in a second group of compounds that were more reactive
than the group of five but did not contribute large quantities of oxidant
under most atmospheric conditions. Due to recent findings on the health
aspects of perchloroethylene, it was deleted from this list. Recently the
OAQPS has recommended to the EPA regional offices that state implementation
plans (SIP) emphasize the use of emission control rather than converting sol-
vent systems to methyl chloroform because it is an exempt solvent.
The Food and Drug Administration (FDA) has published a rule stating that
any aerosol drug product containing methyl chloroform to be used for inhala-
tion is a new drug and subject new drug application. Tolerances for residues
of trichloroethylene in foods are in effect but the food industry has stopped
using this compound as an extractant.
Of the 17 states responding to inquiries regarding standards on regula-
tions for these compounds, only one (Texas) had no standards. Kentucky and
Illinois require consumer product labeling. Twelve states regulate the com-
pounds via hazardous waste or toxic substances regulations. Michigan requires
a license to operate commercial or self-service cleaning plants using per-
chloroethylene. The state plans to include trichloroethylene and perchloro-
ethylene in the Critical Materials Register which requires industry to re-
port use and discharge of the compounds. Virginia requires all companies to
file an inventory of chemicals manufactured or used in manufacturing.
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10.5.2 Standards
Occupational exposure limits for workplace concentrations of the three
compounds have been set by the Occupational Safety and Health Administration
(OSHA) to be 350 ppm (8-hr TWA) for methyl chloroform and 100 ppm (8-hr TWA)
for trichloroethylene and perchloroethylene. These standards are not based on
any of the recent health effects studies of any of the three compounds. How-
ever, OSHA has issued a tentative list of Category I chemicals (including
trichloroethylene) which may be regulated under the proposed generic carcinogen
policy.
The National Institute for Occupational Safety and Health (NIOSH) has
recommended levels of occupational exposure of 350 ppm for methyl chloroform,
100 ppm for trichloroethylene, and 50 ppm for perchloroethylene. NIOSH has
recently issued bulletins on the three subject compounds which cautions
against reliance on the existing standards and recommendations for worker
protection.
Other levels have been suggested by the American Conference of Govern-
mental Industrial Hygienists (ACGIH) and the American National Standards
Institute (ANSI). The ACGIH threshold limit values are the same as those
stated earlier for the current OSHA occupational exposure limits. The ANSI
(Z-37) workplace quality standards for trichloroethylene and perchloroethylene
are the same as OSHA and ACGIH. The ANSI level for methyl chloroform is 400
ppm (8-hr TWA).
10.5.3 Shipping and Transportation Practices
The National Tank Truck Carriers, Inc., have set forth recommendations
for truck transportation regarding tank types, metals for tank construction,
precautions for handling, and procedures for accidental spills. The Depart-
ment of Transportation requires that all shipping containers be tagged with
a ORMA label along with the name and quantity of solvent.
10.6 SOLVENT EMISSIONS
10.6.1 Metal Cleaning Industry
Control of emissions from the metal cleaning industry has been the sub-
ject of three major reports. Information from these reports was summarized
and the control systems recommended by EPA presented. Two control systems were
suggested for the reduction of emissions from cold cleaning operations; the
attainable reductions for high volatility solvents were 55 (+ 20) percent and
69 (+20) percent for the two systems. For opentop vapor degreaser operations,
two systems for emission reduction were suggested. One system may reduce
emissions by 45 (+ 15) percent and the second system by 60 (+ 15) percent.
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The two systems for the reduction of emissions from conveyorized vapor de-
greasers were estimated to have, efficiencies of 25 (+5) percent and 60
(+10) percent.
10.6.2 Dry Cleaning Industry
An evaluation of the solvent (perchloroethylene) losses in the dry clean-
ing industry shows that most machines (transfer and dry-to-dry) average ap-
proximately 7,000 to 8,000 Ib of clothes per drum of solvent (mileage).
Modern transfer machines with carbon adsorbers can obtain greater than 10,000
Ib/drum. Carefully operated dry-to-dry machines can attain mileage figures of
14,000 to 18,000 Ib. Mileage levels of greater than 20,000 Ib can be attained
using modern equipment and extremely careful operation. Factors affecting sol-
vent mileage are discussed and reasons for erratic solvent consumption are
evaluated. A statistical analysis of data from a study of 69 dry-to-dry
machines shows that not over 30.8% of current machines would meet a performance
level of 5 Ib of perchloroethylene emitted per 100 Ib of fabric cleaned
(14,000 Ib of clothes per drum). A similar analysis for data from 193 trans-
fer machines shows that not over 10.4% of current transfer machines would meet
a 14,000 Ib/drum performance level.
10.6.3 Solvent Recovery or Disposal
Reclamation of trichloroethylene, methyl chloroform, and perchloroethylene
by distillation is the most environmentally acceptable method for treating
waste solvent. Recovery by this process can generally occur by two methods:
(a) a contract service; or (b) in-house distillation. With the contract recla-
mation service, the contractor collects the waste solvent, distills the mate-
rial, and returns the reclaimed portion to the solvent user. Large volume
users of these solvents can utilize in-house distillation. The total annual
cost of in-house distillation can generally be recovered from the savings
incurred for the first 350 gal. of recovered solvent. It has been estimated
that in terms of overall reduction in waste solvent volume, reclamation by
the use of distillation can generally result in the recovery of 80 to 85% or
more of the solvent contained in the initial waste solution.
The complete and controlled high temperature incineration of distillation
residues and other sources of these three compounds represents the greatest
immediate potential for safe disposal. There are four general types of incin-
erators commercially available for the destruction of toxic liquid organic
wastes from industrial operations. Multiple hearth, rotary kiln, fluidized
bed, and liquid injection incinerators represent proven technology in liquid
waste disposal techniques. For trichloroethylene, methyl chloroform, and per-
chloroethylene, consideration must be given to the potentially detrimental
products (hydrogen chloride and phosgene) which may be formed during combus-
tion. A promising new technology for the destruction of toxic halogenated
organic wastes is the combustion with molten salts.
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Hazardous waste landfills approved for the disposal of materials such
as trichloroethylene, methyl chloroform, and perchloroethylene are currently
in operation. However, disposal by this method presents the potential for fu-
ture atmospheric and groundwater contamination. Landfills that meet the cri-
teria for a California Glass I hazardous waste disposal site have been suggested
to be acceptable; however, the EPA has stated that most hazardous waste land-
fills are not adequate for the disposal of wastes containing trichloroethylene,
methyl chloroform, or perchloroethylene.
10.6.4 Container Labels
In addition to the Department of Transportation regulations stated earlier,
an American Society of Testing Materials Subcommittee has recommended container
labels for each of the three compounds. The basic label found on each container
has the following information: identification; health and safety information;
precautions; first aid; and handling and storage.
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CONTENTS
11. Proposed Regulatory Options 11-2
11.1 Review of Major Findings 11-2
11.2 Options for Specific Areas 11-5
11.2.1 Air emissions from metal cleaning 11-6
11.2.2 Waste disposal 11-7
11.2.3 Dry cleaning industry 11-8
11.2.4 Water quality 11-9
11.2.5 Container labels 11-10
11.2.6 Dental and medical procedures 11-10
11.2.7 Aerosol products 11-11
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SECTION 11
PROPOSED REGULATORY OPTIONS
In this section, an assessment is presented of the need for limita-
tions on the quantity of trichloroethylene, methyl chloroform, and per-
chloroethylene entering the environment. This assessment will be in the
form of several recommendations which are suggested for consideration
by appropriate governmental agencies as methods for the reduction in emis-
sions of these compounds. These recommendations should not be considered
as an attempt to state future agency policy nor should they, as policy
decisions are, of course, the province of the agency. The recommendations
set forth in this section are based on the studies reported in this re-
view of the three subject compounds.
Prior to a presentation of the recommendations, it is appropriate
to present a brief review and summary of the major findings of this study.
11.1 REVIEW OF MAJOR FINDINGS
All three of the subject compounds are produced in relatively large
quantities. In 1977, the estimated production for all three amounted to
1,548 million pounds. Of this total, perchloroethylene was manufactured
in the largest quantity, 659 million pounds, followed by methyl chloro-
form at 596 million pounds, and trichloroethylene at 293 million pounds.
Over 97% of all trichloroethylene (excluding exports) was used industri-
ally in metal cleaning operations. Approximately 8070 of the annual pro-
duction of methyl chloroform (excluding exports) was used industrially
in metal cleaning operations. Use in adhesives and aerosol products ac-
counted for 14%; 67» was attributed to miscellaneous uses. Perchloroethylene
is used primarily in the textile industry as a cleaning agent and in metal
cleaning operations. If its use as a chemical intermediate and exports
are not considered, approximately 77% of the annual production is used
by the textile industry and about 20% for industrial metal cleaning op-
erations. Small quantities of the three compounds are used in consumer
products directly by general population. However, all of the quantities
used industrially for metal cleaning operations and by the textile in-
dustry as a dry cleaning agent are eventually lost to the environment,
primarily in the form of atmospheric emissions.
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All three of the compounds are globally distributed in the tropo-
sphere primarily as a result of emissions by the users. Atmospheric lev-
els are generally in the low parts per billion (ppb) or parts per tril-
lion (ppt) range. The highest average atmospheric level for any of the
three compounds was approximately 20 ppb, measured at a user site. In
general, average levels are of the order of 1 to 2 ppb or less. In re-
cent studies, methyl chloroform was detected in the stratosphere at an
average level of 79 ppt and perchloroethylene at a level of approximately
6 ppt. In dry cleaning establishments, perchloroethylene levels ranging
from 1 to >1,000 parts per million (ppm) have been detected in the out-
let air vents.
Trichloroethylene, methyl chloroform, and perchloroethylene have
been detected in the drinking water in various cities throughout the United
States. The highest trichloroethylene level was 32 ppb, but in 10 of the
14 cities or areas, the levels were 2 ppb or less. For methyl chloroform,
the highest level was 17 ppb; all other 13 cities were found to have lev-
els of 1 ppb or less. With perchloroethylene, 2 ppb was the highest level
and the remaining 12 cities had levels of 0.4 ppb or less. There have
been recent confirmed reports of trichloroethylene contamination of wells
used for drinking water. Contaminant levels in these wells have been de-
tected up to 20 ppm, and, in one case, apparently results from the dis-
posal of trichloroethylene by a user located near the wells. Nondrinking
water levels of trichloroethylene and methyl chloroform at manufacturing
site outlets ranged from 74 to 535 ppb and 5 to 344 ppb, respectively.
At dry cleaning plants, perchloroethylene levels in the wastewater ranged
from 6 to 1,010 ppm. Of 204 other sites sampled in the United States,
95% showed levels of the three compounds to be less than 6 ppb. The maxi-
mum levels detected were 188 ppb for trichloroethylene, 45 ppb for per-
chloroethylene, and 8 ppb for methyl chloroform.
With regard to the human health effects of these three compounds,
an exposure level at which some type of physiological effect can be con-
sistently observed is approximately 150 ppm for trichloroethylene. When
this level of exposure is maintained for extended periods (e.g., in a
workplace), the effects are dizziness, headaches, and incoordination;
all of these effects are reversible after the individual is removed from
the source of the compound. With similar exposure times to methyl chloroform,
the dizziness, headaches, and incoordination do not generally occur until
the level reaches approximately 350-500 ppm for several hours duration.
