United States
Environmental Protection
Agency
Office of Water
Regulations and Standards (WH-553)
Washington DC 20460
January 1982
EPA-440/4-85-006
&EPA
An Exposure
and Risk Assessment
for Benzene
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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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30272-101
REPORT DOCUMENTATION »• REPORT NO. 2.
PAGE EPA-440/4-85-006
4. Tttte and Subtitle
An Exposure and Risk Assessment for Benzene
7. Author<*>
Gilbert, D. ; Byrne, M. ; Harris, J.; Steber, W. ; and Woodruff, C.
9. Performing Organisation Nam* and Address
Arthur D. Little, Inc.
20 Acorn Park
Cambridge, MA 02140
12. Sponsoring Organization Nam* and Addrms
Monitoring and Data Support Division
Office of Water Regulations and Standards
U.S. Environmental Protection Agency
Washington, D.C. 20460
3. Recipient's Accession No.
s. Report Data Final Revision
January 1982
«.
8. Performing Organization Rept. No.
10. Project/Task/Work Unit No.
11. Contraet(C) or 6rant(6) No.
(0 68-01-5949
(G)
13. Type of Raport & Pariod Covered
Final
14.
15. Supplementary Notea
Extensive Bibliographies
1C. Abstract (Limit 200 words) ~
This report assesses the risk of exposure to benzene. 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 technical
publications assembled in March of 1981.
The assessment includes an identification of releases to the environment during
production, use, or disposal of the substance. In addition, the fate of benzene 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 benzene for
various subpopulations.
17. Document Analysis a. Descriptors
Exposure
Risk
Water Pollution
Air Pollution
b. IdentlAers/OpeivEnded Terms
Pollutant Pathways
. Risk Assessment
Effluents
Waste Disposal
Food Contamination
Toxic Diseases
Benzene
U.S. Environmental Protection
Region V, Library
230 South Dearborn Street
Chicago, Illinois 60604.
c. COSATI Field/Group Q6F 06T
*. AvallaMltty Statement
Release to Public
• ANS«-Z».1«) «„ M.»™~IM. «"»jd
19. Security Class (This Report)
Unclassified
20. Security Class (This Page)
Unclassified
21. No. of Pages
122
22. Price
$13.00
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FOREWORD
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Effective regulatory
Iers anding of the human aim environmental risks associated with the
manufacture, use, and disposal of the chemical. Assessment of risk
wSronint "etui""0 ^dgment ab°Ut the Probability of harm to the
I+,j mi. *fwn \jL pocGTiciaj. 6nviiroTii*iGn13x concsntrs.""
fe°»8' C.?M , Assessment process integrates health effects data
ill8;A CarCl"°gefClty« teratogenicity) with information on exposure
S:.J£?°n:±.±-?0'Ure lnClVde an -valuation of the sources'of lie
as
assessment of risk for humans and aquatic life and is
sr
chapters were comprehensively checked for uniformity in
:
Michael W. Slimak, Chief
Exposure Assessment Section
Monitoring & Data Support Division (WH-553)
Office of Water Regulations and Standards
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EPA-440/4-85-006
March 1981
(Revised January 1982)
AN EXPOSURE AND RISK ASSESSMENT
FOR BENZENE
BY
Diane Gilbert
Melanie Byrne, Judi Harris, William Steber, and Caren Woodruff
Arthur D. Little, Inc.
Charles Delos
Project Manager
U.S. Environmental Protection Agency
EPA Contract 68-01-5949
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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EXECUTIVE CONCLUSIONS"
Excessive occupational exposure to benzene has been shown to be
associated with leukemia, and other serious blood diseases. Acute
toxicity involves central nervous system effects which can result in
death.
Environmental exposures are at least 100 fold below the minitnums
thus far shown to be associated with toxicity from occupational expo-
sures. However, prudent public health policy, by not recognizing thres-
holds for carcinogenic effects, would anticipate some risk at such levels.
Conservatively.applying the EPA Cancer Assessment Group's linear non-
threshold extrapolation to low exposures, the effect of benzene expo-
sure routes on the potential cancer incidence in the total U.S. popula-
tion would be estimated as shown below:
Comparison of Benzene Exposure Routes
(EPA Exposure and Risk Estimates)
Average
Benzene Level
3.3 - 6.5 yg/m
0.025 - 0.17 yg/1
Nationwide
Average Excess Incidence
Lifetime Risk_ (cancers/year)^
2xlO~5 - 5xlO~5
4xlO~8 - 2xlO~7
75 - 150
0.1 - 0.8
possibly 250 ug/day possibly greater than air
90 ug/cigarette 10 800
The assumptions incorporated into the EPA cancer risk extrapolation
suggest that these estimates may exceed the actual risks from the above
tabulated exposure levels (as discussed in Chapters 5 and 7). The
above estimates (or range of estimates) for the population mean do not
reveal the distribution of individual exposures within the population.
