oEPA
United States
Environmental Protection
Agency
Off ice of Water
Regulations and Standards (WH-553)
Washington DC 20460
October 1980
EPA-440/4-81-021
Water
An Exposure
and Risk Assessment
for Pentachlorophenol
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DISCLAIMER
This is a contractor's final report, which has been reviewed by the Monitoring and Data Support
Division, U.S. EPA. The contents do not 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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REPORT DOCUMENTATION 1- «PORT NO. 2,
PAGE EPA-440/4-81-021
4. Tttl* and SuMttlo
An Exposure and Risk Assessment for Pentachlorophenol
1
'-. AuthoKa) Scow, K. ; Coyer, M. ; Payne, E. ; Perwak, J.; Thomas, R. ;
Wallace, D.; Walker, P.; and Wood, M.
. j. Performing Organization Nama and Addraaa
' Arthur D. Little, Inc.
20 Acorn Park
Cambridge, MA 02140
2. Sponsoring Organization Nama and Addraaa
| Monitoring and Data Support Division
Office of Water Regulations and Standards
U.S. Environmental Protection Agency
j Washington. D.C. 20460
3. Raclpianft Accattlon No.
S. Rapeit Oat*
October 1980
a.
8. Performing Organisation Raet Me.
10. Proiact/Taak/Work Unit No.
Task No. 21
U. ContracMQ or Snnt(O) No.
(0 68-01-3857
(0
U. Typa of Raport A Parted Covarod
Final
it.
1 IS. Supplementary Notas
Extensive Bibliographies
L Abatract (Umtt; 200 woMa)
| This report assesses the risk of exposure to pentachlorophenol. This study is part of
a program to identify the sources of and evaluate exposure to 129 priority pollutants.
The analysis is based on available information from government, industry, and
I technical publications assembled in October 1980a
The assessment includes an identification of releases to the environment during
production, use, or disposal of the substance. In addition, the fate of pentachloro-
phfinol in the environment is considered; ambient levels to which various populations
of humans and aquatic life are exposed are reported. Exposure levels are estimated
and available data on toxicity are presented and interpreted. Information concerning
| all of these topics is combined in an assessment of the risks of exposure to penta-
chlorophenol for various subpopulations.
I
t
Exposure
Risk
Water Pollution
Air Pollution
b. Idantmon/Opan Endod Torma
Pollutant Pathways
Risk Assessment
e. COSATl natd/Gioup Q6F 06T
Effluents
Waste Disposal
Food Contamination
Toxic Diseases
Pentachlorophenol
Ik. Availability SUtamant
Release to public
19. Security data (Thla Raport)
Unclassified
Sacurlty Claia (Thla Pago)
scci f led
21. No. of Pagaa
195
22. Prtea
S17.50.
&M ANSI-Z39.in
Sa* Inttntetlent on ffavaraa
OPTIONAL FORM 272 (4-77)
(rormarty NTIS-3S)
Oapartmant of Cofiunareo
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EPA-440/4-81-021
October 1980
AN EXPOSURE AND RISK ASSESSMENT
FOR PENTACHLOROPHENOL
by
Kate Scow
Muriel Cover, Edmund Payne, Joanne Perwak
Richard Thomas, Douglas Wallace, Pamela Walker, and Melba Wood
Arthur D. Little, Inc.
and
Lynn Delpire
U.S. Environmental Protection,Agency
EPA Contract 68-01-3857
Task No. 21
Monitoring and Data Support Division (Wh-553)
Office of Water Regulations and Standards
Washington, D.C. 20460
OFFICE OF WATER REGULATIONS AND STANDARDS
OFFICE OF WATER AND WASTE MANAGEMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. 20460
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FOREWORD
Effective regulatory action for toxic chemicals requires an
understanding of the human and environmental risks associated with the
manufacture, use, and disposal of the chemical. Assessment of risk
requires a scientific judgment about the probability of harm to the
environment resulting from known or potential environmental concentra-
tions. The risk assessment process Integrates health effects data
(e.g., carcinogenicity, teratogeniclty) with information on exposure.
The components of exposure include an evaluation of the sources of the
chemical, exposure pathways, ambient levels, and an identification of
exposed populations Including humans and aquatic life.
This assessment was performed as part of a program to determine
the environmental risks associated with current use and disposal
patterns for 65 chemicals and classes of chemicals (expanded to 129
"priority pollutants") named in the 1977 Clean Water Act. It includes
an assessment of risk for humans and aquatic life and is intended to
serve as a technical basis for developing the most appropriate and
effective strategy for mitigating these risks.
This document is a contractors' final report. It has been
extensively reviewed by the individual contractors ?.nd by the EPA at
several stages of completion. Each chapter of the draft was reviewed
by members of the authoring contractor's senior technical staff (e.g.,
toxicolqgists, environmental scientists) who had not previously been
directly involved in the work. These Individuals were selected by
management to be the technical peers of the chapter authors. The
chapters were comprehensively checked for uniformity in quality and
content by the contractor's editorial team, which also was responsible
for the production of the final report. The contractor's senior
project management subsequently reviewed the final report in its
entirety.
At EPA a senior staff member was responsible for guiding the
contractors, reviewing the manuscripts, and soliciting comments, where
appropriate, from related programs within EPA (e.g., Office of Toxic
Substances, Research and Development, Air Programs, Solid and
Hazardous Waste, etc.). A complete draft was summarized by the
assigned EPA staff member and reviewed for technical and policy
implications with the Office Director (formerly the Deputy Assistant
Administrator) of Water Regulations and Standards. Subsequent revi-
sions were Included in the final report.
Michael W. Slimak, Chief
Exposure Assessment Section
Monitoring & Data Support Division (WH-553)
Office of Water Regulations and Standards
ii
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TABLE OF CONTENTS
LIST OF FIGURES
LIST OF TABLES viii
I. EXECUTIVE SUMMARY 1
II. INTRODUCTION 9
III. MATERIALS BALANCE 11
A. Introduction and Methodology 11
B. Materials Balance 11
1. Production 15
2. Wood Preserving 18
3. Sodium Pentachlorophenate 23
4. Other Uses of Pentachlorophenol and Sodium PCP 23
a. Paints 23
b. Cooling Water Towers 23
c. Tanning 24
d. Textiles 25
e. Other Uses and Releases 25
5. Investigation of POTW's 26
IV. DISTRIBUTION OF PENTACHOLORPHENOL IN. THE ENVIRONMENT 33
A. Introduction 33
B. Monitoring Data 34
1. Introduction 34
2. Water and Sediment 34
3. Humans 41
4. Air 44
5. Food and Feed 44
6. Biota 44
7. Soil 50
8. Miscellaneous Media 50
C. Environmental Fate 50
1. Physicochemical Pathways 50
a. Introduction 50
b. Air 50
c. Water 54
d. Soil 63
e. Treated Wood 67
£. Conclusions 71
iii
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TABLE OF CONTENTS (continued)
2. Biological Pathways 73
a. Introduction 73
b. Freshwater Systems 73
c. Marine Fish 74
d. Terrestrial Organisms 74
e. Conclusions 77
Concentration Estimates 78
1. Introduction 78
2. Air Models . 79
a. Assumptions Used in Air Models 79
b. A't mo spheric Concentrations Due to Wood Treatment
Wastewater Evaporation 79
c. Atmospheric Concentration Due to Volatilization
from PGP-Treated Wood Products 80
d. Atmospheric Concentrations Due to Evaporation from
Cooling Towers 83
e. Atmospheric Concentrations Due to Open Burning of
PCP-Treated Wood .Products 83
f. Ground Level Concentrations in the Plume Downwind
of a Cooling Tower 85
g. Concentrations Downwind of a Wood Treatment Plant
Waste Water Evaporation Pond 89
h. Rainout 90
i. Conclusions 92
3. Water Models 93
a. Introduction 93
b. EXAMS Concentration Estimates 95
4. Summary of Concentration Estimates 100
V. HUMAN EFFECTS AND EXPOSURE 113
A. Effects on Humans 113
1. Introduction 113
2. Metabolism and Bioaccumulation 113
3. Animal Studies 115
a. Carcinogensis 115
b. Mutagensis 115
c. Reproductive and Fetotoxic Effects 116
d. Other Toxic Effects 118
4. Human Studies 120
5. Overview 121
B. Human Exposure 122
1. Introduction 122
2. Ingestion of Food 122
3. Ingestion of Drinking Water 123
iv
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TABLE OF CONTENTS (continued)
4. Inhalation of Air 123
5. Dermal Absorption 126
6. Summary 127
VI. NON-HUMAN EFFECTS AND EXPOSURE 135
A. Effects on Non-Human Organisms 135
1. Introduction 135
2. Freshwater Organisms 136
a. Chronic and Sublethal Levels 136
b. Acute Effects 137
3. Marine Organisms 139
a. Chronic Effects 139
b. Acute Effects 139
4. Other Studies 141
5. Factors Affecting the Toxicity of PCP 141
6. Effects on Terrestrial Biota . 143
a. Plants 143
b. Animals 143
7. Conclusions 144
B. Non-Human Exposure 144
1. Introduction 144
2. Monitoring Data . 144
3. EXAMS Model 145
4. Fish Kill Data 145
5. Exposure to Terrestrial Animals 148
6. Summary 148
VII. RISK CONSIDERATIONS 155
A. Methodology 155
B. Relative Exposure Effects and Risk Comparisons—Humans 155
C. Relative Exposure Effects and Risk Comparisons—Biota 161
APPENDIX A CONTAMINANTS IN PENTACHLOROPHENOL 165
APPENDIX B BIODEGRADATION PATHWAYS AND PRODUCTS 173
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LIST OF FIGURES
Figure
No. Page
1 Materials Balance of Pentachlorophenol 14
2 Production of Pentachlorophenol 16
3 Locations of PCP Manufacturing Plants and
Wood Treatment Plants 17
4 Regional Consumption of Pentachlorophenol by
Wood Preservation Plants (Estimated 1978) 19
3 Materials Treated With Pentachlorophenol
(Estimated 1978) . 21
6 U.S. Consumption of Wood Treated With Penta-
chlorophenol by Region (Estimated 1978) 22
7 Dioxin Formation from PCP Photodegradation 56
8 Proposed Photolysis Pathway for PCP 56
9 NaPCP Photodegradation Products 58
10 Relation of the Apparent Adsorption of PCP to
the pH of the Supernatant Liquid 65
11 PCP Degradation in Various Soils Under Flooded
and Upland Conditions 68
12 Relation Between Degradation Rate of PCP and
Organic Matter Content in Various Soils for
Different Incubation Periods 68
13 Ground Level Concentrations of Pentachlorophenol
in the Plume Downwind of a Cooling Tower—Two
. 'Source Heights 88
14 Ground Level Pentachlorophenol Concentrations in
the Plume Downwind of a Wood Treatment Plant
Evaporation Pond 91
A-l PCP Contaminants—Chlorines at Various
Positions on the Rings 166
B-l Gas Chromatogram of PCP Degradation Products
in Acid Fraction After 5 Days' Incubation in
Anjo Soil 176
vi
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LIST OF FIGURES (continued)
Figure
No. Page
B-2 Proposed Pathway of PCP Degradation in Soil 176
B-3 Suggested Metabolic Fate of PCP in Pseudomonas sp.
Isolated From Soil 178
vii
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LIST OF TABLES
Table
No. Page
1 Summary of U.S. Production and Consumption
of Pentachlorophenol, 1978 12
•2 Summary of Environmental Releases of
Pentachlorophenol (Estimated 1978) 13
3 Summary of FDA-Approved Uses of
Pentachlorophenol in Food-Associated
Products 27
4 PCP Concentrations in POTW Final
Effluent 29
5 Total Pentachlorophenol in Ambient Waters
(Remarked and Unremarked Data) 35
6 Mean Concentrations of PCP in Hater 36
7 PCP in Surface Waters of The Netherlands
(1976-1977) 37
8 Average Concentrations of Pentachlorophenol in
POTW's 38
9 PCP in Water at Various Locations 39
10 PCP in Water and Sediment of a Freshwater
Ecosystem 40
11 PCP Levels in Human Tissue and Urine 42
12 Pentachlorophenol in Human Urine (Florida) 43
13 PCP in Air at Oregon Wood Preserving Plants 45
14 PC? in Food and Feed . 46
15 PCP in Biota 47
16 PCP in Biota 47
17 PCP Concentrations in Fish Tissue as Reported in the
STORET Data Base 49
viii
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LIST OF TABLES (continued)
Table
No. Page
18 Chemical and Fate Properties of Pentachlorophenol 51
19 Results of PCP Irradiation in UV Light
(A>7290 nm) Under Two Conditions 32
20 Stability of NaPCP in Sunlight and Artificial
Light in pH 8 Phosphate Buffer 57
21 Solubility in Water and Henry's Law Constant
of Pentachlorophenol at Different pH Values 60
22 PCP Concentration in Water and Sediments 61
23 Concentration and Percent Removal of Hexachloro-
phene and Pentachlorophenol at Various Stages
Within the Corvallis, Oregon, Sewage Treatment
Plant 64
24 Correlation Coefficients Between Degradation Rate
of PCP and Properties of Soils 69
25 PCP Bioaccumulation in Freshwater Biota 75
26 PCP Bioaccumulation in Marine Biota '" 76
27 Usage Data for Pentachlorophenol by Wood Product 81
28 Dimensions and Production Volumes of PCP-Treated
Wood Products Used in Concentration Estimates 82
29 Estimated PCP Volatilization Loss by Wood
Product Category 83
30 .Typical Operating Values for an Industrial Forced-
Draft, Open, Recirculating-Type Cooling Tower 86
31 Dispersion Coefficients as a Function of Downwind
Distance 87
32 Dispersion Coefficients Used in the Calculations of
Concentrations Downwind of an Evaporation Pond
Releasing PCP into the Air . 90
33 Estimated Upper Limit PCP Daily Load in Industrial
Effluents 94
ix
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LIST OF TABLES (continued)
Table
No. Page
34 . Steady-State Concentrations in Various Generalized
Aquatic Systems Resulting From Continuous PCP
Discharge at 17.1 kg/day . 96
35 Steady-State Concentrations in Various Generalized
Aquatic Systems Resulting From Continuous PCP
Discharge at 0.25 kg/day 97
36 Steady-State Concentrations in Various Generalized
Aquatic Systems Resulting From Continuous PCP
Discharge at 0.07 kg/day 98
37 The Fate of PCP in Various Generalized Aquatic
Systems 99
38 Summary of Estimates of Regionally Distributed
PCP Concentrations in Environmental Media 101
39 Summary of Local-Scale Estimates of PCP Concentra-
tions in Environmental Media 102
•
40 Summary of Levels of Human Exposure to PCP via
Various Pathways 124
41 ' PCP Acute Toxicities (LC) to Freshwater Biota 138
42 PCP Acute Toxicities (LC$Q) to. Marine Biota 140
43 Water Concentrations Estimated by the EXAMS Model
For Different PCP Loading Rates 146
44 Data for PCP-Related Fish Kills, 1970-1976 147
45 . 'Exposure of Humans to PCP 156
46 Exposure Situations for PCP 159
47 Reported Levels of PCP Causing Adverse Effects in
Mammals 160
A-l Dioxin Contaminants Found in PCP 167
A-2 Dibenzofuran Contaminants in PCP 168
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LIST OF TABLES (continued)
Table
No. Page
A-3 Composition and Concentrations of Contaminants in
Pentachlorophenol Preparations 169
A-& Hexa- and Octachlorodibenzodioxin Concentrations in
Domestic PCP 170
B-l Degradation Products of Pentachlorophenol 174
B-2 Concentrations of Pentachlorophenol in 2.5% Malt
Extract Solution (As Culturing Medium) Before and
After 12-day Incubation with Various Fungi 180
xi
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ACKNOWLEDGEMENTS
The Arthur D. Little, Inc., Task Manager for this study was Kate Scow.
Other major contributors were Muriel Goyer (human effects), Jane Metzger
(editor), Joanne Perwak (human exposure), Edmund Payne (monitoring),
Kathy Saterson (biological fate), Richard Thomas (fate), Pamela Walker
(materials balance), Douglas Wallace (aquatic effects) and Melba Wood
(monitoring). Other contributors and reviewers included Diane Gilbert,
Caren Woodruff, Alfred Wechsler, George Harris, and Warren Lyman.
Pearl Hughes was responsible for the typing and preparation of the
final draft report.
The EPA Task Manager for this study was Lynn Delpire. Paul Gammer
of the Special Pesticide Review Division (OPTS) provided considerable
assistance in terms of information, guidance and review. Additional
help was provided by Michal Slimak, Bruno Maestri, George Keitt, and
Mark Segal.
xii
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SECTION I.
EXECUTIVE SUMMARY
INTRODUCTION
The Monitoring and Data Support Division, Office of Water Regulations
and Standards, U.S. Environmental Protection Agency is conducting an on-
going program to identify the sources of and evaluate the exposure to the
129 priority pollutants. This report assesses the exposure to and risk
associated with pentachlorophenol (PCP). It is based on the collection
and analysis of available data using quantitative models, whenever possible,
to estimate environmental concentrations and exposure of humans and other
biota, and to evaluate the overall risk. This assessment is focused on penta-
. chlorophenol and not specifically on its contaminants and degradation products.
MATERIALS BALANCE
Production; Pentachlorophenol and its salts (e.g., sodium pentachloro-
phenate) are commonly used as a fungicide in wood preservatives and, to a
lesser extent, as a bactericide and fungicide in cooling tower waters, rayon
and textile processing, tanning, paints , glues, and in other processes or
products.
Annual production of PCP is 21,300 metric tons (MT) in 1978 and occurs
at only three sites in the U.S.: in the states of Michigan, Kansas and
Washington. Release of the chemical to the environment during both
production and transport between production sites and areas of use is
apparently small, although not all transport practices have been examined.
Most of the PCP produced is consumed domestically; however a small amount
of PCP is exported.
Wood Preserving: Use of PCP is widely distributed throughout the U.S.
Since 80% to 90% of the amount produced is used in wood preserving processes,
a major portion of PCP mass is concentrated in the Southeast quadrant of
the U.S., in the Mid-Atlantic states and in the Northwest where the lumber
industry is located. Two principal wood preserving practices use penta-
chlorophenol—Boulton conditioning and steam conditioning—each associated
with different efficiency in treating waste water. Only one wood pre-
serving plant discharges PCP directly to water; others discharge to POTW's
or remove the PC? in sludge during waste water treatment. Approximately
14 MT of PCP sludge are generated annually by indirect dischargers in the
wood-preserving industry. The remaining plants, with no discharge, use
evaporative technology and generate an estimated 60 MT of PCP in solid
waste. The treated wood is widely distributed throughout the U.S. and
its total contribution of PCP release to the environment is not known.
As much as 344 MT may be released to air through volatilization from wood,
based on estimates.
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Other Uses: Other applications of PCP and its salt (that account
for the remaining 10-152 of PCP use) include application to cooling tower
water as a bactericide/fungicide (estimated to be 230 MT in 1978), use
as a preservative in paints (approximately 800 MT of NaPCP annually) in
tanning (approximately 15 MT annually), in textile processing (approxi-
mately 20 MT of NaPCP annually), and as a domestic herbicide (approximately
600 MT annually). Other uses are as a fungicide in mushroom cultivation,
as a disinfectant, and as a general preservative in numerous construction
materials, in the glue of food packaging, in petroleum industry products,
and' in photographic material. Additionally PCP has been detected in the
paint of imported toys and may be present in toys manufactured overseas
for domestic toy companies
Release of PCP to the Environment; The majority of PCP releases
•during production and use are to air ('620 MT) from wood preservers and
cooling towers and to land (890 MT) from wood preservers and domestic
use as a preserver and herbicide. Discharges to water, direct and
through POTW's,are expected to be small: 12 MT and 5 MT, respectively.
These estimates are based on available information; new data in certain
important areas are likely to alter the distribution. For example, based
on preliminary estimates, as much as 380 MT of PCF may be discharged into
water in POTW effluents; however, this number is associated with a wide
margin of error.
DISTRIBUTION OF PENTACHLOROPHENOL IN THE ENVIRONMENT
The analysis of the distribution of PCP in the environment is comprised
of four parts: (1) monitoring data for PCP in the environmental media,
(2) physico-chemical processes determining PCP concentrations in each
environmental compartment, (3) important biological pathways and (4) esti-
mations of PCP concentrations in air and water.
Monitoring Data; Data from monitoring of pentachlorophenol levels
in various environmental media are too limited to indicate typical U.S.
ambient concentrations. The published data suggest concentrations of
0.01 ug/1 to 147 ug/1 in surface water, both fresh and estuarine, and in
some cases in industrial areas. The highest water concentrations reported
were 82 to 10,500 ug/1 in a culvert near a wood-preserving factory. Rain-
water concentrations (in Hawaii) ranged from 0.002 ug/1 to 0.284 ug/1.
Sediment and organic matter in general exhibited concentrations one to
three orders of magnitude higher than those in surface water. Data were
not available concerning ambient PCP levels in soil and air in the U.S.
Data concerning PCP levels in urine and tissue for the general human
population indicate continual exposure to pentachlorophenol. PCP has
been detected in urine samples for 85% of the U.S. population. PCP resi-
dues have been reported in various food items and in fish and wildlife
species at concentrations of 0-50 mg/kg.
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Physico-Chemical Pathways: The air compartment appears to receive
a large amount of PC? discharge as indicated by materials balance informa-
tion. Pathways for entry into the atmosphere include evaporation from
aeration/evaporation ponds at wood treatment facilities, evaporation and/
or droplet release from cooling towers using PCP biocide, volatilization
from treated wood products, and burning of treated wood. Physical removal
mechanisms, such as rainout, are important processes affecting PCF concen-
trations in the atmosphere. Photolysis also appears to be an important
transformation process on the basis of PGP's behavior in water. The atmos-
pheric lifetime for PCP is estimated to be one month and is assumed to be
determined primarily by physical removal processes.
Releases CD surface water occur through direct discharge and direct
entry from numerous non-point sources including treated wood. In addition,
PCP can be transferred to water from other compartments such as air through
rainout, and soil, throughout runoff and leaching. At low concentrations
in water, PCP appears to be quite readily degraded by microbial action (in
water treatment facilities) and, in clear water, photolyzes rapidly.
Extreme concentrations or turbid conditions could inhibit these two
processes. Sorption onto sediments and larger organic matter is also
likely to occur. Based upon laboratory studies, hydrolysis, oxidation and
volatilization do not appear to affect concentrations in water significantly.
The lifetime of PCP in natural waters is estimated to be one week in con-
ditions that are optimal for photolysis. For systems in which biodegra-
dation is the primary removal mechanism, the lifetime will be longer and
extremely variable, depending on environmental conditions. Once PCP is
adsorbed onto sediment, there appears to be potential for re-release to
water; however, the conditions that would trigger this transfer have not
been investigated.
Pentachlorophenol enters the soil compartment as a result of its use
as a garden herbicide, leaching from treated wood, rainout from the atmos-
phere, and spills around PCP-using industries. Due to its high adsorpti-
vity, especially on organic matter and under acidic conditions, and based
on the results of one laboratory study, PCP does not appear to be very
mobile in soil. Biodegradation is a significant removal process under
both aerobic and anaerobic conditions. Important variables affecting
the degradation rate include temperature, moisture, the presence of
organic matter, and to a lesser degree, the soil cation exchange capacity
and pH. Photolysis and volatilization do not appear to be important
determinants of PCP concentrations in soil.
Wood that has been treated with pentachlorophenol apparently loses,
at a minimum, the amount of chemical residing in the wood's surface layer.
Photolysis may degrade PCP in products exposed to sunlight, while vola-
tilization occurs at a fairly slow rate, estimated at 1.7 x 10-*^g/cm2/sec.
On the basis of this volatilization rate, a lifetime of one year for PCP
residence in wood is estimated. The potential exists for removal of PCP
from treated wood by runoff from surfaces or leaching, however, the overall
importance of this process could not be assessed.
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Biological Pathways; PCP is accumulated in the tissues of biota
at concentrations greater than water concentrations by a factor of one
to 1000. Depending on the species, some of the PCP is metabolized and
may be concentrated in specific organs, such as the liver. Certain
plant species take up PCP and, some species rapidly metabolize the
compound.
Calculated Concentration Estimates: Using simple quantitative models,
estimates were made of ambient air concentrations resulting from the follow-
ing sources: wood treatment waste water evaporation ponds, volatilization
from treated wood, evaporation from cooling towers, and open-burning of
treated wood. Estimated levels were 4.3 ng7m3, 56.0 ng/m3, 36.0 ng/m3
and 40.0 ng/m3, respectively, summing to 136.3 ng/m3. Localized con-
centrations in the immediate vicinity of a cooling tower plume and a
waste water evaporation pond were estimated to be approximately 10u ng/m3,
and 10 ng/m3, respectively.
With use of the computerized EXAMS model, estimates were made of sur-
face water concentrations generated by three discharge rates—0.7, 0.25
and 17.1 kg PCP/day—into six generalized aquatic ecosystems. The cal-
culated water column (total) concentrations ranged from 0.003 ug/1 for
the lowest pollutant loading into a river system to a high of 26,000 us/1
for the highest pollutant loading into a pond system.
HUMAN EXPOSURE TO AND EFFECTS OF PCP
Exposure; Incidences of PCP exposure and toxicity to humans have
been reported for both occupational and non-occupational populations.
Most exposure is occupational involving dermal contact or inhalation of
contaminated water vapor. Eighty-five percent of the general U.S. popu-
lation has PCP residues in the urine indicating continual exposure to the
chemical. Potential routes of exposure include ingestion of food of
drinking water, inhalation and dermal absorption.
Ingestion is associated with relatively low per capita exposure
levels: in food 0.76-1.5 mg/day on average and 18 nig/day maximum; in
drinking water 0.02 yg/day average and 24 ug/day, maximum. Certain foods
with high PCP concentrations include fish, with a maximum exposure level
of 0.1 mg/day, peanut butter with 6.2 mg/day and gelatin with 0.02 mg/day
(high PCP level based on limited sample). The subpopulation exposed to
the maximum levels is expected to be small.
There are numerous potential exposure routes through inhalation of
PCP-contaminated air~bo.th occupational and non-occupational. Exposure
levels of 0.9 mg/day to 14.4 ing/day were estimated for workers in wood
treatment plants. In the vicinity of a cooling tower (<1 km), workers
may be exposed to 14.4 mg PCP/day. Domestic use of PCP in spray form
results in an estimated exposure level of 0.91 mg/day.
The general population is expected to be exposed to ambient levels
of PCP in the air resulting from wood treatment waste water evaporation
(0.09 ug/day), volatilization from treated wood (1.1 yg/day), evaporation
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from cooling towers (0.7 yg/day), and open-burning of treated wood
(0.8 ug/day). The total exposure level from all sources combined is
2.7 yg/day.
Certain subpopulations may be exposed to higher concentrations of
PCP downwind from cooling towers (maximum 2.0 ag/day) and from waste
water evaporation ponds (0.002 mg/day). Subpopulations using PCP indoors
on wood panelling may be exposed to 3.2 mg/day through inhalation of
volatilized PCP.
Exposure to PCP may also occur through dermal absorption. Contact
witha contaminated vater supply has an associated maximum exposure level
of 0.48 yg/day. Direct spilling of PCP on the skin may result in an
exposure level of 170 mg per incident and handling of treated wood, 0.5
mg/day.
Effects; Determination of the effects of pentachlorophenol is com-
plicated by its contamination with varying amounts of polychlorinated
dibenzo-furans. These contaminants and other impurities may comprise from
1% to 15% of the total PCP. However, purified PCP appears to be toxic by
itself as indicated by fetotoxicity and teratogenicity studies.
Teratogenicity and fetotoxicity are the most serious effects of PCP
indicated by available data. Adverse effects were observed following
exposure of rats to 30 mg/kg day during gestation. Purified PCP was more
toxic than technical grade PCP with respect to certain of the observed
effects. A no-effects level of 6 mg/kg/day has been observed; OPTS reports
a lower level of 3 mg/kg/day for fetotoxic effects. Carcinogenicity and
mutagenicity data are much less conclusive due to the small number of
experiments and conflicting data. Chronic dietary exposure to 100 ppm of
technical grade PCP has caused liver lesions in rats. The median oral
lethal dose for rats is 78-205 mg/kg.
Two other routes of exposure, inhalation and dermal absorption, are
important. Inhalation of PCP aerosol has an associated LD5() of 11.7 mg/
kg in rats. Dermal LD50's reported for rats range from 96 mg/kg to 320
mg/kg.
NON-HUMAN EXPOSURE TO AND EFFECTS OF PCP
Exposure; Aquatic organisms are typically exposed to PCP in water
at concentrations less than 100 yg/1. Simulations of water concentrations
resulting from practiced discharge rates are in general agreement with these
exposure levels, with the exception of discharges to the pond system and
at the highest loading rate to the eutrophic lake system. Higher water
concentrations have been measured in industrial areas, the highest at
10,500 yg/1. Even higher concentrations may be found associated with oil
slicks on water surfaces near sources. Incidences of fish exposure to
PC? have been reported in the vicinity of wood preserving plants, pulp
and paper industries, cooling water discharges, and following spraying.
-------
Terrestrial organisms may be exposed Co PCP through contact with
spilled material and ingescion of contaminated plants and aquatic organisms.
No information regarding actual exposure was available.
Effects; The lowest reported effects level for freshwater aquatic
organisms was 1 ug/1 in algae. Sock-eyed salmon exhibited sublethal
effects at 1.74 ug/1. The lowest acute effects level was an LCSO of 15.5
ug/1 for rainbow trout. LCSQ'S reported for freshwater fish and invertebrate
species ranged over two orders of magnitude.
Marine aquatic organisms exhibited lowest effects, at 38 and 43
ug/1 for a fish and invertebrate species, respectively. Only limited
toxicity data were available concerning both acute and chronic effects.
Several water parameters influence PCP toxicity. Toxicity increases
with decreasing pH, increasing temperature and, to a lesser degree, decreasing
hardness.
No information was available concerning the effects of PCP on terres-
trial animals and only limited data on phytotoxicity were found.
RISK CONSIDERATIONS
Risk to Humans; The non-occupational human population potentially
at risk with respect to PCP can be divided into three categories: 1) the
general U.S. population, 2) subpopulations residing in the vicinity of PCP
sources, and 3) subpopulations directly using PCP as a preservative,
bactericide or herbicide.- Calculating margins of safety—the ratio of the
exposure level to the lowest effect level (in this case, of a no-effects
level for rats of 3 to 6 mg/kg)—gives an indication of the significance of
the exposure level in relation to toxicity. The general population is
potentially exposued to PCP through ingestion of food (0.3 mg/kg/day maxi-
mum) and drinking water (0.0004 mg/kg/day maximum), dermal absorption of
water (negligible), and inhalation of nationally distributed air concentra-
tions (0.00005 mg/kg/day). All of these routes are associated with low
exposure levels compared to the following levels. Subpopulations residing
near PC? sources such as cooling towers and wood preserving waste water
evaporation ponds, are exposed through inhalation to higher levels estimated
at 0.001 mg/kg/day to 0.03. mg/kg/day depending on proximity to source.
Subpopulations using PCP directly are exposed to levels estimated at 0.03
mg/kg/day from use of spray,. 0.05 mg/kg/day from breathing fumes from treated
wood indoors, and 2.8 mg/kg from a direct spill on the skin.
Combining several exposure routes—ingestion, inhalation and absorp-
tion—gives a maximum exposure level of 3.2 mg/kg/day if a direct spill
on skin is included; this exceeds the no-effects level set by OPTS.
Eliminating the spill gives a total exposure level of 0.4 mg/kg/day. A
margin of safety of 8.6 is associated with this combined exposure level.
Most other individual exposure routes have associated margins of safety of
at least 100; however, due to the uncertainties of such an assessment,
these are not meant to indicate acceptable levels of exposure.
-------
In addition to the described exposure routes, there is limited
epideniological evidence possibly linking PCP exposure through the
handling of treated packing cases with a higher incidence of leukemia in
Kentucky. The results of further investigation of this possible relation-
ship are expected to be published in the near future.
Risk to Other Biota; Aquatic organisms are likely to encounter
surface water PCF concentrations that may have acute adverse effects on
a few species (certain algae and salmonids) and sublethal effects on a
larger number of species. Acute effects were reported for concentrations
ranging from 15.4 ug/1 to over 100 ug/1 and many ambient water concen-
trations reported also fell within this range. Incidents of fish kills
are common, but usually occur in the vicinity of obvious PCP sources,
probably resulting from concentrations much higher than 100 ug/1* The
paucity of monitoring data makes assessment of risk to aquatic organisms
difficult because of lack of information on regional distribution of
ambient environmental concentrations of PCP.
The limited monitoring data base indicates ambient surface water
concentrations ranging from 0.001 ug/1 to 100 ug/1, with numerous obser-
vations greater than 1.0 ug/1 especially in the Pacific Northwest. No
data are available for many of the U.S. major river basins, such as in
the Southeastern and South Central states, where PCP concentrations are
expected to be high.
Fish kill data and miscellaneous observations of high PCF concentra-
tions in water implicate several industries and activities that may generate
levels of PCP potentially harmful to aquatic life. These include the wood
preserving industry (through holding lagoon spills, runoff from contaminated
soil), the pulp and paper industry, cooling water discharges and spraying of
wood near water. The results of the analysis with the EXAMS model indicate
potentially harmful water concentrations generated by continuous discharge
of 0.25 kg/day into static aquatic systems.
Certain PCP sources warrant further investigation, such as leaching
from treated wood products and PCP-treated paint on products in contact.
with water. In addition, information is needed on typical PCP concentra-
tions in effluents from and the discharge practices of PCF-associated
industries.
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SECTION II.
INTRODUCTION
The Office of Water Regulations and Standards, Monitoring and Data
Support Division, of the U.S. Environmental Protection Agency is con-
ducting a program to evaluate the exposure to and risk of 129 priority
pollutants in the nation's environment. The risks to be evaluated include
potential harm to human beings and deleterious effects on fish and other
biota. The goal of the task under which this report has been prepared is
to integrate information on cultural and environmental flows of specific
priority pollutants and estimate the risk of receptor exposure to these
substances. The results are intended to serve as a basis for evaluating
the magnitude of the risk and developing suitable regulatory strategy for
reducing any such risk when action is warranted.
This report provides a brief, but comprehensive, summary of the
manufacture, use, distribution, fate, effects and potential risk of penta-
chlorophenol (PCF). Making effective use of the information given requires
an understanding of uncertainties regarding the data and qualifications
regarding conclusions presented he-ein.