The effects of perchloroethylene are somewhat different from those observed
for either trichloroethylene or methyl chloroform. With methyl chloroform,
only about 65% of the quantity inhaled is absorbed by the body with the
remainder being immediately exhaled. It appears that even the absorbed
methyl chloroform is largely expired unmetabolized. Trichloroethylene
is readily absorbed (~85%) by the body during inhalation, but it is also
rapidly metabolized by the body so that the actual residence time in the
11-3
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body is relatively short. Perchloroethylene, on the other hand, is readily
absorbed (~90%) during inhalation, but is very slowly metabolized by
the body so that its effects are much more prolonged than those of the
other two compounds. An epidemiological study, in which workers were exposed
to levels of about 150 ppm of methyl chloroform for periods of 1 to 6
years, showed no adverse health effects. There is no evidence of death
occurring among workers as a result of long-term occupational exposure to
any of the three compounds; trichloroethylene and perchloroethylene have
had particularly long usage. Case histories have, of course, shown that
deaths have occurred as a result of occupational exposure, but these
instances result from accidental exposure to very high levels (~7,000
ppm or more). At these levels, the narcotic or anesthetic effects of these
compounds are very rapid and death has resulted from overexposure after
the victim became unconscious. All three compounds can sensitize the heart
to the effects of epinephrine. Of the three, methyl chloroform appears
to be the most potent for inducing this type of sensitization. The precise
dose and exposure level, mechanism, and persons at risk due to sensitization
are unknown. Sensitization with fatal results has been most frequently
reported after exposure to high levels (~7,000 ppm) of methyl chloroform.
Studies by the National Cancer Institute indicate that trichloro-
ethylene and perchloroethylene may be potential carcinogens, attributable
to liver tumor production from oral doses of the compounds in mice but
not rats. Tests conducted with methyl chloroform produced no tumors but
high dosages resulted in animal data that were not suitable for statisti-
cal analysis. Even in view of the early death losses, available data
indicate methyl chloroform is not carcinogenic. For trichloroethylene
and perchloroethylene, the average daily oral doses were approximately
500 and 1,000 mg/kg. The results of the bioassays have created considerable
controversy because of the high dose levels used, the method of dosage,
and that only the mice showed liver tumors. The predominant human exposure
route for these two compounds is generally by inhalation, not oral ingestion
which vitally affects distribution. Toxicology literature contains many
caveats regarding the interpretation of data obtained with inbred mice
having murine tumor viruses and unique detoxification enzyme levels in
the liver. The carcinogen bioassays, with improved experimental design,
are being repeated on all three compounds.
Few studies have been conducted concerning the toxicity of these
compounds towards nonlaboratory animals found in the environment, and
no studies have been conducted on fish or wildlife which serve as a source
of food for humans. Of the reported data, the most sensitive species is
the barnacle which shows an LD _ of 3.5 ppm with trichloroethylene. For
nonmanufacturing or user sites, levels of each of the three compounds
were generally a factor of about 250 or more below the toxic level. At
manufacturing sites, the outfall levels generally showed factors from
about 10 to 110 below the toxic concentration of the most sensitive spe-
cies.
11-4
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The major results of this study can be summarized as follows:
1. Methyl chloroform has been identified in the stratosphere at an
average level of approximately 80 ppt. Theoretical calculations show that,
based on current and projected production volumes, methyl chloroform will
result in an ozone depletion of approximately 20y0 of the extent postulated
for the chlorofluorocarbons. Current calculations estimate an average ozone
depletion of about 13 to 15% for the chlorofluorocarbons.
2. Incidents of well water contamination by trichloroethylene have
been reported and levels of the order of 10 to 20 ppm have been measured
in some of these wells. Contamination apparently occurs by transport of
the trichloroethylene through the soil to underground aquifers, which
lead to the wells. In at least one case, the contamination was apparently
due to disposal of waste trichloroethylene.
3. Trichloroethylene and perchloroethylene have been identified
as a cause of liver cancer in one certain strain of test animal by oral
gavage. However, because of high dose levels used and the method of in-
troduction, considerable controversy has arisen over the results of these
tests, and additional tests are being conducted.
4. High levels of all three compounds have been shown to sensitize
the heart to the effects of epinephrine, which, under certain circumstances,
can lead to death. Of the three compounds, methyl chloroform appears to be
the most potent with respect to sensitization.
5. Aside from the carcinogenicity results and the sensitization
effects, both of which occur at high levels, no adverse health effects
could be identified for the levels normally encountered by the general
public.
6. In dry cleaning establishments, perchloroethylene levels rang-
ing from 1 to >1,000 ppm have been detected in the outlet air vents.
These localized levels are over 1,000 higher than any ambient air lev-
els; however, the data were for levels in the air vents leading to the
atmosphere. No data were found for ambient air levels in the immediate
vicinity of dry cleaning establishments.
11.2 OPTIONS FOR SPECIFIC AREAS
The following subsection presents specific proposed options which
may be considered to reduce the quantities of trichloroethylene, methyl
chloroform, and perchloroethylene introduced into the environment. These
options are deemed the most appropriate based on the information presented
in this study for the production and use, health and environmental impacts,
known environmental levels, and disposal practices for each of the three
compounds.
11-5
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In general, the data show that, at the present time, there is no basis
to recommend a total regulation or cessation of the manufacture or use of
these three compounds. This statement should not be construed as a judgment
that any of these three compounds poses no human or environmental risk from
their manufacture or use, but rather that the data available at this time
are insufficient to conclude that a need exists for the cessation of the
manufacture of these compounds. However, certain options do appear to be
appropriate in certain areas to limit the exposure of these compounds to
humans and the environment. These options are delineated in the following
paragraphs.
11.2.1 Air Emissions From Metal Cleaning
In view of the recent theoretical studies of ozone depletion by methyl
chloroform, it would seem appropriate to reconsider the present EPA policy
with respect to these three compounds. At the present time, the policy for
the control of volatile organic compounds lists methyl chloroform as being
exempt from regulation under state implementation plans (Federal Register,
Friday, July 8, 1977, 35314-35316). While the disadvantages (resulting
from the interchangeability of these solvents) noted in this discussion
are recognized, the recommended policy is intended primarily for the con-
trol of volatile organic compounds which are a constituent in the formation
of photochemical oxidants. The policy is not necessarily designed to take
other atmospheric factors into account.
Other solvents or systems have been proposed as alternatives for
these three compounds in the area of metal cleaning, but none of them
possesses the wide range of flexibility shown by trichloroethylene, methyl
chloroform, and perchloroethylene. Aside from its potential for ozone
destruction, F-113 has a rather low solvency power so that its applica-
bility to many current uses of the three subject compounds would be ques-
tionable. Methylene chloride, in addition to its potential health prob-
lems, is much more volatile than the three subject compounds so that con-
trol of emissions of this solvent would require more stringent conditions
(including added equipment) than that presently necessary for the:current
solvents. Alkaline detergent solutions may be applicable in selected minor
areas, but they are inappropriate for use with electrical equipment and
their general use is often limited by rust and corrosion problems caused
by residual water. Disposal of the aqueous detergent solution poses prob-
lems in the waste treatment process. In effect, available alternative
systems are not generally applicable to many areas of current utilization
and may pose more problems than the three solvents currently under study.
Because of methyl chloroform's proposed role in the depletion of
ozone, it should probably not be placed in a classification of chemicals
for which "it is not necessary that they be inventoried or controlled."
11-6
-------
Therefore, it is suggested that consideration be given to the deletion
of methyl chloroform from the uncontrolled classification and placed
in the same category with trichloroethylene. Perchloroethylene had previ-
ously been placed in the category of low photochemically reactive com-
pounds* These compounds were included in the baseline emission inventories,
and reductions in their emissions were credited toward achievement of the
National Ambient Air Quality Standard. As such, they are subject to reason-
ably available control technology. In the recent policy statement (see
Section 8, "Regulations and Standards"), perchloroethylene was removed
from this classification and apparently placed in the same category as
trichloroethylene. The inclusion of methyl chloroform in the same clas-
sification with trichloroethylene and perchloroethylene would result in
this compound being subject to the same emission controls as those for
the other two compounds.
The discussions and suggestions presented in the preceding paragraphs
were originally set forth in a Draft Final Report by MRI in September 1977.
The Office of Air Quality Planning and Standards, EPA, Research Triangle
Park, North Carolina, was cognizant of the potential stratospheric reactions
with methyl chloroform since the first report in early 1977 of an 8-year
tropospheric residence time. Recently this office has recommended that state
implementation plans (SIPs) emphasize positive emission reduction for all
three solvents rather than substitution of methyl chloroform for either-
of the other two solvents. .
\
According to a recent EPA report, current control technology can re-
sult in a decrease in ambient air emissions on the order of 50 to 60%.
A large portion of the control technologies recommended by EPA (see Section
9) do not require the purchase or use of expensive equipment. Significant
emission reductions can be attained by the employment of careful operating
practices and good maintenance procedures. It is inherent that in order to
attain high solvent emission reductions and to reduce the potential for
human exposure to trichloroethylene, methyl chloroform, or perchloroethylene,
a comprehensive training program must be employed. This training program is
very significant not only for vapor degreasing operations but also for cold
cleaning procedures. Many cold cleaning operations are conducted by un-
trained and nonsupervised workers in small companies. These situations can
lead to increased human exposure and high emission losses unless the personnel
are carefully trained and cognizant of the potential health effects that can
result from the use of these three compounds.
11.2.2 Waste Disposal
In view of the current drinking water contamination problems result-
ing from the apparent transport of solvent by aquifer systems, certain
current methods of waste solvent disposal do not appear to be adequate
in protecting the general public from contact with these solvents.
11-7
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Although not a method of waste disposal, solvent recovery techniques
are currently available which could lead to appreciable recycling of the
solvent and an overall reduction in the quantity of waste solvent to be
discarded. Depending upon the annual volume of solvent employed, in-house
solvent recovery techniques can be cost effective, both in terms of the
reduction in the quantity of solvent to be disposed, and, consequently,
the quantity of new solvent to be purchased. In other cases (low volume
users) where the use of in-house distillation methods would not be cost
effective, contract services are available to recycle waste solvent. Sol-
vent recovery techniques can generally recover over 807» of the solvent
contained in the waste so that the use of these techniques could signifi-
cantly reduce the sheer volume of waste solvent currently discarded.
The use of solvent reclamation will, however, still result in a quan-
tity of distillation residue to be treated. For that quantity of solvent
remaining after reclamation, incineration could be employed as the means
of disposal and assurances be made to maintain the levels of toxic or
corrosive decomposition products at an environmentally acceptable minimum.
Most current state implementation plans allow for the incineration of
photochemically reactive materials, provided that 90% or more of the car-
bon is transformed into inorganic carbon or that the concentration of
organic material following incineration is less than 50 ppm (calculated
as carbon with no dilution).
Contract reclamation and incineration services are generally avail-
able, primarily in the larger metropolitan areas, so that many companies
will be able to readily reclaim or dispose of their waste solvent. How-
ever, companies generating small volumes of waste solvent to be reclaimed
or residue to be destroyed may encounter difficulties in the location
of a service interested in small volumes. In addition, there may be large
geographical areas where no services of either type are available so that
users of these solvents may encounter problems in the location of ser-
vices for the disposal of the waste material. In order to alleviate these
potential problems, assistance may be required by the users. An appropriate
federal agency, through the use of regional offices, could establish and
maintain an information office (or source person) to assist users within
the region in the location(of the nearest contract reclamation or incin-
eration services. In this manner, special problems could also be handled
so that users will be able to dispose of the waste materials in an en-
vironmentally acceptable manner.