Individual exposures may be two orders of magnitude higher than the
means, as described in Chapter 5. Nevertheless, these estimates pro-
vide some indication of the possible overall importance of benzene in
the environment, since for linear nonthreshold risk extrapolations,
incidence is determined by the arithmetic mean exposure. (The above
estimated means and the Chapter 5 and 7 estimates for specific scenarios
are intended to complement each other.)
Prepared by EPA Technical Project Officer based in part on program
considerations.
iii
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It is apparent that cigarettes, food, and ambient air constitute
the most important exposure routes for the non-occupationally exposed
general population. Drinking water appears to comprise less than one
percent of average exposure. Because the food data is very limited,
the exposure via food is uncertain. While its presence at very low
levels may represent a phase equilibrium with contaminated air, its
presence at higher levels, such as in eggs, is believed to occur
naturally. Due to benzene's low potential for bioconcentration, expo-
sure to waterborne benzene via contaminated fish is expected to be less
than via drinking water.
Relatively little risk to aquatic life can be expected to result
from current environmental levels. Benzene is acutely toxic to some
fish and aquatic invertebrates at concentrations above about 5000 ug/1.
Although there is insufficient data to establish a chronic toxicity
criterion, limited data suggest that chronic toxicity to fish may
sometimes occur at concentrations in the range of 100-1000 ug/1. Of
185 ambient water measurements recorded in STORE!, none exceed 1000
Ug/1, and only 5 percent exceed 100 ug/1. No fish kills on file for
the last decade have been attributed to benzene spills or discharges.
Although benzene is a naturally occurring substance, its global
production and environmental burden have been increased by human activ-
ities. Approximately 11 million metric tons of benzene per year are
handled within the U.S. economic system. One half of this is essen-
tially pure benzene, mostly produced from petroleum by catalytic or
thermal reactions, and used almost entirely as a feedstock to synthe-
size other chemicals. The other half is a constituent of hydrocarbon
mixtures, primarily gasoline and other fuels.
Nearly all known environmental releases of benzene are to air,
primarily from gasoline combustion. Less than one percent of the
known releases is to water, primarily from solvent users, petroleum
refiners, and chemical plants. Benzene disposal to land appears to
be negligible; however, the content of some potentially important
solid wastes is not known. It may be noted that the relative pro-
portions of water and air disposal are very roughly equivalent to
the relative proportions of average water and air exposures.
In soil the fate of benzene wastes is somewhat uncertain, and may
involve volatilization, biodegradation, or leaching. In most surface
waters volatilization is expected to dominate over degradation, thereby
bringing benzene into the atmosphere, where it is oxidized. Water in
equilibrium with contaminated urban air having 10 ug/m^ benzene would
have only 0.044 ug/1, and would represent negligible exposure compared
to the air concentration. Nevertheless, such equilibrium may not be
approached quickly, but may require a distance of a few miles to many
dozens of miles, depending on a stream's depth and turbulence. The
absence of substantial levels of benzene in ambient water is thus con-
sistent with both the sparsity of discharges and the high fugacity of
waterfaorne benzene.
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Overall, it can be concluded from the assessment of benzene dis-
posal, fate, exposure, and risk that:
1) Population aggregated exposure through waterborne routes
(drinking water and eating fish) is small compared with
exposure through either air, smoking, or possibly food.
2) Water discharges of benzene are small compared with air
emissions, and thus, even when volatilized, do not sub-
stantially increase nationwide air concentrations.
3) Air contamination with benzene does not cause serious con-
tamination of water, as through rainout.
4) The potential for aquatic life problems downstream of most
benzene dischargers appears to be quite low.
5) Due to benzene's multi-media exposure potential, removal
from one medium (such as water) by transfer to another
(such as air) may not necessarily be of benefit.
Notes on Tabulated Cancer Risk Estimates:
1) Unit risk (dose-response) is taken from EPA (1980) , referenced in
Chapter 5. Other unit risk estimates are described in Chapter 5.
a) Lifetime ingestion of 13.5 yg/day would result in 10 risk.