Pentachlorophenol has numerous uses. The majority of the chemical
produced is used in wood preserving, and a significant amount of data
has been collected concerning this use. However, other uses must be
considered also because their nature provides a greater potential for
exposure to receptors. Very little information is available for certain
of these alternative, yet significant applications regarding the total
quantity involved and typical use concentrations. This lack of informa-
tion makes comparison between different exposure pathways uncertain
(e.g., exposure to PCP in cooling towers vs. treated wood).
Although pentachlorophenol is widely used throughout the U.S., very
little monitoring data exists for levels in soil, water and air. In
order to provide the information necessary for exposure analysis, estima-
tions of concentrations in water and air were calculated using materials
balance as input. The calculations are based on simple calculational
models and many assumptions. Since persistence of PCP in any environ-
mental medium is a complex phenomenon determined by many site-specific
and largely non-generalizeable parameters, the calculated values may not
be indicative of actual concentrations in specific environmental systems.
Pentachlorophenol has associated with it a number of impurities,
including dibenzofurans and chlorinated dioxins. The degree of contami-
nation varies by the PCP product formulation or grade, by the company
producing it, and even by batch of chemical. Although little information
is available describing the toxicity of these compounds, related compounds
are known to be highly toxic (e.g., TCDD). Most toxicology investigations
concern the effects of one of the commercial formulations of PC? and do
not distinguish between toxicity due to PCP itself and that due to its con-
taminants. Some of the variability, in reported toxic concentration
-------
thresholds can be attributed to variability in levels and types of contami-
nants in the material tested. The contaminants in PC? may be important
determinants of the observed effects of exposure to various grades of
PCP. However, the level of effort involved and the limitations of cur-
rently available data precluded distinguishing the risks of exposure to
PCP from the risks of exposure to the accompanying contaminants. There-
fore, the presence of contaminants in PCP introduces another element of
uncertainty into the analysis.
The. report is organized as follows:
Section III presents a materials balance for PCP
that considers quantities of the chemical consumed
in various applications, the form and amount of
pollutant released to the environment, the environ-
mental compartment intially receiving it, and, to
the degree possible, the locations and timing of
releases.
Section IV describes the distribution of PCP in
the environment by presenting available monitoring
data for various media, by considering the physico-
chemical and biological fate processes that transform
or transport PCP, by calculating concentrations for
several critical environmental pathways.
Section V describes the available data concerning
the toxicity of PCP for humans and laboratory
animals and quantifies the likely level of human
exposure via maj or 'known pathways.
Section VI considers toxicological effects and
exposure to non-human biota, predominantly aquatic
biota.
Section VII presents a range of exposure scenarios
for humans and likely exposure conditions for other
biota and correlates these with reported effects
levels from Sections V and VI, in order to assess
the risk presented by various exposures to PCP.
Appendix A discusses the contaminants found in different
grades of pentachlorophenol.
Appendix B presents an overview of available information
concerning PCP biodegradation pathways and products.
10
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SECTION III.
MATERIALS BALANCE
A. INTRODUCTION AND METHODOLOGY
In this section, a materials balance is developed for pentachloro-
phenol. The materials balance considers pentachlorophenol as it is
released from the cultural environment to its first point of entry into
the natural environment. Potential sources of pentachlorophenol releases
were identified by a review of activities in which the material partici-
pates from its production and use in various forms to its ultimate dis-
posal.
For each major source of pollutant release, the amount of material
released was estimated, and the environmental compartments (air, land,
and water) initially receiving and transporting the material were identi-
fied, as were the locations at which the pollutant loadings take place.
There are many uncertainties inherent in this type of analysis: not all
current releases have been identified, past releases were not well docu-
mented, 'and future releases are difficult to predict. Nevertheless,
sufficient information is available to indicate in general terms the
nature, magnitide, location, and time dependence of pollutant loading of
the environment with pentachlorophenol.
B. MATERIALS BALANCE
Pentachlorophenol is produced in the U.S. by chlorination of phenol
in the presence of a catalyst; it can also be formed by the hydrolysis of
hexachlorobenzene, but this process is currently not used. In addition
to several trade names, the material is commonly referred to as "penta"
and PCP.
Pentachlorophenol is toxic to a wide spectrum of life forms, in-
cluding bacteria, algae, fungi, and certain plants. Because of this
property, over 80% of the pentachlorophenol and its co-product, sodium
pentachlorophenate, produced is consumed in the timber and plywood
industry as a wood preservative. PCP is also applied as an industrial
and commercial pesticide and acts as a preservative in paints for wooden
items such as lawn furniture, trailers, and boats.
In 1978, total U.S. industrial demand was 21,300 metric tons (MT)
(U.S. International Trade Commission, 1979). Table 1 shows U.S. production
and consumption patterns for that year. Estimates of environmental re-
leases resulting from production and consumption of PCP are presented in
Table 2, and Figure 1. Manufacture of pentachlorophenol is expected to
increase by 2-3% each year through 1981. The volume of future use of
the chemical is somewhat uncertain due to increasing concern about its
potential for adverse environmental effects.
11
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TABLE 1. SUMMARY OF U.S. PRODUCTION AND CONSUMPTION
OF PENTACHLOROPHENOL, 1978
Supply Consumption
Source/Consumer (MT) Year (MT)
Production—1978 18,140
Domestic Stocks—1978 3,160
Wood Preserving—1978 18,0002
Sodium-PCP 2.5003
Cooling Towers (230)^
Paints (800)
Textiles (20) •»
Tanning (15) •»
Home and Garden 600
Herbicide 200
Total 21,300 21,300
United States International Trade Commission, 1979
2Linsey, 1979
3Versar, 1978
"*MITRE, 1979
( ) Indicates most of this quantity is sodium PCP, therefore, should
not be included in PCP consumption total.
12
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TABLE 2. SUMMARY OF ENVIRONMENTAL RELEASES OF
PENTACHLOROPHENOL (ESTIMATED 1978)
Release (MT/Yr)
Source
Production
Wood Preserving
Preserved Wood
Production of NaPCP
Cooling Towers
Paints
Textiles/Rayons
Pulp and Paper Mills
Tanning
Home and Garden
Herbicide
POTW
Total
Air
50
-
344
*
228.0
_
-
-
**
**
-
Direct
Aquatic
*
insignf2
**
*
2.0
3.0
5.0
2.0
**.
**
-
POTW
*
5.31,2,3
-
*
j.
7
-
i
i
**
%*
-
Land
*
74.51,2,3
*
*
-
9.0
-
6.0
600.0
200.0
18.0
622
14.5
5.3
881.1+
Arthur D. Little, Inc., industrial experts.
2EPA, October 1979.
3Rao, 1978.
At this time, not enough sampling has been done to perrr.it estimates
of gross environmental discharge.
**
Portions of these releases enter directly or indirectly through the
water compartment through groundwater, surface runoff, etc.; however,
due to the uncertain nature of the release, the contribution to water
cannot be quantified.
:It is uncertain whether these industries discharge directly to water or
through POTw's.
13
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Reichold
8,500 M.T.
PRODUCTION
(Capacity)
CONSUMPTION
Wood Preserving
18.0COM.T.
Herbicide
200 M.T.
Home & Garden
600 M.T.
ENVIRONMENTAL
COMPARTMENTS
Water
14.5 M.T.
POTW
5.3 M.T.
Legend:
Land
Water
Air
Note: Boundaries between receiving medium are often undefined and/or changing;
PCP apparently released to one compartment can result in another
Source: Arthur 0. Little. Inc.. based on 1978 estimates
FIGURE 1 MATERIALS BALANCE OF PENTACHLOROPHENOL
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1. Production
The majority of pentachlorophenol consumed in Che United States is pro-
duced domestically and only a small portion of U.S. production is exported.
The chemical is produced industrially in a two-stage process, shown
schematically in Figure 2. PC? is formed by chlorinating phenol at
close to atmospheric pressure. In the first stage of production in the
primary reactor, phenol is maintained at a temperature betveen 65°C and
130°C until the solution stabilizes at 95°C. At this stage, three to
four chlorine atoms are joined while the reactor temperature is held
about 10°C above the final product melting point. ' The entire process
is completed in 5-15 hr.
A byproduct of the chlorination product is an off-gas (HC1 initially
and chlorine gas in the later stages), which is treated by a scrubber-
reactor system utilizing excess phenol. Some of the lower chlorinated
phenols formed are recovered and returned to the primary reactor and
the remaining vapor is pure HC1 gas.
Until 1978, there were four pentachloraphenol producers in the
United States. Dow Chemical, 'U.S.A., has an estimated annual capacity
of 12,000 MT in Midland, Michigan, using equipment exclusively designated
for PCF production; Dow recycles HC1 in the process. Reichhold Chemicals,
Inc., has the estimated capacity to produce about 8,500 MT of PCP annually
at a facility located in Tacoma, Washington. Vulcan Materials Company,
Chemicals Division, has a capacity of about 8,500 MT in Wichita, Kansas.
Monsanto Company's Industrial Chemical Company had a plant capacity of
12,000 MT in Sauget, Illinois, manufacturing phenol in its Gulf Coast
plant; however, Monsanto stopped producing PCP in 1978 due to a shift in
market demand and in order to streamline operations (Linsey, 1979).
Pentachlorophenol production has been steady at approximately 21,500
MT (Linsey, 1979) despite a brief decline in production following a con-
tamination incident in Michigan involving cattle exposed to PCP-treated
wood in their shelters. Following Monsanto's shutdown, compensating
increases in production by the other three companies have maintained
a constant production volume.
Emissions during production are relatively insignificant in volume
and are geographically restricted to the three currently operating
facilities shown in Figure 3 (Versar, 1979). As described, air emissions
are limited by a scrubber mechanism enabling recovery. Incentives for
control are economic, as well as regulatory. An additional release
potential during production is discharge of contaminated cooling waters.
These are treated prior to release; however, industries producing and
consuming PCP have not yet been subjected to effluent guidelines and,
consequently, no sampling data are available upon which to base estimates
of gross annual discharge.
15
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Pl.enol
Chlorine -
Aluminum -
Chloride
(Catalyst)
Primary
Reactor
Pentachlorophenol
HCI &
Excess _
CI2
1
I
I
I
I
1
Chlorine
Scrubber
C6CIXOH
HCI
Recycle to
Chlorine
Plant
Recovery
Source: U.S. EPA 1974.
FIGURE 2 PRODUCTION OF PENTACHLOROPIIENOL
-------
Notes: 1. Battelle for EPA. 1975
2. Forest Service. U.S. Department of Agriculture
FIGURE 3 LOCATIONS OF PULP MANUFACTURING PLANTS AND WOOD TREATMENT PLANTS
-------
Normally PCF is shipped in two forms: first in reusable containers
or drums, which are returned to the manufacturer following delivery and
to be recycled exclusively for PCP transport; and second, in a large cake
weighing.around 2 MI, which is handled by mechanized equipment and trans-
ported in trucks-
Previous studies of pentachlorophenol use and emissions have suggested
that material may be released during or as a result of transport from the
manufacturer to the consumer. Aside from identifying this possible source
of release, however, prior reports have been unable to quantify the release
to the environment and have suggested exploring methods of transport and,
in particular, procedures used by the railroad companies to clean freight
cars after use.
Since PCP is not currently shipped in raw form in railroad freight
cars, this type of release is no longer occurring. This has been veri-
fied by the Forest Service (Gjovik, 1979) and by a manufacturer (Linsey,
1979). The potential for release from trucks remains; however it was
not possible to estimate the contribution due to transport. Accidental
spills at points of origin or destination or while the material is en-
route can occur, but to date no such incidents have been documented.
2. Wood Preserving
The wood preserving industry consumes more pentachlorophenol than
all other consumers combined. PCP is used for cosmetic reasons to pre-
vent discoloration, to enhance toughness, and to prevent attack by wood-
destroying fungi.and insects. Precise estimates of consumption vary
from year to year and depend upon the source (timber industry, manu-
facturer, federal government, etc.), but all are in the same range:
Mannsville Chemical Products reports 78% in 1976 (Versar, 1978);
U.S. EPA (1974) reported 78% in general; manufacturers project as high
as 85% to 93% in 1978 (Linsey, 1979).
The timber industry has reported to EPA that 415 wood preserving
plants are currently operated in the United States by approximately 300
companies (44 FR 62810-62846). Plants are geographically located in a
manner consistent with the natural timber range, with heaviest concentra-
tions in the Midsouth, Southeast and Pacific Northwest as shown in
Figure 4. Wood preserving involves a two-stage process: first the wood
is conditioned to reduce natural moisture content, thereby increasing
permeability; second, the resulting wood is impregnated with PCP. EPA
has designated the first stage as the most significant wood preserving-
related contributor to wastewater flows (44 FR 62810-62846).
Two wood conditioning procedures predominate in the United States,
which, when PCP is used, result in high phenolic concentrations in water.
The Boulton conditioning process heats wood immersed in an oily, acidic
(pH of 4-6) preservative inside of a treatment cylinder. The steam con-
ditioning process steam pressurizes wood, also in a treatment cylinder,
and this is followed by a vacuum cycle to reduce and remove moisture.
13
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Northeast
North Central
Southeast
South Central
Mountain
Pacific
720
1080
4320
6940
ft
2340
3600
I
I
I
0 1000 2000 3000
Total: 18,000 Metric Tons
4000 5000
Metric Tom
6000
Source: Arthur D. Little,Inc.. and American Wood-Preservers' Association (1975)
and U.S. International Trade Commission (1979).
FIGURE 4 REGIONAL CONSUMPTION OF PEiMTACHLOROPHENOL
BY WOOD PRESERVATION PLANTS (Estimated 1978)
19
-------
Approximately 90% of existing wood treatment plants evaporate their
wastewaters and, consequently, have no discharge to water at all. EPA
reports that 11 plants utilizing the Boulton process and 31 steam plants
introduce discharge to POTW's, as allowed by EPA guidelines. (These
regulations are currently being revised.) Only one plant discharges
directly to water on an intermittent basis, at a rate between 10,000 and
14,000 gallons per day; with concentrations of PCP between 10 and 20 mg/1
the total release is estimated to be 3.8 to 26.5 kg annually for 10 to
25 operating days each year. (EPA, proposed, 1979). In the Development
Document for Effluent Limitations Guidelines and Standards-Timber Products
(proposed, 1979), EPA reports sampling results from 65% of the steam
process indirect discharges and 25% of the Boulton process indirect dis-
chargers. The efficiency of wastewater treatment varies; these data
indicate that steam conditioners treated wastewaters with about 81%
efficiency and Boulton conditioners with about 44% (the Boulton had a
lower pretreatment concentration of PCP). Associated discharges to POTW's
by steam and Boulton were, respectively, 5.1 and 0.2 MT of PCP annually
(44 FR 62810-62846).
The majority of constituents removed by wastewater treatment probably
accumulate in sludge. Though inconsistencies exist in sludge data and in
the sludge practices themselves, the quantity of PCP in sludge from wood
preservation can be estimated roughly. Approximately 14.3 MT of PCP
sludge are generated per year by indirect dischargers, for treatment
efficiencies as discussed above (EPA, 1979). The remainder of the indus-
try, with no discharge, produces from the evaporation stage solid waste
containing roughly 60.2 MT of PCP annually (EPA, 1979 and Arthur D. Little,
Inc., estimates 1979). PCP deposited in sludge at industrial sites is
largely believed to remain there (Arthur D. Little, Inc.); although it
decays fairly rapidly in the presence of light, oxygen and microorganisms
(see Section IV-C), conditions conducive to degradation cannot be assumed
to exist at all sludge disposal sites.
Preserved wood is consumed by a variety of applications and is more
evenly distributed geographically than are wood preservation plants.
PCP is applied to wood at the widely published rate of about 0.23 kg PCP
per cubic foot of wood (Rao, 1978). A distribution of wood products
treated with PCP is presented in Figure 5, and regional consumption of
PCP-treated wood is shown in Figure 6. By far, the largest application
is to poles, comprising 57% of the total PCP consumption by the timber
industry. Other applications include fenceposts (13%) and railroad ties
(1.4%). Since these treated products are used out of doors the treated
wood is exposed to environmental conditions (sunlight, rainfall, etc.).
It was not possible to estimate the amount of PCP lost from treated wood
through leaching and runoff. These sources contribute non-point releases
to land, water and POTW's. Approximately 344 MT of PCP is volatilized
from treated wood to the air annually (Arthur D. Little, Inc., estimates).
Assuming that wood consumption is associated with land area, as illustrated in
Figure 6, PC? release from treated wood by the previously described pro-
cesses is expected to be distributed fairly evenly throughout the regions
of the U.S.
20
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Riiiwiv Tin
Pom
Piling
Lumotr
Ftnca Pom
Oth tf
0 1000 2000 3000
Total: 18.000 Metric Tons
4000
5000
Metric Tom
6000 7000 8000 9000 10.000
Source: Arthur D. Little.lnc.,American Wood-Preservers' Association (1975)..and U.S. Forest Service (1979).
FIGURE 5 MATERIALS TREATED WITH PENTACHLOROPHENOL
(Estimated 1978)
21
-------
North
Central
5220 Metric Tons
South-
east
2880 Metric Tons
Northeast
4140 Metric Tons
South
Central
2880 Metric Tons
West
2880 Metric Tons
Source:
Total: 18,000 Metric Tons
Arthur D. Little, Inc.; American Wood—Preserver's Association (1975)>
U.S. International Trade Commission (1979).
FIGURE 6 U.S. CONSUMPTION OF WOOD TREATED WITH PENTACHLOROPHENOL BY REGION
(Estimated 1978)
-------
Another source of release of .PCP would be to the atmosphere through
open-burning of treated wood. This is most likely to occur after some
period of exposure of the wood to environmental conditions so that some
portion of the original FCP will have already been lost through volatili-
zation and leaching. Based on calculations described in Section IV-D,
an estimate of 26 MI of PCP annually is expected to enter the atmosphere
from burning of treated wood products.
3. Sodium Pentachlorophenate
Roughly 9% of the pentachlorophenol produced in the United States
is used in the manufacture of sodium pentachlorophenate. This material
is generally consumed as a fungicide and bactericide. The three most
significant applications are in water cooling towers and as a preserva-
tive in paint and adhesives; each is discussed briefly below.
A. Other Uses of Pentachlorophenol and Sodium-PCP
Although the wood preserving industry consumes as much as 90% of
PCP produced, there are additional applications which, because of their
nature, are likely to result in human exposure and, therefore, merit
discussion.
a. Paints
Pentachlorophenol is added to outdoor paints to enhance the water
resistance of items such as porch furniture, trailers, boats, and outdoor
trim. Occasionally these paints are misused and applied indoors (see
Section V-B ). The paint industry reports consumption of roughly 800 MT
of PCP annually (Linsey, 1979).
Information has been published indicating that PCP may be used in
toy paints (van Langeveld, 1975). Within the domestic toy industry,
procedures have been tested and guidelines established to ensure that
negligible amounts of PCF are used in toy manufacture or are contained
in the final product (Arthur D. Little, Inc., estimates, 1979). However,
van Langeveld (1975) has reported the results of a sampling of 65 commer-
cial toy paints in Europe; nine were found to contain PCP in concentra-
tions of Q.01%-0.27% (detection limit 4 mg/kg). The types of water
colors and finger paints tested are imported into the U.S. Some manu-
facturing .for U.S. toy companies is contracted out to foreign operators.
Some of the toys may also contain paint to which PCP has been added.
At present, data are Insufficient to estimate the volume of PCP involved
in these applications and the magnitude of any resulting releases to the
environment.
b. Cooling Water Towers
Cooling waters used in industrial complexes are warm and well
oxygenated, conditions favorable to growth of microorganisms. When
microorganisms do grow, they promote equipment degradation, decrease
23
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operating efficiency and product quality, and present a potential health
hazard. Proliferation of microorganisms is induced by factors both in-
ternal (system design, temperature, pH, and process materials) and ex-
ternal (water supply quality, site geography, and nature of aerosol
contaminants) to the system (MITRE, 1979). Industrial cooling systems
are decreasingly using adjacent stream waters due to environmental con-
cern over thermal pollution of that media. Recirculating cooling water
networks (especially cooling water towers) are replacing them. In
addition to industrial applications, cooling water systems are also
commonly found commercially in air conditioning systems in office build-
ings and large-scale computer operations (MITRE, 1979).
PCF is used in cooling water systems in two ways, each providing
potential environmental release of the material. First, wooden slats,
treated with PCP, are placed in a grid system to break the fall of
cooling water into droplets and to optimize the heat exchange with the
environment. The quantity of PCP released from this application is
expected to be minor compared with other cooling tower uses.
Secondly, application of PCP to cooling waters themselves was
estimated to be 230 metric tons in 1978 (MITRE, 1979). Recirculating
Na-PCP-treated water has a greater potential for environmental, release
than PCP-treated wood slats. After passing through the industrial system
which increases its temperature, water is depressurized, returned to the
cooling tower and cooled as a result of its exposure to air. During
temperature reduction of the cooling waters, vapor is emitted to the
atmosphere, potentially containing PCP. There are data indicating that
a high percentage of PCP consumed by this application is released to the
air in this fashion. (Conservative estimates would assume that ultimately
all PCP and the waters containing it are emitted to the atmosphere except
that which is discharged during a system washout.) A more thorough
investigation into this type of release is recommended.
Cooling water systems are occasionally washed out to clean the
system and combat the build up of salt and other impurities. Typically
these waters are treated before discharge. Based upon EPA-supplied
effluent data (as yet unpublished) from industrial sites using cooling
towers, it is estimated that 2 MT of PCP is discharged to water by this
use, and the remaining 228 metric tons to air. If the aquatic discharge
is treated, roughly 75% would be deposited in sludge; however, the nature
of treatment practices is poorly documented.
c. Tanning
Pentachlorophenol and sodium pentachlorophenate are frequently
combined with 2,4,5-Trichlorophenol (TCP) during product formulations .
in the leather industry (MITRE, 1979). Tanning is the chemical process
during which natural hides and skins are converted to stable, durable
leather. Because of its natural condition before treatment, leather is
susceptible to infestation by bacteria molds and yeasts; consequently,
PCP is used to protect the material during extended exposure to moisture.
24
-------
Rarely is PCP used by itself. In most instances, PCF supplements the
application of 2,4,5-TCP because PCP is less expensive and the use of
these chemicals together is more effective. Annual consumption of
2,4,5-TCP is more substantial—approximately five times as great as that
of PCP (MITRE, 1979).
On the basis of a survey of approximately 43% of the industry, it
is estimated that approximately 15 MT of PCP is consumed annually (MITRE,
1979); this amounts to less than.0.1% of annual PCP production.
The use of PCP and its sodium salts in the tanning industry is
expected to decline (MITRE, 1979). Particularly at early stages of
treatment in which PCP is applied, improvements have speeded up the
process, decreasing the time the leather is vulnerable to fungal growth;
as a consequence, the MITRE Corporation (1979) suggests that PCP is not
critical for tanning treatments.
Limited monitoring data on tanning industry effluents expected
to become available in the near future would enable rough projections
of PCP discharge directly to waters and/or indirectly to POTW's (EPA,
1979). At this time, however, only conservative estimates are possible
based on knowledge of the application procedure. Preservatives are
introduced in the early stages of tanning (batch soaking), as discussed
above, and in finishing (sprays, pastes). PCP is used more frequently
in the former process; if 80% is used in any of several soakings and 30%
of the PCP in solution is absorbed or decays, then the remainder,
approximately 8 MT per year, is discharged and treated at an assumed
efficiency of 75%. Therefore, about 6 MT of PCP is released in sludge to
to land and 2 MT to waters (MITRE, 1979).
In general, use of leather protectors decreases in winter months
when fungi are less likely to abound.
d. Textiles
As is the case for many other uses of PCP, the chemical controls
fungi and rot fungi when introduced to textiles and is registered with
the EPA for this use (MITRE, 1979). In a study of this industry, MITRE
indicates that all identified users add sodium-PCP to finishing solutions
at concentrations ranging from 0.25% to 0.31% (MITRE, 1979). The total
PCF and sodium-PCP consumed by the industry is about 20 MT annually.
Roughly 60% or 12 MT of this is discharged for treatment (MITRE, 1979).
Sixty-five percent of the textile plants have biological treatment with a
70% efficiency based on BOD removal (U.S. EPA 1980; MITRE 1979). There-
fore 5.5 MT of PCP is discharged to surface water annually.
e. Other Uses and Releases
The most significant consumptive uses and sources of environmental
release that can be identified and quantified given the current state of
knowledge have been discussed in the preceding sections. However,
•7=;
-------
several additional uses and potential sources of release should be noted.
These are relatively minor applications and little is known of their
precise nature at this time, although future studies in these areas may
be appropriate.
PC? is registered with the EPA for use as a disinfectant, for appli-
cation to masonry, agricultural seeds, paper mill systems, and construction
materials such as: asbestos shingle, roof tilesj brick walls, concrete
blocks insulation and pipe sealing compound (Rao, 1978).. The petroleum
industry has injected PCP into drilling muds, gypsum muds and packer
fluids. It is added to photographic solutions to control slime and
fungus (Rao, 1978). PCP is used at concentrations of 15-40 mg/1 in
secondary oil recovery to control microbial growth and optimize recovery
(Rao, 1978).
In Europe, hexachlorobenzene (HCB) is used as a predecessor to PCP
by manufacturers. Because.of similarities in the chemical nature of PCP
and HCB, biotransformation of HCB to PCP occurs with relative ease.
Because of this, some residues of PCP may be attributable to HCB pollu-
tion (Conklin and Fox, 1978).
In the past, PCP has been used as an herbicide, both commercially
and in home and garden applications. The U.S. Department of Agriculture
reports its use by commercial mushroom houses to prevent proliferation
of undesirable microbial life (MRI, 1974). It has been used on non-
crops and dormant crops during •pre-harvest periods. Approximately 200
MI per year is consumed in this fashion (Versar, 1978). The material
can be bought in retail hardware stores for use by homeowners as a bird
repellent and garden insecticide. Approximately 600 MT is consumed
annually by homeowners. Both of these applications are assumed to be
direct releases to the environment as non-point and point sources.
Pentachlorophenol is used as a preservative in many food-associated
products such as adhesives on food packaging, coatings on paper and paper-
board used in food producing, manufacturing, packaging, processing, pre-
paring, treating and transporting. Consequently, the use of PCP in this
area is covered by the Food Additives regulations set forth in Title 21
of the U.S. Code Annotated. A summary of potential PCP applications is
presented in Table 3; where limitations have' been articulated, they are
included.
5. Investigations of POTW's
There are five known sources of PCP release to sewer systems that
will reach POTW's: PCP production plants, textile factories, the leather
tanning industry, approximately 10% of the wood preserving facilities,
and cooling towers. The amount of PCP waste discharged to sewers that
has been accounted for is 9 MT per year from these sources. The wood
preserving industry reports a total discharge of 6 MT per year from only
42 plants of the total 415 operating facilities. An additional 3 MT per
year is associated with leather tanning plants. The discharges from the
26
-------
TABU 3. SUMMARY OF FDA-APPROVED USES OF 7EM7ACHLOROPHENOL
IN FOOD-ASSOCIATED PRODUCTS
Product Description
Substances Used
Racooaand Concentrations/
Paperboard products used in feed
packaging
Preservative for aomoniua algiaace
used in aanufaeeure of ?VC emulsion
polymers
Preservative far wood used in
packaging/transport raw
agricultural produeta
Animal glue
Textile* used in aanufacturing,
processing, packaging, transport.
•tc. of food
lubber articles used in manufacturing.
processing, packaging transport, etc.
of food
Closures with sealing gaskets on
containers for feed
Slimicides used in manufacture of paper
(board) that will contact food
Defoaning agents used in manufacture
of paper (board) that will contact
food
Defoaming agents used in manufacture
of coatings for articles that will
contact food
trncoaced/coated food-contact surface
of paper (board) in packaging, etc.
Resins and polymeric coatings used
as food contact surface in
aanufacturing. packaging, transport, etc.
— — — ^— — — ~_
Potassium - PC?
Sodiua - PCP
Sodiua • PCP
PCP: Sodiua - PCP
Potassium - PCP
Sodiua - PCP
Sodium - PCP
Sodiua - PCP
Potassium - PCP
Sodiua - PCP
Potassium - PCP
Sodium - PCP
Potassium - PCP
Sodium - PCP
Potassium - PCP
Sodium - PCP
Sodium - PCP
Sodium - PCP
i O.SZ by weight
<. SO mg/kg/PCP
Only as a preservative
Only as a preservative
iS.OZ by weight
<_ 0.051 by weight of closure
sealing gasket
Only as a preservative
Only aa a preservative
0.12 by weight in can-sealing
compounds on containers with
_> gallon capacity.
Adhesives of articles used la
packaging transport, etc. of
food
I PCP, Sodium - PCP
Potassium - PCP
Only as a preservative
'The above were taken from various portions of the Food Additive regulations of the Food
and Drug Administration. Title 21, U.S. Code.
27
-------
three remaining sources have not been quantified to date, but it is
expected that production-associated wastes are probably negligible.
Total loadings may be estimated by a doubling of the known discharge
to sewers of 9 MT to 18 MT per year. This accounts for contributions
from textile works and cooling towers, as well as runoff from PCP-treated
putdoor wood products which enters sewage systems in runoff. A total of
18 MT is conservatively estimated to account for all unquantified sources
of PCP.
Most known sources of PCP to sewers are localized. The wood pre-
serving industry is concentrated in the eastern half of the United States,
especially the Southeast and the Northwest. Discharges from other sources,
such as textile facilities, tanning plants and cooling towers, are inter-
mi^tent point sources and more widely distributed. Release of PCP from
treated wood products is expected to be distributed evenly across the U.S.
The amount of PCP that would reach storm sewers from this source relative
to other sources is unknown so it is not possible to rule out an even
distribution of PCP on a national basis. However, based on the assumption
that the wood preservers are significant dischargers to POTW's, any esti-
mations of total sewage PCP loading based upon effluent concentrations
and total U.S. POTW flow will be too high or low, depending on the loca-
tion where the effluents were sampled.
The following sample calculation uses the estimation procedure of
Versar (1979) but with revised numbers. Table 4 presents PCP concentra-
tions detected in POTW final effluents in several cities. Excluding
the Grand Rapids measurement as an outlyer, a mean concentration of 10.5
ug/1 can be calculated. Then the calculation, based on a total flow in
U.S. POTW'S of 26,205 million gallons per day (E?A, 1978) follows:
Total PCP in sewage effluent ° average concentration x flow =
(10..5 ug/1) x (365 days/year) x (26,205 x 10s gal/day) x
(3.785 1 x 10"12 MT/yg) » 380.13 MT
This estimate may be too high due to assumptions of the model such
as using daily flow estimates for 365 days per year. Another factor is
the small amount of data supporting the estimated average effluent con-
centration. Most of the POTW's sampled in Table 4 are located in states
with numerous wood preserving industries which may contribute to effluent
concentrations higher than the national average. Without more data,
however, no firm conclusions can be made concerning the contribution of
POTW discharges to surface water concentrations of PCP. In Table 2,
18 MT describes the amount of PCP contributed to the environment by POTW
sludge. Three hundred eighty MT approximates the amount of PCP discharged
to water in POTW effluents. The discrepancy between the numbers implies
either:
(1) a low efficiency for PCP removal from water onto sludge,
assuming limited disappearance in the system or
28
-------
TABLE 4. PCP CONCENTRATIONS IN POTW FINAL EFFLUENT1
Number of Days
City Concentration (ug/1) Days Sampled
Indianapolis, Indiana
Cincinnati, Ohio
Lewis ton, Maine
Atlanta, Georgia
St. Louis, Missouri
Pottstown, Pennsylvania
Grand Rapids, Michigan
1
1
< 50
< 5
< 5
1
<2502
12
7
4
6
6
6
6
•^Preliminary data to be verified from Burns and Roe POTW study
sponsored by Effluent Guidelines Division.
2Effluent before chlorination.
29
-------
(2) a high efficiency for PCP degradation in POTW sludge,
coupled with a very large combined industrial discharge
to POTW's (»400 MT) leaving only a small fraction be-
hind in sludge.
Assuming a total POTW efficiency of 80%1 (which includes removal at all
treatment levels), then 20% of the total amount of PCP discharged by
industries to POTW's equals the amount leaving in POTW effluents (380 MT)
and sludge (18 MT), totalling 400 MT of PCP annually. From this number
the total industrial input to POTW's is estimated at 2000 MT annually.
Due to the large number of assumptions made in deriving this POTW load-
ing estimate, it was not used as input to the materials balance of PCP
in Table 2.
1 Based on observations in wastewater treatment and POTW treatment of
efficiencies of =100% and 60% averaged (see Sections IV-3-2 and
IV-C-1-c-vi). Excluded from this average was a low efficiency of 4-28%
(observed in one treatment plant) because it was not a typically observed
number, it was derived from a small sample and on evidence of biode-
gradation of PC? in laboratory environments.
30
-------
REFERENCES
American Wood-Preserver's Association. 1975. Wood preservation statistics.
1975. (Published in the 1976 volume of the AWPA Proceedings). Ernst and
Ernst, Washington D.C.
Battelle. 1975. Screening studv to develop background information and
determine the significance of air contaminant emissions from pesticide
plants. Report to EPA, Washington, D.C. Report #540/9-75/026).
Bendtsen, B. Condition of preservative-treated cooling tower slats
after 10-year service. Forest Products Journal 22;4.
Conklin, J. and R. Fox. 1978. "Environmental impact of pentachloro-
phenol and its products—a round table discussion," in K.R. Rao (ed.)
Pentachlorophenol; Chemistry. Pharmacology, and Environmental Toxicology.
Plenum Press, New York. New York.
Gjovik, L. 1979. Forest Products Laboratory. Madison. Wisconsin.
Personal communication.
Linsey, Dennis, 1979. Vulcan Materials, personal communication.
Midwest Research Institute (MRI), 1974. Production, Distribution. Use and
Environmental Impact Potential of Selected Pesticides. Report to
Council on Environmental Quality.
MITRE Corporation, 1974. Analysis of Existing Wood Preserving Techniques
and Possible Alternatives. MITRE Technical Report 7520; McLean, Virginia.
MITRE Corporation, 1979. Use Profiles and Alternatives Assessment of
2,4.5-Trichlorophenol and Pentachlorophenol in Tanneries. Textiles,
Water Cooling Towers. McLean, Virginia. Report to EPA (Contract
#68-01-3965).
Rao, K.R., 1978. Pentachlorophenol; Chemistry. Pharmacology and
Environmental Toxicology. Plenum Press, New York, New York.