11.2.3 Dry Cleaning Industry
Guidelines for the control of volatile organic compounds (VOC),
specifically perchloroethylene, from all dry cleaning systems which use
this solvent have been published by the Office of Air Quality Planning
and Standards (see Section 8). Other solvents used in the dry cleaning
11-8
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industry, petroleum distillate (Stoddard Solvent) and trichlorotrifluoro-
ethane (fluorocarbon-113), were not discussed in this guideline. The
methodology described in the guideline represents the presumptive norm
or reasonably available control technology (RACT) that can be applied
to existing perchloroethylene dry cleaning systems.
Control techniques delineated in the guideline include carbon adsorp-
tion, good equipment maintenance and housekeeping procedures, and waste
solvent treatment. The carbon adsorption units are stated to exhibit collec-
tion efficiencies ranging from 96 to greater than 997o with outlet concen-
tration of 2 to 100 ppm as perchloroethylene. Good equipment maintenance
and housekeeping procedures can reduce solvent consumption in certain
pieces of equipment from 15 kg or more per 100 kg of clothes cleaned to
3 to 5 kg per 100 kg of clothes. Various sources of waste solvent recovery
and treatment methods were presented.
In view of the emission reductions that can be achieved by the imple-
mentation of these guidelines and the activity by the office of Air Quality
Planning and Standards in the control of perchloroethylene emissions from
the dry cleaning industry, it is felt that additional suggestions for con-
trol measures are not desirable at this time.
11.2.4 Water Quality
Amendments and proposed amendments have been published for the con-
trol of levels of these three compounds in water. At the present time,
there is considerable controversy surrounding some of the measures and
new regulations are being proposed for other measures.
With respect to the levels of the three compounds in finished drink-
ing water, methods for the control of chemical contaminants have been
proposed by the Office of Water Supply (see Section 8). Contaminants to
be controlled were trihalomethanes and volatile synthetic organic com-
pounds, including all three of the subject compounds. The proposed regu-
lation (February 1978) inspired considerable debate from the water supply
industry and EPA is preparing detailed responses to the issues raised
during the comment period in an attempt to resolve these differences.
In view of the current activity in this area, it is felt that no options
to modify the proposed regulations are justified.
As previously stated in Section 8, "Regulations and Standards," tri-
chloroethylene was classified as a category C hazardous substance in the
EPA hazardous substance spill program (March 1978). This classification
was based on aquatic toxicity (96-hr LC _) levels in the 10 to 100 mg/
liter range. Neither methyl chloroform nor perchloroethylene were identi-
fied as hazardous substances. The spill program was halted by an industry
law suit and the revised Section 311 rules are ready for final internal
11-9
-------
review. EPA intends to revoke some current Section 311 rules and simul-
taneously issue new regulations designating 299 substances as hazardous.
This list will be the 271 substances designated plus the additional 28
substances proposed in the March 1978 rule. If, as indicated, the new
Section 311 rules will include only the previous list of 299 substances,
trichloroethylene will be the only one of the three compounds designated
as a hazardous substance. Since methyl chloroform and perchloroethylene
have basically the same type of aquatic behavior and aquatic toxicity
levels as trichloroethylene, these two compounds should be evaluated for
inclusion in the same category as for trichloroethylene.
The upcoming regulations on Section 311 will also cover areas desig-
nated in the 1976 toxic pollutant settlement agreement such as hazardous
substance toxicological selection criteria, hazardous substance discharge
potential, determination of harmful quantities, and Section 311 regulatory
applicability. Since this new regulation should be published in the near
future, no options are justified until the full scope of the regulations
can be reviewed.
11.2.5 Container Labels
All three of the subject compounds pose a human health problem in
high vapor concentration. In view of this, all containers of trichloro-
ethylene, methyl chloroform, and perchloroethylene should be adequately
labeled to state the potential dangers involved with these materials.
Most manufacturers and at least some distributors do label or will label
their containers to warn users that personnel should avoid inhalation
of the vapors and skin contact with the chemicals. The label should also
state that a high vapor concentration can cause unconsciousness or death.
It is further suggested that containers be labeled in some manner to state
that exposure to high vapor concentrations of these compounds followed by
strenuous physical activity or high levels of excitement or stress may
result in heart sensitization. This label warning would be of particular
value to personnel with a previous history of heart problems who may en-
counter high concentrations of these compounds. It is suggested that all
containers, including those used for disposal of waste solvent and consumer
products be labeled in a similar manner. It has also been strongly suggested
by at least one equipment manufacturer that all vapor degreasing equipment
be labeled in a similar manner. MRI concurs that such labeling be employed
to warn workers of the potential dangers of these compounds.
11.2.6 Dental and Medical Procedures
On the basis of the health effects data derived in this study, it
is suggested that appropriate agencies should consider the essentiality
of the usage of trichloroethylene in dental and medical procedures. Al-
though these are minor use areas, they represent a mechanism for the direct
11-10
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introduction of trichloroethylene into the human body at levels considerably
above those to which the general public would normally be exposed. In all
cases, alternative materials are currently being utilized, in varying
degrees, in each of these use areas.
11.2.7 Aerosol Products
It is suggested that the use of the three subject compounds in aerosol
products be reviewed by the appropriate agencies. As with the previous case,
this represents a minor use area for each of these compounds, but one that
also represents a mechanism for the potential direct inhalation of these
chemicals. The levels attainable through the use of aerosol products could,
under certain circumstances, reach levels where a decrease in manual dex-
terity, eye irritation, and effects on the central nervous system, primar-
ily as dizziness, could occur. In many instances, other competitive prod-
ucts not containing these compounds are on the market.
11-11
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APPENDIX A
COMMERCIAL PRODUCTS CONTAINING TRICHLOROETHYLENE. METHYL
CHLOROFORM. OR PERCHLOROETHYLENE
A-l
-------
COMMERCIAL NONPESTICIDE PRODUCTS
CONTAINING 1.1.1-TRICHLOROETHANE^
Product
Amway Drain Mate
Amway Dri-fab
Amway Oven-n-grill
Amway Remove
Amway Wonder Mist
Barton's Spot Remover
Carbo-chlor
Carbona No. 10 Special Spot Remover
Carbona Spray Spot Remover
Oressup
Edwal Color Film Cleaner
Enduro Dry Cleaning Fluid
Enduro Spot Remover
Enduro Wig and Toupee Cleaner
Everblum Cleaning Fluid
Glamorene Spot Clean
Gripdust
IBM Adhesive
IBM Cleaning Fluid
IBM-SMS Card Contact Cleaner
IBM Stain Remover
IBM Tape Developer and Cleaner
O.K. Cleaning Fluid
One-Time Rug Frost
PL-100 Safety Solvent
Quik 'n Easy Spot Lifter
Renofab Custom Home Dry Cleaner
Roberts 41-0911
Roberts 41-4001
Roberts 41-4015
Scotts Liquid Gold Cleaner
Sila Slide
Sturman's Dry Cleaner and Spot Remover
Tetra-Sol Spot Remover
Touch-n-glue
Tri-ethane Solvent
Weldwood Nonflammable Brush Contact Cement
Weldwood Panel Adhesive (nonfummable)
Weldwood Standard Solvent
Manufac turer
Percentage 1,1,1-
Trichloroethane
Amway Corp.
Amway Corp.
Amway Corp.
Amway Corp.
Amway Corp.
Dynashine
Sunnyside
Carbona
Carbona
Dolge
Edwal
Midwest Mfg.
Midwest Mfg.
Midwest Mfg.
Albatross
Glamorene
Dolge
IBM
IBM
IBM
IBM
IBM
Albatross
One Time Package Prod.
Precision Labs
Penn Champ
Renofab
Roberts Consolidated, Inc.
Roberts Consolidated, Inc.
Roberts Consolidated, Inc.
Scotts Liquid Gold
Scientific International
Crestwood Products
Midwest Mfg.
U.S. Plywood-Champion Papers, Inc.
P.P.G. Industries, Chem. Div.
Roberts Consolidated, Inc.
U.S. Plywood-Champion Papers, Inc.
Roberts Consolidated, Inc.
>70%
>93%
>65%
>60%
>70%
10%
25%
b/
b/
b/
b/
b/
b/
b/
b/
b/
b/
70%
b/
b/
b/
b/
~ 10%/v
b/
33.3%
b/
b/
100%
b/
b/
b/
a/ Adapted from Reference 1.
b/ Information not available.
A-2
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REGISTERED PESTICIDE USES
OF 1.1.1-TRICHLORO ETHANE3^ /
Application
Target Pests
Commercial - Edible, Indoor Cockroaches, Hornets, Silverfish, Wasps,
Yellowjackets
Commercial - Edible, Outdoor Mud Daubers, Wasps
Commercial - Outdoor Hornets, Wasps, Yellowjackets
Domestic Dwellings - Indoor Hornets, Wasps, Yellowjackets
Domestic Dwellings - Outdoor Hornets, Mud Daubers, Wasps, Yellowjackets
Electric Shaver Heads
Garbage Cans
Mothproofing
Railroad Cars
Stored Tobacco
Stored Tobacco
Tobacco
Tobacco Storage Rooms
Tobacco Warehouses
Trucks
Bacteria
Cats, Dogs
Clothes Moths
Cockroaches, Silverfish
Cigarette Beetle, Tobacco Moth
Cigarette Beetle, Tobacco Moth
Cigarette Beetle, Tobacco Moth
Cigarette Beetle, Tobacco Moth
Cigarette Beetle, Cigarette Beetle, Tobacco
Moth
Cockroaches, Silverfish
&l Adapted from Reference 2.
_b/ 1,1,1-Trichloroethane appears in formulations with other AI in all
uses noted here.
A-3
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COMMERCIAL NONPESTICIDE PRODUCTS
CONTAINING TRICHLOROETHYLENE^/
Product
Manufacturer
Percentage
TrichXoroethylene
Adhes-off
Balkamp Klean and Prime
Bowes Buffing Solution
Carboff
Carbona Cleaning Fluid
Carbona No. 10 Special Spot Remover
Crater 2X Fluid
Crater 5X Fluid
Glamorene Dry Cleaner for Rugs
Instant Chimney Sweep
Lacco Chlorosan
Lash Bath
Mildew Stop Spray
Pedi-Skin Adherent No. 2
Perm-a-chlor SA
TFE Dri-glide Teflon Aerosol
Thoro Dry Cleaner
Trichlor
Harvey Labs, Inc. b/
Loctite Corp..£/ b/
Bowes b/
Holcomb 1-10%
Carbona 44%
Carbona 40%
Texaco, Inc.; Texaco Canada, Ltd. Jj/
Texaco, Inc.; Texaco Canada, Led. J:/
Glamorene ^/
Miracle Adhesives 34%/wt
Los Angeles Chem. 6.4%
RevIon b/
Cardinal Products Corp. 25.9%
Pedinol Pharmaceutical, Inc. b/
Detrex Jj/
Cling-Surface 14%
Thoro .b/
P.P.G. Industries, Chem. Div. 100"
_a/ Adapted from References I and 3.
b/ Information not available.
_c/ Product owned by Balkamp, Inc.