Drinking water intake is assumed to be 2 I/day, although this
may be high (Appendix C).
b) Lifetime inhalation of 1.35 yg/m3 with 50% absorption
efficiency would result in 10~5 risk.
c) Annual incidence is for the entire U.S. population (220
million persons), assuming a 70 year average lifespan.
2) Two estimates are provided for the air concentration averaged over
the entire population. The lower is from Mara and Lee (1978), as
referenced in Chapter 4; the higher is from Chapter 5.
3) The drinking water mean concentration is assumed to be represented
by the National Organic Monitoring Survey. The range of estimates
for the average was generated by assuming either:
a) Benzene not detected implies zero concentrations;
b) Benzene not detected implies a concentration just below
the detection limit.
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Two other EPA surveys support this general magnitude: the Community
Water Supply Survey and the National Organic Surveillance Program
(SRI).
4) The food exposure is an NCI estimate based on very little data
(Chapter 5).
5) The cigarette smoking exposure is as described in Chapters 5 and
7. This risk is applicable to 54 million smokers.
VI
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TABLE OF CONTENTS
EXECUTIVE CONCLUSIONS
LIST OF FIGURES vii
LIST OF TABLES ix
1.0 TECHNICAL SUMMARY 1-1
1.1 Risk Considerations ]__]_
1.1.1 Humans ]__!
1.1.2 Biota 1_2
1.2 Materials Balance 1_2
1.3 Environmental Fate of Benzene - 1_3
1.4 Environmental Monitoring of Benzene 1-5
1.4.1 Human Effects and Exposure 1_6
1.4.2 Biotic Effects and Exposure 1_9
2.0 INTRODUCTION 7-1
References 2-3
3.0 MATERIALS BALANCE 3_j_
3.1 Introduction and Methodology 3_]_
3.2 Production of Benzene 3_3
3.2.1 Direct Production from Oil 3.3
3o2,2 Direct Production from Coal 3_8
3.3 Imports and Exports of Benzene 3-10
3.4 Indirect Sources of Benzene 3-11
3.4.1 Coal Coking 3-11
3.4.2 Petroleum Refining for Gasoline 3-12
3.4.3 Use of Products Contaminated with Benzene 3-12
3.4.4 Natural Gas Well Condensates 3-14
3.4.5 Resource Mining and Processing Operations 3-14
3.4.6 Benzene Releases from Oil Well Drilling 3-14
3.4.7 Benzene Releases from Oil Spills 3-17
3.4.8 Combustion of Petroleum-based Fuels 3-17
3.4.8.1 Benzene in Gasoline 3-17
3.4.8.2 Benzene in Other Petroleum-based Fuels 3-20
3.5 Use of Benzene 3-20
3.5.1 Consumptive Use 3-20
3.5.2 Nonconsumptive Use 3-24
3.5.2.1 Solvent Use 3_24
3.5.2.2 Pesticide Use 3_26
3.6 Transportation and Storage of Benzene 3-26
3.7 Summary 3-27
References 3-31
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TABLE OF CONTENTS (Continued)
Page
4.0 FATE AND DISTRIBUTION OF BENZENE IN THE ENVIRONMENT 4-1
4.1 Introduction 4_^
4.2 Physical, Chemical, and Biological Characteristics
of Benzene 4_j_
4.3 Monitored Levels in the Environment 4-3
4.3.1 Air 4.3
4.3.2 Water 4_5
4,3.2.1 Drinking Water 4_3
4.3.2.2 Ambient Water 4-8
4.3.3 Soil 4_14
4.3.4 Food 4-14
4.3.5 Summary 4-14
4.4 Environmental Fate Modeling - 4-14
4.4.1 Equilibrium Partitioning 4_14
4.4.2 EXAMS Modeling 4_22
4.4.3 Intermedia Transfers 4-27
4.4.3.1 From Air Medium to Surface Waters
or Land 4-27
4.4.3.2 Intermedia Transfers from Water Medium 4-31
4.4.3.3 Intermedia Transfers from Soil Medium 4-33
4.4.4 Intramedia Fate Processes 4-36
4.4.4.1 Air 4.35
4.4.4.2 Water 4-45
4.4.4.3 Soil 4_50
4.4.4.4 Plants 4_52
4.5 Summary 4-52
4.5.1 Intermedium Transfer Processes 4-53
4.5.1.1 Air 4.53