U.S. Code Annotated. Title 21 Food and Drugs, Chapter 1 Food and Drug
Administration.
U.S. Environmental Protection Agency, 1974. Production. Distribution.
Use of Selected Pesticides. Office of Pesticide Programs, Office of Water
and Hazardous Materials; Washington, D.C.
U.S. Environmental Protection Agency, 1979. Development Document for
Effluent Limitations Guidelines and Standards for the Timber Products
Industry, proposed; EPA 440/l-79/023b.
U.S. Environmental Protection Agency, 1979. Environmental Assessment
for the Timber Products Processing Industry. Final Report from Monitoring
and Data Support Division, Office of water Planning and Standards, U.S.
EPA; Washington, D.C.
31
-------
REFERENCES (continued)
U.S. Environmental Protection Agency, 1979. Timber products processing
point source effluent limitations guidelines, pretreatment standards,
and new source performance standards. Federal Register 44(212):62818-
62846.
U.S. International Trade Commission. 1979. Synthetic Organic Chemicals,
Government Printing Office, Washington, D.C.
van Langeveld, E.A., 1975. Determination of pentachlorophenol in toy
paints, Journal of the AOAC. 58:1.
Versar, Inc., 1978. Production and Use of Pentachlorophenol. Draft
Report to the Monitoring and Data Support Division, U.S. Environmental
Protection agency. Contract No. 68-01-3852.
32
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SECTION IV.
DISTRIBUTION OF PENTACHLOROPHENOL
IN THE ENVIRONMENT
A. INTRODUCTION
This section of the exposure assessment describes the distribution
of PCP among different environmental media following release from its
sources. The section contains a discussion of:
(1) monitoring data presenting concentrations of PCP
measured in various media,
(2) physico-chemical fate processes that determine
these PCP concentrations through transformation
or transport,
(3) biological fate processes, and
(4) concentration estimates for several critical environ-
mental pathways.
The overall approach chosen to analyze PCP's environmental distri-
bution was determined by the nature of the chenical's entry into the
environment, its physico-chemical properties, and the availability of
data. The majority of the pollutant loading of the environment with PCP
does not enter through direct discharge but from numerous, often unknown,
non point sources. No particular environmental compartment stands out as
the primary recipient of PCP release, and transfer of the pollutant between
compartments appears to occur. PCP is relatively persistent in most media,
based on its physico-chemical properties, which suggests that physical trans-
port is equally or more important than chemical transformation. Finally,
lack of monitoring data necessitates estimation of PCP environmental con-
centrations for use in the exposure sections. Because fate data are so
limited, these estimates are based on simple calculational models and
many assumptions in some cases.
Several approaches have been described for the environmental fate
and pathways analyses required for an exposure assessment (ALL, 1980).
The critical' pathways approach was used for PCP, making use of estimated
pollutant environmental loadings to different environmental media based
on materials balance data. Information on fate was reviewed in the first
section and used, when applicable, in the estimation of environmental
concentrations. The approach was limited by data gaps concerning load-
ings to certain compartments, (e.g., water) on a national scale and for
the most part, did not address intercompartmental transfers. The results
of this analysis are not inclusive, therefore, nor do they account for
the total mass of PCP entering the environment. The analysis was focused
on what appeared to be the important pathways, largely because of the
availability of data required for estimation. Whenever possible, moni-
toring data were used to verify the results of the estimations.
33
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B. MONITORING DATA
1. Introduction
Monitoring data giving PCP concentrations in various environmental
media are too few to be systematic and indicative of the national distri-
bution of the chemical. Data are scattered, inconsistent and primarily
anecdotal. At best, the information that is available can be used to
verify estimates of environmental concentrations based on fate models.
The following section presents, by environmental medium, the available
monitoring data.
2. Water and Sediment
Tables 5 through 10 summarize levels of PCP found in water and sediment
over the last 10 years as reported in the literature. Monitoring data
available through STORE! were found to be very limited, with a total of
497 observations, 82% of which were remarked data (at the detection
limit) as of March, 1979; for the unremarked data (above detection
limits), 84% of the observations fell between 0.1 ug/1 and 10 yg/1, with
a total range of 0.01 ug/1 to 1QO ug/1. For unremarked and remarked
• data combined, the majority of non-zero observations (approximately 55%)
fell between 0.1 ug/1 and 100 ug/1, with all values less than 100 mg/1.
The data imply that ambient levels of PCP in surface water are
usually below 1 ug/1, with much higher levels in more industrialized
areas. Bevenue et al.'(1972b) analyzed samples of snow, rainwater, and
lake water in Hawaii where PCP is used extensively for wood preservation
and termite control (see Table 6). The authors attributed the consistent
presence of PCP in the area mainly to the use of construction lumber
treated with preservatives containing PCP.
Young et al. (1975) found results comparable to those of Benevue in streams
feeding into the Kaneohe in Hawaii Bay and in the Bay itself (see Table 6).
Mean values for the streams were 0.12 ug/1 and for the Bay 0.07 ug/1.
Values for samples taken near sewage outfalls in the Bay (0.068 ug/1)
did not vary significantly from values for samples collected at other
stations (0.073 ug/D- In the Netherlands, Wegman (1979) reports PCP
levels in five major rivers averaging 0.49 ug/1 in 1976 and 0.93 ug/1 in
1977 (see Table 7).
Preliminary data on PCP concentrations in various POTW treatment
stages are presented in Table 8. Final effluent concentrations varied
from 1 ug/1 to <50 ug/1. Levels in the influent fell within the same
range: from none detected to <50 ug/1. It was not possible to calculate
an average treatment efficiency due to differences in treatment methods
and analytical techniques between POTW plants. For the Pottstown and
Atlanta plants, however, efficiencies calculated were 93% and 100%,
respectively. A study of PC? content in the sewage of three Oregon
cities conducted by Buhler et al. (1973) found the average percentage
of PCP removed at the treatment plants to be 59%. POTW influent ranged
34
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TABLE 5. TOTAL PENTACHLOROPHENOL IN AMBIENT WATERS
(Remarked and Unremarked Data)
_ Percentage of Observations
0.001-0.01
Region
New England
Mid Atlantic
Southeast
Great Lakes
Ohio
Tennessee
Upper Mississippi
Lower Mississippi
Souris and Red of North
Missouri
Arkansas and Red
Western Gulf
Rio Grande and Pecos
Upper Colorado
Lower Colorado
Great Basin
Pacific Northwest
California
Alaska
Hawaii
United States 3 16 19 33 30 80
.-0.01
Ug/1
^
-
-
0
0
— '
_
..
_
0
_
_
_
_
_
_
9
0
_
_
0.01-0.1
ug/1
—
-
-
0
0
-
_
-
_
0
_
_
_
_
_
_
0
32
-
_
0.1-1
yg/1
^
-
—
100
0
-
.
_
_
0
_
_
_
_
_
_
0
17
-
—
1-10
ug/1
^
-
—
0
100
—
_
_
_
67
_
_
_
_
_
_
0
44
-
_
10-100
ug/1
—
—
-
0
0
—
_
-
_
33
_
_
_
_
_
_
91
7
—
_
No.
0
0
0
8
6
0
0
0
0
3
0
0
0
0
0
0
22
41
0
0
Source: STORET: Data from 6/78-6/79.
35
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TABLE 6.
Site/Type of Sample
Drinking water
River below papermill
Lake below papermill
Riverwater below wood
preserving plant
Streams (Hawaii - Kaneohe)
Bays (Hawaii - Kaneohe)
Rainwater (Hawaii)
Kallua
Kaneolie
Walpaliu
Honolulu
Snow
Lake Water
Sewage Influent (Oregon)
Sewage effluent (Oregon)
Willamette River water (Oregon)
Drinking water for Corvallis
Kallhl stream (Industrial area -
Hawaii)
Sand Island outfall (sewage - Hawaii)
Concentration (ug/1)
Ranee
MEAN CONCENTRATIONS OF 1'CP IN WATER
No.
Samples Mean
108 0.07
9
3
0.35
63
29
0.12
0.07
0.02
0.012
0.014
0.1
0.014
0.01
4.3
0.655
2.6
0.01-0.48
ND3 -0.38
0.016-0.008
0.002-0.284
1-5
1-4
0.1-0.7
0.04-0.28
Source
NOMS1
Rudling (1970)2
Rudling (1970)
Renberg (1974)
Young et a.L. (1976)
Young et al. (1976)
Bevenue ejt al. (1972b)
Be venue £t al. (19721))
Bevenue et al. (1972b)
Bevenue et al. (1972b)
Bevenue e£ al. (1972b)
Bevenue e£ al. (1972b)
Bevenue ej^ al. (19721*)
Buhler et_ £1. (1973)
Buhler et al^. (1973)1*
Buhler et al.. (1973)
Buhler e£ a^. (1973)
Bevenue et al. (1972a)
Bevenue et al. (1972a)
NOMS = National Organics Monitoring Survey.
-Recovery = 94%.
3ND = non detectable.
** Aver age recovery = 103%.
-------
TABLE 7. FCP IN SURFACE WATERS OF THE NETHERLANDS
Concentration (Vg/1)
Site
Rhine
Boven Mernede
IJssel
Me use
Me use
Detection limit: 0.01 ng/1
Recoveries > 85%
Source: Wegman (1979)
1976
max.
2.4
2.6
2.00
3.9
1.4
med.
0.73
0.49
0.55
0.38
0.32
0.494
1977
max.
11
9.6
10
8.9
10
med.
1.1
1.0
1.0
0.79
0.78
0.934
37
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TABLE 8. AVERAGE CONCENTRATIONS OF PENTACHLOROPIIENOL IN POTW'S
• cl
Type of Sample
Influent
Effluent Pre
Chlorination
Final Effluent
% Removal
Primary Sludge
oa Waste Activated
Sludge
Flotables
Combined Sludge
Gravity Thickened
Overflow
Digested Sludge
Heat-treated Sludge
Heat Treatment Decant
Secondary Effluent
(Chlorinated)
Number of Days
Sampled
93
112
1
12
50
<50
3
1
2
1
<50
<50
5
100
ND
30
<50
25
ND
ND
15
93
ND
ND
<27
<250
<18
1000
ND
<250
60
NA
ND
ND
NA
Average concentration In pg/1.
Source: Preliminary data from Burns and Roe POTW Studies for Effluent Guidelines Division
U.S. Environmental Protection Agency.
-------
TABLE 9. PCP IN WATER AT VARIOUS LOCATIONS
Mean Concentration
in 24-hr. Samples (ug/1)
Location /Type
of Sample
r.orvallis Sewage Plant1
Corvallis
Eugene
Salem
Non-Potable Water, Hawaii2
Water (industrial area)
Sewage
Points on Naylors Creek3
Culvert (factory area)
Manoa Rd.
Manor Rd.
Garret t Rd.
Influent
1.4
4.1
4.6
Concentration
Mean
0.655
2.6
Concentration
Mean
6171
179
150
43
Output g/10000
Effluent POD., 24 hr.
1.0 5.5
3.3 26.0
4.4 33.6
(Ug/1)
Range
0.168 - 1.143
(ug/1)
Range
82 - 10,500
120 - 240
71 - 230
38 - 49
Oil sample at factory outlet 5.38 x 106 5.3 x 10s - 5.45 x 10s
lBuhler et al. (1973)
2Bevenue et aJU (1972a;
3Fountaine et al. (1975)
39
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TABLE 10. PCP IN WATER AND SEDIMENT1 OF FRESHWATER ECOSYSTEM
Water(p g/1)
Sediment (dry)(pg/kg)
Leaf Litter (dry)
Sample Date
2/27/7S2
4/24/75
6/28/75 •
8/05/75
10/11/75
12/6/75
2/7/76
5/3/76
8/11/76 3
10/22/76
1/5/77
2/22/77
4/27/77
Mean
10.3
7.8
18.3
2.25
2,8
21.2
18
6
2.8
0.5
36.5
88
7.8
Range
6-19
6-15
2-82
1-3
<1-10
1-76
10-29
2-18
0.1-11
2.3-1
16-81
29-147
5-16
Mean
162.2
254.8
474.2
116
269.5
253.6
117.6
36
487
440.3
209
1518
156.8
Range
2-800
21-1160
5-1300
10-207
24-927
11-900
10-313
7-96
142-857
166-994
250-277
1518
4-250
Mean(ng/ke)
6400 1 250
2550 ± 650
5200 ± 300
5800 1 1200
3470
1680 ± 12
6000 1 1000
1
Six sices on the lake and inlet stream were sampled.
Recovery of PCP Background levels in control pond
water
sediment
leaf litter
water
sediment
90 ± 15%
90 ± 38%
62 ± 4%
95
113
10%
25%
0.5 pg/1
5 pg/kg
50 pg/kg
0.28 pg/1
3.3 pg/kg
SOI
ce
1.
77)
i. t
-------
from 1 yg/1 to 5 ug/1 PCP, effluent ranged from 1 ug/1 to 4 ug/1 PCP,
and the Willamette River samples ranged from 0.1 ug/1 to 0.7 ug/1 PCP.
Bevenue et al. (1972a) reported PCP levels of 2.6 ug/1 at the Sand Island
outfall in Hawaii (see Table 9).
Fountaine et al- (1975) studied the effects of untreated industrial
effluents in a stream running through an industrial district with several
manufacturing (including wood-preserving) plants in Pennsylvania; they
found PCP levels ranging from 0.038 mg/1 to 10.5 mg/1 (see Table 9).
The authors believe that theit findings result from direct discharge into
the stream, with the additional possibility of chronic seepage from PCP-
saturated soil in the factory area.
Similar measurements of industrial waste outputs have been reported
by Pierce et al. (1977 and 1978) (see Table 10).
-------
TABLE 11. PCP LEVELS IN HUMAN TISSUE AND URINE
Population and Sample
Exposed workers - urine (Japan)
Non-exposed workers - urine (Japan)
General population - urine (Florida)
Occupational workers - urine (Florida)
General Population - adipose tissue
Concentration
fug/kg and ug/1)
Mean
4.9
119.9
26.3
Occupational population - urine (Hawaii) 1802
Non-occupational population - urine (Hawaii) 40
Occupational/non-occupa.tional population 217
- urine
Combination of the above three groups 587
(Hawaii)
Occupational worker exposure - urine -
by wood preserving methods (Oregon)
Dip 2830
Spray 980
Pressure 1240
U.S. General Population - urine 6.3
Range
1100-5910
10-50
2.2-11.2
22.2-270
12-52
3-35700
ND-1840
3-38642
120-9680
130-2580
170-5570
ND-193
Reference
Bevenue (1967a)
Bevenue (1967a)
Cranmer (1970)
Cranmer (1970)
Shafik (1973)l
Bevenue (1967b)2
Bevenue (1967b)
Bevenue (1967b)
ND-38642 Bevenue (1967b)
Arsenault (1976.
Kutz (1978)
Detection limit
Detection limit
Detection limit
^Detection limit
5 ug/kg.
3 ug/1.
5 ug/1.
5-30 ug/1.
-------
TABLE 12. PENTACHLOROPHENOL IN HUMAN URINE (FLORIDA)
Sample Origin
1 General Population
2 General Population
3 General Population
4 General Population
5 General Population
6 General Population
7 Carpenter
8 Boat Builder
9 Sprayman
10 Sprayman
Concentration ug/1
Replicate Range*
2.2 - 2.3
2.7 - 2.9
2.9 - 3.0
5.0 - 5.3
5.2 - 5.5
10.6 - 11.2
22.2 - 25.5
55.0 - 60.1
131 - 136
259 - 270
Mean2
2.2
2.8
2.9
5.1
5.3
10.8
24.1
57.3
133
265
*Four replicates of each sample.
2Varlation of the method was ±5%.
Source: Cranmer and Freal (1970).
-------
In a study of workers exposed to PCP in the wood preserving industry,
Arsenault (1976) reports FCP levels of 120-9680 ug/1 in urine, urith a
mean of approximately 1683 ug/1- In a hospital where two infant deaths
occurred due to PCF exposure, hospital diapers were found to contain
an average of 61937 ug/1 as a result of cleansing in a mildew preventa-
tiye. Samples of serum of nurses handling the linen revealed a level
of 5400 ug/1 PGP.
4. Air
Limited information is available on the levels of PCP in air, although
work by Bevenue .et al. (1972a) has reported PCP levels of 0.002-0.284 ug/1
in rainwater in Hawaii. In a study of 25 wood preserving companies in
Oregon, Arsenault (1976) reported PCP levels in the air of the plants
ranging from Q..003 mg/m3 to 0.063mg/m3 (see Table 13). In Sweden, Levin
and Nilson (1977) collected samples of air containing wood dust in trim-
ming and grading plants, where boards treated with PCP were cut; with a
recovery rate of 70%, they reported a mean value of 157,000 mg/m3 PCP.
5. Food and Feed
Levels of PCP in food sold over the counter were examined as a part of
FDA's ongoing Market Basket Studies (see Table 14). Heikes (1979)
reported an average of 18 ug/kg with a range of 1.8-62 ug/kg, in peanut
butter samples. The same, study also reported finding.PCP on the Mason
jar lids used in home canning. Between August 1974 and July 1975,
Johnson and Manske examined a wide range of products typically found in
the diet of 16-19 year olds. The products were purchased at random
locations, cooked, and then analyzed. PCP levels ranged from below
detection levels to 40 ug/kg, and detectable amounts were found in
dairy products, grain and cereal, leafy vegetables, foot vegetables,
garden fruits, fruits, and sugars and adjuncts. Grain and cereal, root
vegetables, and sugars had the highest mean concentrations: 1, 1, and
6 ug/kg, respectively.
In Michigan in 1977 several dairy herds were quarantined because
of the suspicion of possible PCP contamination from exposure to wood
treated with PCP. Lamparski et §1. (1978) analyzed milk collected from
the herds and found no evidence of PCP content at detection limits of
10-15 ug/1.
6. Biota
The premise that the distribution of PCP in the aquatic environment
is widespread would appear to be supported by reported levels of PCP (see
Tables 15-17). Zitco et al. (1974) collected fish samples from the St.
Croix and St. John estuaries and off the New Brunswick coast and bird
eggs from White Horse and Hospital Island. PCP levels in biota from
these relatively clean sample sites ranged from less than 0.5 ng/g to
10.33 ng/g.wet weight and averaged 2.23 ng/g. Rudling (1970) examined
fish in Sweden collected downstream from a pulp mill's effluent and
44
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TABLE 13. PCP IN AIR AT OREGON WOOD PRESERVING PLANTS
Concentration fme/m3)
Wood Preserving Process Mean Range
Dip .019 .003 - .063
Spray .006 .003 - .012
Pressure .014 .004 - .028
Source: Arsenault (1976).
-------
TABLE 14. PGP IN FOOD AND FEED
Sample
Dairy
Grain and Cereal
Leaf vegetables
Root vegetables
Garden fruits
Fruits
Sugars
Peanut butter
Bovine milk
Concentration (ug/1) and ug/kg)
Mean
0.5
1
T
1
T
T
6
18
ND
Range Reference
10 Johnson and Manske (1977)1
10 - 13 Johnson and Manske (1977)
13 Johnson and Manske (1977)
10 Johnson and Manske (1977)
10 Johnson and Manske (1977)
11 Johnson and Manske (1977)
10 - 40 Johnson and Manske (1977)
1.8 - 62 Heikes (1979)2
Lamparski et aj,. (1978) 3
IT ° average below detection limit. Samples collected through U.S. in
FDA's Market Basket Study.
2Market Basket Study - U.S. population.
^Michigan dairy herds, detection level « 10 ug/1.
46
-------
TABLE 15. PCP IN BIOTA
Sampling Site/Type
Lake (Sweden) - mg/kg
Pike
Perch
Eel
Mean
0.2
0.15
3.0
Concentration
Range
Reference
Rudling (1970)1
Coastal Estuaries (New Brunswick,
Canada) (ng/g wet weight)
Cod 0.82
Winter Flounder
Sea Raven 2.5
Silver Hake 1.75
Atlantic Salmon
White Shark Liver 10.83
Double-Crested Cormorant Egg 0.36
Herring Gull Egg 0.51
Fish Food 2.23
Zitco (1974)
1.77-3.99
0.54-1.26
Detection limit
Recovery:
Pike 87%
Perch 81%
Eel 91%
.1
-------
TABLE 16. PCP IN BIOTA
Lake (Mississippi)1'2
Mean
Concentration
(ng/g dry weight)
2/27/75 2500 ±200
4/24/75 1380 ± 20
6/23/75 130 - 70
10/11/75 Trace
12/6/75 651 ±650
2/10/76 87 ± 22
5/3/76 Trace
Recovery level = 62 - 4% Background level » 50 ng/g
Muscle Gills Liver
10/11/763
Sunfish-1
Sunfish-2
1/6/77
Sunfish-1
Sunfish-2
Bass-1
Bass-2
Bass-3
Catfish-1
4/27/77
Sunfish-1
Sunfish-2
Catfish-1
Catfish-2
Recovery level «
5
4
9,400
6,400
7,000
17,000
16,000
19,000
900
1,000
8,200
1,500
• ± -3%
N.A.1*
N.A.
48,400
N.A.
42,000
N.A.
N.A.
N.A.
N.A.
N.A.
N.A.
N.A.
26
150
130,000
N.A.
200,000
140,000
325,000
214,000
14,600
14,900
50,600
20,200
AAssumed to be combined values for sunfish, bass, catfish,
SPierce et al. (1977).
3Pierce and" Victor (1978)
^N.A. = not analvzed. 48
-------
TABLE 17. PCP CONCENTRATIONS IN FISH
TISSUE AS REPORTED IN THE
STORET DATA BASE1
Major River Basin
Lake Michigan
Lower Mississippi
Pacific Northwest
Western Gulf
S. Central Lover
Mississippi
Alaska
Concentration (mg/kgj
Range Mean
0.0022 0.002
0-1.3 0.478
0.005-50.O3 16.38
0 0
0 0
5.0 5.0
No. of
Observations
28
48
33
2
1
!For years 1976-79.
2All data are remarked.
3All data except for two observations are remarked.
49
-------
found PCP levels ranging from 0.2 mg to 3.0 mg of PGP per kg of tissue.
The STORE! data base reports tissue concentrations ranging from 0 mg/kg
to 50 mg/kg.
Pierce (1977 and 1978) studied a fresh water lake located below a
wood treating plant in Mississippi from 1975 to 1977. Observations over
this time period, which included two extensive fish kills, indicated per-
iodic releases of PCP from the watershed. In the first study, PCP con-
centrations in fish ranged from 87 ng to 2500 ng/g dry weight tissue,
while in leaf litter concentrations ranged from 1680 ng to 6400 ng PCP/g
dry weight. In their second study, the authors reported ranges from a
mean of 15.5 ng/g wet weight to a mean of 29400 ng/g wet weight tissue.
7. Soil
Although several authors refer to possible soil contamination as
a source of PCF levels in water samples, very little data are available
on actual measurements of PCP in soil. Fountaine (1975) says, "It is
at least possible that some of the PCP discharge might not be a result
of the present factory process but might be a result of the saturation
of the factory area with excess PCP." Pierce et al. (1978) state., "The
increase in PCP concentrations observed in February 1976 followed a
period of heavy rainfall, indicating that PCP was leached from the
contaminated watershed area..." Stark (1969) reported levels as high
as 1.5" PCP on a contaminated lake shore in Sweden. The detection
limit was .05 vg/kg with 80-100% recovery.
8. Miscellaneous Media
Von Langeveld (1975) examined PCP levels in the Netherlands in samples
of children's paints (i.e., watercolors, finger paints) and reported levels
ranging from 0.01 to 0.27 m/1 in nine out of sixty-five samples. The
detection limit was 4 mg/1.
C. ENVIRONMENTAL FATE
1. Physico-Chemical Fate Processes
a. Introduction
The following section describes, by environmental medium, the major
physical and chemical fate processes affecting PCP concentration and
distribution following its release. The media considered are air, water,
soil and wood that has been treated with preservative. Table 18 presents
some general chemical properties of PCP and lists the fate processes dis-
cussed in the following section for each medium.
b. Air
i. Atmospheric Photolysis
Very little information is available relating to the photolysis of
PC? in the atmosphere. Two references (GSb et a^., 1975 and Crosby and
50
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TABLE 18. CHEMICAL AND FATE PROPERTIES OF PENTACHLOROPHENOL
Chemical Structure of
Pentachlorophenol
Fate Processes
Air
Photolysis
Free Radical Oxidation
Rainout
Water
Hydrolysis
Photolysis
Oxidation
Volatilization
Biodegradation
Adsorption/Sedimentation
Chemical Properties
Molecular Weight 266.35
Melting Point
Boiling Point at
760 torr
Vapor Pressure at
20°C
190°C
310°C
1.1 - 1.7 x 10-4* torr
Solubility in Water 14 mg/L
20°C
Acid Dissociation
Constant
Log octanol/water
partition coefficient
pKa • 4.74
5.01
SOURCE: Versar (1979).
Soil
Sorption
Leaching
Hydrolysis
Photolysis
Volatilization
Biodegradation
Treated Wood
Photolysis
Volatilization
Leaching
-------
Hamadmad, 1971) Indicate chac PCP is probably photolyzed in the absence
of water, though the mechanisms for this are not well understood.
In one experiment (Gal) et al., 1975), PCP was sorbed onto a silica
gel or deposited as a film on a glass surface and then irradiated in
the presence of an oxygen stream. "It was observed that the conversion
rates of the substances absorbed on particulate matter were far higher
than with those deposited as solids or thin films on a glass surface."
This was attributed to a shift in absorption bands due to adsorption
onto particles, as well as to the greater dispersion of pesticide mole-
cules in the adsorbed phase resulting in greater contact of the pesticide
with oxygen. C02 and HC1 were formed during irradiation of PCP with wave-
lengths X >290 nui. No values were given for the intensity or spectrum
of light used; therefore it is not possible to relate the rates of
degradation in the environment to those determined experimentally
(Table 19).
TABLE 19. RESULTS OF PCP IRRADIATION IN UV LIGHT
(X >290 nm) UNDER TWO CONDITIONS
Initial Remaining _ , , »1
irradiation Solid Solid Products (mg)
Condition Time (Days) Material Material O>2 HC1 Cl2
(mg) (mg)
In oxygen stream 7 80 69 15 6 n.d.
Adsorbed on silica gel 102
4 26
7 12 n.d. n.d. n.d
L0ther compounds could have been formed but not detected by analytical
methods.
nci.d. m not detected.
Source: Gab et al., 1975.
In another experiment (Crosby and Hamadmad, 1971), PCP was dissolved
at a concentration of 1 g/1 in an organic solvent and irradiated at 25*C.
The PCP solution turned pale yellow after exposure to sunlight for 7 days.
When.:jPtCP>-;,was exposed as a film on glass, the same thing occurred. No
decomposition products were detected by gas-liquid chromatography or
thin-layer chromatography analysis. Similar PCP solutions were irradiated
in the laboratory with a low-pressure mercury arc lamp radiating at 253.7
nm. (Note that this wavelenghth is below the atmospheric .cutoff for solar
radiation of ^290 nm.) After 32 hours, 60% PCP, 30% tetrachlorophenol,
and 10% of another phenolic substance were found. The experimenters report
that "although definite photodecomposition [in PC?] was observed, both in
solution and in solid films, light probably is relatively unimportant in
loss...from the environment." This implies that other processes are acre
52
-------
significant than photodegradation for PCF loss. The authors did not dis-
cuss these processes, nor their reasoning for the statement.
Though it is difficult to draw any conclusions from these experi-
ments, photolysis of POP in water suggests that this may occur in the
atmosphere also. Because of normal atmospheric humidity, there is water
vapor in the atmosphere, and PCF is likely to adsorb onto aerosols due
to its low vapor pressure and high partition coefficient. These parti-
cles could serve as nuclei for water droplet formation or could be washed
out by rain. PCP has been found as a constituent of rainfall (Bevenue
et_aJL., 1972). Photolysis of sorbed PCP in the presence of oxygen also
occurs by UV light. Sunlight intensity in the atmosphere will be much
greater than in water, leading to a higher photolysis rate. Also, the
results from the first experiment (Gab e_t aL., 1975) indicate that the
presence of oxygen and UV light at wavelengths found in the atmosphere
are sufficient for PCP degradation in either the sorbed or film state,
but no light intensity was given. Results of both experiments indicate
the formation of degradation products similar to those found in water
photolysis.
On the basis of these considerations, the conservative assumption
that PCP photolyzes in the atmosphere has been adopted. In water, a
characteristic time can be taken to be approximately a week, but since
no strong argument can be made for photolysis lifetimes in air in the
range of hours or days, other removal processes have to be considered
in order to determine a characteristic lifetime of PCP in air.
ii. Atmospheric Free Radical Oxidation
Though no direct information was found regarding the susceptibility
of pentachlorophenol to free radical oxidation in the atmosphere, this
is not expected to be an important fate process. Data from Darnall
_et_al. (1976), the State of California Air Resources Board (1976) and
Hendry and Kenley (1979) indicate that related compounds such as benzene,
chlorobenzenes, nitrobenzenes, and phenol have low reactivity with respect
to the OH radical in the air. The non-reactive rating is uncertain but
can be reasonably estimated. The rate constant for OH radical oxidation
of PCF is expected to be <10~7/sec, based on the reactivity of these
similar compounds (<5 x 1010 cm3/mole-sec) and the global average OH con-
centration of 1.8 x 10~18 mole/cm3. A similar analysis can be applied
to ozone oxidation. The rate constant for benzene would be 4.5 x 10"1-/
sec based on average ozone concentrations. If the similarity between PCP
and benzene is valid, then ozone oxidation does not appear to 'be a signifi-
cant atmospheric removal process.
iii. Rainout
Rainout of FCP from the atmosphere is an environmental pathway that
has to be considered. There are no data concerning the rate or frequency
of the occurrence or the concentration of PCF in rainwater except for
local situations (concentrations are calculated later in Section IV.E).
53
-------
iv. Persistence
The residence time of pentachlorophenol in the atmosphere is depen-
dent on its chemical reactivity, as veil as on various atmospheric pheno-
mena. Since PCF does not appear to be substantially degraded through
photolysis or free radical oxidation, physical transport processes appear
to the most important determinants of its atmospheric persistence. Time
scales associated with major atmospheric processes have been estimated
by Junge (1977) and Slinn (1978). For precipitation or nucleation scaveng-
ing of a generalized air-borne pollutant, they reported a time scale of
one week and for the vertical mixing time of the troposphere, also one
week. Based on these observations, one month was assumed as conservative.
estimate of the lifetime of PCF in the atmosphere.
c. Water
Pentachlorophenol is a moderately strong organic acid with a piCa of 4.74.
PCP will therefore undergo a dissociation reaction with water, as shown in
equation
OH 0-
K - 1.82 x 1(T5 M
From the dissociation constant, it can be calculated that PCP is exten-
sively dissociated over the pH range (5-8) characteristic of natural
waters. The ratio of pentachlorophenate anion to pentachlorophenol con-
centration is approximately 1.8 at pH 5, 18 at pH 6, 180 at pH 7 and
1800 at pH 8. The degree of dissociation affects the distribution of PCP
in aquatic environments since the anion has a much greater water solubility
than the parent acid (Table 21). The apparent values of other physical
chemical parameters such as the Henry's law constant (Table 21) and octa-
mol:water partition coefficient will also be pH dependent and these in
turn will result in pH dependent behavior with regard to chemical reac-
tion, adsorption onto biota or sediments and volatilization.
Unfortunately, the pH of the aquatic medium is not always stated in
conjunction with reported experimental or monitoring data on PCP. This ac-
counts for some apparent discrepancies in reported values. For example,
the value of the octanol:water partition coefficient cited by Versar (1980)
(Table 18) as 102,000 or log P - 5.01, probably refers to the relatively
water insoluble PCP itself and would be appropriate for water with pH <_ 3.
The values given by Branson and Blau (1979) as 490 at 18°C (log P « 2.69)
and 980 at 70 8C (log P » 2.99) are probably "mixed", constants, reflecting
the higher hydrophilicity of the (unknown) fraction of the PCP that was
dissociated under the experimental conditions.
i. Hydrolysis
The covalent bond of a substituent attached to an aromatic ring is
usually resistant to hydrolysis because of the high negative charge-
density of the aromatic nucleus. For example, the synthesis of penta-
chlorophenolate anion from hexachlorobenzene requires treatment of the
hexachiorobenzene with concentrated alkali at 130"C-!-200°C. It can be
54
-------
assumed that more extreme conditions would be necessary for further
hydrolysis of the pentachlorophenolate anion. These are conditions not
normally found in the natural environment. Consequently, hydrolysis is
not an important mechanism for the removal of PCP from the environment
(USEPA, 1979a).
ii. Photolysis
Pentachlorophenol in water is photodegraded by sunlight. PCP ab-
sorbs ultraviolet light in the solar spectrum, with maximum absorption
occurring at a wavelength of 320 nm. In simulated sunlight, PCP at
concentrations of 100 mg/1 in a pH 7.3 borate-phosphate buffered solu-
tion was degraded totally in approximately 20 hours. Total degradation
occurred in a similar solution exposed to natural sunlight for 5-7 days
(Wong and Crosby, 1978). During one release event (Pierce and Victor,
1978), PCP appears to have been photodegraded into tetrachlorophenol
before reaching the water into which it flowed. This occurred while PCP
was in a solution with fuel oil or while in a holding pond.
Although it has been reported that sunlight will not degrade PCP in
the absence of water or some other solvent (Arsenault, 1976), evidence
exists to contradict this statement (Gab e£ al.., 1975).
Several intermediate products will be formed as a result of PCF
photodegradation (Wong and Crosby, 1978; Kaufman 1978a; Crosby and Wong,
1976). In naturally alkaline waters, it is possible that chlorinated
dioxins could be formed photochemically if the PCP concentration were
sufficiently high for bimolecular interaction. The production of dioxins
would depend then on the photolysis rate and concentration. The con-
centration though is usually too low for dioxin formation (Crosby and
Wong, 1976) (see Figure 7).
Test compounds irradiated in simulated and natural sunlight generate
octachlorodibenzodioxins (OCDD) and hexachlorodibenzodioxins (HCDD), but
no di-, tri-, or tetrachlorodibenzodioxins (Crosby and Wong, 1976). These
latter compounds are also unstable in ultraviolet light so may degrade
too rapidly for detection even if they are formed. The presence of HCDD
indicates that the more stable OCDD is being photodegraded. Pure PCP in
an aqueous solution of NaOH at a PCP (pentachlorophenate anion) concentra-
tion of 10 mg/1 irradiated in simulated sunlight for 16 hours generated
26 mg/1 of OCDD and 5 mg/1 of HCDD. HCDD and OCDD are also trace contami-
nants in technical grade PCP (Arsenault, 1976), and so may be present be-
fore they are formed as photodegradation products.