A-4
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REGISTERED PESTICIDE USES
OF TRICHLOROETHYLENKa»b/
Application
Commercial - Inedible, Outdoor
Domestic Dwellings - Outdoor
Feed Stores
Grain Elevators
Grain Mills
Grain Storage Areas
Grain Terminals
Mothproofing
Seed Stores
Stored Corn
Stored Grain
Target Pests
Bees, Hornets, Wasps, Yellowjackets
Bees, Hornets, Wasps, Yellowjackets
Angoumois Grain Moth, Confused Flour
Beetle, Flies, Granary Weevil, Indian
Meal Moth, Mosquitos, Rice Weevil,
Sawtoothed Grain Beetle
Same as last entry
Same as last entry
Same as last entry
Same as last entry
Clothes Moths, Moths
Angoumois Grain Moth, Confused Flour
Beetle, Flies, Granary Weevil, Indian
Meal Moth, Mosquitos, Rice Weevil,
Sawtoothed Grain Beetle
Stored Grain Insects
Angoumois Grain Moth, Confused Flour
Beetle, Flies, Granary Weevil, Indian
Meal Moth, Mosquitos, Rice Weevil,
Sawtoothed Grain Beetle, Stored Grain
Insects
a/ Adapted from Reference 2.
b/ Trichloroethylene appears in formulations with other AI in all uses
noted here.
A-5
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COMMERCIAL NONPESTICIDE PRODUCTS
CONTAINING PERCHLOROETHYLENEJ/
Product
Manufacturer
Percentage
Perchloroethylene
Amway Remove
Carbona Spray Spot Remover
Command Safety Solvent
Detrex Perk
Dowper
Glamorene Spot Clean
One-Time Rug Frost
Parsons Lethogas Fumigant
Perchlor
Safe-t-solve Solvent Cleaner
Schalk's Spot Dry Cleaner
S.I.R. Safety Solvent
Solvoway Rug Shampoo
Talbot's Mar-hyde
Techna-solve
Ucon-12
Ultramar Oil Dispersant
Zipola
_a/ Adapted from Reference 1.
b/ Information not available.
Ainway Corp.
Carbona
Uncle Sam
Detrex
Dow
Glamorene
One-Time Package Prod.
Parsons Chem.
P.P.G. Industries, Chem. Div.
Consolidated Chem., Inc.
Schalk
Scientific International
Uncle Sam
Talsol
Dolge
*
Ultramar Chem.
High Chem.
<20%
16%
100%
b/
b/
0.004%
100%
b/
b/
b/
15%
b/
b/
b/
b/
A-6
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REGISTERED PESTICIDE USES OF PERCHLOSOETHYLENEJU^
Application
Arborvitae
Target Pests
Aphids, Bagworm, Carnation Bud Mite,
Carnation Shoot Mite, Clover Mite,
Cottoneaster Webworm, Cottony'cushion
Scale (crawlers), Cyclamen Mite,
Dipterous Leafminers, European Pine
Shoot Moth, European Red Mite, Fall
Webworm, Flea Beetles, Hemlock Chermes,
Holly Bud Moth, Lecanium Scales (crawlers),
Obliquebanded Leafroller, Obscure Root
Weevil, Omnivorous Leaftier, Pearslug,
Pine Needle Scale (crawlers), Privet Mite,
San Jose Scale, Soft Scales, Tent Cater-
pillars, Twospotted Spider Mite, Western
Oak Looper
Azalea
Beef Cattle
Beverage Plants
Same as last entry
Cattle Fever Tick, Ear Tick, Gulf Coast
Tick, Horn Fly, Lice, Lone Star Tick, Winter
Tick
Blow Flies, Drosophila, Flying Moths,
Gnats, House Fly, Mosquitos
Birch
Aphids, Bagworm, Carnation Bud Mite, Car-
nation Shoot Mite, Clover Mite, Cottoneaster
Webrowm, Cottonycushion Scale (crawlers),
Cyclamen Mite, Dipterous Leafminers, European
Pine Shoot Moth, European Red Mite, Fall Web-
worm, Flea, Beetles, Hemlock Chermes, Holly
Bud Moth, Lacanium Scales (crawlers), Oblique-
banded Leafroller. Obscure Root Weevil,
Omnivorous Leaftier, Pearslug, Pine Needle
Scale (crawlers), Privet Mite, San Jose
Scale, Soft Scales, Tent Caterpillars,
Twospotted Spider Mite, Western Oak Looper
A-7
-------
REGISTERED PESTICIDE USES OF PERCHLOROETHYLENE^^
(continued)
Application
Target Pests
Boxwood
Camellia
Carnation
Chrysanthemum
Commercial - Outdoor
Commercial - Edible, Indoor
Same as last entry
Same as last entry
Same as last entry
Same as last entry
Hornets, Wasps, Yellowjackets
Angoumois Grain Moth, Ants, Blow Flies,
Carpet Beetle, Cheese Mite, Cheese Skipper,
Cigarette Beetle, Clover Mite, Cockroaches,
Confused Flour Beetle, Crickets, Drosophilia,
Drugstore Beetle, Firebrat, Fleas, Flies,
Flour Moths, Flying Insects, Flying Moths,
Gnats, Grain Beetles, Grain Mite, Grain
Moths, Granary Weevil, Hornets, House Fly,
Indian Meal Moth, Meal Moth, Mediterranean
Flour Moth, Mosquitos, Rice Weevil,
Sawtoothed Grain Beetle, Scorpions, Silver-
fish, Spider Beetles, Spiders, Vinegar Fly,
Wasps, Yellowjackets
Commercial - Edible, Outdoor Angoumois Grain Moth, Ants, Blow Flies,
Cadelle, Carpet Beetle, Cockroaches,
Confused Flour Beetle, Drosophila,
Drosophila Gnats, Flying Moths, Gnats,
House Fly, Indian Meal Moth, Mediterranean
Flour Moth, Mosquitos, Silverfish
Commercial - Inedible, Indoor Angoumois Grain Moth, Ants, Blow Flies,
Brown Dog Tick, Cadelle, Carpet Beetle,
Cigarette Beetle, Cockroaches, Confused
Flour Beetle, Crickets, Drosophila Gnats,
Firebrat, Fleas, Flies, Indian Meal Moth,
Mediterranean Flour Moth, Mosquitos,
Roaches, Silverfish, Spiders, Vinegar Fly,
Waterbugs
A-8
-------
REGISTERED PESTICIDE USES OF PERCHLOROETHYLENB^/
(continued)
Application
Commercial - Inedible, Outdoor
Confectionary Companies
Dairies
Department Stores
Domestic Dwellings - Indoor
Domestic Dwellings - Indoor
Target Pests
Angoumois Grain Moth, Bees, Blow Flies,
Carpet Beetle, Cigarette Beetle, Cock-
roaches, Confused Flour Beetle, Gnats,
Hornets, House Fly, Indian Meal Moth,
Mediterranean Flour Moth, Mosquitos,
Silverfish, Spiders, Vinegar Fly, Wasps,
Yellowjackets
Cockroaches, Flies, Gnats, Meal Moth,
Mosquitos, Silverfish
Same as last entry
Same as last entry
Angoumois Grain Moth, Ants, Blow Flies,
Cadelle, Carpet Beetle, Cheese Mite,
Cheese Skipper, Cigarette Beetle, Clover
Mite, Cockroaches, Confused Flour Beetle,
Crickets, Drosophila Gnats, Fleas, Flies,
Flying Insects, Flying Moths, Gnats, Grain
Beetles, Grain Mite, Granary Weevil, Hornets,
House Fly, Indian Meal Moth, Mediterranean
Flour Moth, Mosquitos, Rice Weevil,
Scorpions, Silverfish, Spider Beetles,
Spiders, Wasps, Yellowjackets
Ants, Brown Dog Tick, Carpet Beetle,
Cigarette Beetle, Cockroaches, Confused
Flour Beetle, Crickets, Drugstore Beetle,
Firebrat, Fleas, Flies, Gnats, Indian
Meal Moth, Mosquitos, Rice Weevil, Roaches,
Sawtoothed Grain Beetle, Silverfish,
Spiders, Waterbugs;
A-9
-------
REGISTERED PESTICIDE USES OF PERCHLOROETHYLENE-
(continued)
Application
Domestic Dwellings - Outdoor
Douglas Fir
Target Pests
Angoumois Grain Moth, Ants, Bees, Bermuda
Grass Mite, Blow Flies, Brown Dog Tick,
Cadelle, Carpet Beetle, Chiggers (Redbugs),
Chinch Bug, Cigarette Beetle, Clover Mite,
Cockroaches, Confused Flour Beetle, Crickets,
Cutworms, Digger Wasps, Drosophila,
Drosophila Gnats, Hornets, House Flies,
indian Meal Moth, Lawn Pillbugs, Mediter-
ranean Flour Moth, Rhodesgrass Scale, Sod
Webworms (Lawn Moths), Sowbugs, Spiders,
Springtails, Ticks, Wasps, Yellowjackets
Aphids, Bagworm, Carnation Bud Mite,
Carnation Shoot Mite, Clover Mite,
Cottoneaster Webworm, Cottonycushion
Scale (crawlers), Cyclamen Mite,
Dipterous Leafminers, European Pine
Shoot Moth, European Red Mite, Fall
Webworm, Flea Beetles, Hemlock Chermes,
Holly Bud Moth, Lecanium Scales (crawlers),
Obliquebanded Leafroller, Obscure Root
Weevil, Omnivorous Leaftier, Pearslug,
Pine Needle Scale (crawlers), Privet Mite,
San Jose Scale, Soft Scales, Tent Cater-
pillars, Twospotted Spider Mite, Western
Oak Looper
Elm
Feed Stores
Same as last entry
Angoumois Grain Moth, Confused Flour
Beetle, Flies, Granary Weevil, Indian
Meal Moth, Mosquitos, Rice Weevil,
Sawtoothed Grain Beetle
Food Processing Plant
Food Processing Plant - Edible
Flies, Gnats, Mosquitos
Angoumois Grain Moth, Blow Flies, Carpet
Beetle, Cigarette Beetle, Cockroaches,
Confused Flour Beetle, Drosophila, Flies,
Flying Moths, Gnats, House Fly, Indian
Meal Moth, Meal Moth, Mediterranean
Flour Moth, Mosquitos, Silverfish,
Vinegar Fly
A-10
-------
REGISTERED PESTICIDE USES OF PERCHLOROETHYLENE-
(continued)
a.b/
Application
Target Pests
Gladiolus
Goats
Golf Courses
Grain Elevators
Aphids, Bagworm, Carnation Bud Mite,
Carnation Shoot Mite, Clover Mite,
Cottoneaster Webworm, Cottonycushion
Scale (crawlers), Cyclamen Mite,
Dipterous Leafminers, European Pine
Shoot Moth, European Red Mite, Fall
Webworm, Flea Beetles, Hemlock Chermes,
Holly Bud Moth, Lecanium Scales (crawlers),
Obliquebanded Leafroller, Obscure Root
Weevil, Omnivorous Leaftier, Pearslug,
Pine Needle Scale (crawlers), Privet Mite,
San Jose Scale, Soft Scales, Tent Cater-
pillars, Twospotted Spider Mite, Western
Oak Looper
Lice, Sheeptick
Angoumois Grain Moth, Blow Flies, Carpet
Beetle, Cigarette Beetle, Cockroaches,
Confused Flour Beetle, House Fly, Indian
Meal Moth, Mediterranean Flour Moth,
Mosquitos, Silverfish, Vinegar Fly