4.5.1.2 Water ' 4.53
4.5.1.3 Soil 4-53
4.5.2 Intramedium Fate Processes 4-55
4.5.2.1 Air 4-55
4.5.2.2 Water 4-55
4.5.2.3 Soil 4-55
4.5.3 Critical Pathways for Specific Sources of Benzene 4-55
References 4-57
5.0 HUMAN EFFECTS AND EXPOSURE 5_1
5.1 Human Effects 5_]_
5.1.1 Pharmacokinetics 5-1
5.1.1.1 Absorption 5-1
5.1.1.2 Distribution 5-2
5.1.1.3 Metabolism and Excretion 5-7
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TABLE OF CONTENTS ('Continued)
5.1.2 Acute Effects 5_10
5.1.3 Chronic Effects 5-10
5.1.3.1 Pancytopenia 5-10
5.1.3.2 Leukemia 5-14
5.1.4 Summary of Effects on Humans 5-18
5.1.4.1 Ambient Water Quality Criteria —
Human Health 5-18
5.1.4.2 Additional Health Effects 5-21
5.1.5 Estimated Dose/Response Relationship for Cancer 5-22
5.1.6 Discussion of Available Data 5-24
5.1.6.1 Infante Study 5-24
5.1.6.2 Aksoy Study 5-26
5.1.7 Application of Dose/Response Models to Estimation
of Human Risk _ 5-26
5.2 Human Exposure 5-31
5.2.1 Introduction 5-31
5.2.1.1 Populations Exposed through Contaminated
Drinking Water and Foodstuffs 5-31
5.2.1.2 Population Exposed through Inhalation 5-34
5.2.1.3 Percutaneous Exposure 5-35
5.2.2 Comprehensive Exposure Scenarios 5-37
5.2.3 Summary 5-40
References 5-41
6.0 3IOTIC EFFECTS AND EXPOSURE 6-1
6.1 Effects on Biota 6-1
6.1.1 Introduction 6-1
6.1.2 Mechanisms of Toxicity 6-1
6.1.3 Freshwater Organisms 6-2
6.1.4 Marine Organisms 6-7
6.1.5 Factors Affecting the Toxicity of Benzene 6-8
6.1.6 Conclusions 6-8
6.2 Exposure of Biota to Benzene 6-10
6.2.1. Exposure Route 6-10
6.2.2 Fish Kills 6-10
6.2.3 Monitoring Data 6-11
6.2.4 Exposure 6-11
References 6-14
7.0 RISK ESTIMATES FOR BENZENE EXPOSURE 7-1
7.1 Humans 7_j_
7.2 Biota 7.3
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TABLE OF CONTENTS (Continued)
Page
APPENDIX A. Vehicle Release of Benzene A-l
APPENDIX B. EXAMS Scenarios B-l
APPENDIX C. Liquid Consumption for Exposure Estimates C-l
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LIST OF FIGURES
Figure
Page
1-1 Summary of Benzene Materials Balance, 1978 1-4
3-1 Producers of Benzene from Petroleum and Coal, 1978 3-6
3-2 Materials Balance for Benzene in Gasoline 3-19
3-3 Materials Balance for Benzene 3-29
4-1 Distribution of Unremarked Benzene Concentrations by
Ambient Water Quality Station, 1977-81 4-9
4-2 Distribution of Remarked Benzene Concentrations by
Ambient Water Quality Monitoring Stations ~ 4-9
4-3 Schematic of Environmental Compartments Selected for
Estimation of Equilibrium Partitioning of Benzene 4-20
4-4 Results of EXAMS Modeling of the Environmental Fate
of Benzene in a Turbid River 4-23
4-5 Results of EXAMS Modeling of the Environmental Fate
of Benzene in a Clean River 4-24
4-6 Results of EXAMS Modeling of the Environmental Fate
of Benzene in an Oligotrophic Lake 4-25
4-7 Results of EXAMS Modeling of the Environmental Fate
of Benzene in a Eutrophic Lake 4-26
4-8 Percentage of Benzene Reduction at Downstream
Distance from Aquatic Discharges 4-34
4-9 Dispersion Modeling Results for Each Type of Source
Category 4.39
4-10 Degradation Pathways for Benzene 4_47
4-11 Major Fate Preocesses for Benzene 4-54
4-12 Critical Pathways for Benzene (Released Amounts for
1978 Materials Balance) 4-56
5-1 Metabolic Pathway of Benzene in Liver 5-8
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3-12 Summary of Annual Environmental Releases of Benzene
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• LIST OF TABLES
™ Table
No.