Degrading PCP also forms other compounds, lower chlorinated phenols,
tetrachlorodiols, and nonaromatics, as it degrades into final products
such as C02, HC1, H and chloride ions. A pathway for PCP degradation
and a list of products corresponding to these compunds are shown in
Figure 8 (Wong and Crosby, 1978); Kaufman, 1973a). PCP-OCH3 had also
been found in the aquatic environment as a product of PCF degradation
and it is speculated that this compound forms in the sediment in the
water (Pierce and Victor, 1978).
Arthur DLitrie !nc
-------
C!
PCP
Source: Crosby and Wong, 1976.
OCOD
FIGURE 7 OIOXIN FORMATION FROM PCP
PHOTOOEGRAOATION
(IX)
Small
Fragments
(e.g..HCl.C02)
I PCP
II 2,3,4,6-tetrachlorophenol
III 2,3,5,6-tetrachlorophenol
IV tetrachlororesorcinol
V tetracnlorohydroquinone
VI tetrachlorocatechol
VII trichlorobenzoquinone
VIII 3,5.6 trichloro-4-hvdroxybenzoquinone
IX 2,3-dichloro-5, 6-dihydroxybenzoquinone
X 2,5-dichloro-3, 6-dihydroxybenzoquinone (cnloranilic acid)
XI 2,3-dichloromaleic acid
Sources: Wong and Crosby. 1978.
Kaufman, 1978a.
FIGURE 3 PROPOSED PHOTOLYSIS PATHWAY FOR PCP
56
-------
Sodium pentachlorophenate (NaPCP), the sodium salt of PC?, is quick-
ly degraded in the presence of ultraviolet light and daylight. Degrada-
tion is almost complete in 16 hours with a sun simulating lamp (Stehl
ejt jd., 1971) (see Table 20). NaPCP has been shown to degrade rapidly in
shallow streams exposed to sunlight. NaPCF is sensitive to wavelengths
in the solar spectrum between 290 nm and 330 nm. The degradation process
appears to follow first-order kinetics with a velocity constant k»3.4 x
10-Vsec (Hiatt et. al., 1960; Monakata and Kuwahara, 1978) at I»0.04W/cm2
between 290 and 330 nm. The degradation rate equation is
klQt
dt oL
where k • a velocity constant, sec"1 ,
I0 a light intensity, w/cm ,
a * absorption coefficient ,
L » water depth ,
t « time , and,
c ° concentration .
Hiatt et al. (1960) reported Io»0.56 w/cm2 between 290 nm and 330 nm at
Cleveland at noon in midsummer. .This value is apparently high by a
factor of five or more, since solar intensity outside the atmosphere is
only 0.135 w/cm2. At sea level, 'sun at Zenith, incident light intensity
over the whole spectrum is 0.106 w/cm2 (Loferski, 1956). Consequently,
this equation may not be applicable to environmental conditions. The
0.04 w/cm2 value seems more realistic.
TABLE 20. STABILITY OF NaPCP IN SUNLIGHT AND ARTIFICIAL
LIGHT IN pH 8 PHOSPHATE BUFFER
Light Source Exposure Time % Degradation
Control 0 0
Fluorescent Black Light 16 hr 7.8
Mineral Light 16 hr 18.7
G.E.R.S. Sunlamp 16 hr 93.9
Daylight 12-16 hr l 45.6
Calculated from a total of 5 days, of which 3.5 days were rainy and
1.5 days (12-16 hr) had sunlight.
Source: Stehl et al. , 1971.
57
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The reported products of NaPCP photodegradation are shown in Figure 9,
Q
Cl
Q
Cl
C!
I 2,5 dichloro-3-hydroxy-6-pentachloropehnoxy-p-benzoquinone
II 2,4,5,6-tetrachlororesorcinol
III 2.5 dichloro-3-hydroxy-6-(2',4';5',6'-tetrachloro-3'- hydroxyphenoxy)•
p-benzoquinone
IV 3,4,5 trichloro-6-(2',3',4',5'-tetrachloro-6'-hydroxyphenoxy)-0-benzoquinone
V a 3-ring chloro, hydroxy compound
VI chloranilic acid
FIGURE 9 NaPCP PHOTODEGRADATION PRODUCTS
58
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Conclusion; Fentachlorophenol has been shown to photolyze in water
under conditions found in the environment. Degradation products formed
may include octachlorodibenzodioxins and hexachlorodibenzodioxins,
though these may also be present as contaminants in technical grade PCP.
Final degradation products are C02, HC1, H and chloride ions. The
sodium salt of PCP also photodegrades in water, and degradation products
are similar to those of PCP. No degradation rate constants applicable
to environmental conditions were found; however, a week seems to be a
reasonable lifetime to expect based on reported experiments.
iii. Oxidation
Although there is no specific information about the oxidation of
PCP, it can be assumed that this chemical behaves in the same manner
as other highly chlorinated organic compounds. Chemicals within this
class are usually resistent to oxidation even at .high temperatures not
commonly found in the natural environment (Morrison and Boyd, 1973).
For this reason, oxidation is assumed not to be an important chemical
process in the degradation of PCP under ambient conditions (USEPA, 1979a)
iv. Volatilization
Pentachlorophenol is not expected to volatilize from water at an
appreciable rate. The vapor pressure of PCP at 20°C is 1.1 x 10"1* torr
(1.4 x 10-" atm) and its solubility at pH6 is 75 mg/1 (.28 mole/m3) (see
Table 21). The Henry's Law coefficient is estimated to be (MacKay, 1976;
MacKa^ and Yuen, 1979). H - (Vapor Pressure)/(Solubility) " 5.2 x 10~7
atm-mVmole. At higher pH values, H is lower, as shown in Table 21. If
the value of H is less than about 3 x 10~7 atm-m3/mole, the substance is
less volatile than water and its concentration will increase as water
evaporates. Humidity ih'the air will lower the volatilization rate of
water somewhat so the lower limit is set at about 10-7. Therefore, a
substance in the range of H»10~7 to 10-6 atm-m /mole can be considered
involatile, or may volatilize very slowly at a rate dependent on H.
For these reasons, volatilization from water will not be considered
as an intermedia transfer process. This does not preclude PCP input into
air during spraying or mechanical agitation, as might .be the case in use
in cooling towers or aeration/evaporation ponds.
59
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TABLE 21. SOLUBILITY IN WATER AND HENRY'S LAW CONSTANT OF PENTACHLORO-
PHENOL AT DIFFERENT pH VALUES
% Water Solubility Apparent
pH Dissociated (mg/l)/mole/m3 H^atm-mf/mole
pH 3 1.8 14 0.053. 2.7 x 10"6
pH 5 64 34 0.13 1.1 x 10-"6
pH 6 95 75 0.28 5.2 x 10"7.
pH 7 99.5 1,950 7.32 2.0 x 10"8
pH 8 99.95 19,300 72.5 2.0 x 10"9
Note: Vapor pressure » 1.1 x 10"1* torr (1.4 x 10~7 atm) for. pentachlorophenol.
Increased solubility as a function of (pH) is due to increased
fraction of pentachlorophenate anion.
Source: Branson and Blau, 1979.
v. Biodegradation and Adsorption
Very little is known about the biodegradation of PGP in natural
waters. Most of the PC? emitted to a body of water is though to be absorbed
by the suspended particulates, the sediment, and the leaf litter.
In one study in which the background concentration of PCP in a
control pond was treasured, the concentration of PCP was shown to be 0.5
yg/1 in water and suspended particulates, 5 ug/kg in the sediments and
50 ug/kg in fish and leaf litter (Pierce et «1., 1977). This division
of PCP among the suspended particulates, the sediment, and the leaf
litter is typical of the way PCP partitions in the aquatic environment.
Little will go to the suspended particulates unless there is an unusually
large suspended particulate load, more will go to the sediment, and most
will be absorbed by the leaf litter.
The same study investigated the concentration distributions in an
aquatic ecosystem after a sudden large spill of PCP into its waters.
Concentrations were measured at six sites starting approximately 2
months after the spill and continuing every 2 months for a year and a
half. Except at the first sampling time, the concentration of PCP in
the sediment was far more than the concentration found in the water.
At one site, the concentrations in the two media differed by a factor
of a hundred (see Table 22). The low level of PCP that continued to be
found in the water was attributed to the continuous inflow of PCP from
the contaminated watershed area connecting the source of PCP and the
lake under study.
Yet still further evidence that PCP has a short life time in the
water was found 2 months after the spill. The fish kill immediately
after the spill was described as extensive to total Air and Water control
60
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TABLE 22. PCP CONCENTRATIONS IN WATER AND SEDIMENTS
Samole Site
Sample
Date
2/27/75
4/24/75
6/28/75
8/5/75
10/11/75
12/6/75
2/7/76
5/3/76
Water1
Sediment2
Water
Sediment
Water
Sediment
Water
Sediment
Water
Sediment
Water
Sediment
Water
Sediment
Water
Sediment
1
9
800
11
1,160
13
1,300
»
-
10
927
76
163
29
100
18"
96
2
11
<5
6
36
8
5
_
-
5
471
25
900
_
-
_
-
3
6
22
8
21
2
5
3
10
-------
Commission, Mississippi, 1975). However, within 2 months, a repopulation
of the fish in the lake demonstrated that the concentration of PCP in
water had drastically and rapidly declined. This could be attributed to
acclimitization, though levels in the lake were also low, as Table 22
shows.
Throughout this investigation, the concentration of PCP in the leaf
litter remained very high, even considerably higher than the concentration
of PCP in the sediment. In a separate study (Pierce et al.. 1974) it was
shown that PCP-contaminated leaf litter released 10% of the PCP to water
after a 24-hour equilibrium period. These results suggest that leaf
litter and sediments once contaminated with PCP can serve as a continual
source of pollution to the aquatic environment.
vi. Water Treatment
There are some discrepancies in the available data concerning the
effectiveness of wastewater treatment on the removal of PCP from process
wastes. Vela and Kasper (1973) reported an unsuccessful search for micro-
organisms capable of degrading PCP in industrial waters while Kirsch and
Etzel (1973) reported some PCP degradation in laboratory cultures of
mixed bacterial populations. Other investigators (Kincannon et al.,
1967, Reiner et al. 1978, and Vela and Rainer, 1976) have concluded from
their studies that PCP is removed in wastewater treatment.
In other studies, the effectiveness of activated sludge on the
removal of pentachlorophenol was shown to be dependent upon the type of
PCP, whether a pure sample or mixed samples of commercially available
PCP preparations. Kirsch and Etzel (1973) examined the feasibility of
biological treatment of PCP-containing wastes by using aerated continuous
flow systems and a contrived, soluble, PCP-supplemented waste. The average
degradation for PCP for 19 days of operation was 99.4%. On the 19th day,
the high-purity PCP was replaced by a blend of composite of five commercial
PCP solutions and a very noticeable decrease of the biodegradability of PCP
was observed. Kirsch (undated) found the same result when commercial grade
pentachlorophenate replaced "high grade" pentachlorophenate in experi-
mental waste treatment.
In an investigation of biological treatment of-PCP waste in a sewage
treatment plant, Arsenault examined mixtures of PCP in aeration lagoon
influent under aeration conditions (Arsenault, 1976). In two separate
experiments, the concentration of pentachlorophenol dropped from 39.5
mg/1 to 0.5 mg/1 in 3 days and from 81.0 mg/1 to 0.6 mg/1 in 30 hours.
These results show that secondary treatment is effective in reducing the
concentration of pentachlorophenol.
An on-site testing of the efficacy of pentachlorophenol removal by
water treatment was conducted in Corvallis, Eugene, and Salem, Oregon
(Buhler ejc_al_., 1972). The level of PCP in 24-hour composite samples of
sewage influent was collected simultaneously from these three cities- and
was shown by gas chromatography to be 1-5 ug/1. Composite effluent values
62
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from the same sewage treatment plant showed 1-4 ug/1 POP, representing a
4-28% removal. Examination of water from Willamette River just upstream
from Corvallis, Oregon, showed a considerably smaller concentration, only
0.10-0.70 ug/1* However, conventional processing of raw Willamette River
water at the nearby drinking water treatment plant showed a removal of
60% of the PCP originally present in the water. At the Corvallis, Oregon,
sewage treatment plant, water samples were taken at each stage of the
treatment plant to help determine the most efficient stage for the removal
of chlorophenol. As Table 23 shows, most of the PC? was removed by the
trickling filter, a finding suggesting that PCP was subjected to substantial
biodegradation.
d. Soil
i. Adsorption and Leaching
Adsorption: PCP is adsorbed most strongly onto soils that are
strongly acidic, regardless of the species of clay mineral or the organic
matter content (Choi et al.. 1974). Choi et al. (1974) studied 13 soils
of different clay and organic matter makeup, with concentrations of PCP
varying from 12.5 mg/kg to 500 mg/kg. The soils were divided into three
groups according to the pH: 4.6 to 5.1, 5.6 to 6.3, and 6.7 to 6.8 for
groups one, two and three, respectively. For group one, the adsorption
relationship was linear over the concentration range used. For the middle
group the relationship was curvilinear, while group three showed practi-
cally no adsorption. Since the initial PCP solution was alkaline, PCP was
almost completed dissociated. When this solution was added to the group
one acidic soil, PCP anions underwent protonation. At concentrations
greater than the solubility of PCF, then precipitation occurred (Choi et
al., 1974).
For the second group in which a moderate amount of adsorption occurred,
the pH of the soil-PCP system was 5.6 or greater. Therefore, PCP was
completely dissolved and mostly dissociated. However, the pH of the clay
surface was lower than the pH of the external solution (liquid phase) in
the case of partly neutralized soils. Consequently, it was possible for
PCP molecules to exist at the clay surface even when the pH of the liquid
phase was high enough for complete dissociation. PCP adsorbed on the soil
would be PCP molecules and/or anions (Choi et al., 1974).
For group three where the pH is 2 units or more greater than the pKa
of PCF, there was no adsorption or precipitation. Apparently, these soils
do not adsorb the PCF anions.
PCF adsorption onto soils is apparently a function of the pH of the soil.
Figure 10 graphically illustrates this relationship. As pH increases,
the percent of PCF adsorbed decreases. However, it is interesting to
note the difference in adsorptivity among the soil types at a given pH
value. The magnitude of adsorption appears to be related to the nature
of soil colloids. The decreasing order to adsorption is humus-rich
63
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TABLE 23. CONCENTRATION AND PERCENT REMOVAL OF
HEXACHLOROPHENE AND PENTACHLOROPHENOL AT
VARIOUS STAGES WITHIN THE CORVALLIS,
OREGON,SEWAGE TREATMENT PLANT1
Concentration3 Percent
Stage Sampled in Plant
After grit chamber
(influent)
After primary clarifier
After trickling filter
After chlorination
Out to river (effluent)
lime
Sampled2
9:00
10:00
10:30
11:00
13:00
HCP
22.2
21.6
6.4
6.8
7.3
PCP
0.91
1.10
0.51
0.49
0.33
HCP
• • •
2.7
71.4
69.4
67.1
PCP
• • •
0.0
44.0
46.2
63.7
1Samples collected on September 24, 1969.
2Sampled at the times indicated to compensate for flow times between
the various stages of operation
3Mean of duplicate extractions and analyses.
Source: Buhler etal., 1972.
64
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100
f 50
i
5.0
575
6.0
PH
7-P
Note: Numbers represent different soil types.
Source: Choi, et el.. 1974.
FIGURE 10 RELATION OF THE APPARENT
ADSORPTION TO THE pH OF
THE SUPERNATANT LIQUID
(Initial concentration: 100 ppm)
65
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allophanic (Nos. 575 and 509), allophanic (No. 576), montmorillonitic
(No. 124), and halloysitic soil (No. 585). Humus seems to adsorb more
PC? Chan inorganic clays, and allophanic clay does so compared .with
crystalline clay (Choi ec al. 1974).
Much research has been done concerning adsorption of PCP on the
organic fraction of soil. An increase in organic matter increases the
adsorption of PCP in soils. (A more detailed review of this subject is
given in the Section IV.C.d.iv. below).
Leaching; Leaching does not appear to be a significant mode of
transport for PCP due to the chemical's high affinity for binding to
organic matter in soil and its low solubility in water. Any leaching
that does occur is by the movement of the oil-based solution. In addition,
some leaching may take place in alkaline or in inorganic clay soils with
a low organic fraction; however, no specific information on this subject
was available.
In one test, leachates were captured from soil that was composted
with PCP-containing sludges from a wood preservation process at concen-
trations of 100, 200, and 300 mg/1 of PCP (Arsenault, 1976). Concentra-
tions in the leachates were 0.19, 0.067 and 0.108 mg/1, respectively, less
than 0.1% of the original amount or concentration of PCP. Consequently, it was
concluded that there is not significant migration of PCP through the soil.
ii. Photolysis
No information was found concerning the photolysis of PCP in soil.
It is assumed, however, that this would be only a minor degradation
process since only small amounts would be exposed on the soil surface.
Photolysis of PCP in soil will, therefore, not be considered further as
a degradation process.
iii. Volatilization
PCP sorbs strongly onto soils and sediments, especially those with
high organic matter content. Therefore, loss from soil by volatilization
is not expected to be a major transfer pathway. In an experimental setup
measuring photodegradation in soil, losses by volatilization accounted
for only 0.5% or less of the PCP added to the soil (Kaufman, 1978).
iv. Biodegfadation
The rate of biodegradation of PCP is largely dependent upon the
temperature, aeration, moisture, and organic content of the soil; somewhat
dependent on the cation exchange capacity and soil pH; and not dependent
upon the soil texture, clay content, or degree of base saturation. Kuwatsuka
and Igarishi (1975) reported a weak correlation of PCP biodegradacion
rates with free iron content and phosphate adsorption coefficient, but
little correlation with available phosphorus content. Their conclusion
concerning free iron content can be contrasted with Kaufman's (1978M
66
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finding chat the rate of degradation of PGP is not influenced by free
iron oxides.
The effect of flooding and anaerobic conditions on PCP degradation
in rice paddies and upland adjacent fields was investigated under field con-
ditions (Kuwatsuka and Igarishi, 1975). It was shown that the half-life for
PCP under flooded conditions ranged from 10 days to 70 days, while under
upland conditions the range was 20 to 120 days. The time required to
degrade 90% of the PCP present was 80 days or more under flooded con-
ditions and 50 days or more under dry conditions (see Figure 11 and
Table 24).
Temperature also plays a key role in the rate of PCP degradation in
soil. At higher temperatures, PCP disappeared more quickly under anaer-
obic (flooded) conditions than it did under aerobic conditions.
The most influential factor in the degradation of PCP is the amount
of organic material present in the soil. In a laboratory study, Kuwatsuka
(1972) found that the half-life of PCP at an initial concentration of 100
mg/kg at 30°C was 10 to 40 days under flooded conditions in arable soil,
whereas almost 100% was present in soils with low organic matter content
after 2 months (see Figure 12). Kuwatsuka and Igarishi (1975) showed
that a forest subsoil with only trace organic matter retained almost 100%
of the initial PCP concentration after 50 days under both water conditions.
Young and Carroll (1951) also observed that PCP decreased more rapidly in
soils containing a higher organic matter content. Results found by
Watanabe (1973a) and Ide et al. (1972) revealed that PCP disappeared
quickly in mature paddy fields, but very slowly in a newly reclaimed
field and in soil collected from an immature field. No reasons for this
behavior were given, but it may be due to the presence of adapted popula-
tions.
The same investigators found that additional applications of PCP to
the paddy fields resulted in accelerated degradation and that no PCP
degradation occurred in submerged soils that had been sterilized. These
results indicate that PCP degrades more quickly in soils with high organic
matter and that the degradation process is related to the microbial activity
of the soil. A final study by Kaufman (1978b) showed a more rapid degrada-
tion of PCP in paddy soil under flooded conditions than in previously aerobic
soils placed under anaerobic conditions, thus showing that the rate of degra-
dation is dependent on an established anaerobic population.
Appendix B presents more detailed information on biodegradation products
and pathways for pentachlorophenol.
e. Treated Wood
i. Photolysis
Pentachlorophenol on the surfaces of treated wood products exposed
exposed to sunlight is photolyzed (USEPA, 19~8c, Lamparski et al..
1980). PCP concentration on wood poles treated with PCP/oil solution
on the sun-exoosed side of the wood and the northern side of the wood
-------
20
30
40
10
20
100 pom 30°
H
30
40
SO 0
Days
Now Letters indicate different soil types.
Source: Kuwatsuku (1972).
FIGURE 11 PGP DEGRADATION IN VARIOUS SOILS UNDER
FLOODED AND UPLAND CONDITIONS
SO
100
T T
1234567
C%
Source: Kuwatsuku (1972)
FIGURE 12 RELATION BETWEEN DEGRADATION RATE OF
PGP AND ORGANIC MATTER CONTENT IN
VARIOUS SOILS FOR DIFFERENT INCUBATION
PERIODS (days)
68
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TABLE 24. CORRELATION COEFFICIENTS BETWEEN DEGRADATION
RATE O'F PCI' AND PROPERTIES OF SOILS1
Flooded Conditions
Incubation period (days)
Soli. Property
Total Carbon Content
Clay Content
C • E • C •
Available Phosphorus
Content
Free Iron Content
pll (II 0)
Phosphate absorption
Coefficient
Upland Conditions
5
***0.839
0.182
***0.831
0.392
**0.889
0.392
10
***0.815
0.457
*0.574
0.365
*0.633
*0.630
20
**0.625
0.352 .
*0.599
*0.499
***0.858
0.420
30
***0.827
0.432
*0.525
*0.589
0.409
0.432
5
**0.817
0.046
**0.926
*0.675
0.091
0.181
10
**0.814
0.264
**0.763
*0.642
0.597
0.539
20
*0.539
0.194
0.368
0.144
0.358
0.444
30
0.383
0.152
0.333
0.198
0.387
0.15)
***0.877
*0.730 ***0.908
***0.922 ***0.937
**0.821
0.368
0.251
*** ** * indicate significance levels of O.I, 1, and 5%, respectively
Data on Tochigi soils under flooded and upland conditions were not Included.
Applied amount +residual amount „ 1
Degradation rate = Applied amount
Incubation Period
Source.: Ide etal., 1973.
-------
(shaded side) differed by 2.4 ng/in2. On the sunny side PCP was
found on the surface ac .7 r.g/in2 and on the shady side at 3.1 ng/in2.
On wood poles treated with a PCP/cella mixture, the differences were even
greater. PCP was found on the south side on .the surface at a concentra-
tion of 0.2 ng/in2. On the north side the concentration of PCP was 2.8
ng/in2. This is a difference of 1.74 ng/in2 in three years, or .58 ng/
in2/yr. This figure probably does not represent the actual photolysis
rate since initial conditions were not known and some portion of the
difference observed may be attributable to other causes.
Experiments with PCP added to filter paper showed that exposure to
ultraviolet light for 7 days degrades more than 90% of 7500 ng PCP initially
initially applied (USEPA, 1978c). There is some evidence that hexachloro-
benzene and certain dioxins may be degradation products of PCP photolysis
(U.S. EPA 1980a).
Experiments were performed to determine the effects of sunlight on
chlorinated dibenzo-p-dioxin formation from PCP in wood treated with
different types of PCP (Lamparski et al., 1980). Yellow pine was treated
with Dowicide EC-7 anti-microbial PCP, purified PCP, and technical PCP
in two types of carrier solutions, methylene chloride and P-9 oil.
Samples were exposed to natural sunlight and a GE Model RS sunlamp that
approximates the natural sunlight. Results of the experiments showed
that EC-7 behaved similarly to very pure PCP. An increase in octachloro-
dibenzo-fp-dioxin (OCDD) concentration was noted in the solutions using
methylene chloride,peaking after about 20 days and was due to photolysis.
Hexa-CDD and hepta-CDD were also found, and temporal variation was similar
to that of OCDD, and were apparently a photodegradation product of OCDD.
Temporal behavior of OCDD formation in the PCP/P-9 oil mixture was similar
to that of the PCP/MC mixture, though total OCDD concentrations were
significantly less (by a factor of about 20) in the PCP/P-9 oil mixture.
The higher content in the PCP/MC solution was attributed to photolytic
reactions of the PCP with the methylene chloride. This did not occur in
the PCP/P-9 oil solution. No information was reported concerning the
concentration of PCP as a function of time.
In conclusion, PCP residing on wood surfaces exposed to light is
likely to be photodegraded. It should be noted that the amount of PCP
held in the surface layer of treated wood is small relative to the unavail-
able amount held in the body of the wood. Unless PCP solution continues
to migrate out from underlying layers, of wood, the PCP concentration on
the wood surface will decrease due to photolysis (Arsenault, 1976).
11. Volatilization
The vapor pressure of pentachlorophenol, 1.1-1.7 x 10"** torr at 20°C
and 3.1 x 10~3 torr at 50°C, suggests that PCP say be volatilized from
wood surfaces (USEPA, 1978a). Walls in a room treated with a PCP wood
preservative released the chemical into the air, with concentrations
reaching 1 ng/m3 air on the first day after treatment and 160 ng/m air
on the fourth day (Gebefugl et al., 1970). Since no information was
given about the size of the room, treated surface/enclosed volume rates,
or air exchange rates, it is not possible to compute the volatilization
rate.
70
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The EPA (1978c) reports that evaporation of PCP, with a vapor pressure
of 1.6 x 10- torr, from a treated surface in which it is adsorbed vields
a vapor density of 2.3 x 10~9 g/cm3 in the immediate vicinity of the
surface. This yields a calculated rate of evaporation of 1.7 x 10"10
g/cm /sec or 53.6 g/m2/yr, though no method for this calculation was given
^ue to the high adsorption forces for PCP on wood, PCP may be volatilized
much more slowly. Therefore, these values should be considered an upper
bound on the rate. The results of more recent investigations on this
subject are expected to be available in the near future (U.S. EPA 1980a).
In wood treatment, the PCP concentration in the finished products
is about 8 kg/m (see calculation developed subsequently in IV-D-2-c for PCP
atmospheric concentrations due to volatilization from treated wood products)
So, in the top 1 mm of surface of distribution, the "concent-ration" is 8 kg/m3
x 10- m- 8 g PCP/mz surface. The upper limit value of the volatilization
rate indicates that this PCP would be depleted in O.lSyr or 1.8 months
One year is, therefore, expected to be a conservative estimate for the
lifetime of PCP in wood surfaces.
iii. Leaching
No information was available that would indicate the propensity for
PCP to leach out of treated wood into surrounding soil or water. Although
PCP has a high affinity for organic matter, it may behave differently in
wood, especially under saturated conditions. If its adsorption to wood
is also pH dependent, alkaline conditions may cause its release from, wood.
These statements are speculative and experimental verification is required
before conclusions regarding PCP's behavior in wood can be made.
f. Conclusions
Based on the results of the laboratory and field studies of penta-
chloroohenol in air, water, soil and treated wood described in Section
IV-B-1., some generalizations can be made concerning the pollutant's
behavior in the environment. These conclusions are based on limited
data and are subject to the usual difficulties in extrapolating experi-
mental results to natural systems.
The air compartment appears to receive a large amount of PCP discharge,
however, the total mass entering the atmosphere cannot be accurately esti-
mated at this time (see Section III). Pathways for entry into air include
evaporation from aeration/evaporation ponds at wood treatment facilities
used instead of direct discharge to water, evaporation and/or droplet
release from cooling towers using PCP biocide, volatilization from treated
wood products and burning of treated wood. Physical removal mechanisms,
such as rainout, are important processes affecting PCP concentrations in
the atmosphere. Photolysis appears to be an important transformation
process based on PCP's behavior in water. Free radical oxidation does
not appear to affect PC?. The atmospheric lifetime for PCP was estimated
at one month and was assumed to be determined primarily by physical removal
processes.
71
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Surface water is also an important compartment to consider in PCF
pathways analysis. Certain FCP users practice direct discharge and there
is potential for direct entry from numerous non-point sources including
from treated wood. In addition, transfer of PGP from other compartments
such as air through rainout, and soil, throughout runoff and leaching,
can occur. Monitoring data and fish kill incidents indicate the presence
of PGP in water over the past ten years (see Sections IV-A and VI-B).
Unfortunately, data are few and scattered, and do not indicate the
national distribution of the pollutant in surface waters. At low con-
centrations in water, PGP appears to be quite readily degraded by microbial
action (in water treatment facilities) and, in clear water, photolyzes
rapidly. Extreme concentrations or turbid conditions could inhibit these
two processes. Sorption to sediments and larger pieces of organic matter
is also likely to occur. Hydrolysis, oxidation and volatilization do not
appear to affect concentrations in water significantly. The lifetime of
PCP in natural waters in which PGP fate processes take place was estimated
at one week, in conditions optimizing photolysis. For systems where
biodegradation is the primary removal mechanism, the lifetime will be
longer and extremely variable, depending on the conditions. Once PCP is
adsorbed onto sediment, there appears to be potential for re-release to
water; however, the conditions that would trigger this transfer have not
been investigated.
Pentachlorophenol enters the soil compartment as a result of its
use as a garden herbicide, leaching from treated wood, rainout from the
atmosphere, and spills around PGP-using industries. No monitoring data
of PCP levels in soil were available to indicate typical concentrations.
Due to its hieh adsorptivity, especially on organic matter and under
acidic conditionstand based on the results of a laboratory study, PCP
•does not appear to be very mobile in soil. Biodegradation is a signifi-
cant removal process under both aerobic and anaerobic conditions. Impor-
tant variables affecting the degradation rate include temperature, mois-
ture and the presence of organic matter, and less so, the soil cation
exchange capacity and pH. Photolysis and volatilization do not appear
to be important soil processes in relation to PCP concentrations. Trans-
fer of PCP from soil to water may occur through runoff and physical
transport of PGP-adsorbed surface soil.
Wood that has been treated with pentachlorophenol apparently loses,
at a minimum, the amount of chemical residing in the wood's surface layer.
Photolysis degrades PCP in products exposed to sunlight, although no rate
information was available. In addition volatilization occurs at a fairly
slow rate, estimated at 1.7 x 1Q-10 g/cm2/sec. Based on this volatiliza-
tion rate, a lifetime of one year for PCP residence in wood was estimated.
The potential for removal of PCP from treated wood resulting from runoff
from surfaces or leaching exists, however, information that would indicate
the overall importance of this process was not available. Further investi-
gation of this potentially significant pathway to water and soil is essen-
tial because of the large amount of PCP used as a wood preservative and
the widespread national distribution of treated wood products.
72
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2. Biological Pathways
a. Introduction
This section concerns the biological pathways for PCP, and particu-
larly its uptake and metabolism in higher organisms. The topics discussed
include potential for uptake, bioaccumulation, metabolism, and elimination
of PCP in both aquatic and terrestrial organisms.
b. Freshwater Systems
The potential for bioaccumulation of PCP is indicated by the log of
the octanol/water partition coefficient, log P » 5.01. This potential
is confirmed by a number of laboratory studies, which have indicated that
PCP is accumulated significantly by aquatic organisms, particularly, those
from higher trophic levels. Lu e_t al. (-1978) examined the fate of radio-
labeled PCP in two model ecosystems, one simulating a fresh water system
and the other a terrestrial/aquatic system simulating a lake and its
shoreline. For the first system, the results showed that the radiolabeled
PCP and its metabolites were rapidly accumulated after 3 days in the food
chain organisms, and most of the parent compound was stored intact. In
the terrestrial/aquatic model with the same species, PCF was applied at
a rate of approximately 1.0 kg/ha, and dispersed by the feeding activities
of salt marsh caterpillars. In this system, however, bioaccumulation
factors were considerably higher (by a factor of 3 to >100) than in the
aquatic model. PCP was also metabolized to a greater extent (primarily
by reductive dechlorination) in the terrestrial/aquatic system. No
explanation was offered for the difference, in results for the two models.
Other studies have confirmed the propensity of PCP to accumulate in
the tissues of exposed organisms. Glickman e_t al. (1978) found that radio-
labeled PCP was rapidly taken up by rainbow trout; residues accumulated
to 16 mg/kg in the liver. High concentrations (250 mg/kg) of PCP were
detected in the bile, primarily as the glucuronide conjugate. In another
study, guppies (Lebistes reticulatus) were killed by 3 mg/1 PCP in 16-18
hours, the bioaccumulation factor during this period was approximately
35 (Stark, 1969).
Kobayashi and Akitake (1975) exposed goldfish to 0.1, 0.2, and 0.4
mg/1 of radiolabeled PCP. The respective bioaccumulation factors measured
after death were 1,000, 570, and 278. In each case, the residues found
in the dead 'specimens were approximately 100 mg/kg, a finding indicating
a. maximum tolerance level for this species. Even during exposure, PCP
was excreted rapidly by the goldfish; accumulation occurred when the rate
of absorption exceeded the rate of excretion.
In a study by Halias (NDC ), guppies accumulated PC? up to 0.1% of
their weight before dying from toxic effects. Of the PCP residues, 99%
were metabolized, leading the author to suggest chat the metabolites,
and not PCP per se. were toxic to fish.
73
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PCP residues were found in three species of fish in a lake receiving
effluents from a pulp mill (Rudling, 1970). Lake concentrations averaged
about 3 ug/lf while PCP residues in perch, pike, and eel ranged between
0.15 and 3.0 mg/kg. In another field study, Pierce et_ al. (1977) examined
the effects of a major PCP discharge to a man-made lake in Mississippi.
After an initial fish kill (described as. extensive to total), residues
in small fish returned to background levels within 10 months. However,
this work does not provide any information regarding possible biomagnifi-
cation in the aquatic food chain, as no predator fish were examined for
PCP residues.
Holmberg e_t al. (1972) exposed the anadromous yellow eel (Anguilla
anguilla) to PCP in freshwater and seawater to compare uptake in the
different media. The eels in freshwater were exposed for 4 days, and
the test organisms in saltwater for 8 days, both at concentrations of
100 ug/1. The respective bioaccumulation factors were 90 and 300, although
uptake was initially.more rapid in freshwater. The authors attributed the
difference in the factors to the unequal exposure periods, and possibly
the higher pH in the seawater (8.1, as opposed to 7.1 in freshwater).
(For a discussion of the influence of pH on PCP activity, see Section VI.A.)