Angoumois Grain Moth, Confused Flour
Beetle, Flies, Granary Weevil, Indian
Meal Moth, Mosquitos, Rice Weevil,
Sawtoothed Grain Beetle
Grain Mills
Grain Storage Areas
Grain Storage Facilities
Same as last entry
Same as last entry
Angoumois Grain Moth, Blow Flies, Gnats,
House Fly, Meal Moth, Mediterranean
Flour Moth
Grain Terminals
Angoumois Grain Moth, Confused Flour
Beetle, Flies, Granary Weevil, Indian
Meal Moth, Mosquitos, Rice Weevil,
Sawtoothed Grain Beetle
A-11
-------
REGISTERED PESTICIDE USES OF PERCHLOROETHYLENE^.^
(continued)
Application
Target Pests
Hawthorn
Hogs
Holly
Horses
Aphids, Bagworm, Carnation Bud Mite,
Carnation Shoot Mite, Clover Mite,
Cottoneaster Webworm, Cottonycushion
Scale (crawlers), Cyclamen Mite,
Dipterous Leafminers, European Pine
Shoot Moth, European Red Mite, Fall
Webworm, Flea Beetles, Hemlock Chermes,
Holly Bud Moth, Lecanium Scales (crawlers),
Obliquebanded Leafroller, Obscure Root
Weevil, Omnivorous Leaftier, Pearslug,
Pine Needle Scale (crawlers), Privet Mite,
San Jose Scale, Soft Scales, Tent Cater-
pillars, Twospotted Spider Mite, Western
Oak Looper
Hog Louse
Aphids, Bagworm, Carnation Bud Mite,
Carnation Shoot Mite, Clover Mite, Cotton-
easter Webworm, Cottonycushion Scale
(crawlers) Cyclamen Mite, Dipterous
Leafminers, European Pine Shoot Moth,
European Red Mite, Fall Webworm, Flea
Beetles, Hemlock Chermes, Holly Bud Moth,
Lecanium Scales (crawlers), Obliquebanded
Leafroller, Obscure Root Weevil,
Omnivorous Leaftier, Pearslug, Pine Needle
Scale (crawlers), Privet Mite, San Jose
Scale, Soft Scales, Tent Caterpillars,
Twospotted Spider Mite, Western Oak Looper
Cattle Fever Tick, Ear Tick, Gulf Coast
Tick, Horn Fly, Lice, Lone Star Tick,
Winter Tick
A-12
-------
REGISTERED PESTICIDE USES OF PERCHLOROETHYLENE:
. (continued)
a,b/
Application
Target Pests
Juniper
Aphids, Bagworm, Carnation Bud Mite,
Carnation Shoot Mite, Clover Mite, Cotton-
easter Webworm, Cottonycushion Scale
(crawlers) Cyclamen Mite, Dipterous
Leafminers, European Pine Shoot Moth,
European Red Mite, Fall Webworm, Flea
Beetles, Hemlock Chermes, Holly Bud Moth,
Lecanium Scales (crawlers), Obliquebanded
Leafroller, Obscure Root Weevil,
Omnivorous Leaftier, Pearslug, Pine Needle
Scale (crawlers), Privet Mite, San Jose
Scale, Soft Scales, Tent Caterpillars,
Twospotted Spider Mite, Western Oak Looper
Kennels
Lawns
Lilac
Brown Dog Tick, Drosophila, Fleas, Flies,
Gnats, Mosquitos, Wasps
Bermuda Grass Mite, Brown Dog Tick,
Chiggers (Redbugs), Chinch Bugs, Clover
Mite, Crickets, Cutworms, Digger Wasps,
Drosophila, Fleas, Lawn Pillbugs, Rhodes-
grass Scale, Sod Webworms (Lawn Moths),
Sowbugs, Springtails, Ticks
Aphids, Bagworm, Carnation Bud Mite,
Carnation Shoot Mite, Clover Mite,
Cottoneaster Webworm, Cottonycushion
Scale (crawlers), Cyclamen Mite,
Dipterous Leafminers, European Pine
Shoot Moth, European Red Mite, Fall
Webworm, Flea Beetles, Hemlock Chermes,
Holly Bud Moth, Lecanium Scales (crawlers),
Obliquebanded Leafroller, Obscure Root
Weevil, Omnivorous Leaftier, Pearslug,
Pine Needle Scale (crawlers) , Privet Mite,
San Jose Scale, Soft Scales, Tent Cater-
pillars, Twospotted Spider Mite, Western
Oak Looper
A-13
-------
REGISTERED PESTICIDE USES OF PERCHLOROETHYLENE-
(continued)
Application
Locust
Maple
Target Pests
Same as last entry
Aphids, Bagworm, Carnation Bud Mite,
Carnation Shoot Mite, Clover Mite, Cotton-
easter Webworm, Cottonycushion Scale
(crawlers) Cyclamen Mite, Dipterous
Leafminers, European Pine Shoot Moth,
European Red Mite, Fall Webworm, Flea
Beetles, Hemlock Chermes, Holly Bud Moth,
Lecanium Scales (crawlers), Obliquebanded
Leafroller, Obscure Root Weevil,
Omnivorous Leaftier, Pearslug, Pine Needle
Scale (crawlers), Privet Mite, San Jose
Scale, Soft Scales, Tent Caterpillars,
Twospotted Spider Mite, Western Oak Looper
Mills
Mothproofing
Noncrop Areas
Office Buildings
Ornamental Turf
Peanut Bins - Empty
Angoumois Grain Moth, Blow Flies, Gnats,
House Fly, Meal Moth, Mediterranean Flour
Moth
Clothes Moths, Moths
Flies, Gnats, Mosquitos
Cockroaches, Flies, Gnats, Meal Moth,
Mosquitos, Silverfish
Chinch bug, Sod Webworms (Lawn Moths)
Cockroaches, Confused Flour Beetle, Flies,
Granary Weevil, Indian Meal Moth, Saw-
toothed Grain Beetle
Peanut Elevators Same as last entry
Peanut Shelling Plants - Edible Same as last entry
Peanut Storage Areas - Empty Same as last entry
Pet Bedding Brown Dog Tick
Pet Sleeping Quarters Brown Dog Tick
A-14
-------
REGISTERED PESTICIDE USES OF PERCHLOROETHYLENB^'
(continued)
Application
Target Pests
Pine
Aphids, Bagworm, Carnation Bud Mite,
Carnation Shoot Mite, Clover Mite,
Cottoneaster Webworm, Cottonycushion
Scale (crawlers), Cyclamen Mite,
Dipterous Leafminers, European Pine
Shoot Moth, European Red Mite, Fall
Webworm, Flea Beetles, Hemlock Chermes,
Holly Bud Moth, Lecanium Scales (crawlers),
Obliquebanded Leafroller, Obscure Root
Weevil, Omnivorous Leaftier, Pearslug,
Pine Needle Scale (crawlers), Privet Mite,
San Jose Scale, Soft Scales, Tent Cater-
pillars, Twospotted Spider Mite, Western
Oak Looper
Poplar
Railroad Boxcars
Same as last entry
Angoumois Grain Moth, Blow Flies, Gnats,
House Fly, Meal Moth, Mediterranean
Flour Moth
Rhododendron
Aphids, Bagworm, Carnation Bud Mite,
Carnation Shoot Mite, Clover Mite, Cotton-
easter Webworm, Cottonycushion Scale
(crawlers) Cyclamen Mite, Dipterous
Leafminers, European Pine Shoot Moth,
European Red Mite, Fall Webworm, Flea
Beetles, Hemlock Chermes, Holly Bud Moth,
Lecanium Scales (crawlers), Obliquebanded
Leafroller, Obscure Root Weevil,
Omnivorous Leaftier, Pearslug, Pine Needle
Scale (crawlers), Privet Mite, San Jose
Scale, Soft Scales, Tent Caterpillars,
Twospotted Spider Mite, Western Oak Looper
Roses
Schools - Indoor
Same as last entry
Cockroaches, Flies, Gnats, Meal Moth,
Mosquitos, Silverfish
A-15
-------
REGISTERED PESTICIDE USES OF PERCHLOROETHYLENE-
(continued)
Application
Seed Stores
Sheep
Spruce
Target Pests
Angoumois Grain Moth, Confused Flour
Beetle, Flies, Granary Weevil, Indian
Meal Moth, Mosquitos, Rice Weevil, Saw-
toothed Grain Beetle
Sheeptick
Aphids, Bagworm, Carnation Bud Mite,
Carnation Shoot Mite, Clover Mite,
Cottoneaster Webworm, Cottonycushion
Scale (crawlers), Cyclamen Mite,
Dipterous Leafminers, European Pine
Shoot Moth, European Red Mite, Fall
Webworm, Flea Beetles, Hemlock Chermes,
Holly Bud Moth, Lecanium Scales (crawlers),
Obliquebanded Leafroller, Obscure Root
Weevil, Omnivorous Leaftier, Pearslug,
Pine Needle Scale (crawlers), Privet Mite,
San Jose Scale, Soft Scales, Tent Cater-
pillars, Twospotted Spider Mite, Western
Oak Looper
Storage Bins
Stored Grain
Tobacco Warehouses
Warehouses
Angoumois Grain Moth, Blow Flies, Gnats,
House Fly, Meal Moth, Mediterranean
Flour Moth
Angoumois Grain Moth-, Confused Flour
Beetle, Flies, Granary Weevil, Indian
Meal Moth, Mosquitos, Rice Weevil,
Sawtoothed Grain Beetle
Brown Dog Tick, Cigarette Beetle,
Cockroaches, Tobacco Moth
Angoumois Grain Moth, Blow Flies, Con-
fused Flour Beetle, Drosophila, Flying
Moths, Gnats, House Fly, Indian Meal
Moth, Mediterranean Flour Moth, Mosquitos,
Rice Weevil, Sawtoothed Grain Beetle
A-16
-------
REGISTERED PESTICIDE USES OF PERCHLOROETHYLENB^-k-'
(concluded)
Application
Warehouses - Edible
Willow
Target Pests
Angoumois Grain Moth, Blow Flies, Carpet
Beetle, Cigarette Beetle, Cockroaches,
Confused Flour Beetle, House Fly, Indian
Meal Moth, Mediterranean Flour Moth,
Mosquitos, Silverfish, Vinegar Fly
Aphids, Bagworm, Carnation Bud Mite,
Carnation Shoot Mite, Clover Mite,
Cottoneaster Webworm, Cottonycushion
Scale (crawlers), Cyclamen Mite,
Dipterous Leafminers, European Pine
Shoot Moth, European Red Mite, Fall
Webworm, Flea Beetles, Hemlock Chermes,
Holly Bud Moth, Lecanium Scales (crawlers),
Obliquebanded Leafroller, Obscure Root
Weevil, Omnivorous Leaftier, Pearslug,
Pine Needle Scale (crawlers), Privet Mite,
San Jose Scale, Soft Scales, Tent Cater- •
pillars, Twospotted Spider Mite, Western
Oak Looper
al Adapted from Reference 2.
b/ Perchloroethylene appears in formulations with other AI in all uses
noted here.
A-17
-------
REFERENCES
1. Clinical Toxicology Commercial Products File. United States Consumer
Product Safety Commission. Washington, D.C. September 13, 1978.
2. Pesticide Product Information on Microfiche. Technical Services Divi-
sion. Office of Pesticide Programs. United States Environmental
Protection Agency. Washington, D.C. October 1976.