I 1-1
Comprehensive Exposure Scenarios for Benzene !_8
| 3-1 Materials Balance for Benzene, 1978
3-2 Producers and Production of Benzene, 1975-79 3_4
3-3 Benzene Releases from Direct Petroleum Production, 1978 3.7
3-4 Producers of Benzene from Coke
°f S°lid »«f Containing
_ 3-13
3-6 Benzene in Contaminated Solvents
3—16
3-8 Estimated Benzene Content of Fuels
3-9 Summary of Consumptive Uses of Benzene, 1978 3.22
3-10 Materials Balance for Benzene in Chemical Feedstocks 3-23
3-25
3-28
4-2
4-2 Levels of Benzene in Air
4"3 Air Near
4-4 Levels of Benzene in Air for Human Activities 4.7
4-5 Concentrations of Benzene by Major Basin in 1980
4-10
^— v Levels Of Ran^ai-.^ -,•_ rr-*. — XT
water Near and In
4-12
4-7 Levels of Benzene in POTW Sampling Data
4-13
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LIST OF TABLES (Continued)
Table
No. Page
4-8 Levels of Benzene in Influents to Sewage Treatment
Plants 4-15
4-9 Levels of Benzene in Soil near Chemical Plants 4-16
4-10 Foods Reported to Contain Benzene 4-17
4-11 Values of the Parameters Used for Level I
Calculation of Equilibrium Concentrations of
Benzene Using MacKay's Fugacity Method 4-19
4-12 Equilibrium Partitioning of Benzene Calculated
Using MacKay's Fugacity Method - 4-21
4-13 Half-lives for Transformation and Transport of
Benzene for Several EXAMS Scenarios 4-28
4-14 Exposure Analysis Summary for Benzene from EXAMS
Model Runs 4-29
4-15 Rough Estimates of Ambient Ground-level Benzene
Concentrations (8-Hour) Average Per 100 g/s
Emission Rate from a Chemical Manufacturing Plant 4-38
4-16 Rough Estimates of 8-Hour Worst Case Benzene
Concentrations Per 100 g/s Emission Rate Using the
PAL Dispersion Model for a Chemical Manufacturing Plant 4-41
4-17 Concentrations of Hydroxyl Radicals and Ozone in
Atmosphere of Different Environmental Settings 4-42
4-18 Oxidation Rate Constants and Half-lives of Benzene
in Different Environmental Settings 4-42
4-19 Half-Life of Benzene in the Lower Troposphere 4-44
4-20 Benzene Biodegradation Rates 4-48
4-21 Microbial Species Isolated from Soil Capable of
Degrading Benzene 4-51
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LIST OF TABLES (Continued)
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Table
No.
5-1 Estimates of the Saturation Half-life of Toluene and
Benzene between Blood and Tissue 5-4
5-2 Toluene Concentrations in Air and Blood 5-6
5-3 Summary of Benzene Exposure and Related Hematotoxicity 5-11
5-4 Leucopenic Effects of Benzene 5-13
5-5 Carcinogenicity of Benzene in Experimental Animals 5-20
5-6 Comparison of Input Data for Calculation of Risk of
Leukemia from Benzene Exposure - 5-25
5-7 Predicted Excess Lifetime Leukemias per Million
Population due to Benzene Ingestion (Inhalation),
Based on the Study of Infante and Coworkers 5-27
5-8 Predicted Excess Lifetime Leukemias per Million
Population due to Benzene Ingestion (Inhalation), 5-28
Based on the Study of Aksoy and Coworkers
5-9 Estimated Benzene Exposure through Ingestion 5-33
5-10 Estimated Benzene Exposure through Inhalation 5-36
5-11 Summary of Estimated Benzene Exposure and Routes 5-38
5-12 Comprehensive Exposure Scenarios for Benzene 5-39
6-1 Effect of Benzene on Aquatic Flora 6-3
6-2 Acute Toxicity of Benzene to Invertebrates 6-4
6-3 Toxicity of Benzene to Freshwater Organisms 6-5
6-4 Toxicity of Benzene to Saltwater Organisms 6-6
7-1 Potential Risk Estimates for Benzene Exposure Scenarios
Using Different Models 7-2
C-l U.S. Beverage Consumption in 1979 C_2
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ACKNOWLEDGEMENTS
The Arthur D. Little, Inc. task manager for this study was Diane
Gilbert. Contributing authors were Judi Harris and Caren Woodruff
(environmental fate), Melba Wood and Ed Payne (monitoring data and
analysis), William Steber and Larry Partridge (human effects),
Melanie Byrne (biotic effects and exposure), John Ostlund (risk
analysis), Diane Gilbert (materials balance and human exposure) and
Muriel Goyer (risk). This report was reviewed by Alfred Wechsler
(program manager), Alan Eschenroeder and Muriel Goyer. Editing
was performed by Laura Williams and documentation by Nina Green.