The available data on PCP bioaccumulation in freshwater organisms
are summarized in Table 25.
c. Marine Fish
* In a study of PCP uptake by sheepshead minnows, Parrish e_t al. (1978)
found that juveniles had substantially higher bioaccumulation factors than
adults or egg/embryos, in addition to a more rapid rate of uptake. Schimmel
et al. (1978) performed residue analysis on dead specimens of two fish and
two shrimp species from 96-hour toxicity bioassays. A longer-term experi-
ment was also conducted on the Eastern oyster, (a filter feeder and hence
a better accumulator than most species) for 28 days. Equilibrium concen-
trations were attained in 4 days, but depuration to non-detectable levels
was equally rapid, occurring in 4 days also. The data from these studies
are summarized in Table 26.
d. Terrestrial Organisms
Lu et al. (1978) applied radiolabeled PCP to a model terrestrial
ecosystem, and found that only 1% had entered into animals after 20 days,
and 48% into the soil. Corn plants (Zaa mays) accumulated PCP rapidly,
and metabolized 84% of the uptake. The prairie vole (Michrotus ochregaster)
at the top of the food chain, had consumed virtually all of the plant and
animal material in the system after 5 days of exposure. Tissue residues
accounted for 0.5% of the total PCP dose applied to the system, and ranged
from 135 yg/kg in the uterus to 26 yg/kg in the skin.
In a field ecosystem study, Vermeer e_t al. (1974) examined uptake
and effects of PCP and other pesticides on organisms in an 8000-ha rice
field. Residues of PC? in birds, fish, and snails were measured after
74
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TABLE 23. PC? BXOACCUMULATION IN FRESHWATER BIOTA
Species
PC? Concentration
in media (ug/O
Bloaccum. Exposure
Factor Period Reference
Gambusla affinis
(aquatic system)
Cambuaia af finis
(terr. /aquatic sys.)
Snail (Physa sp.)
(aquatic system)
Snail (Physa sp. )
(terr. /aquatic sys.)
Daphnta magna
(aquatic system)
Daphnia magna
(terr. /aquatic. sys.)
Mosquito (Culex pipiens) larvae
(aquatic system)
Mosquito (Culex pipiens) larvae
(terr. /aquatic sys.)
Alga (Oedogonium cardiacum)
(aquatic system)
Alga (Oedogonium eardiacum)
(terr. /aquatic sys.)
Rainbow trout (Salmo gairdneri)
Cuppy (Lebistes reticulatua) 3
Goldfish (Carassius auratus)
Goldfish (Carassius auratus)
Goldfish (Carassius auratus)
Snail 2
Perch (Perca fluviatilis)
Northern pike (Esox lueius)
Yellow eel (Anguilla angullla)
Yellow eel (Anguilla angullla)
freshwater
Yellow eel (Anguilla anguilla)
seawater
2.7
1.0 kg/ha
2.7
1.0 kg/ha
2.7
1.0 kg/ha
2.7
1.0 kg/ha
2.7
1.0 kg/ha
20
,000
100
200
400
.000
3
3
3
100
100
2.96
132
1.21
21
1.65
204
16
21
1.5
5
%0.35
•05
1,000
570
278
50
50
67
1.000
90
300
72 h
•
72 h
72 h
72 h
72 h
24 h
18 h
120 h
20 h
6 h
30 h
Indefinite
Indefinite
Indefinite
4 d
8 d
Lu et al. (1978)
Lu et al. (1978)
Lu et al. (1978)
Lu et al. (1978)
Lu et al. (1978)
Lu et al. (1978)
Lu et al: (1978)
Lu et al. (1978)
Lu et al. (1978)
Lu et al. (1978)
Glickman et al.
(1978)
Seark (1969)
Kobayaahi and
Akltake (1975)
Kobayaahi and
Akitake (1975)
Kobayaahi and
Akitake (1975)
Weinbach and
Nolan (1956)
Rudling (1970)
Rudling (1970)
Rudling (1970)
Holaberg et al. (1972)
Holaberg et ai. (1972)
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TABLE 26. PCP IllOACCUMULATION IN MARINE BIOTA
Species
Sheepshead minnows (Cyprinodon varlegatus)
juveniles
iidul r.s
eggs/embryos
l.ongnose kllllflsh (Fiindulls slmllls)
Striped mullet (Mugll cephalus)
**4
^ Crass slirlmp (Palaemonetes pufilo)
Brown shrimp (Penaeus aztecus)
Eastern oyster (Crassostrea virglnlca)
Eastern oyster (Crassostrea virglnica)
PCP
Concentration
(nB/1)
18
18
18
88
85
85
76
49
2.5
25
Bioaccuuiu-
lation
Factor
48
27
26
41
79
3.0
0.45
78
41
Exposure
Period
28 d
151 d
138 d
96 h
96 h
96 h
96 h
28 d
28 d
Reference
Parrlsh et art.. (1978)
Parrlsh et_ al. (1978)
Parrlsh et al. (1978)
Parrlsh et_ al. (1978)
Schlmmel et al. (1978)
Schlmmel et al. (1978)
Schlmmel e£ al. (1978)
Schlmroel et al. (1978)
Schlmmel et al. (1978)
Schlnunel et al. (1978)
-------
applications of 4 kg/ha NaPCP, resulting in a concentration of 4 mg/1.
Fish found dead after applications contained 31-59 mg/kg PCP, while fish
collected alive from unsprayed ditches contained 2-13 mg/kg PCP. In dead
snails (Pomacea sp.), residues of 37 mg/kg PC? were found. Birds in the
area were found to contain PCP residues ranging from 0.04 mg/kg in the
purple gallinule (Porphyruls martinica). which feeds on rice seeds, to 10.0
mg/kg in a common egret (Egretta alba). which feeds on insects, fish and
amphibians. Fifty (out of 279) snail kites, which feed almost exclusively
on Pomacea, were found dead after NaPCP spraying. Concentrations of PCF
in their brains, livers and kidneys were 11, 46 and 20 mg/kg respectively.
In a study of PCP fate in cotton, Miller and Aboul-Ela (1969) found
that the toxicant accumulated to concentrations of 2 mg/kg in cottonseed
kernels of closed bolls. In kernels of open bolls on the same plants,
however, PCP was not detected, indicating that it may be translocated
from hulls to developing seeds.
Hilton et al. (1970) applied PCP to sugarcane in 6-mg doses per
plant, and found that 84% was retained by the leaves. When the leaves
abscised naturally, virtually all of the remaining PCP was lost from the
plant. Roots exposed to PCP in solution absorbed 99% of the toxicant,
while the remaining 1% was delivered to the stalk and suckers.
Rice seedlings in one experiment absorbed 3% of PCP applied to the
soil at a concentration corresponding to agricultural application.
Residues in the seedlings were determined to be 90% PCP, and most of the
remainder unidentified conjugates (Hague et al., 1978).
e. Conclusions
PCP has a high propensity to accumulate in the tissues of both
aquatic and terrestrial biota. Reported bioconcentration factors in
fish range from 3 to 1,000, depending on the species, duration of
exposure, aqueous PCP concentration, and.environmental factors such as
salinity and pH. Studies in which biochemical analyses were performed
indicate that PCP is metabolized to a large extent in fish tissues. The
metabolites are apparently toxic as well, which in some species are not
tolerated above a certain level. There is some evidence that PCF bio-
magnifies in food chains, but no conclusive data on this aspect are
available.
Little 'information is available on the characteristics of PCF uptake
in terrestrial ecosystems. Sugarcane and corn plants have been observed
to accumulate PCP strongly, although plants vary in their tendency to
metabolize the toxicant. PCP may also concentrate selectively in certain
tissues, such as the leaves or roots, depending on the type of exposure.
77
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D. CONCENTRATION ESTIMATES
1. Introduction
This section presents estimations of PC? concentrations in environ-
mental media based on simple calculational procedures using materials
balance, fate , and in some cases, monitoring data as input. Only the
air and water compartments were considered. Soil was excluded due to
the complexities of the medium and lack of simple calculational models.
This does not mean to imply that soil is not an important environmental
compartment for PCP residues. There is a significant potential for
release of the pollutant to soil through garden herbicide .use and leach-
ing from treated wood.
The air compartment is an important recipient of PCP discharge as
discussed in Sections III and IV-B. Important sources to air include
evaporation of wood treatment facility wastewater, volatilization from
treated wood surfaces, cooling tower water evaporation, and open burning
of PCP-treated wood. For an assumed steady-state input of PCP, estimations
were made of air concentrations on a national scale resulting from each
source category. In addition, the propensity for transfer of PCP from
air to water (or soil) through rainout was calculated. Last of all, two
local-scale PCP concentration estimations were calculated:
1) in a plume downwind from a cooling tower using PCP as
a biocide,
2) in a plume downwind from a wastewater evaporation pond.
The water compartment is potentially a significant recipient of PCP
release although the sources are numerous, widespread, and often
undefined. Reports of PCP-caused fish kills (see Section VI-B) indicate
PCP contamination of water at harmful concentrations. The most signifi-
cant user of PCP, the wood preserving industry, does not commonly practice
direct discharge to surface water. The amount of PCP associated with
other users which do discharge is relatively small. The amount discharged
to POTW's based on available data, is small and would be reduced 50% to
100% by treatment processes. An unknown amount of PCP held in storage
lagoons has the potential for release through leakage or overflow. There
is an additional potential for indirect entry into water from non-point
sources through runoff or leaching from soil in herbicide-treated areas,
leaching out of treated wood products and rainout from contaminated air.
Due to insufficient monitoring to characterize total PCP releases
to water, no attempt was made to estimate concentrations in water on a
national scale. Concentrations were, however, estimated on a local scale,
making use of typical effluent concentrations and flow data associated
with industries practicing direct discharge. The computerized EXAMS
(Exposure Analysis Modelling System) model vas implemented to simulate
concentrations in water and sediment of six types of generalized aquatic
systems. The model is discussed in greater detail in the following section.
78
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2. Air Models
a. Assumptions Used in Air Models
Concentration calculations made in this section are based on three
main assumptions:
(1) The atmospheric lifetime for PC? is one aonth. The time
scale for removal of chemicals from air due to nucleation
and/or precipitation scavenging is approximately one week
(Junge, 1977; Slinn,1978). PCP is probably photolyzed
in air, but a time scale for this is not known. One
month is, therefore, a conservative estimate.
(2) Ninety percent of the PCP from fugitive emissions is
released into the air over an area one-half the size
of the continental United States. This is based on
production patterns of PCP-treated products and an
assumed relationship between use of PCP-treated
products and population. Eighty-two percent of •
wood treatment plants are located in the eastern
half of the country (Section III). Ninety percent
of the population occupies about one-half of the
land area of the U.S., and PCP use is assumed to be
directly related to population.
(3) The altitude at which PCP mixing occurs is assumed
to be 1 km. This value characterizes the vertical
extent of surface-based pollution on a time scale
of days, and as such is a conservative assumption
on the basis of the 1-3 month residence time.
These assumptions give a mixing volume of 4.7 x 1015m3 in which at any
time one month of PCP release will reside. In view of the possible
invalidity of any of these assumptions or others used on the modelling
order of magnitude bounds will be placed on the estimated concentrations.
b. Atmospheric Concentrations Due to Wood Treatment Wastewater
Evaporation
In a study of the effects of PCP on a stream, oil slicks on the
water surface were found to contain up to 5450 mg/1 of PCP, while the
water contained up to 10.5 mg/1. On the basis of these two values, an
oil/water partition coefficient of about 520 is indicated. Octanol/water
partition coefficients for PCP are given as 490 at 18°C and 980 at 70°C
(Branson and Blau, 1979). An average value of 550 will be used in the
following calculations.
In the wood preserving industry approximately 150 1 of water is
used per m3 of wood treated (USEPA, 1979a). The wastewater effluent
contains approximately 1 gm/1 of oil and grease and 20 ag/1 of PC?.
79
-------
(USEPA, 1979a). From these values it can be estimated that there is approxi-
mately 150 g of oil and grease and 3 g PCP in the effluent stream per m3
of wood treated. Before disposing of wastewater, most plants practice
oil/water separation to remove the oil and grease, which is then recycled
or disposed. The remaining water is sent to either a cooling tower or a
holding pond equipped with aerators and sprayers where vaporization takes
place.
Though some plants do discharge treated water to POTW's or streams.
most practice some treatment through the methods described. As the water
evaporates from the cooling towers or ponds, the PCP contained in the
water is also assumed to evaporate.
Using values given above, and computing the partitioning of the PCP
between the process water and the oil and grease, about 2 g PCP/m3 treated
wood remains in the process water at a concentration of 0.013 g/1 (13 mg/1),
and 1 g PCP/m3 wood is removed along with the oil and grease. Production
of PCP-treated wood in the main categories is. about 1.8 x 106 m3/yr,
giving 3.6 x 103 kg/yr of PCP input to air via wastewater. evaporation.
In a similar analysis, Branson and Blau (1979) assumed 200 1/m3 for process
water use and the effluent water contained 28 ag/1 of PCP, or 5.6 g/m3
(4.2 g/m3 if the previous estimate of 150 1/m3 is used), a concentration
similar in magnitude to the 2 g PCP/m3 wood derived above. An inconsis-
tency In the reported analysis (Branson and Blau, 1979) appears though,
since it states that 0.18% of the total amount of PCP used ends up in the
treated water. The values of 28 mg/1 PCP in treated water, 200 1/m3
water use, and 8 kg PCP/m3 wood indicate only a 0.07% loss. A loss of
0.18% of the total amounts to 3 x 10** kg/yr while the 0.07% figure indi-
cates 1.2 x 10** kg/yr. Nevertheless, these loss estimates are narrowly
within the same order of magnitude.
Eighty two percent of the wood treatment plants are located in the
eastern half of the country, as shown previously in Figure 3. Figure 4
shows that a corresponding amount of PCP is used and presumably lost in
the regions containing the preponderance of these plants.
Eighty-two percent of the range estimating PCP atmospheric loading
due to wastewater evaporation (3.6 x 103 - 3.0 x 10** kg) amounts to
3.0 x 103 to 2.4 x 101* kg PCP lost annually in the eastern region alone.
Based on the dilution volume and lifetime in the atmosphere for PCP
assumed, 250-2000 kg of PCP is dispersed in an atmospheric volume of
4.7 x 101S m3. The resulting PCP concentrations range from 5.2 to 43
x 10-ll g/m3 cr 0.05 to 0.40 ng/m3. An order of magnitude of error
either way in these estimates gives a range of 0.005 ng/m3 to 4.3 ng/m3.
c. Atmospheric Concentrations Due to Volatilization From PGP-Treated
Wood Products
Treated wood products account for approximately 8-0% to 90% of PCP use
in the United States (see Materials Balance). The 1976 production levels
of PCP-treated wood products are shown in Table 27. Sizes assumed for
30
-------
pieces in each of the categories of wood products are shown in Table 28.
The surface area and volume from which PCP is assumed to volatilize is
also shown. The PCP is assumed to be distributed evenly through the
wood, all of the PCP is assumed to volatilize from only the top 1 mm of
surface, and no PCP is assumed to be degraded photolytically or metaboli-
cally. This is a conservative assumption since PCP probably escapes via
other routes or is degraded to some extent.
TABLE 27. USAGE DATA FOR PENTACHLOROPHENOL BY WOOD PRODUCT
Product Category
Wood Poles
Amount
Treated
(m3)
1,034,410
Lumber, timber, plywood 392,890
Fence posts 257,600
Crossarms
Pilings
Cross ties
Millwork
Source: U.S. EPA (1980b).
128,600
10,420
540
283,200
TOTAL
Total PCP
Used (Kg)
(106kg)
10.8
2.6
1.8
0.91
0.09
0.05
0.45
16.6
% Total Rate
(kg/m3)
65%
15.6%
10.6%
5.5%
0.5%
0.2%
2.7%
4.9-12.7
4.9-8.1
4.9-8.1
4.9-8.1
4.9-13.8
5.6-8.1
Four product types—poles, lumber, fenceposts and crossarms—account for
most of the PCP use as a wood preservative.
.The total volume of treated wood from which PCP is assumed to vola-
tilize per year is found to be 3.6 x 10U m3 as shown in Table 28. The
concentration in wood is used to determine the total amount of PCP vola-
tilized (see Table 29). The upper limit is used. The total amount of
material volatilizing each year can then be estimated as 3.44 x 105kg,
or roughly 2% of the total amount of preservative applied. Based on
the atmospheric lifetime assumptions of one month adopted previously,
the total amount of preservative in the air at any one time is one
twelfth this amount, or "2.9 x lO^kg.
SI
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TABLE 28. DIMENSIONS ANI) PRODUCTION VOLUMES OK PCP-TREATED WOOD 1'KODUCTS
USED IN CONCENTRATION ESTIMATES
PER PIECE
oo
M
Category
I'olea
Lumber
Fence posts
Crossarms
Surface Area
Dimensions (ra) (in2)
.4
.1
.2
.1
dla x 10 long
x .1 x 2.44
dia x 2 long
x .1 x 2.44
12.5
1.0
1.25.
1.0
Volume
(n.3)
1.25
0.25
0.063
0.025
Volatilization
Volume (in3)
1.25 x 10~3
1 x 10~3
1.25 x 10~3
1 x 10~3
No
Pieces
8.3 x
1.57 x
4.1 x
5.14 x
105
107
106
106
Total Volatilization
Volume (m3)
1.03 x
1.57 x
5.17 x
5.14 x
10*
ID*
103
io3
Total: 3.6 x 10
Source: Arthur D. Little, Inc., estimates.
-------
TABLE 29. ESTLMATED ?CP VOLATILIZATION LOSS BY WOOD PRODUCT CATEGORY
Volume From Which PC? Concentration Total PGP
Category PCP Volatilizes in Wood Lost
(m3) (kg/m3) (kg)
Poles 1.03 x 10" 12.7 1.3 x 10s
Lumber 1.57 x 10* 8.1 1.3 x 10s
Fenceposts 5.17 x 103 8.1 4.2 x 10"
Crossarms 5.14 x 103 8.1 4.2 x 10U
Total 3.44 x 105
Based on assumptions stated previously 2.6 x 10^ kg will be disper|ed in
4.7 x 1015 m3 of air, giving a concentration estimate of 5.6 x 10~3 g/m3.
An order of magnitude error either way in this estimate yields a range
of approximately 0.6 to 56 ng/m3.
d. Atmospheric Concentrations due to Evaporation from Cooling Towers
Each year, 2.3 x 10^ kg of pentachlorophenol is used in the treat-
ment of cooling tower waters (MITRE, 1979). It is difficult to predict
the relative amounts of this material that might be volatilized or be
discharged with the cooling water into holding ponds or directly into
water bodies after once through the cooling cycle. The conservative
assumption is that all of this PCP escapes into the atmosphere, along
with the evaporated water and steam from cooling towers.
The previously adopted assumptions regarding atmospheric dilution
and emission are assumed. In addition removal processes such as deposition
and rainout from the plume are assumed not to occur. Consequently 17250 kg
of PCP will be dispersed in 4.7 x 1015 m3 of air, giving an average concen-
tration estimate of about 3.6 ng/m3 due to evaporation of PCP in cooling
tower waters. Order of magnitude uncertainty in this estimate gives a
range from0,4ng/m3 to 36 ng/m3.
e- Atmospheric Concentrations Due to Open Burning of PCP-Treated
Wood Products
No information was found regarding the fraction of the original amount
of PCP in wood which is released during open burning. Experiments have
been done, however, on the incineration of PCP in a wood-burning furnace
of the type used to dispose of wood scrap and sawdust treated with sodium
pentachloro.phenate from woodworking operations (Ahling and Johansson,
1977). Though these cases may seem to be similar, it is not possible to
draw an analogy between the cases of burning in a furnace and open
burning.
83
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la a pilot-scale furnace, waste PCP solution was injected into the
combustor at 50 to 70 g/hr with high excess air. The PCF residence time
was 3.5 seconds and the temperature was "600°C. 52 mg PCP remained per
kg PCP charged to the furnace. At a temperature of 700°C the remainder
was 23 mg/kg and at 800°C it was 16 mg/kg. The heat load on the furnace
(heat removed that would otherwise-contribute to fuel and PCP decomposi-
tion) affected the product yield. In a full scale furnace running at
2 to 11 g PCP/hr, PCP remainder was between 1.6 mg/hr (645 mg/kg) at a
low load to 79 mg/hr (7100 mg/kg) at a high load. Therefore 0.6% to
0.7% of the original PCP remained in the flue gas. The high PCP emission
rates were attributed to excessively high loading, even though temperature
drop was moderate. The periods or regions where temperature in the furnace
is less than 700°C would account for most of the emission. At 750-800°C,
the destruction of PCP is more reliable.
Primary variables in the comparison between furnace incineration
and open burning are: initial amount of PCP available for burning (either
kgPCP/kg wood or as kgPCP/hr); residence time of PCP in the hot combustion
zone; temperature; equivalence ratio; and modes of 02 transport to the
wood surface. Two types of processes are possible. PCP may oxidize,
leading to the formation of various combustion products, or it may pyro-
lyze, a thermal degradation that occurs in the absence of oxygen. It may
evaporate unchanged.
With respect to the variables mentioned above, open burning is sig-
nificantly different from combustion in a furnace. There is likely to
be more PCP in wood than was injected into the furnace as a PCP solution.
Wood is treated with PCP at concentrations up to 8 kg PCP/m3 wood or
.014 kg PCP/kg wood (pine wood at 554 kg/m3). In the furnace tests up
to 11 g PCP/hr were injected. In an open fire, more than a kg of wood
would be burned per. hour; thus, more than 11 gPCP/hr would be in the
burning wood.
In the open burning case, PCP could remain in regions of high
temperature longer than 3.5 seconds since the material is tightly absorbed
into the wood and remains at high temperatures for a longer time, both
inside the wood, on the glowing surface, and in the flame. It is also
quite possible though that PCP may evaporate or boil off quickly and
escape.
Temperatures in open burning in some regions may be considerably
higher than 'the 700°C-800°C existing in the furnace. Surface temperatures
of burning wood approach 1000'C.
In the furnace tests, much excess air, and therefore oxygen, was
available to the burning wood and PCP. This is a significant factor
leading to increases of the oxidation in the furnace, thereby reducing
the amount of unhurried hydrocarbons. Lower availability of oxygen is
likely to occur in open burning with unreacted PCP introduced into the
air, because of incomplete reaction.
34
-------
The lack of available oxygen,taken along with the increased amount
of PCF in the wood, will tend to decrease the fraction of PCF reacted in
open burning. These uncertainties suggest that the furnace test results
should not be used to estimate the PCP burned or released in open waste
fires.
In order to estimate the atmospheric loading from the release of
PCP. by open burning, scrap timber, lumber,* and plywood are assumed to
be the only products burned. Fenceposts, utility poles, and crossarms
will not be burned to any great extent, whereas wood scraps from timber,
lumber, and plywood of little economic use are likely to be disposed of
by burning. Of annual PCP use, 15.6% or 2.6 x 106 kg, goes into the
timber, lumber, and plywood category (U.S. EPA 1980b). If 1% of
this total is assumed to be disposed of by burning, 2.6 x 10** kg/yr could
be put into the air. Conclusions from the discussion above indicate that
no quantitative estimates can be made of the PCF actually oxidized or
pyrolyzed vs. the amount that is merely evaporated unchanged. The poten-
tial, therefore, exists for up to 100% of this 2.6 x 10** kg of PCP to
enter the atmosphere each year.
Following previously stated assumptions, the atmospheric concentra-
tions due to open burning are estimated to be "0.4 ng/m3. if the assumed
amount of scrap burned is increased to 10% of the total 2.6 x 106 kg of
PCP use, the atmospheric concentration is increased'to 4 ng/m3. When
order of magnitude uncertainty is included, the resulting estimate ranges
from 0.04 ng/m3 to 40 ng/m3.
f. Ground-Level Concentrations in the Plume Downwind of a Cooling Tower
Pentachlorophenol is used as a biocide in cooling tower waters.
Blocides may be injected continuously or used intermittently as a shock
treatment (Shair and Dorrington, 1976). It is possible that the PCP may
be vaporized from the cooling'water and then be dispersed in the atmos-
phere or that it may be concentrated in the cooling tower blowdown.
However, owing to the increased vapor pressure of PCP at higher tempera-
tures (1.6 x KH* torr at 25°C and 3.1 x 10~3 at 50°C) and to the higher
volatility of PCF in steam and hot water (USEPA, 1978a), it seems reason-
able to assume that some, if not all, of the PCP will be emitted into the
atmosphere. The conservative assumption adopted is that the relative con-
centration of PCF in this plume is the same as that in the makeup water.
PCP is-an effective biocide at a concentration of about 0.01% (USEPA,
197Sc). In this analysis, the water is assumed to be treated with PCP
to 100 mg/1. NaPCP is used at concentrations of 5-85 mg/1 (USEPA, 1978a)
and chlorophenols in general at about 30 mg/1 (Glover, 1975). It is
possible that higher concentrations may be used in the makeup water; in
this case concentrations in the plume will increase by a similar amount.
The most common type of industrial cooling tower is the forced draft,
open recirculating type (Matson, 1977). Typical specifications for a
cooling tower of this type are shown in Table 30. Water is used in these
35
-------
units as a low-level heat sink and is cooled by evaporation and heat
exchange with air in a cooling tower. Makeup water is added to compen-
sate 'for evaporation and drift, the entrained water droplets in the air
leaving'the cooling tower. The evaporating water and drift cause the
plume.
. TABLE 30. TYPICAL OPERATING VALUES FOR AN INDUSTRIAL FORCED-DRAFT,
OPEN RECIRCULATING-TYPE COOLING TOWER
Operating Characteristic
Makeup water
Slowdown rate
Evaporation rate
Drift rate
Recirculating water rate
Cooling tower AT across tower
Cooling tower heat load
SOURCE: Matson, 1977.
The ground-level concentrations of PCP in the cooling tower plume
can be calculated. Since a large amount of heat is released in the plume,
it is assumed to be bouyant. The initial height of the plume is assumed
to be 10 m. The adjusted source height, due to bouyancy, is given by
(Briggs, 1969).
h - hs + 1.6
V *
2/3
where
h - initial source height, 10m,
g - acceleration, of gravity, 9.8 m/sec.
H • heat load of cooling tower, 146 x 105W,
p - density of air, 1.23 kg/m3,
e • specific heat, about 1.465 J/kg'K for air/steam,
P
T - ambient temperature, 300°K,
U,, • wind speed, 3 m/sec, and
- distance downwind, » lOh when x > lOh ,
86
-------
The adjusted source height for the plume becomes,.in this case, 120 m.
For a Gaussian concentration distribution in the plume, ground level PCP
concentration Cc (x,o,o) can be computed from (Slade, 1968):
Cc (x, o, o) » Q.
ITO a U \ exp
y z w \ r
2 z
where
Q - mass input, 0.045 kg PCP/sec,
? » horizontal dispersion parameter, m.
o =» vertical dispersion parameter, m.
z
U • mean wind speed, 3 m/sec, and
h » source height, 10 m or 120 m.
This equation models a dispersing plume being carried along steadily and
uniformly by the wind. Dispersion coefficient ay and az are dependent
on meteorological conditions and downwind distance. Values used are
given in Table 31.
TABLE 31. DISPERSION COEFFICIENTS AS FUNCTION OF DOWNWIND DISTANCE
(PARTLY SUNNY DAY, WIND 3 M/SEC)
x, km
0.3
50
30
0.5
84
51
0.7
112
73
1.0
150
110
3.0
375
360
5.0
670
650
7.0
890
920
10.0
1200
1400
Source: Slade, 1968.
Values of PCP concentration at ground level downwind of a cooling
tower were computed for source heights of 10 m and 120 m (buoyant plume)
and the plots of the results are shown in Figure 13. Maximum concentra-
tions appear within a kilometer or two of the tower and then decrease
with distance. Many other factors will affect the dispersion process,
including rainout, terrain induced dispersion, large-scale atmospheric
turbulence, and possible reactivity in the plume. These factors, which
have not been modelled, would tend to reduce concentrations.
The results of the computations can be scaled linearly in order to
reflect increased or decreased PCP concentrations in the makeup water.
Values from Figure 13 should then be adjusted accordingly.
87
-------
10
,-3
.c
SI
I
I ID"4
u
"3
o
o
1
1 ID'5
10'
,-6
Nonbouyant Plume Source Height• 10m
Bouyant Plume Source Height • 120m.
1
I
I
I
468
km Downwind
10
FIGURE 13 GROUND-LEVEL CONCENTRATIONS OF PENTACHLOROPHENOL
IN THE PLUME DOWNWIND OF A COOLING TOWER -
TWO SOURCE HEIGHTS
33
-------
The concentration estimates in a plume downwind of a cooling tower on
the order of 10** ng/m3 are considerably higher than those estimated for other
particular atmospheric inputs as compared to 10 ng/m
g. Concentrations Downwind of a Wood Treatment Plant Waste Water
Evaporation Pond
Wood treatment plants treat effluent and then discharge this treated
waste into evaporation ponds to achieve zero effluent discharge into
streams and other water bodies (USEPA, 1979a and 1979b). This effluent
contains pentachlorophenol. As the water in the ponds evaporates, some
of this PCP may evaporate along with the water. Although volatilization
appears to be a minor fate process, another pathway for removal of PCP
from pond water is adsorption to sludge or sediment in the bottom of the
pond. Some ponds are equipped with mechanical aerators to enhance PCP
and water evaporation. For this analysis, the conservative assumption is
adopted that all the PCP in the waste water evaporates into the air in
order to obtain an upper limit for air releases and to compute PCP con-
centrations in the plume downwind from an evaporation pond.
The ponds are designed to contain all process water used by a plant
in addition to water that may enter the plant site through precipitation;
therefore, in continuous operation, these ponds must be capable of evapora-
ting water at least at the rate it is used by the plant. Therefore,
the daily water use is assumed to be evaporated as it is used. As an
example, a daily process water throughput of 3.8 x 10- 1 is assumed.
Furthermore, this water will contain 2.8 mg/1 PCP (Branson and Blau, 1979)
when it is discharged_into a 4 x 10** m2 pond. Thus, in steady-state
operation, 1.23 x 10~3 kg PCP/sec is evaporating.
Concentrations downwind from an area source discharging continuously
into the air can be estimated (Slade, 1968) assuming a virtual point source
located five area source diameters upwind. For the example chosen, the
diameter of the source is "220m and the virtual point source is 1.1 km
upwind. Standard Gaussian dispersion formulas can be employed to estimate
centerline ground-level concentrations downwind from a surface source.
The equation is (Slade, 1968):
C(x,o,o) - jj
TOx°y Uw
where
Q - release rate of pollutant, 1.23 x 10~s kg/sec,
a ° horizontal dispersion coefficient
y
o
vertical dispersion coefficient, and
based on virtual source
1.1 km upwind and the
, , , , / assumed stabilitv
Uw - wind speed, 3 m/sec. conditions
39
-------
.5
1.6
240
1
2.1
310
2
3.1
430
3
4.1
570
4
5.1
700
Dispersion coefficients used are shown in Table 32. The results of
the calculations are shown in Figure 14.
TABLE 32. DISPERSION COEFFICIENTS USED IN THE CALCULATIONS OF
CONCENTRATIONS DOWNWIND OF AN EVAPORATION POND
RELEASING PGP INTO THE AIR
Dispersion Coefficient1
Actual km downwind
Model km downwind
ff . m 175 240 370 510 670
1Based on partly sunny day; 3 m/sec wind.
Source: Slade, 1968.
Terrain induced dispersion, large scale atmospheric turbulence, and
rainout or deposition are neglected in the calculations, thereby giving
upper limit concentrations in the ng/m3 range at distances greater than
1 kilometer.
h. Rainout
Dissolution in water droplets and subsequent rainout is considered
here as a possible atmospheric loss mechanism. PCP has been found in rain-
water in Hawaii at concentrations of about 8 ng/1-284 ng/1 (Bevenue et al.,
1972b) (see Table 6). Concentrations of PCP in rainwater can be estimated
from a knowledge of concentration in air and the non-dimensional Henry's
Law coefficient . For equilibrium conditions (Slinn ejt al., 1978):
C , C*tr
rain « —::—
where
C
rain » concentration in rainwater,
C . » concentration in air, and
H • non-dimensional Henry's Law coefficient.
90
-------
10'7
n
4
c
H 10"
5
6
I 10-9
1
eo
•»
I
i
-------
H can be computed from (Neely, 1976):
where
P » vapor pressure of PCP at 208C, 1.7 x 10"1* torr, upper
value of range reported,*
P • partial pressure or air, 760 torr (1 atm.),
M - molecular weight of PCP, 266.35,
29 • average molecular weight of air,
°air » density of air, 1.23 kg/m3, and
Xg » solubility of PCP, .014 g/1 -0.014 kg/m3*.
The non-dimensional H is then computed to be 1.8 x 10~**, and
C . - 5556 C .
rain air
For equilibrium between water and air, the air concentration required to
cause a concentration of 8-284 ng/1 in rainwater is, using the values of the
Henry's Law coefficient computed above, between 0.002 to 0.063 ng PCP/m3 air.
The cumulative air concentration estimated from release rates of PCP from
burning, volatilization from treated produced wastewater evaporation,
and cooling tower use is between 0.5 and 136 ng/m3. The ranges for the
inputs were 0.04 Co 40, 0.06 to 56, 0.005 to 4.3, and 0.4 to 36 ng/m3,
respectively. The air concentrations estimated from rain data are some-
what lower than the cumulative estimate, though the rain-based estimate
still falls partially in the lower range of the cumulative estimate.
PCP concentration in the rain in Hawaii was attributed to the large
use of PCP-treated building materials. The general agreement noted here
tends to support the validity of the estimates derived above, especially
considering that the estimated concentration based on volatilization from
treated products was 0.06 to 56 ng/m3, which is quite similar to the
estimate based on rain data.
i. Conclus-ions
Inputs to the air compartment seem to occur steadily over a large
area. Estimates were derived of PCP input to air from evaporation of
92
-------
wood treatment facility waste water, volatilization from treated wood
products, PCP-treated cooling tower water evaporation, and open burning
of PCP-treated wood. Total inputs to the air were estimated as 3.0 x
103 to 2.4 x 10U kg/yr, 3.4 x 10s kg/yr, 17250 kg/yr, and 2.6 x 10* to
2.6 x 10s kg/yr, respectively. This produced concentration estimates
due to each source of 0.005 - 4.3, 0.06 - 56,0.04- 36, and 0.04 0.40
ng/m3, respectively. A cumulative concentration estimate is then 0.15 to
Ub ng/m3. The lower range of this estimate is in general agreement with the
upper range of air concentration estimates computed based on PC? concentrations
in rain in Hawaii, where PCP treated wood is extensively used. This estimate
gave 0.002 to 0.063 ng/m3.