3. Waters, E. M., H. B. Gerstner, and J. E. Huff. Trichloroethylene - I.
An Impact Overview. Oak Ridge National Laboratory. Report No. ORNL/
TIRC-76/2. Contract No. W.7405-eng-26. May 1976.
A-18
-------
APPENDIX B
RESULTS OF THE WRITTEN QUESTIONNAIRE
B-l
-------
SURVEY OF INDUSTRIAL PROCESSING DATA
Midwest Research Institute (MRl) is presently conducting a program
for the Office of Toxic Substances of the U.S. Environmental Protection
Agency under Contract No. 68-01-4121. The primary purpose of this program
is to assimilate information relative to the production/formation, use and
release into the environment of trichloroethylene (TCE) and methyl chloro-
form (1,1,1-trichloroethane), which is abbreviated as MC.
In addition to industries that directly produce or use these sub-
stances, we have identified the following chemicals whose manufacture may
produce small amounts of either trichloroethylene or methyl chloroform as
a by-product, a component of waste material, or an impurity in a product.
* Perchloroethylene
* Vinyl Chloride
* Vinylidene Chloride
The MRI study is based on available information in the literature
and private communications with industry personnel, via telephone, letters,
and questionnaire. In order to attain a statistically reliable overview of
the industrial situation on the subject, it is important that we contact as
many industries as possible. We, therefore, respectfully solicit your co-
operation in completing this questionnaire; your early response (within
4 weeks) will be sincerely appreciated.
If your department cannot supply the requested information, please
forward to other departments which can respond to this questionnaire. If
any questions should arise concerning this questionnaire, please contact
Charles E. Mumma at (816) 753-7600 (Ext. 415).
Please return the completed questionnaire to:
Midwest Research Institute
425 Volker Boulevard
Kansas City, Missouri 64110
Attn: Charles E. Mumma
Thank you very much for your assistance and cooperation.
B-2
-------
QUESTIONNAIRE PREPARED FOR OFFICE OF TOXIC SUBSTANCES,
U.S. ENVIRONMENTAL PROTECTION AGENCY
(Please fill in the details and check the appropriate blanks.)
1. Parent Corporation Name:
Mailing Address:
2. Person to contact regarding information supplied in questionnaire.
Dr/Mr/Ms:
Address:
Zip Code_
Telephone: __
3. If your company manufactures, or has manufactured within the past 10
years, any of the chemicals listed in the cover letter please com-
plete the following form:*
Listed
Chemical Production Site: City or Town and State
b.
c.
d.
* If additional space is needed, please use the back of this sheet.
B-3
-------
4. For the product(s) listed in Item 3, please state the year span during
which they were manufactured and the type(s) or grade(s) produced.
Years Produced
Product From To Type(s) or Grade(s)
5. Does your company export or import TGE or MG?
Specify imported products: .
Specify exported products: _______________
6. What type(s) of container(s) is(are) utilized for the transportation
of the finished product to the customer? What is principal method of
transport (rail, truck, etc.)?
7(a) Have chemical analyses been made on any of your by-products* or
process waste materials to determine the presence of TGE or MG?
TGE MC
yes no yes no
* By-products are also referred to as co-products.
B-4
-------
(b) If the above answer is "no," then based on your experience, do you
think that any TCE or MC may be contained in any of your by-products*
or process waste materials?
TCE MC
yes no yes no
8. Where would the TCE or MC occur?
a. In by-product(s)? b. In process waste materials?
TCE: TCE:
yes no yes no
MC: MC:
yes no yes no
9. For each "yes" answer to any category in Questions 7 and 8, please
identify compound(s) by name(s) and form(s) (i.e., solid, liquid or
gas). Also, please indicate the plant location(s) for each.
Compound(s) Form(s) Plant Location(s)
If additional space is required, please use the back of this sheet.
* By-products are also referred to as co-products.
B-5
-------
10» For each item listed in Question 9, please indicate the approximate
concentration level of each compound(s) and where the material appears
(i.e., by-product, or process waste material). If any compound appears
in two or more instances, please distinguish between the entries.
Compound(s) Concentration Level Where Material Occurs
11. To the extent possible, within the constraints of proprietary considera-
tions, for each product identified in Item 3, please describe briefly
the production process used and the current utilization of production
capacity.
Process Description (e.g., Approximate Current Utiliza-
raw materials and major re- tion of Plant Production
Product actions, or U»S» Patent Number) Capacity %
B-6
-------
12(a) What are the emission levels in air, water, and soil near plant site?
If no analyses are routinely performed, please identify your answers
with either "measured" or "best estimate" under remarks:
C one ent rat i on Uni t s Remarks
Air _________
Water (effluent) ...-,-. _____ _____________________
Soil (e.g., landfill) , .
(b) What waste disposal techniques do you use? (Please identify correspond-
ing production process).
Please describe techniques briefly and also comment on their effective-
ness in preventing the release into the environment (e.g., landfill,
waste pond, deep-well injection, incineration). If incineration is
used, please indicate operating conditions such as temperature, reten-
tion time, gas scrubbing procedure, etc.
13. To the extent possible within the constraints of proprietary considera-
tions, please indicate in as much detail as possible, the end uses of
the TCE and MC manufactured by your company.
B-7
-------
14. To your knowledge, in what industry or industries would TCE or MC
occur as a manufacturing process by-product or process waste material?
Any assistance you can provide in this area would be sincerely appre-
ciated*
B-8
-------
This written questionnaire was submitted during 1976 to the six manu-
facturers of trichloroethylene and methyl chloroform. A discussion and sum-
mary of the replies to this written inquiry are presented in the following
paragraphs.
1. Vulcan Material Companyt Vulcan produces methyl chloroform and
perchloroethylene, but does not manufacture trichloroethylene. No methyl
chloroform occurs in by-products. The waste materials are used as feed ma-
terial for a perchloroethylene plant. Water effluent and vented air contain
methyl chloroform. The perchloroethylene plant wastes, containing hexachloro-
benzene and hexachlorobutadiene, are either land-filled or incinerated.
Vulcan estimated that the soil (e.g., landfill) near their plant sites con-
tained no methyl chloroform.
2. Diamond Shamrock Chemical Company; Diamond produces trichloro-
ethylene and perchloroethylene but no methyl chloroform. Trichloroethylene
and methyl chloroform are reported to be present at < 50 to 100 ppm in the
by-products (hydrogen chloride and perchloroethylene) but not in the process
waste materials. The trichloroethylene contains < 50 ppm of methyl chloro-
form. The air near the plant site is reported to contain < 50 ppm of tri-
chloroethylene and < 10 ppm of methyl chloroform. The water effluent has
been analyzed to show < 1.0 ppm trichloroethylene and < 0.1 ppm of methyl
chloroform. Diamond estimated that the solvent concentration in the soil
was very low.
3. PPG Industries, Inc.; PPG manufactures trichloroethylene, methyl
chloroform, and perchloroethylene. The company reported that neither tri-
chloroethylene nor methyl chloroform occur in by-products, but that they
are present in process waste materials. Trichloroethylene is present in
still bottoms at a concentration of < 0.1% and in aqueous effluent (ppm).
Methyl chloroform is contained in still bottoms at < 0.17» and in aqueous
effluent (ppm). The still bottom waste is disposed of in an incinerator.
The other three companies contacted did not respond to this written
inquiry, even after repeated follow-up requests.
B-9
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APPENDIX C
STATISTICAL ANALYSIS OF NCI CARCINPJgNESIS DATA
CARCINOGENESIS BIOASSAYS OF TRICHLOROETHYLENE,
PERCHLOROETHYLENE. AND METHYL CHLOROFORM
C-l
-------
The following data are statistical tables from the National Cancer In-
stitute Carcinogenesis Bioassay reports for trichloroethylene, methyl chloro-
form, and perchloroethylene. Copies of the final NCI-approved reports are
available, but tests are being repeated. High levels of deaths in some groups
have made statistical statements difficult, according to the draft report.
C-2
-------
Table XXIVa. Exact Statistical Tests Comparing Proportions of Animals (Not
Adjusted for Age) with Observed Hepatocellular Carcinoma of the Liver
among Pooled Control and Trichloroethylene-Treated Rats
Comparison
Male Rats
Female Rats
Veh. Low High Exact
Cont. Dose Dose Test
r/n r/n r/n P
Veh. Low High Exact
Cont. Dose Dose Test
r/n r/n r/n P
Dose-Response
Veh. Control
Dosed vs.
Veh. Control
Low Dose vs.
Veh. Control
High Dose vs.
Veh. Control
High Dose vs.
Low Dose
1/99 0/50 0/50
1% 0% 0% 1.000
1/99 0/100
1% 0% 1.000
1/99 0/50
1% 0% 1.000
1/99 0/50
1% 0% 1.000
0/50 0/50
0% 0% 1.000
0/98 0/48 0/50
0% 0% 0% 1.000
0/98
0%
0/98
0/98 0/48
0% 0%
0/98
0%
I 1.000
1.000
0/50
0% 1.000
0/48 0/50
0% 0% 1.000
Comparison
Chi-square df
Chi-square df
Among High Dose.
Low Dose and
Vehicle Control
Dose-Response Trend
Vehicle Control
Deviation from Trend
Vehicle Control
1.02 2 1.000
0.83 1 0.749
0.19 1 1.000
1.00 2 1.000
1.00 1 1.000
0.00 1 1.000
r = Number of animals with observed mark.
n = Number of animals examined histopathologically for the mark.
P = Exact probability of exceeding or equaling observed test
statistic under null hypothesis.
df = Degrees of freedom.
C-3
-------
Table XXVII. Exact Statistical Tests Comparing Proportions of Animals (Not
Adjusted for Age) with Observed Hepatocellular Carcinoma or Neoplastic
Nodule of the Liver among Pooled Control and Trichloroethylene-Treated Mice
Male Mice
Untr. Veh. Low High Exact
Cont. Cont. Dose Dose Test
Comparison r/n r/n r/n r/n P
Dose-Response 5/77 26/50 31/48
Veh. Control 6% 52% 65% 0.000
Dose-Response 5/70 26/50 31/48
Untr. Control 7% 52% 65% 0.000
Dosed vs. 5/77 57/98
Veh. Control 6% 58% 0.000
Dosed vs. 5/70 57/98
Untr. Control 7% 58% 0.000
Low Dose vs. 5/77 26/50
Veh. Control 6% 52% 0.000
Low Dose vs. 5/70 26/50
Untr. Control 7% 52% 0.000
High Dose vs. 5/77 31/48
Veh. Control 6% 65% 0.000
High Dose vs. 5/70 31/48
Untr. Control 7% 65% 0.000
High Dose vs. 26/50 31/48
Low Dose 52% 65% 0.145
Veh. Con. vs. 5/70 5/77
Untr. Control 7% 6% 0.686
Female Mice
Untr. Veh. Low High Exact
Cont. Cont. Dose Dose Test
r/n r/n r/n r/n P
1/80 4/50 11/47
1% 8% 23% 0.000
2/76 4/50 11/47
3% 8% 23% 0.000
1/80 15/97
1% 15% 0.001
2/76 15/97
3% 15% 0.004
1/80 4/50
1% 8% 0.072
2/76 4/50
3% 8% 0.169
1/80 11/47
1% 23% 0.000
2/76 11/47
3% 23% 0.000
4/50 11/47
8% 23% 0.034
2/76 1/80
3% 1% 0.887
(continued)
C-4
-------
Table XXVII. Exact Statistical Tests Comparing Proportions of Animals (Not
Adjusted for Age) with Observed Hepatocellular Carcinoma or Neoplastic
Nodule of the Liver among Pooled Control and Trichloroethylene-Treated Mice
(continued)
Comparison Chi-square . df P Chi-square df P
Among High Dose,
Low Dose and
Vehicle Control 52.02 2 0.000 17.76 2 0.000
Dose-Response Trend
Vehicle Control 47.85 1 0.000 16.96 1 0.000
Deviation from Trend
Vehicle Control 4.16 1 0.041 0.80 1 0.367
Among High Dose,
Low Dose and
Untreated Control 47.31 2 0.000 14.41 2 0.001
Dose-Response Trend
Untreated Control 43.43 1 0.000 13.41 1 0.000
Deviation from Trend
Untreated Control 3.89 1 0.049 0.99 1 0.344
r = Number of animals with observed mark.
n = Number of animals examined histopathologically for the mark.