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1.0 TECHNICAL SUMMARY
The Monitoring and Data Support Division, Office of Water Regulations
and Standards of the U.S. Environmental Protection Agency is conducting
risk assessments for pollutants which may enter and traverse the environ-
ment thereby leading to exposure to humans and other biota. The program
is in response to Paragraph 12 of the NRDC Consent Decree. This report
is a risk assessment for benzene using available data and quantitative
models were possible to evaluate overall risk.
1-1 RISK CONSIDERATIONS
1.1.1 Humans
To assess the risks associated with the production and use of benzene
to various human subpopulations, the results of exposure analysis for three
comprehensive exposure scenarios were coupled with a series of mathematical
risfc models. Despite predominantly negative carcinogenic data for studies
with laboratory animals, evidence that benzene is a probable leukemogen
for man is convincing. Risk estimates were therefore based on human
epidemiological studies of occupational situations.
Four risk extrapolation models were applied to the dose-response
data to indicate the range in the predicted number of possible excess
cases of leukemia that might result from chronic human exposure to ben-
zene. The range of predicted risk obtained for the human exposure levels
of interest is indicative of the inherent uncertainty associated with
the mathematical models currently used for risk extrapolation purposes
There is presently no scientific concensus for selecting the most appro-
priate model for extrapolating high exposure levels associated with
occupational exposure. Each of the models is formulated in such a way
that the curves pass through the origin; that is, some finite response
can be predicted at doses greater than zero. The no-threshold concept
xs_scientifically debatable; however, it has been the position of some
scientists and of government regulators that thresholds to careinogens
do not exist. By taking this position, the predicted risks tend to be
conservative, i.e., an overstatement of the risk.
The range of potential excess cases of leukemia predicted b> the four
mathematical models applied is described below for each of the three
scenarios. The total human dose was computed on a milligrams per day
basis, assuming that the response is dependent on absorbed dose but is
independent of exposure route.
• Scenario A. Urban/suburban exposure (includes inhalation of
typical urban air, food and drinking water ingestion and gas
station use) combined with risk models, yielded a range of 5
to ,560 potential excess leukemias per million people exposed.
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• Scenario _B. Rural/remote exposure (includes inhalation of
typical rural air; food and water ingestion and gas station
use) combined with risk models, yielded a range of _3 to 420
potential excess leukemias per million population exposed.
• Scenario C. Exposures near user/manufacture sites (includes
inhalation of air with industrial scale benzene levels, and
includes food and water ingestion and gas station use, as
above) combined with risk models yielded a range of 21 to
1119 potential excess leukemias per one million people
exposed.
It is noteworthy that drinking water appears to contribute less
than 1% to the total exposures that result in the range of potential
excess lifetime leukemias cited above. If one excludes residence near
a user/manufacturing site, consumption of contaminated food appears to
account for more than one-half of the total exposure (and thus of the
risk) in the above three scenarios. Some uncertainty exists, However,
in the food exposure pathway. Available data are incomplete; in the
absence of data, it was Accessary to assume that reported concentrations
in certain foods were representative of all food groups utilized in
estimating total intake. It is unknown how representative the reported
concentrations are for foods in general. Exposure via gas station
usage and inhalation of ambient air levels account for the balance of
total benzene intake in the three exposure scenarios examined.
Additional risks of 3240 to 106,000 potential excess leukemias could
exist for the 54 million people that smoke (i.e. 6_0 to 1960 per 106 popu-
lation exposed), based upon 50% absorption of 90 yg benzene per cigarette,
the consumption of 1.6 packs per day and the use of the models described
above.
1.1.2 Biota
Biotic risks from benzene exposure could result from such events
as spills of the chemical or gasoline. Despite the number of such
spills, however, no fish kills have been reported. Ambient benzene
levels are generally below reported effects levels; and, in the case
of more concentrated effluent discharges, disturbances would occur to
local populations only, rather than on a large-scale ecological basis.