In addition, ground level concentrations in the plume downwind from
a cooling tower using PCP as a microbiocide and downwind from a waste water
evaporation pond were computed. Estimates were about 10s ng/m3 and 10 ng/
m3, respectively, for distances less than a few kilometers.
3. Water Models
a. Introduction
The EXAMS model has been developed by EPA Athens Environmental
Research Laboratory in order to help assess the behavior of a pollutant
in various characteristic aquatic systems UJ.s. EPA 1980c). The output'of the
model includes:
(1) simulations of steady-state concentrations and pollutant
mass distribution among water, sediment and biota in
different compartments (e.g. water column, bed sediment),
(2) percentage of system-loading removed by each chemical
and biological kinetic process, and
(3) concentration die-away time following cessation of dis-
charge.
As input the model requires the pollutant's physico chemical properties,
environmental reaction rate constants, and loading rate to the system.
The assumptions of the model include a continuously discharging source
at a constant level, a box of water made up of a system-defined number
°f well-mixed compartments, and first-order rate kinetics in all processes.
A more thorough discussion of the model is given in Lassiter, et al. (1978)
and Baughman and Burns (1980).
Input data for PCP was derived from two sources. The chemical
property and rate data were compiled specifically for the model by EPA
(Versar, 1980). The loading data were derived from effluent concentra-
tion and flow data characteristic of various industry categories that
discharge PCP. Table 33 lists upper limit PCP loads calculated from
effluent guidelines discharge data. The data can not be assumed to
represent worst case discharge levels for each industry because they are
derived from a small number of plants and days sampled. On the other
hand, unless other information was available, the assumption was made
that the sampled concentration and flow data represent practices typical
l?rooerries were for the undissociated aolecule. PCP
-------
TABLE 33. ESTIMATES OF UPPER LIMIT PCP DAILY LOAD
IN INDUSTRIAL EFFLUENTS1
Industry
Leather Tanning
Textiles
Wood Preserver
Flow (MGD)2
0.300
1.0
0.0143
PCP Concen-
tration (mg/1)
15.0
0.066
20
Daily Load
(ks/dav)
17.1
0.25
0.07*
1Loadings are estimates of upper limit amounts based on a very limited
sample of data from effluent guidelines.
2MGD • million gallon per day
3Average number of days of discharge per year » 10 - 25 days.
''Discharge averaged out over entire year.
94
-------
for every day of the year. This may result in too high a loading rate
but, until more detailed discharge data become available, this assumption
is justified.
A major drawback of using the EXAMS model for PGP relates back to
the discharge practices of the pollutant's major users. Only one wood
preserving plant practices direct discharge and the other industry cate-
gory dischargers account for a relatively small amount of the PCP pollu-
tant load. Most sources are non-point sources and estimating their
release rates is difficult. Therefore, the results of the model apply
only to a small number of known situations and cannot be assumed to be
representative of widespread conditions.
b. EXAMS Concentration Estimates
Tables 34-37 present the output from the EXAMS model (U.S. EPA 1980c).
Steady-state maximum concentrations of PCP in the six different components of
each aquatic system are listed for the three discharge rates of 17.1 kg/day
(Table 34), 0.25 kg/day (Table 35) and 0.07 kg/day (Table 36). Table 37
presents the percentage of total PCP loss attributable to each transfor-
mation or transport process and the estimated time for self-purification
for each of the six aquatic systems. These values are independent of
loading rate but dependent on the physico-chemical characteristics of
PCP and system characteristics.
In general, the results show higher concentration accumulation in the
water compartments of the pond and two lake systems than in the three
river systems. Suspended .sediment concentrations are approximately 2 to
2.5 orders of magnitude greater than dissolved concentrations in water.
Bottom sediment concentrations are similar to water concentrations, some-
times slightly greater and sometimes less than dissolved water levels,
depending on the particular system. Plankton concentrations are approx-
imately 15 to 20 times above dissolved water concentrations.
Table 37 describes the steady-state distribution of PCP between water
and sediment, and the percentage transformed by each process. Physical
transport processes account for almost all losses in the river systems
and for most of the loss from the pond and oligotrophic lake systems.
According to the model, biodegradation is very significant in the
eutrophic lake system. Chemical processes account for one-third of the
PCP disappearance in the oligotrophic lake system. The estimated time
for self-purification ranged from 96.64 days in the river system to
695.5 days in the oligotrophic lake. Persistence is a complex phenomenon
dependent on many site-specific non-generalizable variables. All of
these values are merely estimates and may not be indicative of the life-
time of PCP in specific natural aquatic ecosystems.
Further discussion of the EXAMS concentration simulations is found in
Sections VI-B and VII-C.
95
-------
TABLE 34
STEADY-STATE CONCENTRATIONS IN VARIOUS GENERALIZED AQUATIC SYSTEMS RESULTING FROM CONTINUOUS PCP DISCHARGE AT. 17.1 kg/day*
MAXIMUM CONCENTRATIONS
*x>
SYSTEM IJOADING
fund (0.713 kg/hr)
(17.1 kg/«luy)
Cut ruplilc
l^ike
OligotropMc
Lake
River
Tiubid
River
Coaatal Plain
River
WATER WATER
DISSOLVED TOTAL
(OR/ I) (an/1)
21.38 26.36
0.121 0.228
0.584 1.14
7.04 X 101* 7.84 X id*
7.04 X 101* 7.84 X 10*
6.91 X 103 7.84 X 103
BOTTOM
SEDIMENT
(-R/D
0.249
.
5.56 X 10
•a
1.43 X 10
1.71 X lO*
3.69 X 16"
S.99 X 10*
BOTTOM
SEDIMENT
78.38
0.235
3.06
4.63 X 10*
4.42 X 103
9.25 X 10*
PLANKTON
(MH/B)
3.92 X 10*
-
2.14 X 10
1.07 X 10
12.83
12.83
128.25
BERTIIOS
(VK/ft)
TOTAL
STATE
TION (
4.49 X 103 583.
99.75
249.38
3.06
6.48
37.75
420.
3240.
0.
0.
7.
STEADY-
ACCUMULA-
k«>
33
42
0
784
784
840
TOTAL
DAfLY LOAD
(kg/day)
17.1
17.1
17.1
0.713
0.713
0.713
All data simulated by EXAMS Model (see text for further Information).
-------
TABLE 35
STEADY-STATE CONCENTRATIONS IN VARIOUS GENERALIZED AQUATIC SYSTEHS RESULTING FROM CONTINUOUS VKV UISCIIARCE AT 0.25 kg/day'
MAXIMUM CONCENTRATIONS
SYSTEM LOADING
WATER WATER BOTTOM
DISSOLVED TOTAL SEDIMENT
(OR/1) (.K/l) (OR/I)
Piind 1.04 X 1112 kg/hr 0. 113 0.38 . 3.65 X 10*
(0.25 kK/«lay)
Km roplilc
vo Lake
-~i
Ol Igulruplilc
Lake
Klwur
Turbid
Hiver
Coastal
Plain Hlwr
-1 -3 -S
1.8 X 10 3.33 X 10 8.13 X 10
-J .9 .1.
8.3 X 10 1.67 X 10 2.08 X 10
1.03 X ID* 1.14 X 10* 2.50 X 10b
-S -S -b
1.03 X 10 1.15 X 10 5.21 X 10
•h - b -5
1.01 X 10 1.15 X 10 3.02 X 10
MAXIMUM
IN DEPOSITS
SEDIMENT PLANKTON BENTHOS
-------
TABLE 36
STKAUY-STATK CONCENTRATIONS IN VARIOUS GENERALIZED AQUATIC SYSTEMS RESULTING FROM CONTINUOUS PCP DISCHARGE AT 0.01 kg/day
I
MAXIMUM CONCENTRATIONS
SYSTEM LOADING
I'oud 2.92 X I0~3kg/hr
(0.07 kg/ Jay)
Cutiophic
Lake
Ollgotroplilc
OO Lake
Rlvur
TurblJ
Rivtir
Coastal Plain
Klvur
HATER WATER
DISSOLVED TOTAL
ta/l) (ma/1)
8.88 X id2 0.108
7.92 X 10S 9.33 X 10*
2.39 X 103 4.67 X id3
2.89 X 106 3.21 X 106
2.89 X 106 3.2 IX 10*
2.83 X 10S 3.21 X 10S
BOTTOH
SEDIMENT
<»«/!>
1.02 X 10*
2.28 X ID*
5.83 X 105
7.00 X l6?
1.46 X 106
8.46 X 106
MAXIMUM
IN DEPOSITS
SEDIMENT
(«K&K)
0.321
9.58 X id"
1.2S X 102
1.90 X 10*
1.79 X 10S
3.79 X lO**
PLANKTON
.
1.60 X 103
8.75
43.75
5.25 X 102
5.25 X 102
0.525
BENTHOS
(MR/8)
18.38
0.408
1.02
TOTAL STEADY-
STATE ACCUMULA-
TION (kn>
2.39
1.72
14.0
1.25 X 102 3.33 x 10*
2.67 X 10- 3.311 X id1
0.155
3.21 X 102
TOTAL
DAILY LOAD
(kR/day)
0.07
0.07
0.07
2.92
2.92
2.92
X10'J
x id1
xid1
All data simulated by EXAMS model (see text fur further Information).
-------
TABLE 37. THE FATE OF PCP IN VARIOUS GENERALIZED AQUATIC SYSTEMS1
% of PCP % of PCP Time for
Residing. in Residing in % Transformed % Transformed % Lost System Self-
Water at Steady- Sediment at by Chemical by Biological ' % Volatll- by Other 2 Purification
State _ Steady-State Processes Processes ized _ Processes (day) 3
90.62
98.87
98.99
93.98
94.84
85.19
9.38
1.13
1.01
6.02
5.16
14.81
6.05
3.99
33.31
0.01
0.01
0.09
12.84
88.69
0.09
0.09
0.09
0.92
0
0
0
0.19
0
0
81.11
7.32
66.41
99.9
99.9
98.99
158.3
103.9
695.5
111.7
96.64
580.7
Pond
Eu trophic Luke
Ol igotrophlc Lake
Kiver
Turbid River
Coastal 1'laJn
Kiver
'All ilata simulated by the EXAMS model (see text for further information).
^IncludiiiK loss through physical transport out of system.
3Estimate- for removal of ca. 75% of the toxicant accumulated in system. Estimated from the results of the
half-lives for the toxicant in bottom sediment and water columns, with overall cleansing time weighted
according to the toxicant's Initial, distribution.
-------
4. Summary of Concentration Estimates
Through use of simple calculational models for air and a computerized fate
model for water, estimates were made of concentrations in these media
resulting from PC? emissions. The results are of two general types:
1) concentrations by source category evenly distributed across the
United States or large U.S. regions that represent the sum of contrib-
utions from numerous point sources; and 2) concentrations for local
sites in the vicinity of single point sources. Tables 38 and 39 sum-
marize the concentration estimates, regional and local, respectively.
100
-------
TABLE 3H. SUMMARY OF ESTIMATES OF REGIONALLY DISTRIBUTED PCP CONCENTRATIONS IN ENVIRONMENTAL MEDIA
Source Medlum Concentration
Wood Treatment Air 4.3 ng/m3
Waste Water Evaporation
Volatilization From Treated Wood Air 56.0 ng/m3
Evaporation From Cooling Towers Air 36.0 ng/m3
Open Burning Of Air 40.0 ng/m3
Treated Wood
Summation Of Air 136.3 ng/m3
All Sources
All estimates are upper limit concentrations.
-------
TABLE 39. SUMMARY OF NEAR-FIELD ESTIMATES 01' PCF CONCENTRATIONS IN ENVIRONMENTAL MEDIA
Source
Cooling Tower
Flume
Waste water
Evaporation
Pond
Any source:
0.07-17.1 kg/day
discharge
0.07-17.1 kg/day
discharge
0.07-17.1 kg/day
discharge
0.07-17.1 kg/day
discharge
0.07-17.1 kg/day
discharge
0.07-17.1 kg/day
discharge
Upper limit concentrations.
•Medium
Concentration
Air
Air
Pond
Eutrophic
Lake
Ollgotrophic
Lake
River
Turbid River
Coastal Plain River
4 3
•»• 10 ng/ro
* 10 ng/ro3
(1)
107.9 - 26362 |ip./t
0.1 - 227.9
0.005 - 1.4
0.003 -0.784
0.003 - 0.784 ug/Jl
0.032 - 7.84 |ig/£
0.032 - 7.84 ug/l
"Range of maximum values in total water compartment of EXAMS,
-------
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Bevenue, A., J. Wilson, L. Casarett, and H. Clemmer. 1967b. A survey
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Ill
Arthur D Little inc.
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SECTION V.
HUMAN EFFECTS AND EXPOSURE
A. EFFECTS ON HUMANS
i. Introduction
Pentachlorophenol (PCF) is an antimicrobial aeent widely used for
the preservation of wood. Most commercial PC? formulations contain from
85% to 99% PCP, as well as different chlorophenol impurities and minor
amounts of highly toxic polychlorinated dibenzo-p-dioxins and dibenzo-
furans. The quantity and proportion of contaminants in the technical
product differ somewhat from batch to batch but generally include:
tetrachlorophenol (5-10%), trichlorophenol (1%), chlorinated phenoxy-
phenols which act as dioxin precursors (i5%) and polychlorinated dibenzo-
p-dioxins and dibenzofurans (range 10- 1000s mg/kg) (Report of the Ad Hoc
Study Group on Pentachlorophenol Contaminants, 1978; Nilsson et al..
1978). The most toxic dioxin known, 2,3,7,8-tetrachlorodibenzo-p-dioxin,
has not been found in commercial PCP formulations. The presence of toxic
contaminants in commercial PCP formulations obfuscates the true toxic
effects of PCP itself. However, the few studies available that have
toxicologically characterized purified PCP suggest that PCP is a toxic
chemical in its own right.
2. Metabolism and Bioaccumulation
The pharmacokinetics of pentachlorophenol have been studied in man,
monkey, rabbits, rats and mice. In man, the half-lives for absorption
and elimination from plasma or an oral dose of 0.1 mg PCP/kg were 1.3
± 0.4 hr and 30.2 ± 4.0 hr, respectively. Approximately 74% and 12% of
the dose were eliminated in urine within 7 days as PCP and PCP-glucuronide.
An additional 4% of the dose was excreted in feces as PCP and its glucuro-
nide (Braun et al., 1978).
A similar pattern is observed in rats. Larsen and co-workers (1972)
reported excretion of 68% of an orally administered dose of ll*C-PCP in
urine and 9-13% in feces of rats within 10 days of dosing. Tissue analy-
sis at 40 hours post-exposure showed highest ^C-activity present in liver
(0.23% of administered dose), kidney (0.18%) and serum (^ 0.15%).
In another study, oral administration of 10 or 100 mg/kg 1UC-PCP to
rats resulted in the excretion of 80 and 64% of the respective doses in
urine. At the 100-mg/kg dose, luC-activity in urine consisted of unchanged
PCP (75%), tetrachlorohydroquinone (15.6%) and PCP-glucuronide (9.4%).
The overall elimination of radioactivity was biphasic in both sexes at
the lower dose and in males given 100 mg/kg PCP> elimination was mono-
phasic in females at the higher dose (Braun and Sauerhoff, 1976). A
similar response was observed following intraperitoneal administration
of PCP to rats (Ahlborg, 1978).
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Jakobson and Yliner (1971) reported excretion of both unchanged and
conjugated PCP in the urine (72-83% of the dose) and feces (8-21%) of
female NMRI mice within 4 days of intraperitoneal or subcutaneous adminis-
tration of 1J*C-PCP. The only breakdown product detected was unconjugated
tetrachloro-p-hyd roquinone.
In rabbits dosed orally with 1J*C-PCP-Na, considerable amounts of
PCP-glucuronide plus small amounts of chloranil and free PCP were detected
in urine (Tashiro et al., 1970).
Unlike man, rodents, and rabbits, the rhesus monkey excretes essen-
tially all (68-78%) of an orally administered l**C-PCP dose in urine as
unchanged PCP. An additional 12-20% of the dose is excreted in feces and
most probably reflects biliary excretion and enterohepatic circulation of
PCP. The half-life values for elimination of PCP from plasma were 83.5
hours for females and 72 hours for males,while half-life values for
urinary excretion were 92.4 and 40.8 hours, respectively, indicating sex-
related differences in the plasma clearance and urinary excretion of PCP
in rhesus monkeys (Braun and Sauerhoff, 1976).
Thus, the pharmacokinetic profile of PCP in monkeys is different from
that in man, rodents and rabbits. Humans, rats and mice excrete PCP more
rapidly than monkeys; in addition, rats and mice metabolize PCP to tetra-
chlorohydroquinone and PCP-glucuronide while monkeys excrete it as unchanged
PCP in the urine. The rat model, therefore, appears to more closely reflect
the pharmacokinetics of PCP in man.
Contamination of human tissues with pentachlorophenol appears to be
ubiquitous in industrialized societies. Sources of PCP residues in human
tissues have not been conclusively established. Biotransformation of hexa-
and pentachlorobenzene to PCP may contribute to the contamination of human
tissues with PCP (Koss and Koransky, 1978).
In an analysis of 416-418 human urine samples from the general popu-
lation of the United States, 84.8% were positive for pentachlorophenol.
The average residue detected was 6.3 ug/1 with a maximum detected value
of 193 ug/1 (Kutz et al.. 1978). The limit of detection was 5 ug/1.
Other investigators have reported urinary residues of up to 50 ug/1 in
the general population (Bevenue et al.. 1967; Akisada, 1965).
Urinary PCP residues in 271 occupationally exposed individuals ranged
from 3 ug/1 to 35700 ug/1, with a mean value of 1244 ug/1 (Bevenue et al..
1967). The urine of PCP-wood-treaters contained an average of 2300 ug/1
PCP over a one-year period. A mean decrease of 60% (range 39-79%) in
urinary concentration was noted in six of these workers 18 days after
cessation of work-related exposure (Casarett et al., 1969). Similarly,
Begley et al. (1977) reported that blood (5.14 mg/1) and urine (1.31 mg/1)
content of PCP decreased by more than 50% in 18 occupationally exposed
individuals during a 20-day vacation period and subsequently increased
again with renewed work exposure.
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PC? content of 18 adipose tissue samples from the general population
ranged from 12 to 52 ug/kg with a mean value of 26 ug/kg (Shaf ik, 1973) .
Ohe (1979) noted slightly higher residue levels of PCF in human adipose
tissue of the general population in Japan; i.e. , the PGP content of 25
samples ranged from undetectable to 570 ug/kg, with a mean value of 140
ug/kg.
PCP has also been detected in seminal fluid.' Levels detected averaged
50 ug/1 (range 20-70 ug/D (Dougherty and Piotrowska, 1976).
3. Animal Studies
a. Carcinogenesis
Innes et al. (1969) administered technical pentachlorophenol (Dowi-
cide 7) by gavage to two hybrid strains of mice [(C57BL/6 x C3H/Anf) FI
and (C57BL/6 x AKR Fi ] at doses of 46.4 mg/kg on days 7-28 of age and at
130 mg/kg (17 mg/kg /day) in the diet of animals up to 18 months/of age.
No significant increase in tumor incidence above control values was
observed. Schwetz et al. (1978) also noted no alteration in tumor inci-
dence or duration of lifespan in rats fed up to 30 mg/kg/day of purified
PCP for 22-24 months.
In a tumor promotion study, 20% PCP in benzene was applied to the
backs of dimethylbenzanthracene- initiated mice twice weekly for 15 weeks.
Survival rates for PCP- and benzene- treated mice were 82.9% and 75%,
respectively. The average number of papillomas per survivor was 0.04
for PCP-treated group compared with 0.07 papillomas in the control group
(Boutwell and Bosch, 1959).
bj _ Mutagenesis
The literature contains conflicting reports concerning the mutageni-
city of pentachlorophenol. Andersen et al. (1972) reported that PCP was
incapable of inducing point mutations in eight histidine-requiring mutants
of Salmonella typhimurium. These tests did not employ activation using
liver microsomes. PCP also produced negative mutagenic responses in a
host-mediated assay (Buselmaier et al. , 1973) and in a sex-linked recessive
test with Drosophila (Vogel and Chandler, 1974).
Fahrig and associates (1978), however, reported a significant increase
in forward mutations and mitotic gene conversions in the yeast, Saccaromyces
cerevisiae MP-1, following exposure to 400 mg/1 PCP for 3.5 hr. No positive
controls were run. These investigators also examined the expression of
recessive color genes in a mammalian "spot" test. Progeny of female
C57BL/6JHan mice mated to rotation bred T-stock males are susceptible to
color spots in the adult coat if exposed in utero to a mutagenic agent.
The incidences of color spots in progeny were 1.3% (2/157), 0.6% (2/316)
and 0.1% (1/967) from dams injected with 100, 50 or 0 mg/kg PCP on the
tenth day of gestation. The statistical significance of these data
the incidence of treatment-related maternal toxicity and control results
were not stated making interpretation of the results 'difficult .
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Thus, although there are conflicting reports on the mutagenic potential
of PC? in the literature, the data currently available are insufficient
to support the mutagenicity of PCP.
e. Reproductive and Fetotoxic Effects
In a series of experiments, Schwetz «t al. (1974) examined the
effects of purified (>98%) and commercial grade (88.42} PCP1on rat
embryonal and fetal development. In one study, dosages of 5, 15, 30
and 50 mg/kg/day of purified PCP and 5.8, 15, 34.7 and 50 mg/kg/day of
commercial grade PCP were administered by gavage to pregnant Sprague
Davley rats on days 6-15 of gestation. At the 5 mg/kg and 30 mg/kg
dosage levels, the amounts of commercial PCP administered (5.8 and 34.7
mg/kg) were adjusted in order to provide 5 mg/kg and 30 mg/kg of PCP.
Dose-related decreases in maternal body weight gain were noted with
both PCP samples and were statistically significant at the top two treat-
ment levels. No other signs of maternal toxicity were noted. In progeny,
purified PCP exerted a more pronounced effect than commercial grade PCP.
Fetal resorptions were increased with both grades of PCP and were statis-
tically significant (p <0.5) in dams given 15, 34.7 or 50 mg/kg/day of
commercial PCP or 30 or 50 mg/kg/day of purified PCP. Resorption rates.
were 9, 27 and 58%, respectively, for commercial PCP and 98 and 100%,
respectively, with purified PCP compared to 4.2% resorptions in controls.
The no-effect dosages for fetal resorptions were 5.8 mg/kg/day commercial
and 15 mg/kg/day of purified PCP.
The sex ratio of surviving offspring was significantly altered among
dams receiving 30 mg/kg (purified) and 50 mg/kg (commercial) PCP; the
majority of survivors were males. (U>so is higher in males than females.)
Decreases in fetal body weight were seen in rats in the 34.7 and 50 mg/
kg/day commercial PCP treatment groups and in the 30 mg/kg purified PCP
group; crown-rump length was also decreased in the latter group. There
were no survivors among the animals that received 50 mg purified PCP/kg/
day. Dosages of 15 mg/kg/day or less of either grade had no effect on
fetal body measurements.
The incidences of anomalies in fetuses of dams treated with either
grade of PCP on days 6-15 of gestation were not significantly different
from control. However, the occurrence of subcutaneous edema, dilated
ureters, and anomalies of the skull and vertebrae increased with
increasing PCP dose.
However, a second experiment by these investigators (Schwetz et al.,
1974) showed that the developing, rat embryo was more susceptible to the
toxic effects of a given dose of PCP during the period of early organo-
genesls (days 8-11). Pregnant rats were administered 0 to 30 mg/kg/day
of purified or 34.7 mg/kg/day of commercial PCP on days 8 through 11 or
days 12 through 15 of gestation. Both samples at the given dose of PCP
caused a significant decrease in the rate of maternal weight gain and
a significant increase in the incidence of. fetal resorptions (45%
1Including 4 ug/g hexachlorodibenzo-p-dioxin, known to be toxic to the
rat embryo and fetus (Schwetz et al. 1974).
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commercial, 91% purified compared to 7% control) when given on days 8
through 11 of gestation but had no effect on these two parameters when
administered on days 12 through 15 of gestation. In addition, signifi-
cant incidences of fetal anomalies were associated with the administration
of PCF during early organogenesis: subcutaneous edema (82% commercial,
100% purified compared to 7% control) as well as skeletal anomalies in
the development of ribs, vertebrae and stemebrae. No increase in anoma-
lies was associated with the administration of commercial PCP during late
organogenesis (days 12-15). Administration of purified PCP during this
period, however, resulted in a significant increase in the incidence of
subcutaneous edema (70% vs. 36% in controls) and variations in sternebral
development.
Schwetz and co-workers (1978) also conducted a single generation
reproduction study with Sprague Dawley rats. Animals were fed 0, 3 or
30 mg/kg/day of purified PCP for 62 days prior to mating, throughout
gestation and up to 21 days postpartum. Ingestion of 30 mg/kg resulted
in a significant decrease in the percentage of pups that were born alive
(91 versus 97% for controls) and significantly decreased survival to days
7, 14 and 21 of lactation,but had no effect on fertility. A significantly
increased number of litters showed skeletal anomalies at this dose, the
average litter size was decreased, and mean neonatal body weight was
significantly less than controls. No adverse effects were noted at doses
of 3 mg/kg/day.
Comparable effects were not observed when a larger (60 mg/kg), but
single oral dose of purified PCP was given to pregnant Charles River CD
strain rats on either day 8, 9, 10, 11, 12 or 13 of gestation. Body
weight of fetuses from dams treated on days 9 or 10 "as significantly
reduced and three malformations were observed in 3 of 59 fetuses treated
on days 9 of gestation (Larsen et al., 1975).
Chou and Cook (1979) reported recently in a meeting abstract that
intraperitoneal injection of either 0, 0.4, 4 or 40 mg/kg of technical
PCP or purified PCP adjusted to provide the same level of PCP to pregnant
Sprague Dawley rats on days 3, 6, 9, 12 and 15 of gestation resulted in
increased fetal resorptions and lower maternal weight gain in dams treated
with the highest dosage of either sample of PCP. The effect was reportedly
more pronounced with purified PCP. No values were given. No teratogenic
response was noted and performance of pups was comparable to control values.
Hinkle (1973) reported that daily oral administration of 1.25 mg/kg
to 20 mg/kg PCP to golden Syrian hamsters on days 5 to 10 of gestation
resulted in fetal deaths and/or resorptions in three of six test groups.
No data were provided.
In summation, fetotoxic and teratogenic effects have been produced
in rats following oral administration of 30 mg/kg/day or greater of pento-
chlorophenol during gestation. Purified PCP was somewhat more toxic than
commercial grade PCP with respect to the incidence of fetal resorptions,
growth retarded fetuses, and the incidence of skeletal and soft tissue
11:
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anomalies, particularly during early organogenesis. Comparable effects
were not observed following a single but higher oral dose of PCP.
d. Other Toxic Effects
Toxicological findings concerning PCP are complicated by the presence
of varying amounts of contaminants in the technical material. The oral
LDso (30% lethal dose) for PCP in .male rats has been reported as 78 mg/
kg (Deichmahn et al., 1942), 90 mg/kg (Gabrileyskaya and.Laskina, 1964),
146 mg/kg (Gaines, 1969) and 205 mg/kg (Schwetz et al., 1974) The last
value was for a purified sample of PCP; the LDso in female rats for this
material was 135 mg/kg, a finding indicating male rats are more tolerant
of the acute toxic effects of PCP than are female rats. Age-related
differences were also noted between adult (150 mg/kg) and 3-4-day-old
rats (65 mg/kg) with a commercial PCP sample (Dow Chemical Co. data cited
in Schwetz et al., 1978).
OtherLD50 values for PCP following oral administration are 130 mg/
kg for the mouse (Pleskova and Bencze, 1959), 168 mg/kg for the hamster
(RTECS, 1977) and 250 mg/kg for guinea pigs (Gabrilovskaya and Laskina,
1964). The lowest reported oral lethal dose in man in 29 mg/kg (RTECS,
1977). Acute signs of intoxication are vomiting, fever, elevated blood
pressure, increased respiratory rate, tachycardia and hyperglycemia
(Knudsen et al., 1974).
Hoben _et al. (1976) reported PCP more toxic in rats by the inhalation
route than by ingestion. The LD50 for inhaled PCP aersol was 11.7 mg/kg
in male rats. Exposure to 5 mg/1 PCP dust for 1 hour, however, did not
kill male and female rats (Reichhold Chemicals, 1974).
PCP may also be absorbed through skin. Dermal LDso values of 96,
105 and 320 mg/kg have been reported for rats (Demidenko, 1966; Noakes
and Sanderson, 1969; Gaines, 1969) and 261 mg/kg for mice (Pleskova and
Bencze, 1959). Minimal irritation of intact and abraded skin have been
observed in rabbits (Dow, 1969). Commercial but not purified PCP samples
have produced chloroacne in the rabbit ear bioassay (Johnson et al.., 1973);
another rabbit ear bioassay test, however, indicated no discemable dif-
ference in results of exposure to various grades of PCP (Shelton, 1978).
Rabbit eyes exposed to solid PCP showed slight conjunctival and iritic
congestion (Dow, 1969).
With respect to the toxic effects of long-term exposure, only one
chronic feeding study is available on PCP. Schwetz pr al. (1978) fed
weanling Sprague-Dawley rats 0, 1, 3, 10 or 30 mg/kg/day purified PCP
in the diet for 22-24 months. The study of male rats was terminated
after 22 months due to high mortality in both control and treated groups.
Ingestion of 30 mg/kg/day of PCF produced a significant decrease In body
weight in females; a significant increase in serum glutamic pyruvic
transaminase activity in both male and female rats; an increase in the
specific gravity of urine among female rats at the end of 1 year but not
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at 2 years; and-an-accumulation of pigment in the liver and kidneys.
Pigment accumulation was also noted in females at the 10 mg/kg level.
No other significant differences were observed. Tumor types and inci-
dences were comparable in test and control groups.
Several subchronic feeding studies have also been reported. Kim-
brough and Linder (1978) fed male and female Sherman rats 0, 20, 100 or
500 mg/kg of diet either technical grade or purified PCP for 8 months. None
of the animals died during the study and no toxic manifestations were
evident except a reduction in body weight gain in animals fed the highest
mg/kg dose. Liver weights were significantly increased in rats fed 500
mg/kg of technical PCP. Morphologically, females were more severely
affected than males. Livers of females were characterized by vacuolation
of the hepatocytes, an increase in fibroblasts and other mononuclear cells
within the sinusoids, bile duct proliferation, periportal fibrosis,
degenerated liver cells, increased mitotic figures and an accumulation
of brown pigments in macrophages and in Kupffer cells. Similar but less
pronounced effects were observed in females at the 100 mg/kg level.
The predominant lesion in males given 100 mg/kg and 500 mg/kg consisted
of enlarged pleomorphic hepatocytes, which had foamy cytoplasm or cyto-
plasm with large vacuoles. Only mild alterations were noted in rats at
the 20 mg/kg level.
In contrast, purified PCP caused slightly enlarged liver cells, with
occasional eosinophilic cytoplasmic inclusions at 500 mg/kg but no altera-
tion in the livers of rats fed the two lower concentrations. Rats receiving
500 mg/kg purified PCP also exhibited thickened walls in the hepatic central
veins of the liver.
Johnson and co-workers (1973) also noted more severe toxic effects
in rats fed 0, 3, 10 or 30 mg/kg/day of technical PCP than those observed
in rats similarly treated with the purified material for 90 days. Tech-
nical PCP resulted in focal heptocellular degeneration and necrosis at
30 mg/kg and liver damage at the two lower treatment levels. No liver
lesions were associated with treatment with purified PCP.
Similar findings in rats have been reported by Knudsen et al. (1974)
Kimbrough and Linder (1975) and Goldstein (1977). Savolainen ana
Pekari (1979) reported that the administration of 20 mg/1 of technical
FCP in the drinking water of male Wistar rats for up to 14 weeks resulted
in a significant liver concentration of PCP (56-65 ug/g wet tissue), which
remained stable during the 14-week period. PCP also accumulated in peri-
renal fat (61 ug/8 v^t tissue at 14 wk) and brain (< 10 ug/g). The major
portion of the PCP-body burden, however, was cleared within 4 weeks after
switching to a PCP-free diet. Transient biochemical changes in brain
enzymes were also noted during PCP treatment.
Goldstein (1977) recently examined the differences between the
hepatic effects produced by commercial and purified PCF with respect to
drug metabolizing enzymes and presence of porphyria. Female Sherman rats
were fed pure of technical PCF at levels of 0, 20, 100 or 500 mg/kg of diet for
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8 months. Technical PCP produced hepatic porphyria and increased hepatic
aryl hydrocarbon hydroxylase activity, glucuronyl transferase activity,
liver weight, cytochrome p-450, and microsomal heme, but no N-demethylase
activity. The peak of the CO-difference spectrum of cytochrome p-450 was
shifted to 448 nm, and there was a dramatic increase in the 455/430 ratios
of the ethyl isocyanide difference spectrum. Enzyme changes were observed
at 20 mg/kg of technical PCP; porphyria occurred at 100 and 500 mg/kg.
Pure PCP had no significant effect on these parameters at any dose level
except for an increase in glucuronyl transferase at 500 mg/kg. Both pure
and technical PCP, however, decreased body weight gain comparably at 500
mg/kg. These results suggest that the liver changes associated with
feeding technical grade PCP to rats stem.from toxic contaminants rather
than from PCP itself.
Thus, the toxicity of PCP cannot be readily divorced from the effects
of contaminants in commercial formulations. Technical PCP is moderately
toxic to mammalian species following acute ingestion or dermal exposure.
Long-term dietary exposure of rats to 20 mg/kg or more of technical grade
PCP is associated with liver lesions, porphyria and enhanced hepatic
enzyme activity. Dietary levels up to 30 mg/kg/day of purified PCP,
however, did not enhance the incidence of tumors in rats after 2 years.
4. Human Studies
Several cases of human poisoning with PCP or its sodium salt are cited
in the scientific literature (Knudsen et al., 1974; Haley, 1977; Robson
&t al., 1969; Bevenue et al., 1967). PCP causes rapid uncoupling of
oxidation and phosphorylation, cycles with a resulting increase in metabolic
rate. Symptoms include fever, profuse sweating, dyspnea, congestion of
ocular and nasal mucosae, abdominal pain, headache, fatigue and tachycardia
(Young and Haley, 1978; Knudsen «. al., 1974)
Uede et al. (1962) noted irritated throats, facial flushing and hand
and leg weakness in four families 'after drinking and bathing in water
from a well containing 12.5 mg/1 PCP. Recovery occurred with 2-3 days.