P = Exact probability of exceeding or equaling observed test
statistic under null hypothesis.
df = Degrees of freedom.
See section on statistical methodology for explanation of tests.
C-5
-------
TAhl.E 3
ANALYSES OK Tllli INCIDENCE <>l' i'KIMAKY TUMORS AT
SPECIFIC SITES JN MALE RATS TREATED WITH TETKACIILOKOETIIYI.KNE'1
n
I
o\
TOI'OliltAI'IIY: Mold-Ill II.OCY
All Sites: llbmanglosarcoma''
P Values0
Kelatlve Ri.sk(lint reated Control)*1
Lower Limit
Upper Limit
Relative Rlt;k(Veh icle Control) d
Lower Limit
Upper Limit
Weeks to First Observed Tumor
Pituitary: Chromophobe Adenoma or
Carcinoma11
P Valued
Departure from Linear Trend
Relative KlskUlntreated Control)*1
Lower Limit
Upper Limit
Relative Rlsk(Vchlcle Control)*1
LoDer Limit
Upper Limit
Week:; Lt> Fi.rut Observed Tuiiior
Pituitary: Chromophobe Adenuiaa '
P Values0
Kelative Kliik(l)nt real ed Control)*1
• Lower Limit
llppi-i l.lmli
Relative Rlsk(Vehlcle Control)*1
l.ouer Limit
Upper Limit
Weeks to l'ir;:t Observed Tumor
a
Number of luitiiir-hfai* 1 n/. - an im.i 1 :;/nuu>her
c
UIJTKEATlill
CONTROL
2/20(0.10)
N.S.
—
93
4/19(0.21)
P - 0.002(N)
V = 0.036
— -
93
3/19(0.16)
P - 0.008(N)
93
i - i -t i
ot :ut Jiaa 1 ti oK\t*.\h
VI-'IIICLK LOW
CUIITKOI. IMISIC
1/20(0.05) 2/50(0.04)
N.S. N.S.
0.400
• 0.032
5.277
0.800
0.045
46.273
70 . 67
0/20(0.00) 1/49(0.02)
N.S. P = 0.019*(N)
0.097
0.002
— o.yl3
Infinite
0.023
Infinite
112
0/20(0.00) 1/49(0.02)
N.S. N.S.
O.I'J'J
0.003
. 1.1)17
Infinite
0.023
Infinite
112
1 *l / 11 f f / 1- • 1 \t*
iinti JH j '^t»/ "tJ uy ii**""!!^ «
:U al iiin: (proportion) .
•
i-il.il'ltvr l<*\i.il f S\r 1~ lilt f' ,-^r-}\r •, it — fi i-m i t rt ,* f* I
MICH
IMISE
1/50(0.02)
N.S.
0.200
0 . 007
3.681
0.400
0.005
30.802
103
0/44(0.00)
P « 0.007*(N)
0.000
0.000
0.459
'
___
0/44(0.00)
P " 0.024*(N)
0.000
0.000
0.709 .
i
—
r ii c r lT»»ir
dose-related trend in proportions when it is below 0.05, otherwise M.S. - not til^nIf leant. Departure from
linear trend i?; nul >-d when it i:> below O.05 lor any comparison. beneath the doije ftroup Incidence Is the
ptoli.-ihl I i cy level lor lUe l-'i:iher enact (conditional) lest fur the coiupuirlsun of that dose (-ruup with the
lei i .ichloroet hylene uni ii-ated control jji oup (*) and the vehicle control i;roup (**) when cither Is below
0.05. otherwise tl.S. - r.ot s i|;n 11 'icaiit .
(M) l.e.is incidence in the do.se j;roup(:;) than In a control i;roup re:iultu In a negative Indication.
Relative Ri.'ik of the treated t'.i'oup ver.su.£i the control j^ronp Is shown along with tin: lower and upper limit
of the '}'->/. coiiMdeiice lnterv.il lor that Relative Risk.
-------
TAI1LI-: 4
ANALYSES 01' Till: 1NCIDKNCK OK PIUMARY TUMORS AT
Sl'liClKIC SlTi:s IN 1-h'MALE RATS TKliATliO WITH TETRACHLOKOIiTIIYLtNli"
TOI'OCRAI'IIY : MORIMIOI.or.Y
Mammary Gland: Mbroadenoma
P Values;0
Relative Risk(Untreateil Control)''
Lower Limit
Upper Limit
kelative Kisk(VchiO I.e Control)
l.'iv/i-r Limit
Upper Limit
Weeks In Kirst Observed Tumor
All Sllet. : lleu.iiig I i>::.i rcoiua1'
1- Values0
Relative l( IskOInt re.ited Control)11 •
Lower Limit
Upper l.lnit
Relative Risk(Vehicle Co tor any coinpiiri son. Ueneatb the doae group Incidence is 'the
probability leve.l lor tbe Usher exact (conditional) test for the comparison of that dose group with the
Cttr.ichliirui-ihyli-iif mil realed eontrol n1"""!' (*) ai>tl tlllj vehicle control i;lo"|) (**) when either is below
0.05. otherwise N.S. - not significant.
(N) Less In:: Ideiice in the .lose |;roup(s) than In a control group results in a negative indication.
Relative Risk of I he treated Kr""P versus the control group Is shown along wilh the lower and upper limit
of the 05Z conlidence interval for that Relative Risk.
-------
TABLE 7
ANALYSES OF THE INCIDENCE OF HEPATOCELLULAR CARCINOMA
IN MALE MICE TREATED WITH TETRACHLOROETHYLENEa
TOPOGRAPHY: . MORPHOLOGY
Liver: llepatocellular Carcinoma
I' Values0
Departure from Linear Trend
Relative Risk(Pooled Untreated Control)
Lower Limit
Upper Limit
nui|> incidence is the probability level for the Fisher exact
(conditional) test for the comparison of that dose group with the pooled untreated control group (*) and the pooled
vehicle control group («•*) when either is below 0.05.
Relative Risk of the treated group versus the control group is shown along with the lower and upper limit of 95%
confidence interval for that Relative Risk.
-------
TABLE 8
ANALYSES OF Till' INCIDENCE OF HEPATOCELLULAR CARCINOMA
IN FEMALE MICE TREATED WITH TCTRACHLOROETHYLENE3
I
VD
TOPOGRAPHY: MORPHOLOGY
Liver: Hepatocellular Carcinoma
P Values0
Departure from Linear Trend
Relative Risk(Pooled Untreated Control)
Lower Limit
Upper Limit
Relative. Risk(Pooled Vehicle Control)
. Lower Limit
Upper Limit
Weeks to First Observed Tumor
POOLED
UNTREATED
CONTROL
4/97(0.04)
P < 0.001
P = 0.011
POOLED
VEHICLE
CONTROL
2/99(0.02)
P < 0.001
P = 0.006
•
LOW
DOSE
19/48(0.40)
P < 0.001*
P < 0.001**
9.599
3.425
35.988
19.594
5.024
164.707
41
HIGH
DOSE
19/43(0.40)
P < 0.001*
P < 0.001**
9.599
3.425
35.988
19.594
5.024
164.707
50
Dosed groups received time-weighted average doses of 386 and 772 mg/kg by gavage.
b .
Number of tumor-bearing animals/number of animals examined at site (proportion).
"Beneath the incidence of each of the controls is the probability level for the Cochran-Armitage test for dose-related
trend in proportions when it is below 0.05, otherwise N.S. - not significant. Departure from linear trend is noted when
it is below 0.05 for any comparison. Beneath the dose group incidence is the probability level for the Fisher exact
(conditional) test for the comparison of that dose group with the pooled untreated control group (*) and the pooled
vehicle control group (**) when either is below 0.05.
Relative Risk of the treated group versus the control group is shown along with the lower and upper limit of the 952
confidence interval for that Relative Risk. •
-------
Table 5. Statistical Analyses of the Incidence of Tumors at Specific Sites in Matched Controls and
1,1,1-Trichloroethane-Treated Rats
o
i
Topography: Morphology
Total Animals: All Tumors ^
P Values0
Weeks to First Observed Tumor
Pituitary: Chromophobe
Adenoma"
P Values0
Weeks to First Observed Tumor
Thyroid: Follicular-Cell
Adenoma or Carcinoma"
P Values0
Weeks to First Observed Tumor
Adrenal: Cortical
Adenoma"
P Values0
Weeks to First Observed Tumor
Matched
Control
3/20(15)
N.S.
72
0/20(0)
N.S.
— —
0/20(0)
N.S.
_ —
0/20
N.S.
MALE
Lowa
Dose
6/48(12)
N.S.
28
0/48(0)
N.S.
___
0/48(0)
N.S.
_ —
3/49(6)
N.S.
28
High3
Dose
6/50(13)
N.S.
50
0/48(0)
N.S.
_,_
0/50(0)
N.S.
1/50(2)
N.S.
106
Matched
Control
7/20(35)
N.S.
58
3/20(15)
N.S.
84
2/20(10)
N.S.
103
2/19(11)
N.S.
85
FEMALE
Low3
Dose
7/50(14)
N.S.
64
2/48(4)
N.S.
71
0/50(0)
N.S.
— —
1/48(2)
N.S.
99
High3
Dose
9/50(18)
N.S.
56
1/48(2)
N.S.
90
1/49(2)
N.S.
97
2/49(4)
N.S.
106
3Low- and high-dose groups received 1,1,1-trichloroethane in corn oil by gavage five times per week in doses
of 750 and 1,500 mg/kg body weight respectively.
"Number of tumor-bearing animals/number of animals examined at site (percent) .
°Beneath the incidence of the matched controls is the probability level for the Armitage test for positive
dose-related trend in proportions when it is below 0.10, otherwise N.S. - not significant. Beneath the dosed
group incidence is the probability level for the Fisher exact (conditional) test for comparison of that dosed
group with the matched control group when it is below 0.10( otherwise N.S. - not significant.
-------
Table 8. Statistical Analyses of the Incidence of Tumors at Specific Sites in Matched Controls and
1,1,1-Trichloroethane-Treated Mice
Topography: Morphology
Total Animal: AH Tumors'3
P Valuesc
Weeks to First Observed Tumor
Hematopoiet ic System:
Malignant Lymphoma"
o P Valuesc
i
fW
l_l
Weeks to First Observed Tumor
Liver: Hepatocellular
Adenoma or Carcinoma,
or Neoplastic Nodule"
P Valuesc
Weeks to First Observed Tumor
Matched
Control
2/15(13)
N.S.