1.2 MATERIALS BALANCE
The materials balance of benzene is somewhat unusual in that nearly
equivalent quantities originate from "indirect" as well as from "direct"
sources. Direct sources are petroleum refineries and coke plants; in
1978, including imports and inventory withdrawals, direct sources
totaled 5,451,100 kkg. Indirect benzene sources include gasoline and
other petroleum fuel refining, distribution and use, use of solvents
contaminated with benzene, coal coking, and mining and resource pro-
1-2
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cessing. These sources totaled 5,754,600 kkg of benzene in 1978.
Environmental releases resulting from these source operations were
27,000 kkg.
The major use of benzene is as a chemical feedstock. This amounts
to 5,251,000 kkg. A small volume is exported (151,000 kkg) and only
9600 kkg are used directly as a solvent, Benzene is included in gaso-
line (4,665,800) and other fuels (959,400 kkg), and in other solvents
(22,600 kkg). The environmental releases resulting from the use of
benzene (including losses during transport and storage) were 246,100
kkg. Chemical transformations and fuel combustion accounted for des-
truction of 10,739,200 kkg. The overall materials balance (see Figure
1-1) had a discrepancy of only 1.0% of the total available benzene.
(All materials balance data given are for 1978).
The materials balance developed for benzene using 1978 production
and use figures shows total environmental releases of 246,100 kkg. Of
this amount, 95.5% was emitted to air, 0.5% was discharged to water and
0.2% was land disposed (3.8% of releases could not be assigned to a
specific medium). The largest source (72%) of benzene emission was
the combustion of gasoline and other fuels. Transport and storage of
gasoline, petroleum refining, and the use of benzene as a chemical feed-
stock also led to significant (21%) air emissions. Chemical production
using benzene feedstocks and refinery production of benzene accounted
for 76% of water discharges, to which petroleum refining contributed 94%
of land discharges.
1.3 ENVIRONMENTAL FATE OF BENZENE
Benzene is a moderately volatile organic chemical with a relatively
high water solubility, and a low chemical reactivity because of its
stable ring structure. The environmental fate of benzene has been
analyzed for inter- and intra-medium processes.
The most significant intermedia fate process is volatilization from
either water or soil to air. Of limited overall importance are: rainout
from air to soil or water, soil adsorption from water or desorption
into water from soil and surficial runoff to water. Within the air
medium, the dominant fate process is oxidation by hydroxyl radicals.
Both soil and water biodegradation by microbial species may be important
in some habitats, however, it is not universally important.
Thus, the three critical pathways that determine the ultimate fate
of benzene released to the environment and act to reduce the total
environmental benzene load are:
• Atmospheric sources (95.5% of total) -»• oxidative destruction.
• Aquatic sources (0.5%) * volatilization -»• oxidative destruction.
• Land sources (0.2%)-* volatilization -- oxidative destruction.
1-3
-------
SOURCES OF BENZENE
USES
Direct
Refineries
Coke Plants
Imports
Inventories
5,451,100 kkg
TOTAL SOURCES
Indirect
Gasoline Refining & Imports
Other Fuels
Coal Coking
Contaminated Solvents
Oil Spills
Resource Mining/Processing
5,574,600 kkg
11,025,700 kkg
Total Sources-Source Releases-Uses
11,025,700 - 27,000 - 11,143,800 =
Source Discrepancy = -145,100
Source Discrepancy
Chemical Feedstock
Solvents
Exports
Gas and Fuel Consumptii
11,143,800 kkg
ENVIRONMENTAL RELEASE
From Direct Sources
4700 kkg
From Indirect Sources
22,300 kkg
From Uses
245,500 kkg
Direct Source Releases + Indirect Source Releases = Total Source Releases
4700 + 22,300 =
Total Source Releases « 27,000 kkg (see above)
Total Environmental Releases = 272,500 kkg
FIGURE 1-1 SUMMARY OF BENZENE MATERIALS BALANCE, 1978
1-4
-------
I
I
I
I
Oxidative destruction has a short half-life (<4 days in urban
settings) as does volatilization from water (0,3 days by EXAMS model).
Although no half-life is available for volatilization from soil, this
process proceeds rapidly. Some portion of the amounts released will
remain within the initial media as ambient levels until either biodegra-
dation or entrance to a critical pathway occurs.
In summary, the bulk of benzene releases occurs in the one medium
in which they are most speedily broken down and this destruction is
the ultimate fate of most of the released benzene. However, rate limits
to the oxidative destruction and to the intermedia transfer processes
do act along with benzene's basic chemical properties to retain some
benzene in water that is adsorbed onto sediments or to remain airborne.