A similar case was reported by Chapman and Robson (1965) in a 4-year-old
child>who had bathed daily for 13 days with water from a PCP-contaminated
holding tank. She was hospitalized with fever, intermittent delirium,
acidosis, aminoaciduria and ketonuria but recovered completely.
Most cases of human exposure, however, are through direct dermal
contact with PCP, from industrial exposure in wood treatment plants or
inhalation of water vapor containing PCP in industrial cooling towers,
paper pulp mills and tanneries.
Bevenue e_t al. (1967) reported reddening and development of painful
sensations in the hands of a male 10 minutes after immersion of his hands
in a solution containing 0.4% PCP. The pain persisted for 2 hours. One
month after the episode, urinary PCP levels had returned to background
levels.
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Local skin irritation and chloracne have also been associated with
dermal contact to PCP (Nomura, 1975; Knudsen et al., 1974). Johnson
et al. (1973) however, demonstrated that the acnegenic agent was present
in technical but not purified PCF, an observation suggesting dioxin con-
taminants as the causative agent.
A case of fatal aplastic anemia has been reported following dermal
exposure to PCF for approximately one year (Roberts, 1963).
Begley et al. (1977) noted evidence of abnormal but reversible
renal function in 18 workers at a wood treatment plant. Creatinine
clearance and phosphorus reabsorption values were depressed prior to
a 20-day vacation period but showed significant 'improvement during
vacation, an occurrence suggesting that PCF exposure transiently reduced
both the glomerular filtration rate and tubular function.
At least 24 industry-related PCF fatalities have been reported.
At autopsy, the following changes are generally found: edematous brain,
heart dilatation, tubular degeneration of the kidneys, edematous lungs
with congestion and intra-alveolar hemorrhages, and a slightly congested
liver with centrilobular degeneration (Knudsen et al.. 1974).
5. Overview
Pentachlorophenol appears to be an ubiquitous contaminant of human
tissues in industrialized societies; some 85% of human urine samples
from the general population of the United States are positive for penta-
chlorophenol. PCP may be absorbed through the skin, by inhalation, or
by ingestion of contaminated food or drink. The pharmacokinetics of PCP
in man, however, show it to be readily excreted in urine, either unchanged
or as the glucuronide conjugate.
lexicological data on pentachlorophenol are complicated by the
presence of varying amounts of polychlorinated dibenzo-p-dioxins and
dibenzofurans in commercial formulations. Although pure PCP has not
been fully characterized toxicologically, PCP does appear to be toxic
in its own right. Acute LD50 values vary according to the contaminant
content of the test material, but man would appear to be more susceptible
than rodents and females more susceptible than males. Dietary exposure
to 100-500 mg/kg technical PCF for 90 days is associated with pronounced
liver lesions in rats; only mild alterations were seen at 20 mg/kg.
Purified PCP produced no significant adverse effects in rats fed 3-10 mg/
kg/day for up to 2 years.
No oncogenic effects were noted in either mice or rats fed 17 mg/kg/
day and 30 mg/kg/day, respectively, of PCP for two years. Currently avail-
able data are insufficient to support the mutagenicity of PCP.
Reproductive effects, however, have been observed in rats orally
exposed to 30 mg/kg/day or more during gestation. Purified
PC? was somewhat more toxic than commercial grade PCP with respect to
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Che incidences of resorbed fetuses, skeletal and soft-tissue anomalies
and fetal growth retardation, particularly during early organogenesis.
Comparable effects were not observed following a single but higher oral
dose (60 mg/kg) of PCP.
B. HUMAN EXPOSURE
1. Introduction
The use of pentachlorophenol as a pesticide results in numerous
opportunities for human exposure. As discussed previously in Part A of
this chapter, PCP is commonly found in human urine, even in subjects who
have not been occupationally exposed to the chemical. This has been
taken by some as evidence of exposure, although the precise route or
combination of routes is unknown. Detrick (1977) has suggested that PCP
found in the body may be the result of the metabolism of other chlorinated
compounds, such as hexachlorobenzene. This section discusses PCP exposure
situations and quantifies the expected exposure to PCP whenever possible.
It does not, however, consider occupational exposures such as those of
pulp and paper mill workers or tannery workers. The'exposure routes con-
sidered here are ingestion of food and drinking water, inhalation of air,
and dermal absorption.
2. Ingestion of Food
Pentachlorophenol is not widely found in food. The FDA (1977), as
part of the Total Diet Studies, reported PCP in 11 of 360 composite
samples. Residues of 0.004-0.017 mg/kg were found in dairy products,
grains and cereals,*root vegetables, and sugars and adjuncts. On the
basis of these data, the FDA estimated an average intake of 0.76 mg/day
for a typical 15-20-year-old male, the USEPA (1978a) has calculated an
average intake of 1.5 mg/day and a maximum of 18 mg/day based on average
and maximum residues reported in the Total Diet Studies. However, these
average intakes are based on the mean of the positive samples and are
not actually representative of the average intake, since the actual
incidence of PCP detection in food was low. As an example, PCP was
detected in one composite sample of dairy products. However, in a
smaller sample in Michigan, Lamparski e£ al., (1978) found no PCP in milk.
Various other food substances have been tested individually for
PCP content. Section IV-B discussed levels of PCP in fish and showed a
range of about 1-5 mg/kg wet weight. An average consumption of fish of
21.4 g/day (USDA, 1978) would result in an exposure of ff.l mg/day,
assuming a maximum level in fish of 5 mg/kg. Peanut butter has been
indicated in the recent market basket study as a source of PCP in food.
Heikes (1979) reported PCP in seven peanut butter samples at concen-
trations of 1.8-62 mg/kg, with an average of 18 mg/kg. The maximum
sample was traced to a jar lid; however, most jar lids do not contain PCP. The
author suggested that PCP may be a breakdown product of pentachloronitrobenzene
i::
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which was also found in peanut butter. For an estimated daily consumption
of 100 g of peanut butter, a maximum consumption of 6.2 mg/day FCP can be
estimated. A more typical exposure from'this source would be much lower,
perhaps about 0.5 mg/day.
PC? has also been detected in gelatin. Firestone (1977) suggested that
the chemical may have contaminated the hide used in making gelatin, since PCP
is used as a preservative during hide processing. Levels of 0-8.3 mg/kg were
found in 15 samples of gelatin, with higher levels found in that imported from
Mexico. Such high concentrations of PCP in gelatin are expected to be rare so
this exposure level represents a worst case. Using the maximum contamination
of 8.3 mg/kg PCP in gelatin powder and a maximum consumption of 200 g of pre-
pared jello per day, an ingestion of 24 ug/day can be estimated.
Another potential exposure route for humans is through ingesting
food packaged in containers in which PCP was used as a. preservative in
glue. The propensity for different food types to absorb this PCP is
unknown; however, the concentrations and total amount of PCF available
in glues are probably small.
Thus, average intake of PCF in food has been estimated to be
1.5 mg/day. Persons consuming large amounts of peanut butter or gelatin
would have potentially larger intakes, perhaps as much as 24 mg/day.
3. Ingestion of Drinking Water
PCP has been found in drinking water in the United States at low
concentrations. EPA (1978b) sampled 113 finished waters in 1976 as part
of the National Organics Monitoring Survey. FCF was found in 86 of 108
samples, with a mean of 0.07 ug/1 and a maximum of 0.70 ug/1. However,
the median was less than 0.01 ug/1, the minimum detectable limit. In a
more recent survey supplementing the NOMS program, FCP was detected in
eight cities out of 135 systems surveyed (U.S. EPA, 1980). Detected
concentrations in finished water were somewhat higher than the NOMS
results, ranging from 1.3 ug/1-12.0 ug/1. Assuming an intake of 2 I/day,
exposure to most persons would be less than .02 ug/day, while the
maximum would be 24 ug/day.
4. Inhalation of Air
Monitoring data for PCP in air is very limited. No information is
available on ambient levels, and information on levels indoors is scarce.
In pressure treatment plants and lumber mills using dip and spray treat-
ment, Arsenault (1976) reported concentrations of 0.003-0.063 mg/m3 PC?
in areas where workers spent most of their time. Near the PC? source,
however, levels ranged from 0.004 mg/ni3 to 1.000 mg/m3. Assuming a
breathing rate of 1.8 m3/hr for 8 hours, exposure levels of 0.9 mg/day
and 14 mg/day, respectively, can be calculated. These results are
shown in Table 40. Though exposure in occupational settings is not
considered in detail here, these data may provide an upper limit for
exposure resulting from home use of PCP. The use of PCP in lumber yards
in spray form is probably the most comparable to home use of PCP in terms
of exposure; thus the maximum value of 0.063 mg/m3 will be used. For an
assumed breathing rate of 1.3 m3/hr for 8 hours, this presents an
exposure of 0.91 mg/day. However, a homeowner would most likely not be
continually exposed to this level.
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TABLE 40.
Exposure Route
Ingestion
SUMMARY OF LEVELS TO HUMAN EXPOSURE VIA
VARIOUS PATHWAYS
Exposure
Level (mg/day)
Average intake from food
Average intake from food (EPA)
Maximum intake from food (EPA)
Intake from fish (maximum)
Average intake from peanut butter
Maximum intake from peanut butter
Maximum intake from gelatin
Intake from drinking water (maximum)
Intake from drinking water (typical)
Inhalation
Working Subpopulation
Wood treatment factions
o general work area
o near PCP source
At cooling tower site
Use of PC? spray
General Population - national
Evaporation of wood preserving wastewater
Open burning of treated wood
Evaporation from cooling towers
Volatilization from treated wood
Total (summation of above)
General Population - local
Downwind of cooling tower (1 km)
Downwind of cooling tower (8 km)
Downwind of wood preserving wastewater evaporation
pond (
-------
Exposure levels for the general population can be estimated using
the PCP concentrations in air calculated in Section IV-D. Nationally
distributed upper limit ambient concentrations contributed from wood
treatment wastewater evaporation, volatilization from treated wood,
evaporation from cooling towers, and open-burning of wood, are 4.3 ng/m ,
56 ng/m^, 36 ng/m3 and 40 ng/m3, respectively. For an assumed breathing
rate of 20 m^/day, exposure levels of 0,09 ug/day, 1.1 ug/day, 0.7 ug/day,
and 0.8 ug/day, respectively, can be calculated. These values, summed,
give rise to a national exposure of 2.6 ug/day for the general population.
Likewise, the exposure of sub-populations downwind from cooling
towers and wood preserving wastewater evaporation ponds can be estimated
based on concentration estimates from Section IV-D. The upper limit plume
concentrations estimated were 1.0 x 10^ ng/m3 (at a 1-km distance from a
tower), and 100 .ng/m3 (up to -4 km distance from evaporation pond).
Exposure levels calculated based on these concentrations are 2,000 ug/day,
and 2 ug/day, respectively, assuming 20 m3/day and a 24-hour exposure.
If one assumes that the exposure within 1 km of a cooling tower applies
only to an occupational subpopulation and that their exposure period equals
8 hours, then the resultant exposure level for this group is 14,400 ug/day.
The USEFA (1978a) has estimated a daily exposure to 9,000 ug PCP for
workers directly exposed to a cooling tower plume. It is unlikely, however,
that humans would be directly exposed to the plume. The levels do indicate
the magnitude of the potential for human exposure through inhalation of
plume vapor and justify the need for further investigation of this path-
way. Measurement of PCP concentrations in plumes would quickly verify the
results of the concentration calculations.
While there have been no measurements of PCP in the air in the home,
two reports in EPA's Pesticide Episode Review System (PERS) (U.S. EPA, 1976)
may be relevant. One involved a painter exposed to "drift" while treating
a roof. The other involved a man spraying PCP in a crawl space beneath a home.
He developed weakness, headache, double vision, tachycardia, nausea and
hyperpyrexia, and subsequently recovered. The route of exposure cay
have been dermal, as well as inhalation, though, the fact that the
location was a crawl space suggests the latter. Furthermore the lack
of dilution air volume may have resulted in a higher exposure than that
estimated above.
Exposure of persons to PCP-treated wood, especially indoors, should
also be considered. PERS (USEPA, 1976) reports several incidents of
effects resulting from inhalation in treated rooms or houses. In some
cases, the subjects had not applied the chemical so that inhalation was
suggested as the likely route of exposure. The symptoms ranged from
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malaise to peripheral nerve manifestations. Gebefugl et al., (1976)
measured air concentrations in enclosed areas treated with PGP according
to the label-directions in Germany. These authors found concentrations
of 1-60 ug/m PCP in the air. USEPA (1978a) used this maximum and a
breathing rate of 1.0 m, /hr. for 20 hours to estimate an exposure of 3.2
mg/day in this situation. Outdoor exposure to PCP-treated lumber would
result in a substantially lower inhalation exposure.
5. Dermal Absorption
The estimation of exposure of persons through dermal absorption of
PCP depends upon the assumptions used in the calculations. Unfortunately,
since little is known about the permeability of the skin to different
chemicals, only gross estimates of the exposure are possible. EPA
(1978a) has used an estimate of 10% dermal absorption of PCP. However,
numerous assumptions must be made in the use of this value, primarily
in assuming the volume of .the liquid in contact with the skin. The use
of permeability constants may decrease the uncertainty. Therefore, in
this section, a permeability constant of 0.01 cm/hour is used for PCP,
similar to that which has been measured for phenol (Blank, 1979, personal
communication). Though the validity of this assumption for PCP has not
been tested, it does present a moderately high rate constant compared
with those that have been measured, and thus represents a conservative
approach to estimating exposure by dermal absorption.
The major sources of dermal exposure are occupational; the general
public is exposed to low concentrations of PCP in water. Assuming daily
contact (total body) with water for 0.2 hrs. through bathing and dish-
washing, exoosure levels of 0..0004 ug/day (at a mean PCP concentration of
0.01 ug/1) and 0^043 ug/day (at maximum PCP concentration of 12.0 Ug/1) can
be estimated.
Home use of PCP can also result in dermal exposure. The USEPA
(1976) reported numerous incidents of perons spilling or splashing
the solution on themselves. The symptoms observed were not usually
described, but Bevenue et al. (1967) reported a burning sensation and
skin irritation resulting from such an exposure. This type of exposure
would not be chronic in most cases, however, since it is accidental, the
extent of the exposure can vary widely. For the purposes of estimation,
a 5% solution of PCP was assumed to have been spilled on 10% of the body
surface area and to have remained there for 10 minutes. When the per-
meability constant of 0.01 cm/hour is assumed, the maximum estimated
exposure is 170 mg.
The handling of treated wood may also result in PCP exposure.
While persons such as carpenters, lumber yard workers, and loading dock
workers handling crates would be exposed continually in this manner,
homeowners would also be exposed occasionally. USEPA (1976) mentions
a few incidents of this nature, without specifying the symptoms. USEPA
(1978a) estimated the exposure to .construction workers by assuming that
6 months after treatment, the concentration of PCP in the wood surface
126
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would be 0.5 mg/square foot. It was also assumed that the worker handled
wood without gloves 40 times/day, and that the skin area exposed was 0.25
sq. ft., and that absorption was 10% effective. The resultant exposure
was 0.5' mg/day.
6. Summary
Table 40 summarizes all the exposure levels calculated in the
preceding section. The route of exposure to PCP for the largest number
of people is through drinking water. While residues of PCP have been
reported in food, the incidence appears to be low. The prevalence of
high levels in gelatin is unknown. A typical exposure through drinking
water was estimated to be 0.02 ug/day, and a maximum of 24 pg/day.
The typical total dietary exposure was estimated at 1.5 mg/day and a
maximum of 18 mg/day. However these estimates do not apply to as large
a subpopulation as the drinking water estimates. Consumption of peanut
butter in addition to other foods that contain maximum residues may
contribute up to 24 mg/day for very limited subpopulations.
Other exposures considered here involve the use of PCP (herbicide
or wood preservative) by the consumer or contact with PCP-treated wood.
The maximum exposure through the use of PCP, as estimated here, appears
to result from accidental spillage and dermal exposure. When various
assumptions are made, the validity of which is unknown, an exposure of
170 mg/spill was estimated. Inhalation from treated wood indoors and
during application may result in exposures of 1-3 mg/day. Inhalation
of estimated ambient levels of PCP in the atmosphere (the summation of
concentrations from four direct sources) has an associated exposure
level of 6 vg/day for the general population. Subpopulations in the
vicinity of 2.6 PCP sources may be exposed to significantly higher levels.
It should be pointed out that persons using PCP will be exposed
through both the dermal and inhalation route. With appropriate pre-
cautions, the dermal route can be eliminated. However, it is not
likely that inhalation exposure can be totally avoided.
127
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133
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SECTION VI.
NON-HUMAN EFFECTS AND EXPOSURE
A. EFFECTS ON NON-HUMAN ORGANISMS
i. Introduction
This section provides information about the levels of pentachloro-
phenol that disrupt normal behavior and metabolic processes, as indicated
by laboratory and field studies. The effects of the sodium salt of this
compound, NaPCF, and of certain Dowicide chemicals containing PCP are
also considered, as they are frequently used in bioassays because of
their availability and solubility.
Several factors introduce a certain amount of inconsistency in bio-
assay results. The various grades of PCP range from less than 80% pure
to 99+% pure, depending on the intended use of the material. Dovicides
G and GS-T are pesticides (molluscicides) containing approximately 70-80%
PCP, in addition to other chlorinated ingredients. These impurities may
modify the toxicity of PCP, depending on their composition and relative
concentrations (see Appendix A).
The type of bioassay used can'also significantly influence the
results. Tests conducted under static conditions are normally less
reliable than continuous-flow experiments because there is less control
of toxicant concentrations. However, continuous-flow conditions may not
be suitable for testing certain kinds of organisms, such as larval fish
and free-floating invertebrates. In both kinds of bioassays, the toxi-
cant concentrations are often determined nominally (i.e., by diluting a
measured amount of the substance) instead of by direct periodic measure-
ment during the bioassay. Nominal determination of concentrations does
not account for toxicant evaporation, adsorption onto particles or the
test tank, or absorption by the test organisms, and so may produce signifi-
cant overestimations of lethal and sublethal levels, particularly in static
tests.
Water parameters, such as temperature, hardness and pH, have been
shown to influence the toxicity of PCP to various aquatic organisms.
Thus, variations in these parameters between experiments could yield
conflicting or misleading results. Other factors include the species
and developmental stage of the organism being tested. Since some species
and stages may be more sensitive to PCP than others, it is not always
valid to extrapolate the data from studies of related organisms.
135
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2. Freshwater Organisms
a. Chronic and Sublethal Effects
Low levels of toxicants that remain for extended periods are generally
considered to represent "normally" polluted conditions in natural water-
ways. Under these circumstances, aquatic biota may become acclimated to
the toxicant, or they may exhibit behavioral alterations such as increased
respiration, loss of equilibrium, or reduced spawning and hatch success.
Prolonged exposure, even to low concentrations of PGP, may ultimately
result in mortality. Whether or not fish are killed by chronic exposure
to PCP, certain effects, such as reduced spawning, may still endanger
local populations.
Webb and Brett (1973) have studied underyearling sockeye salmon
(Oncorhynchus nerka) in 12-week tests of growth rate and food conversion
efficiency and 2-week tests of swimming performance. Growth rate and
food conversion efficiency were closely related: the EC50 values (50%
of organisms demonstrating the stated effect) were 1.74 ug/1 and 1.80 ug/1
respectively. Swimming performance, however, was unhindered at the
highest exposure concentration (50.0 ug/1)• Since the- effects of these
levels on natural populations are-not known, they should not-necessarily
be considered sublethal or harmful.
Matida et al. (1970) found that the growth of rainbow trout (Salmo
gairdheri) was "markedly retarded" after 4 weeks of exposure to PCP con-
centrations exceeding 8 ug/1, with slight retardation occurring at 3 ug/1.
Solutions containing 34 ug/1 of PCP created the same effect in sweet-
fish after 13 weeks of exposure. In the 2 ug/1 solution, however, the
experimental sweetfish grew more quickly than the control fish in 0 ug/1-
The cause of this positive effect was not surmised by the authors; con-
ceivably the low levels of PCP had a biocidal effect on the natural para-
sites and diseases of the sweetfish. Another seemingly paradoxical
phenomenon was the variable effect of PCP on swawning by sweetfish. In
20 ug/1, spawning was delayed up to 2 weeks, while fish exposed to 34
ug/1 spawned 7-10 days before the controls. Macroscopic inspection of
ovaries and testes revealed no differences in fecundity and virility
between experimental and test fish, and no explanation for the variation
was given.
In acute toxicicy tests, Reinert (1976) observed behavioral changes
preceding death in rainbow trout. At concentrations between 10 ug/1 and
32 ug/1, the trout exhibited abnormal respiration, followed by partial
and total loss of equilibrium and death. Bluegill sunfish had the same
symptoms in 65-100 ug/1 PCP.
Chapman (1969) conducted a variety of tests on rainbow trout in
various pre-adult stages. After 3-6 weeks of exposure to 30-100 ug/1
NaPCP, trout alevins had retarded growth, increased yolk catabolism, and
increased mortality compared with controls. The maximum dry weight of
alevins reared in NaPC? decreased approximately 62 for each 10 ug/1 in-
crease in PCP concentration.
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Whitley and Sikora (1970) observed an increase in respiration rates
in sludgewonns (Tubifex tubifex) exposed to 250-1,250 ug/1 PCP. This
effect was attributed to the toxicant's tendency to interfere with
oxidative phosphorylation. Respiration was affected to a greater degree
at pH's exceeding 8.5, although the toxlcity of the solution'increased
with decreasing pH.
Among the most sensitive freshwater organisms tested was the alga
(Chlorella pyrenoidosa). Huang and Gloyna (1968) observed substantial
destruction of chlorophyll at a concentration of 1 ug/1 PCP; extrapolation
of the data indicated that 7 ug/1 would cause death. Blackman et al.
(1954) exposed duckweed (Lemna minor) to PCP and determined an ECso
level (inducing chlorosis) of 800 ug/1. The minimum level reported to
cause chlorosis was 121 ug/1.
b. Acute Effects
Acute toxicity is defined as toxicant-induced mortality over a short
period, generally within 96 hours. Although fish in natural waterways
are more likely to be exposed to lower concentrations that may result in
chronic or sublethal effects, industrial discharges and spills can
temporarily result in levels high enough to cause fish kills (see Section
B of this chapter).
The acute effects of PCP on freshwater finfish have been studied for
at least fifteen species, and this work provides a fairly reliable data
base, which has been compiled and condensed in Table 41. It should be
noted that the LCSO values given were derived under a variety of con-
ditions. Such factors as exposure period (between 24 and 96 hours), age
of test fish, differences in certain water parameters, and bioassay type
(static or flow-through) may account for some of the variation in a given
species' sensitivity. (Factors contributing to variability in PCP toxicity
and fish sensitivity are discussed in greater detail in Part 5 of this
section.)
Reported LC50 values for PCP and PCP salts range from 15.4 ug/1 for
the rainbow trout to 1,740 ug/1 for the flagfish. As with many toxicants,
the salmonids are apparently somewhat more sensitive as a group to PCP
than other fish. However, the reliability of this generalization with
respect to field situations is uncertain. Two normally hardy fish, the
bluegill and the goldfish, were found to be relatively sensitive to
NaPCP in a static bioassay by Inglis and Davis (1972).
LC50 values for the freshwater invertebrates tested ranged from 240
ug/1 for the OncomeIania snail, to 10,000 ug/1 for another snail species,
Pseudosuccines collumnea. However, only four species are represented in
the literature, and further testing could possibly reveal a broader range
of sensitivities among the invertebrates. The available data are also
summarized in Table 41.
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TABLE 41. PCP ACUTE TOXICITIES (LC5(J) TO FRESHWATER 3IOTA*
PC? Concentration
Range (ug/1)
15.41 - 2302
.203 - 303
SO3 - 220
63* - 90s
64.2s - 150
68 - 86
120
130 - 135
138
160 - 170
210 - 370
390
510 - 630
1,000
1.1302
1.7402
Vertebrates
Rainbow trout (Salmo gairdneri)
Bluegill sunfish (Lepomis macrochirus)
Goldfish (Carassisu auratus)
Sockeye salmon (Oncorhynchus nerka)
Coho salmon (Oncorhynchus kisutch)
Sweetfish (Plecoglossus altivelis)
Channel catfish (Ictalurus punctatus)
Carp (Cyprinus carpio)
Brook trout (Salvelinus fontinalis)
Southern top-mouthed minnow (Pseudorasbora pary
Fathead minnow (Pimephales promelas)
Channa gachua
Japanese killifish (Oryzias latipes)
Lamprey (Petromyzon marinus)
Zebrafish (Brachydanio rerio)
Flagfish (Jordanella floridae)
240
310
680
833
5909
4,000
4,000
10,000
lReinert (1976)
2Fogels and Sprague (1977)
3Inglis and Davis (1972)
"Webb and Brett (1973)
,5Davis and Eoos (1974)
'Hanumante and Kulkarni (1979)
Invertebrates
Snail (Oncomelania sp.)
Sludgeworm (Tubifex tubifex)
Daphnid (Daphnia magna)
Snail (Pseudosuccines collumnea)
138
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3. Marine Organisms
a. Chronic Effects
The only marine finfish tested in a chronic exposure bioassay was
the sheepshead minnow (Parrish .et al., 1978). In continuous-flow
conditions, adverse effects were observed in concentrations as low as
88 yg/1. Concentrations exceeding 88 ug/1 caused significant mortality
in adult fish during the 151-day test period. At 195 ug/1, hatching
success and survival of second generation fish were also reduced.
The lowest concentration of PCP reported to cause sublethal effects
in invertebrates was 40 ug/1, an EC50 level for abnormal development in
the Eastern oyster (Borthwick and Schimmel, 1978). Rubinstein (1978)
observed inhibition of feeding in the lugworm (Arenicola cristata) at
at 80 ug/1.
The grass shrimp (Palaemonetes pugito) has been extensively studied
for its reactions to various concentrations of PCP. Brannon and Conklin
(1978) found that the exuviae (molted exoskeletons) of grass shrimp
increased in dry weight with exposure to 100-1,000 ug/1 PCP. It is
possible, however, that this is an adaptive response rather than a sub-
lethal effect. In a chronic bioassay, Conklin and Rao (1978) tested the
sensitivity of shrimp to PCP during different stages of ecdysis, or shell
molting. Shrimp in the later proecdysial stages were found to be more
susceptible to PCP than during early proecdysial or intennolt periods.
During 66 days of exposure to 436 ug/1 PCP, 63% of the test shrimp died
within 24 to 48 hours of ecdysis. Increased respiration rates were
observed (as in sludgeworms) at a concentration of 5.0 ug/1 by Cantelino
et al. (1978). Exposure to 10-20 mg/1 caused an initial increase in
oxygen consumption, which now was followed by a decline leading to death.
b. Acute Effects
Available data on acute toxicity to marine biota were somewhat
limited, and covered only a small range of concentrations for finfish.
The lowest reported LC50 for a vertebrate was 38 ug/1 for the pinfish,
by Borthwick and Schimmel (1978). The highest LC50 was 422 ug/1 for the
sheepshead minnow, as observed by Parrish et al. (1978).
The most sensitive invertebrate tested was apparently the Pacific
oyster, with an LCc;0 of 48 ug/1. The highest LC50 recorded was for the
shrimp (Palaemon elegans) in the adult stage at 10,390 ug/1- However,
the same species also exhibited median mortality at 84 ug/1 as first
instar larvae in the same study. On the basis of such limited data for
both vertebrates and invertebrates, it is not possible to identify
particularly susceptible species, with the possible exception of the
pinfish and' the oyster. The data are summarized with references in
Table 42.
139
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TABLE 42. PGP ACUTE TOXICITIES (LC5Q) TO MARINE BIOTA*
PCP Concentration
Range (ug/1)
38* - 53.22
1122 - 123
2401 - 422
306
Vertebrates
Pinfish (Lagodon rhomboides)
Striped mullet (Mugil cephalus)
Sheepshead minnow (Cyprinodon variegatus)
Longnose killifish (Fundulus similis)
483
84 - 10,390"
112 - 1,790"
195
250
363 - 5,090"
436s- 3,650s
Invertebrates
Pacific oyster (Crassostrea gigas)
Shrimp (Palaemon elegans)
Sand shrimp (Crangon crangon)
Brown shrimp (Penaeus aztecus)
Atlantic oyster (Crassostrea virginica)
Shrimp (Palaemone.tes varians)
Grass shrimp (Palaemonetes pugio)
*Data compiled from EPA (1978), except where noted.
^orthwick and Schimmel (1978)
2Schimmel et_ al. (1978)
3Woelke (1972)
"van Dijk e£ al. (1977)
5Conklin and Rao (1978)
6Reinert (1976)
140
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4. Other Studies
In an attempt to understand the impact of PCP on ecosystems, some
researchers have devised methods to expose micro-communities to con-
trolled levels of the toxicant. Tagatz et il. (1977, 1978) conducted
tests on estuarine communities composed of annelids, arthropods, mollusks,
and echinoderms. Ecocommunities were simulated by pumping seawater (with
its plankton) into constant-head boxes with drains leading to a screened
box, which collected animals from the effluent. PCF was metered at
different concentrations into seawater flowing into each box.
In the first experiment, exposure concentrations were 7, 76, and
622 yg/1 PCP for 9 weeks. At the lowest concentration, the only signifi-
cant effect was a reduction in the number of mollusks compared with the
control system. At 76 yg/I, annelids and arthropods decreased as well,
while almost no animals survived at 622 yg/1.
In a second test, Dowicide G-ST (79% NaPCP) was used in concentra-
tions of 1.8, 15.8, and 161 ug/1 for 13 weeks. Although 1.8 yg/1 had no
effect, mollusks again were the most sensitive organisms in the macro-
benthic community at higher concentrations, and the total number of
benthic species declined.
Cantelmo and Rao (1978), using similar methods, found an increase
in the biomass and density of nematodes in 76 yg/1 as a result of the
biocidal- effects of PCP. However, concentrations of 161 yg/1 and 622
yg/1 were more harmful than beneficial. With increasing concentration
there was a shift in relative abundance of espistrate feeders to deposit
feeders. The general effects of PCP in all ecocommunity studies were
reductions in the biomass and density of organisms, as well as changes
in species composition. The latter effect could be the result of vary-
ing sensitivity between species, as well as alterations in the food
supply caused by the algicidal properties of PCP.
5^ Factors Affecting the Toxicity of PCP
There are several variables in a natural aquatic environment that
may strongly influence the availability and toxicity of PCP to biota.
Among the most important parameters are pH, water temperature and
hardness. The relationship between fish size and sensitivity has also
been studied, in addition to .differential susceptibility to PCF in male
and female snails. The interaction of PCP with other aqueous chemicals
may modify its toxicity either by synergy or inhibition; however, such
relationships remain to be studied in detail.
The pH of the water is perhaps the most significant and certainly
the most studied of the parameters affecting PCP toxicity. As a weak
acid, PC? dissociates only partially at a neutral pH (7.0). Even the
dissociation of the sodium salt (most often used in bioassays) is pH
.dependent; at pH's above 7.4 it is 99% ionized (Davis and Hoos, 1974).
Kaila and Saarikoski (1977) found that lowering the pH from 7.5 to
141
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6.4 Increased Che toxicity of PCP to crayfish by a factor of 5.9, Indi-
cating that the nonionized form of PCF was more toxic, and by implication,
more available for metabolism. The authors also suggested that the resis-
tance of the crayfish may have been diminished by the acidic water.
Whitley (1968) found that the LC50 values for Tubifex worms doubled
with each successive increase in pH between 7.5, 8.5, and 9.5. A study
on fathead minnows by Crandall and Goodnight (1959) found similar effects
of pH on PCP toxicity.
Whitley and Sikora (1970) observed two different effects of pH which
occurred at opposite ends of the pH range. As described in Part 2 of
this section, Tubifex worms exhibited significantly increased respiration
rates at pH levels exceeding 8.5. The toxicity of PCP,. however, increased
with decreasing pH as in other experiments. The authors suggested that
two separate mechanisms may be responsible for the two effects, and
attributed .the increased respiration response to PGP's effect on the
uncoupling of phosphorylation. The mechanism for toxicosis was not
suggested, although presumably the nonionized form of PCP affects
metabolic systems differently.
Crandall and Goodnight (1959) also studied the effect of temperature
on the toxicity of PCP to minnows. Survival times decreased significantly
in response to a temperature increase from 10° to 26°C. The effect was
attributed to the variable rates of metabolism as a result of the fish's
poikilothermia. Asano &t al. (1969) found that a 10°C rise in temperature
reduced the median lethality period (LTM) and LC50 by factors of 2.23 and
4.82, respectively. In a bioassay with three species of marine shrimp,
van Dijk et al. (1977) corroborated these findings using temperature
variations of 5 to 25°C.
The data of Ruesink and Smith (1975), however, are completely at
odds with these three studies. In 48- and 96-hour bioassays with fat-
head minnows, they found that PCP was more toxic by a factor of 1.5 to
1.8 as the temperature was reduced from 25° to 15°C. A suggested explana-
tion was that the rate of detoxification and excretion may decrease more
rapidly than the rate of absorption with decreasing temperature. Since
no temperatures below 15°C were used in the test, however, these findings
should be verified by further research.
Only one study testing the effects of water hardness on PCP toxicity
was found. The data of Reinert (1976) indicate that rainbow trout and
bluegill are significantly (P - 0.05) more susceptible in soft water
(47 mg/1 hardness) than in hardwater (218 mg/1). The respective 96-hour
LCgg's for trout and bluegill in hard water were 23 and 88 yg/1; in soft
water, 15.4 and 79 ug/1. No explanation was offered for these results.
The size of the test fish may have some effect on its sensitivity,
but experimental data are inconclusive. Matida et al. (1970) stated
that the "median tolerance limit increases with the size of fish."
Adelman £t al. (1976) found that the size of goldfish had no significant
142
-------
effect on LCso levels, while lethal threshold concentrations were slightly
higher for smaller fish. This relationship was not evident in fathead
minnows. In a bioassay with lake trout (Cristivotner namaycush), Good-
night (1942) concluded that "within reasonable limits the size of the
fish...does not greatly affect the toxicity" of PCF or NaPCP. From the
evidence presented, it appears that the relationship between size and
sensitivity to PC?.probably varies from species to species.
In an experiment conducted by Hosaka e_t al. (1969), Oncomelania
snails were collected once a month for 7 months, with the males and
females separated. Each group of snails was then exposed to several
concentrations of NaPCP for 48 hours. By the fifth month females were
more resistant than males, while the LC50's were the same in one group
of snails collected in June (the sixth month). The females particularly
became more sensitive between April and June, the time coincident with
an egg-laying period. Sexual and reproductive factors remain to be in-
vestigated for other species.