80
2/15(13)
N.S.
80
0/15(0)
P = 0-035
—
MALE
Lowa
Dose
2/47(4)
N.S.
89
0/47(0)
N.S.
—
0/47(0)
N.S.
—
High3
Dose
6/49(12)
N.S.
50
2/49(4)
N.S.
64
4/49(8)
N.S.
—
Matched
Control
4/18(22)
N.S.
80
3/18(17)
N.S.
80
0/18(0)
N.S.
—
FEMALE
Low3
Dose
2/48(5)
N.S.
54
1/48(2)
N.S
90
0/48(0)
N.S.
—
High3
Dose
3/50(6)
N.S.
26
0/50(0)
N.S.
—
0/50(0)
N.S.
—
aLow- and high-dose groups received 1,1,l-trichloroethane in corn oil by gavage five times per week in time-
weighted average doses of 2,807 and 5,615 mg/kg body weight, respectively.
"Number of tumor-bearing animals/number of animals examined at site (percent).
cBeneath the matched controls incidence is the probability level for the Armitage test for positive
dose-related trend in proportions when it is below 0.10, otherwise N.S. - not significant.
Beneath the dose group incidence is the probability level for the Fisher exact test for comparison of that
dosed group with the control group when it is below 0.10, otherwise N.S. - not significant.
-------
SUBJECT INDEX
absorption, human 5(8-9, 102-103,
176 )£/
adsorption, carbon 7(5-6, 9-10)
air concentrations
manufacturing sites 7(3, 5)
user sites 7(5, 10)
U.S. sites 7(10, 14)
non-U.S. sites 7(14, 17)
stratospheric 7(17-18)
allergic effects 5(55, 136, 147,
210-211)
alcohols, as substitutes 4(14-16)
alkaline cleaners 4(21-24)
aquatic plants
toxicity to 6(26)
accumulation 6(26-27)
atmospheric emissions, total 3(101-
102)
bioaccumulation 5(63, 136, 205);
6(32-33)
bioassay, NCI 5(60-63, 149-151, 214,
216, 219)
birds, toxicity to 6(28, 30)
carcinogenicity 5(60-63, 149-151,
214-219)
cats, subacute effects on 5(53, 185,
196, 200)
chemical properties 3(5-18)
trichloroethylene 3(12-14)
methyl chloroform 3(13-15)
perchloroethylene 3(15-17)
consumption, by end use 3(19-21,
24, 26, 28, 30, 91)
metal cleaning 3(61-71)
dry cleaning 3(72-74)
miscellaneous 3(74, 77-78); 5(228)
future U.S. 3(79-81, 82-85)
contamination
drinking water 7(29-31)
groundwater 7(3 0-33)
degradation, atmospheric
tropospheric 6(4-11)
stratospheric 6(13-15)
degradation/biotransformation
5(13, 15-19, 106-107, 177)
degradation, hydrolytic 6(15-18)
dogs, effects on 5(49, 130)
acute exposure 5(200-201)
subacute exposure 5(53, 131,
201)
dry cleaning industry
consumption by state 3(74-76)
solvent losses 3(97,.99, 100);
9(12, 14-26)
emission reduction from 9(26-28)
enzymes, effect on 5(31-32, 110-
113, 121, 124, 186-188, 221)
epidemiology, human 5(65, 159-163,
226-228)
excretion 5(19-26, 108-110, 177-
185)
exports, U.S. 3(21, 23, 26-27, 28,
32, 81, 83, 85, 92)
exposure
aquatic species 6(27-29)
plants 6(26-27)
exposure, human
calculated levels 5(7, 102-104,
176, 177); 7(35, 37-46)
occupational 5(7, 65, 157, 226-
227)
accidental 5(67-69, 159, 228)
fish
toxicity to 5(51, 200); 6(20-24)
accumulation 6(23, 25-26)
fluorocarbons
F-ll 4(30)
F-113 4(16, 17-19, 30)
food, levels in 7(35-36)
greenhouse effect 6(20)
aj Each section of this report is numbered separately. The number outside
the parentheses designates the section number, while those inside desig-
nate the specific pages.
SI-1
-------
guinea pigs, effects on
acute 5(50, 130)
subacute 5(52, 130, 201)
half-life
biological 5(19-20, 104-105, 177-
178)
tropospheric 6(11-12)
heart, effects on 5(40-41, 118, 151,
220)
histology 5(133, 149)
hydrocarbons, as substitutes 4(11-
14, 17, 28)
hydrolysis 3(13, 16); 6(15-18)
imports, U.S. 3(21, 22, 26, 28, 31,
81, 83, 85, 91)
incineration 9(30-33)
ketones, as substitutes 4(14, 17)
kidney, effects on 5(38-39, 122,
195)
labels, container 9(34, 36-38)
liver, effects on 5(31, 36-37, 121-
123, 193-194)
lungs, effect on 5(39-40, 124-125,
188)
metabolism 5(13-18, 106-108, 177,
220)
metal cleaning
solvents in 3(61-71)
solvent emission 3(92-99); 9(3-5)
control systems 9(5-13)
methylene chloride 4(15-16, 19-21)
mice, effects on
acute 5(47-48, 131, 198-199)
carcinogenic 5(60, 214)
chronic 5(60, 131, 205)
subacute 5(51, 131, 196-197)
monkeys, subacute effects 5(54, 131)
mutagenicity 5(57-59, 148, 213-214)
natural sources 3(85); 6(3)
options, regulatory 11(5-11)
phosgene 3(12-14, 16)
photolytic reactions 3(15)
physical properties 3(7-9)
production, methyl chloroform
from vinyl chloride 3(39-41, 88)
from vinylidene chloride 3(42-43,
88-89)
from ethane 3(43-44, 89)
SI-2
sites 3(34)
quantities, U.S. 3(25, 48, 51,
53, 58)
future 3(82 )
alternatives 4(4-5, 7)
production, perchloroethylene
from ethylene dichloride 3(45,
90)
from hydrocarbons 3(45-46, 89)
from acetylene 3(46-47, 90)
sites 3(35)
quantities, U.S. 3(29, 49, 51,
53, 54, 57-60)
future 3(84)
alternatives 4(5-6, 8)
production, trichloroethylene
from ethylene dichloride 3(33,
36-37, 86)
from acetylene 3(37-39, 86-87)
from ethylene 3(54-56)
sites 3(32)
quantities, U.S. 3(20, 48, 50,
52, 54, 57)
future 3(79)
alternatives 4(3-4, 7)
rabbits, effects on
acute 5(50, 131, 200)
chronic 5(55)
subacute 5(53, 132, 200)
rats, effects on
acute 5(48, 131, 199)
chronic 5(54, 60)
subacute 5(51, 132, 199)
regulations, federal
Consumer Product Safety Commis-
sion 8(9)
Department of Defense 8(9)
Department of Transportation
8(21)
Environmental Protection Agency
8(3-7)
Food and Drug Administration
8(8)
General Services Administration
8(9-11)
regulations, state and local
8(9-15)
-------
sediment
reactions in 6(18)
concentration 7(34)
sensitization 5(55, 151, 210, 220)
sewage treatment, effects on
6(19-20)
soil
reactions in 6(18)
concentrations 7(34)
solvent
interchangeability 4(24-27)
reclamation 9(28-30)
stabilizers 3(17-18); 5(64-65, 155)
toxicity of 5(224)
standards
OSHA 8(15-17)
NIOSH 8(16, 17-18)
ACGIH 8(18, 19)
ANSI 8(18, 20)
foreign countries 8(20-21)
Stoddard solvent 4(11-14)
substitutes
cold cleaning 4(9-16)
vapor degreasing 4(16-21)
synergistic effects 5(63, 151, 221)
synonyms 3(6, 10-12)
teratogenicity 5(56, 147, 211)
terrestrial plants, toxicity 6(28,
31)
trade names 3(6, 10-12)
transport, human 5(9, 104-105,
176-179)
troposphere
reactions in 6(4-11)
residence times 6(11-12)
uptake, human 5(7-8, 125-130, 176)
water
volatilization from 6(15-18)
drinking water levels 7(18-21)
marine levels 7(26-27)
nondrinking water levels 7(21-26)
wastewater levels 7(27-29)
SI-3
-------
TECHNICAL REPORT DATA
(Please read Inumctionson the revene before completing)
. REPORT NO.
EPA 560/11-79-009
3. RECIPIENT'S ACCESSION-NO.
A. TITLE AND SUBTITLE
An Assessment of the Need for Limitations on Tri-
chloroethylene, Methyl Chloroform, and Perchloroethylene
S. REPORT DATE
July 1979
6. PERFORMING ORGANIZATION CODE
7. AUTHOR(S)
Thomas W. Lapp, Betty L. Herndon, Charles E. Murama,
Arthur D. Tippit, and Robert P. Reisdorf
8. PERFORMING ORGANIZATION REPORT NO.
9. PERFORMING ORGANIZATION NAME AND ADDRESS
Midwest Research Institute
425 Volker Boulevard
Kansas City, Missouri 64110
10. PROGRAM ELEMENT NO.
11. CONTRACT/GRANT NO.
68-01-4121
12. SPONSORING AGENCY NAME AND ADDRESS
Environmental Protection Agency
Office of Toxic Substances
Washington, D.C. 20460
13. TYPE OF REPORT AND PERIOD COVERED
Final
14. SPONSORING AGENCY CODE
IS. SUPPLEMENTARY NOTES
Dr. Stanley C. Mazaleski, Project Officer
16. ABSTRACT
Information on the manufacture, use, distribution, health impacts, ecological
effects, monitoring data, and current regulations and standards for trichloro-
ethylene, methyl chloroform(1,1,1-trichloroethane), and perchloroethylene (tetra-
chloroethylene) has been assessed. Emission control and solvent recovery techn-
niques were evaluated, population exposure levels were calculated, and technical
alternatives for the use of the compounds were identified and assessed. Estimated
production for the three compounds was 1,644 million pounds in 1978. All three
compounds are globally distributed in the troposphere (primarily as a result of
emissions by users). Methyl chloroform has been detected in the stratosphere and
has been postulated to participate in the ozone depletion process. An extended
review is presented of the health effects resulting from exposure to the compounds.
Results of studies of acute and chronic exposure, absorption, metabolism, organ
effects, mutagenicity, carcinogenicity, teratogenicity, epidemiology, and many
other effects are discussed. Environmental fate and effects of each compound
are summarized and evaluated. Published monitoring data are presented and
potential population exposure levels have been calculated. Based on the findings
of Che study, several regulatory options are presented for the control of these
compounds. One of the principal options was removal of methyl chloroform from
the category of air quality exempt solvents and placement in the restricted
category with trichloroethylene.
17.
KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS
b.IDENTIFIERS/OPEN ENDED TERMS
c. COSATi Field/Group
Trichloroethylene
Methyl chloroform
1,1,1-Trichloroethane
Perchloroethylene
Tetrachloroethylene
Air pollution control
Industrial wastes
Transport properties
Organic compounds,
chlorinated
Toxicology
Epidemiology
Environmental survey
Water pollution
13. DISTRIBUTION STATEMENT
Unlimited distribution
19. SECURITY CLASS (This Reporr/
Unclassified
21. NO. OP PAGES
642
20. SECURITY CLASS (This page)
Unclassified
22. PRICE
EPA Form 2220-1 (R»v. 4-77) PREVIOUS EDITION is OBSOLETE
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