The presence of other chemical substances in the water may increase
or decrease the toxicity of PCP. The only substances tested so far have
been carbaryl and arecoline, a direct-acting cholinergic agent (Sta'tham
and Lech, 1975). The toxicity of pentachlorophenol to rainbow trout was
significantly increased in fish that were pre-exposed to these compounds,
even though carbaryl by itself caused no mortality during 48 hours of
exposure to a 1 mg/1 concentration.
Various bioassays on PCP toxicity have used different grades of the
toxicant, which could be a significant factor in LC50 variability.
Technical grades of PCP may contain less than 80% of PCP; commercial
grades a higher pro-portion; and reagent grades in excess of 99.8% PCP.
Depending on the toxicity of these impurities, experimental results
under otherwise identical conditions can vary widely. For a
discussion of the contaminants found in PCP, see Appendix A.
6. Effects on Terrestrial Biota
a. Plants
The only study available on PCP toxicity to land plants was done by
Sund and Nomura (1963). The respective LC5g values for radish (Raphanus
sativus) seeds and grass (Sorghum sudanense) seeds were 7.190 and 5,400
Ug/kg. Blackman et al. (1954) observed inhibition of radial growth in
the mycelium of the fungus, Trichoderma viride, at 585 ug/kg.
b. Animals
No data on PCP effects on terrestrial animals were available, aside
from scattered information in Vermeer e_t al. (1974). See Section VI-3
for a discussion of this study.
143
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7. Conclusions
According to Che literature surveyed, the lowest concentration of
POP at which effects have been observed in an aquatic organism is 1 ug/1,
which caused destruction of chlorophyll in the alga, Chlorella pyrenoidosa.
The sockeye salmon exhibited reduced growth and food conversion efficiency
at 1.74 and 1.30 ug/1, respectively. The lowest reported LC$Q is 15.4
Ug/1, for the rainbow trout. Oncomelania snails were apparently the most
sensitive freshwater invertebrate tested, for which the LC50 values
ranged from 240 ug/1 to 390 ug/1.
Among the marine organisms, the pinfish and the Pacific oyster were
the most susceptible to PGP, with respective LCso's of 38 ug/1 and 48
Ug/1. -Three species of marine shrimp were found to be substantially more .
sensitive during the larval stages than as adults.
PCP has been shown to affect estuarine ecosystems adversely by
reducing biomass and species diversity and composition.
The toxicity of PCP is affected by several water parameters. The
data' generally indicate that toxicity increases with decreasing pH,
increasing temperature, and decreasing hardness. Factors of uncertain
importance are fish size and interactions, with other aqueous chemicals..
The study of PCP toxicity could be expedited by the adoption of a standard
grade of PCP for use in aquatic bioassays, as purities of different grades
range from less than 80% to 99+% PCP.
B. NON-HUMAN EXPOSURE
1. Introduction
Fish kill data indicate that PCP sometimes reaches concentrations in
natural systems high enough to have lethal effects on aquatic organisms.
Unfortunately, monitoring data reporting ambient PCP levels in surface
water are too few to support more than speculation on exposure of aquatic
biota to PCP.
2. Monitoring Data
The data provided by STORET on PCP levels in ambient waters of U.S.
river basins- are extremely limited, indicating that PCP is an infrequently
monitored parameter. The California and Pacific Northwest basins (with
41 and 22 measurements, respectively) are the only areas with even a
remotely adequate data base. Remarked and unremarked measurements ranged
from 1 ng/1 to 100 mg/1, with the majority of values between 1 ug/1 and
100 ug/1* Levels in California were fairly evenly distributed between
10 ng/1 and 10 ug/1. The Pacific Northwest had substantially higher
values than California, with 91% of the data in the 10-100 ug/1 range.
144
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Ambient concentrations in surface water from sources other than the
STORE! system are also few and inconclusive. Because these data are
commonly accompanied by a description of the location (e.g., near wood
preserving plant), source of the contamination (e.g., run-off following
storm), they provide examples of concentrations that fish may be exposed
to in the field. The highest reported PCP concentrations were measured
in an industrial area and ranged from 82 ugYl to 10,500 ug/1 (see
Table 6). A higher concentration of 5450 mg/1 was found in an oil sample
at a factory outlet (Table 6). Most of these miscellaneous observations,
however, were consistent with the concentrations reported in STORE!,
usually less than 100 ug/1.
3. EXAMS Model
The EXAMS model (U.S. EPA 1980) was used to simulate concentrations of PCP in
natural aquatic systems based on realistic loading rates. The results
are discussed in detail in Section IV-D-2 (see Tables 34-37). The maximum
values generated by the model for water concentrations are summarized
in Table 43. Most of the data are fairly consistent with measured ambient
concentrations reported in STORE! and elsewhere: less than 100 ug/1.
At the highest loading, 17.1 kg/day, concentrations are higher than
typical measured concentrations, especially in the pond and eutrophic
lake systems. The highest measured concentration reported, 10,500 US/1,
was greater than the highest EXAMS value.
The results of the EXAMS model estimate the significance of build-up
of PCP concentrations based on reported dishcarge rates. Due to data
limitations and the level of effort that would be required, the generalized
aquatic systems models in EXAMS were used without adjustment that might
more.accurately simulate aquatic systems into which PCP is actually dis-
charged. System influences on concentrations were very noticeable.
Maximum estimated concentrations for rivers were lower than those for
static systems, the small pond system achieved the highest concentrations,
and the eutrophic lake had higher levels than the oligotrophic lake.
Bottom sediment concentrations were approximately three to fourteen times
the water concentrations.
If the EXAMS model is assumed to simulate reasonably the concentra-
tions accumulating in different aquatic systems during continuous PCP
discharge, then the results can be used to gain further insight into the
impact of PCP effluents on aquatic systems in general. The simulated
concentrations do not, however, represent the worst case because the
model assumes reduction of pollutant concentrations at the transformation
rates entered as input data as well as loss through the physical transport
mechanisms appropriate to each system.
4. Fish Kill Data
Table 44 provides information on the location and activities associ-
ated with fish kills attributed to PCP between 1970 and 1976. Unfor-
tunately, no data on PCP concentrations were available in the fish kill
145
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TABLE A3. WATER CONCENTRATIONS ESTIMATED BY THE EXAMS MODEL FOR
DIFFERENT PCP LOADING RATES (|ig/l)
Concentration (iifi/1)
l'l,T Loading Eutrophic Oilgotrophic Turbid Coastal
(kg/day) Pond Lake Lake River River Plain River
0.07 107.9 (87.5)1 0.1 (0.079) 0.005 (0.002) 0.003 (0.002) 0.003 (0.002) .032 (.028)
0.25 385.4 (312.5) 3.33 (1.75) 0.016 (0.008) 0.011 (0.010) 0.011 (0.010) 0.115 (0.101)
17.1 26362 (21375) 227.9 (121.2) 1.14 (0.584) 0.784 (0.704) 0.784 (0.704) 7.84 (6.91)
'First number is total PCP concentration, number in parenthesis is dissolved PCP concentration).
-------
TABLE 44. DATA FOR PCP-RELATED FISH KILLS, 1970-1976
Year River
Nearest City
No.
Killed1" Cause
1970
1970
1971
1972
1972
1972
1972
1973
Cahaba R.
Caney Cr..
Saquoit Cr.
-
-
Big Piney R.
Shipbuilder's Cr.
Mill Cr. & tribs
Centreville, AL
Conroe, TX
Clayville, NY
PA
OR
Cab oo 1, MO
Webster, NY
Webster, NY
65
30
3
3
563
115
10
1
Lumber treatment
Railroad pilings
Paper plant slime control-
Possible contamination
from mushroom growers
Runoff from lumber company
. Chemical industry operations
Publishing Company
Cooling water from
copying machines
1973 Mill Cr. & tribs.
1974
1974
1974
1974
1974
1975
1976
1976
1976
1976
Brickyard Cr.
Napa R.
San Leandro Cr.
Dryden L. outlet
Anderson Cr.
Cedar Cr.
1976 Cowskin Cr.
1976 Mtn. Fork R.
1976 Bear Cr. Res.
197" Port of Stockton
1977 Texaco Canal &
Crawford Canal
Webster, NY
Red Bluff, CA
CA
Calistoga, CA
San Leandro, CA
Dryden, NY
MO
Anderson,.CA
GA
AR
Cedartown, GA
Wichita, KS
Mena, AR
Bear Creek, AL
Stocktor, CA
Paradis, LA
.018
7
3.1
1.6
1
7
1
9
2
0.2
25
8
38
unknown
Cooling water from
copying machines
Cans thrown into creek
PCP spraying on bridge
PCP spraying on bridge
Runoff from power plant
cooling tower
Paper industry
Discharge from pallet company
Rail operation -
preservative spill
Chemical operations
Paper industry
Wood preservative discharged
from holding lagoon at lumber
lumber company
PCP discharge from co.
treating logs with creosate
NaPCP from petroleum
operation.
thousands.
Source: United States Environmental Protection Agency (USE?A) 1979a. Reports
of fish kills, 1970-1976. Data files or Monitoring ana Liaca Support
Division
-------
reports; moreover, the presence of other toxic chemicals cannot be ruled
out. It is possible that, in some cases, synergy between PCF and other
toxicants increased the magnitude of the fish kill beyond the effect of
PCP alone. Lumber and wood product industries were the most frequent
sources of spills (from holding lagoon overflows), discharges, and run-
of-f from plant sites. During use as a wood preservative near water, PCP
also caused fish kills. Another source of PCP was discharge of cooling
water used in power plants and copying machines. With regard to geo-
graphical distribution, the reported fish kills were not concentrated in
any one region of the country.
5. Exposure to Terrestrial Animals
All of the information on PCP exposure to land animals were taken
from a.field study by Vermeer et al. (1974) in rice field of Surinam,
South America. The study, area was an 8000-hectare rice-growing project,
where some dozen pesticides were used heavily. Applications of NaPCP
were the heaviest, at a volume of 50,000 kg per year. The concentration
of NaPCP in the rice fields averaged about 4 mg/kg following application.
Among the terrestrial animals found at the study site were 33 species of
birds, a frog (Pseudis paradoxa). and the spectacled caiman. Six times
as many dead snail kites (Rostrhamus sociabilis) were found at a roost
close to the rice fields as in a roost further away. The most likely
exposure route was the ingestion of contaminated Pomacea snails. Dead
specimens of egret, heron, and josana were also found, but there was no
basis for comparison with mortality rates in unaffected birds.
•
PCP is normally not used directly on crops or in rice fields on a
large scale in the U.S. Application rates for use as a garden herbicide
are lower and the area typically treated is not as large as an agricul-
tural field. Thus exposure incidents such as the one previously described
are unlikely to occur in the U.S. This does not rule out small-scale
exposure of local invertebrate and bird populations to PCP used as a
garden herbicide. In addition, there may be exposure to PCP spilled on
soil and plants surrounding wood treatment plants. Another pathway is
ingestion of contaminated fish. Accumulation of PCP up to three o'rders
of magnitude (depending on the species) above water concentration has
been reported (see Section IV-C).
6.' Summary
Aquatic organisms are typically exposed to PCP in water at concen-
trations less than 100 ug/1. Simulations of water concentrations result-
ing from practiced discharge rates show agreement with these exposure
levels, with the exception of discharges to the pond system and at the
highest loading rate to the eutrophic lake system. Higher water concentrations
have been measured in industrial areas, the highest at 10,500 ug/1- Even
higher concentrations may be found associated with oil slicks on water
surfaces near sources. Incidences of fish exposure to PC? have been
reported in the vicinity of wood preserving plants, pulp and paper indus-
tries, cooling water discharges, and following spraying.
143
-------
Terrestrial organisms may be exposed to PC? through contact with
spilled material and ingestion of contaminated plants and aquatic
organisms. No information regarding actual exposure was available.
149
-------
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and swimming performance in underyearling Sockeye Salmon (Oncorhynchus
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Whitley, L.S. and R.A. Sikora. 1970. The effect of three common
pollutants on the respiration rate of cubificid worms. J. Water Poll.
Control Fed: 4(2, part 2):R57-R66.
152
-------
Whitley, L.S. 1968. The resistance of tub ificid worms to three common
pollutants. Hyrobiologia .32:193-205.
Woelke, C.E. 1972. Development of receiving water quality bioassay
criterion based on the 48-hour Pacific oyster (Crassostrea gieas)
embryo. Wash. Dept. Fish. Tech. Rep. 9^:1-93, as cited in Borthwick and
Schimmel (1978).
153
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SECTION VII.
RISK CONSIDERATIONS
A. METHODOLOGY
The desired output of the risk assessment is the quantification of
risks to various subpopulations of humans and other classes of biota.
This requires careful identification of the subpopulations at risk and
the populations exposed, evaluation of the ranges in each subpopulation's
exposure consideration of the effects levels or dose response data for
the species of concern and/or proxies for these species and extrapola-
tion of effect levels from dose/response data for laboratory animals to
the human subpopulations at risk.
In this risk assessment for PCP, exposure levels that might result
from several human exposure scenarios are compared with levels of PCP
exposure that have caused effects in laboratory animals. For a number
of reasons, no attempt has been made to extrapolate dose-response
relationships for humans. The risks most clearly associated with
exposure to PCP are the reported teratogenic and reproductive effects.
At present, there appears to be no generally accepted basis for extrapo-
lation of teratogenesis data froa laboratory animals to humans. As a
result, the discussion or risk for humans is qualitative only. For the
exposure scenarios, possible exposures of humans derived from a number
of scenarios, and the "safety factors" are computed from the ratio of
effects to exposure levels. These provide an indication of the signifi-
cance of PCP as a potential environmental hazard to humans.
In the case of risks to other forms of biota, insufficient data are
available on most toxic effects and on exposure values to permit quanti-
tative risk estimates. However, potential risks to various species are
described and presented herein.
B. RELATIVE EXPOSURE EFFECTS AND RISK COMPARISONS—HUMANS
Table 45 presents a series of possible non-occupational exposure
scenarios for humans, with an indication of the possible exposure routes
and levels and key assumptions used in developing the exposure estimates.
Data used in developing the estimates in this table were described in
other sections of this report. The size of the subpopulation associated
with these exposures is described qualitatively and is only meant to
indicate the relative distribution of each exposure scenario in the
population.
The maximum exposure to PCP in food would 0.4 mg/kg/day. Contri-
butions from drinking water, even for the maximum contamination level,
are relatively small. It should be noted, however that residues in food
are not commonly found in sampling studies. Therefore, the maximum possi-
ble exposure is probably only valid for a very small subpopulation.
155
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TABLE 45. EXPOSURE OF HUMANS TO PCI'
Exposure
Ol
ICxpouure Koute
and Med 1 um
Ingest ion
l'0t>d
Diet - "Typical"
Maximum
(ing/day)
1.53
183
mg/kK /day1
0.025
0.3
Subpopulatlon
small
very small
Assumptions2
Typical 5-20 yr male,
average residues.
Typical 15-20 yr. male,
maximum residues
Typical 15-20 yr. male.
I'M uh - Maximum
I'eanut butter
"Typical"
Maximum
Gelatin Maximum
Total Maximum
Drinking Water
Typical
Maximum
0.1
0.00002
0.024
a 60-kg person (woman).
2Sue Section V for more detail.
^Includes drinking water
0.002
0.5
6.2
0.024
0.008
0.1
0.0004
0.4
0.0004
very small
probably small
very small
probably small
very small
large
very small
maximum residues
Maximum concentration in fish
of 5 nig/kg and an average
consumption of 21.4 g/day.
Concentration of 5 mg/kg,
consumption 100 g/day
Concentration of 62 mg/kg,
consumption 100 g/day
Concentration of 8.3 mg/kg in
gelatin; consumption 200 jello/
jelly/day
Concentration of 0.01 mg/1,
consumption - 2 I/day.
Concentration of 0.01 mg/1,
consumption - 2 I/day.
-------
TABLE 45. EXPOSURE OF HUMANS TO PCP
(Continued)
Exposure Route
ami MedJiim
Exposure
(ing/day) me/kg /day Subpopulation Assumptions2
Inhalation
Downwind of cooling
tower (1 km)
0.03
very small
Upper limit concentration of 1.00 |ig/ma,
Inhalation, 20 in3/day.
Ui
Downwind of cooling 0.06
tower (8 km)
Home use of PCP-
Mcixlmiuu
Air Jn PGP treated
rooms
Outdoors-general
population
Dermal Bathing,
dishwashing
Typical
Maximum
0.001
small
1
3.2
0.003
0.02
0.05
0.00005
small
very small
large
0.0000004
0.00048
Home use-spill
maximum 170
Handling of treated
UltOll — (J-J
2.8
0.008
large
small
very small
small
Upper limit concentration of
3 KB/'"3, inhalation of 20 m3/day
Concentration of 0.07 mg/ra3, breath Ing;
rate - 1.8 m3/hr, exposure time - 8 hri
Concentration of 0.16mg/m3, breathing:*-
rate - 1.0 m3/hr, exposure time - 20 hi
See Section V
Concentration of 0.01 ug/1, permea-
bility constant 0.01 cm/hr, total
body immersion - 0.2 hr/duy.
Concentration of 12.0 Pg/1 permea-
bility constant 0.01 cm/hr, total
body immersion - 0.2 hr/day.
Concentration of 50,000 mg/1, permea-
bility of 10% body surface area, for
10 minutes/spill.
Concentration of 0.5 mg/ft at wood
surface, absorption 10%,.40 contacts
of 0.25 sq. ft/contact
-------
Exposure through normal inhalation or dermal absorption also
appears to be quite low. However, certain situations present the
potential for considerably higher exposures, primarily use-related
activities. The home use of PCP can result in an estimated maximum
exposure of 0.02 mg/kg/8 hrs. In addition, spills of PCP may result
in direct dermal exposure, perhaps as much as 170 mg, as well as
inhalation exposure. However, these exposures would not be recurring
ones.
Other use-related situations can result in chronic exposure. For
example, the use of PCP-treated wood indoors may result in an inhalation
exposure of 0.05 mg/kg/day. The continued use of PCP in these situations
would result in a chronic exposure. In addition, persons living close
to cooling towers may be exposed to maximum levels of 0.03 mg/kg/day.
Table 46 combines the estimates' shown in Table 45 into daily total
doses for three scenarios. In the worst case situation, food can be
the largest contributor to exposure on a chronic basis. This is also
true under more typical circumstances. However, it should be reiterated
that the magnitude of the subpopulation experiencing these exposures is
not known. For example, the exposure of persons to 0.00002 mg/day in
drinking water is probably much more typical than exposure to 1.5 mg/day
in food. In the case of persons living close to cooling towers, inhala-
tion may represent the more significant exposure pathway.
Table 47 indicates levels of exposure to PCP at which adverse
effects have been observed in'laboratory animals. (These data are
discussed in more detail in Section V.) Fetotoxic and teratogenic
effects have been observed in the rat following exposure to 15-30 mg/kg.
This exposure is critical primarily during specific phases of gestation,
and does not necessarily have to be a chronic exposure to result in
teratogenic effects. With the apparent effect level of 6 mg/kg for these
effects, the safety factor for the exposure estimates can be evaluated.
The worst case situation described in Table 46 would result in an
exposure to 3.2 mg/kg/day, providing a safety factor of 1.7 over the
reported effects level (6 mg/kg). However, this number exceeds the
OPTS no effects level of 3.0 mg/kg/day (U.S EPA 1980). Most of the
exposure in this scenario can be attributed to a spill of PCP. Thus,
such an incident would be of concern during pregnancy. When the spill
is excluded, the exposure in this case would be only 0.4 mg/kg, associ-
ated with high residues in food. The safety factor in this case would
be 8.6. Though it is likely that these situation are extremely rare,
the exposure routes mentioned above should be examined more closely in
order to determine actual exposures and the size of the subpopulations
associated with each.
Other non-occupational exposure routes provide a safety factor of
at least 100. This is not to say, however, that they represent acceptable
levels of exposure since there are considerable uncertainties in all
aspects of such an assessment.
153
-------
TABLE 46. EXPOSURE SITUATIONS FOR PCI*
Exposure Situation/Pathway
Maximum Exposure
'Food
Drinking Water
Inhalation - Ambient
Dermal - Home Use - Spill
TOTAL
Exposure
(ing/day)
(mg/kg/day)
0.4
0.0004
2.8
3.2
i-
Ul
v£>
Exposure of Typical Person1
Food
Drinking Water
Inhalation Ambient
Dermal
TOTAL
1.5
0.00002
0.003
0.003
1.5
0.025
0.025
Exposure of Person Living
Near Cool Ing Tower
Food
Drinking Water
Inhalation
Dermal
TOTAL
1.5
0.00002
2
0.003
3.5
Tt Is not known how "typical" these exposures are; the levels In drinking water are known
to be low and numerous locations have been sampled. No monitoring data Is available for
air. Limited data are available for food, and the detection of PCP was hot widespread.
-------
TABLE 47. REPORTED LEVELS OF POP CAUSING ADVERSE EFFECTS IN MAMMALS
Adverse Effect
Care inogenesIs
Fel.otoxiclty
Teratogenesis
Liver Lesions
Median Oral
Lethal Dose
Median Inhala.tlon
Lethal Dose
Median Dermal
Lethal Dose
Species
Rat
Mouse
Rat
Rat
Rat
Rat
Rat
Rat
Lowest'Reported
Effect Level
15 mg/kg
30 mg/kg (days 8-11)
100 ppm (diet)
78-205 mg/kg
11.7 mg/kg
96-320 mg/kg
No Apparent
Effect Level
30 mg/kg/day (diet)
17 mg/kg/day (diet)
5.8 mg/kg1
OPTS lias decided on 3 mg/kg/day as a no effects level for fetotoxic effects In rats
(U.S.EPA 1980).
-------
The above discussion has dealt with general human exposure scenarios
and reported teratogenic effect levels for laboratory animals. There is
also some very limited epidemlologieal evidence of a link between PCP
exposure via treated wood and leukemia. •. In a study in Kentucky, 140
workers handling packing cases treated with PCP (average concentrations
of 127.4 ug/kg), appear to have an abnormal incidence of leukemia (Dlckson,
1980. Pesticide and Toxic Chemical News, 1980). 'Since the dioxin contami-
nants have also been implicated, the evidence regarding PCP is unclear.
The results of this study should become available in the near future and should
enable a mere thorough consideration of this possible risk of PCP exposure.
C. RELATIVE EXPOSURE EFFECTS AND RISK COMPARISONS—BIOTA
The monitoring data provided by STORE! and other sources were
insufficient to permit estimation of the potential for harmful exposure
of aquatic organisms to pentachlorophenol on a national level. Measured
concentrations in major river basins ranged from 1 ng/1 to 100 ug/1.
Data were heavily skewed by the preponderance of observations from
California and the Pacific Northwest. Levels in California were fairly
evenly distrlbured between 10 ng/1 and 10 ug/1* while 91% of the measure-
ments in the Pacific Northwest were in the 10 ug/1 to 100 ug/1 range.
It is worth noting that both river basins are locations of wood preserving
industries.
Simulation of water concentrations generated for known PCP discharge
rates through use of the EXAMS model yielded levels (of total PCP) ranging
from 3.2. x 10~6 mg/1 (at a PCP discharge of 0.07 kg/day) in a riyer
system to 26.36 mg/1 (at a PCP discharge of 17.1 kg/day) in a pond system.
Most concentrations for all systems excluding the pond were less than 1.0
mg/1. Again, it should be noted that these concentrations are based on
numerous assumptions described in Sectin IV-D-2, including the unconser-
vative assumption that PCP leaves the system at the rates entered as input
to the model. Not all transfer and transformation reactions can be expected
to take place at all sites of PCP discharge. At the two highest loadings
for the pond and lake systems, 17.1 kg/day and 0.25 kg/day, the simulated
total PCP concentrations violated or were only slightly less than the
freshwater criterion level for PCP of 14 ug/1 recommended by EPA (USEPA,
1978). At the lowest loading of 0.07 kg/day, the estimated concentration
of PCP exceeded the freshwater criterion in the pond system and was slightly
below it in the oligotrophic lake system. In the river systems, none of
the estimated concentrations of PCP exceeded the criterion level, even
at the highest loading; however, in the coastal plan river system the
estimated concentration was only slightly under the freshwater criterion.
From the toxicity data, it appears that PCP concentrations greater
than 1 yg/1 may cause chronic or sublethal effects in aquatic biota.
Levels exceeding 10 ug/1 could be lethal to many species over varying
periods of exposure.
161
-------
One species of alga, Chlorella pyrenoidosa. has been adversely
affected by PGP concentrations as low as 1 yg/1. Rainbow trout were the
most susceptible of the freshwater fish, with a 96-hour LCSQof 15.4 ug/1;
other salmonids were found to be comparatively sensitive as well. Among
the marine organisms the plnfish and the Pacific oyster were the most
susceptible to PCP, with respective LC50's of 38 and 48 ug/1* Most fish
were sensitive in the ranges of 10-300 ug/1. In most aquatic animals,
larval and juvenile stages are periods of decreased resistance to most
toxicants.
Among the factors that influence PCP toxicity, pH is perhaps the
most significant. Since PCP is more toxic in its nonionized form, a
lower pH increases risk to biota. From the limited evidence, it appears
also that higher temperature and softer water increase PCP toxicity;
however, these effects remain to be verified by further research. Where
PCP occurs in the water, fish will generally be more susceptible in warmer,
softer, and more acidic waters.
When environmental variables (e.g., pH, hardness) that may modify
PCP's toxicity in natural ecosystems are not considered and on the basis
of a very limited monitoring data base, certain freshwater fish and inver-
tebrate species appear likely to encounter PCP at concentrations to which
they are sensitive, greater than 1.0 ug/1. According to the EXAMS model,
the currently practiced discharge rates of 0.25 kg/day and 17.1 kg/day
(see Table 33) may result in water concentrations on the order of 0.1 to
26 mg/1, especially in the more static aquatie systems such as ponds
and lakes. Lower practiced discharge rates do not appear as lively
according to the model, to generate concentrations at levels harmful to
biota except In small ponds. Discharges are assumed less likely co-be
released into ponds than into larger, more resilient aquatic systems.
Exceptions may be contained ponds that are considered as holding lagoons;
however, these are not natural systems and the EXAMS model would not be
applicable to them. It should be pointed out again that the estimated
loading rates are based on small samples of effluent concentrations and
flow rates represent neither the highest known rates of PCP discharge
Into water, nor typical discharge practices.
Fish kill data and miscellaneous observations of high PCP concen-
tratations in water implicate several industries and activities that may
generate levels of PCP potentially harmful to aquatic life. These include
the wood preserving industry (through holding lagoon spills, runoff fvom
contaminated soil), the pulp and paper industry, cooling water discharges
and spraying of wood near water.
Individual continuous industrial discharges on the order of 0.25
kg/day and 17.1 kg/day may result in harmful concentrations in certain
aquatic systems. No information on effluent levels or discharge practices
was available for a number of PCP-associated industries. In addition,
since currently available effluent data are based on a limited number
of observations, they may not reflect widespread discharge practices.
Further investigation is warranted on disposal practices for cooling
waters from cooling towers and machinery, in particular.
162
-------
The PC? contribution to water from treated wood and from boat paints*
treated with PGP also requires further investigation. Treated wood dis-
tribution is widespread throughout the U.S. and an estimated 18,000 MT
of PCP is consumed annually by the wood preserving industry alone, although
the percentage of the total mass coming in contact with water is unknown.
There is a potential for leaching out of the chemical from wood submerged
in water (as dock posts or on boat bottoms); however, no fate data were
available to permit estimation of the significance of this process.
163
-------
REFERENCES
Dickson, D. 1980. PCP- dloxins found to pose health risks. Nature
283:418. '
PCP seen as possible link to leukemia: EPA unsure of next step. Pesti-
cide and Toxic Chemical News. January 30, 1980. pp. 25-26.
U.S. Environmental Protection Agency. 1978. Criterion Document Penta-
chlorophenol. Draft.
U.S. Environmental Protection Agency. 1980. Draft document of Position
Document 213; Wood Preservative Pesticides: Pentachlorophenol. Special
Pesticides Review Division, Office of Pesticides and Toxic Substances;
U.S.EPA, Washington, D.C.
164
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APPENDIX A. CONTAMINANTS IN PENTACHLOROPHENOL
The contaminants in commercial pentachlorophenol could play a role
in the environmental importance of PCP. Commercial technical grade penta-
chlorophenol contains contaminants, mostly other chlorinated phenols,
dioxins, and dibenzofurans (see Figure A-l).* The chlorinated phenols
include 2,3,4,6, tetrachlorophenol, traces of trichlorophenol, chloro-
phenoxy phenols, chlorodiphenyl ethers, chlorohydroxy diphenyl ethers,
and traces of even more complex phenol reaction products. The principal
chlorodioxins and chlorodibenzofurans are those containing six to eight
chlorine atoms. The highly toxic 2,3,7,8 tetrachlorodibenzo-p-dioxin
(TCDD) isomer has not been identified as a contaminant of PCP manufactured
.in the U.S.
Octachlorodibenzodioxin (OCDD) is the principal dioxin contaminant.
There are two heptachlorodibenzodioxins and both have been found in PCP.
Of the ten possible hexachlorodibenzo-p-dioxin isomers possible, six have
been detected. (See Table A-l for a listing.)
Several dibenzofurans have also been detected in PCP. These include
tetrachlorodibenzofurans, pentachlorodibenzofurans, and a hexachloro-
dibenzofuran (see Table A-2).
The relative concentrations of these contaminants in PCP are shown
in Tables A-3 and A-4. The composition of PCP from various sources varies
somewhat.
Commercial processes exist that enable the production of PCP with
greatly reduced concentrations of contaminants. However, the production
of a purified product is more costly, and may result in byproducts that
are more difficult to handle. Disposal of the highly concentrated
residual waste that contains the removed contaminants is problematic.
For every 5000 units of PCP manufactured, approximately 10% of this amount,
or 500 units, of bottom residues are produced; these may contain the -follow-
ing compounds at varying concentrations: octa-, hepta-, and hexa-chloro-
dibenzodioxins and chlorodibenzofurans, tetrachlorophenol, trichlorophenol,
chlorophenoxy phenols, hydroxy diphenyl ethers, hexachlorobenzene, chlori-
nated biphenyls, chlorinated polymers, and other compounds. These figures
indicate that approximately 2000 tons/year of residual wastes requiring
disposal are generated.
The removal of contaminants during production may not be as complete
as one might expect. Many of these contaminants are also degradation
products of PCP and can be expected to be formed in the environment.
Therefore, the initial removal of these contaminants during production
does not assure that they will not enter the environment.
*
Most of the information in this appendix is based on the Adhoc Study
Croup on Pentachlorophenol (1979) and USEPA (1978). Some, data in the
Lables was obtained from USEPA (1978).
165
-------
cr>
Clilbrodloxln
Chloroplienoxy Chlorophenol
Clilorofuran
Chlorophenyl ether
Chloroplienoxy Chlorophenol
Oil
I Oil
Chlorodlhydroxy dlphenyl ether
FIGURE A-l. PCP Contaminants - Chlorines at Various Positions on the Kings
-------
Octachlorodibenzodioxin
Heptachlorodibenzodioxins
1,2.3,4,6,7,9
1,2,3,4,7,8,9
Hexachlorodibenzodioxins
1.2,3,7,8,9
1,2,3,6,7,8
1,2,4,6,7,9
1,2,4,6,8,9
1,2,3,6,7,9
1,2,3,6,8,9
Polychlorodibenzodioxin
TABLE A-l. Dioxin Contaminants round in PC?
167
-------
hepcachlorodibenzofuran
hexachlorodibenzofuran
1,2,3,6,7,8
pentachlorodibenzofurans
2,3,4,6.7
1,2,4,7,8
2,3,4,7,8
tetrachlorodibenzofurans
2,3,6,7
2,4,6,7
Chlorodibenzofuran
TABLE A-2. Dibenzofuran Contaminants in PCP
168
-------
TABLE A-3. COMPOSITION AMI CONCENTRATIONS OP CONTAMINANTS
IN HENTACIILOHorilKNOL PREPARATIONS
PCP 1-
Coonerclal MiniHanln Cooi»oslte Duwlcldu
*:.'!!:«!i:ill Compoalte PCP nu/kB jag/kB KC-7'(nm/kfl) l} PCP^ JLi«B./kj&). fliPd*;!2 "U/Kjl
Piinl.iir.il loro|>lu:iiul B5-90Z
l,:li.,,:l,loi,,,,li,;iiol 5-10X
Trli:liluru|i|iunnl IX
Cliliirliiutril I'huiioxy Phenol a 5X
Ocliicliloroilllii-iizodloHln "1000 ng/kg
Hi:|>tui:lilorudltii.-nZMdloxln
1.2.1.4.6.7.9
lli!x»i:li lurod 1 liunzod 1 ox 1 n
1.2.1.7.8,9
1.2.1.6,7.8
1.2,4,6,7,9
1.2.4.6,8.9
1.2,1,6.7.9 ~ 100 ng/kg
1.2.3.6.8.9 ng/kg
I'viiiaclilurodlliL-nzodloxlii
Tel rai-lilorutiilionzodloxln No
Oc l iicli I orod 1 henzu f u ran
llu|il:uclilorudllii!nzof uran
lluxaclilorodlbvnzofuraii
Huiiliichlurudlbunzofuraii
Tul raclilurudlliunzofiiriin
''Ilirec unulysus.
Two anulyuutj.
8-J.8X H8.4X
10. 2X 4.4X
< IX .IX
6.2X
1180 1170 5.5.8.0.15.0 250.2500
520 199 I.I. .6. 6.5 125
171
63
8 II .15, .03,1.0 4
0
5
1
1
No No No No
260 137 .2..: .l.
-------
TABLE A-4. HEXA- AND OCTACHLORODIBENZODIOXIN
CONCENTRATIONS IN DOMESTIC PCP'S
Concentration (mg/kg)
Sample
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
Manufacturer
Vulcan
Vulcan
Vulcan
Vulcan
Relchold
Reichold
Reichold
Reichold
Monsanto
Monsanto
Monsanto
Dow
Dow
Dow
Dow
Dow
Dow
Hexachlorodioxin
10
ND
15
16
20
17
23
ND
15
12
15
ND
ND
ND
16
16
21
Octachlorodioxin
1700
ND
2500
3600
700
600
900
ND
1400
1100
1900
2
2
ND
1500
1800
3400
SOURCE: USEPA (1978)
170
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