1.4 ENVIRONMENTAL MONITORING OF BENZENE
Data have been collected for benzene concentrations in water, air,
soil, and foodstuffs. Because of the traditional concern over benzene
inhalation, especially in occupational situations, the most extensive
data base covers air levels.
Air levels are typically between 1 and 3.5 yg/m3 in areas remote
from sources and between 4 and 160 yg/m3 in urban areas where the number
of sources (cars and industrial plants) is high, compared with 4.5 yg/m3,
which is a usual level in more residential areas. Atmospheric levels
have been directly correlated with traffic volumes. Service stations
are cited as a major source of benzene releases, with the levels for
both rural and urban stations in the 1-32 yg/m3^ range. The levels near
chemical plants have been as high as 824 yg/m3, however, they are more
typically around 14 yg/m3 for chemical plants and 9 yg/m3 at refineries.
The few data on benzene in drinking water indicate a median level
of less than 2 yg/1 for those samplesxthat tested positively; to be
conservative, a level of 2 yg/1 was taken as a representative level of
benzene in drinking water. For both food and water, the term "conservative"
implies a higher level than may actually occur.
Most ambient and effluent levels in surface waters fell between 0
and 10 ug/1. However, the mean concentrations (104-638 yg/1) in Missouri,
Kansas, and Michigan were as much as seven times higher than in other
areas. The high values were generally reported in the vicinities of
chemical plants and refineries. Benzene levels in raw wastewater were
between <1 and 143 yg/1; removal averaged about 90%, with 3 of 5 plants
achieving 100% removal. These data and sludge concentrations indicate
that benzene is volatilized during aeration; biodegradation may also take
place to a limited extent.
Few soil data were available. Levels between 13 and 115 yg/kg
were reported in samples taken near chemical plants producing or using
benzene. &
1-5
-------
Benzene has been detected in fruits, nuts, vegetables, dairy pro-
ducts, meat, poultry, eggs, fish and several beverages. Only a few
of these items have been quantitatively analyzed and it is hypothesized
that benzene may even be a naturally-occurring flavor component. Eggs
have the highest documented lex-els (500-1900 ug/kg) , followed by haddock
(100-200 ug/kg) and Jamaican Rum (120 ug/kg). Cooked meats have levels
of less than 10 ug/kg higher than those levels found in raw meats.
1.4.1 Human Effects and Exposure
Benzene is readily absorbed by all routes of exposure, with the
rate of absorption dependent on both concentration and membrane perme-
ability. Absorption via the lungs is rapid; most reports indicate a
respiratory retention in humans of.approximately 50% of inhaled benzene.
The average skin permeability to benzene vapor is estimated to be 0.002
m3/(m2_nr). Dermal absorption of liquid benzene is much faster than that
for vapor; the estimated absorption rate for liquid benzene through
skin is 550 mg/m2/hr.
Once absorbed, benzene is widely distributed to all tissues, with the
rate of uptake by a tissue determined by the relative blood perfusion
of that tissue. A large fraction of absorbed benzene is excreted un-
changed in expired air, with the actual proportion dependent on dose and
species. Estimates of the fraction excreted by humans range from 12 to
50%. Metabolic conversion of retained benzene occurs predominantly in
the liver. The major metabolites include phenol, catechol and their
sulfo- and glucuronic conjugates.
Single exposures to high levels (64,000 mg/m3) of benzene are lethal
within 5 to 10 minutes for man. Severe but non-fatal acute exposures pro-
duce headache, nausea, a staggering gait, paralysis and convulsions.
Less severe exposures may produce giddiness and euphoria.
The relationship between chronic human exposure to benzene and hema-
tological disorders, most notably pancytopenia and leukemia, has been
extensively documented in the literature. Despite predominantly negative
animal carcinogenicity data, there is strong evidence to suggest that
benzene is a probable leukemogen in humans. However, case reports of
benzene-associated leukemia generally relate to occupational exposures
in industries where workers were exposed to rather high benzene concen-
trations (300-1200 mg/m3) sufficient in themselves to produce pancytopenia
and its variants. Pancytopenia, a deficiency of all cellular elements of
the blood, in its most severe form, is a result of aplastic anemia.
Furthermore, in any of the reported cases of benzene associated leukemia,
occupational exposures to other organic solvents occurred concurrently
with benzene exposure.
A dose-effect relationship between exposure and the incidence of
these diseases is more difficult to establish due to uncertainties of
occupational exposures. Several assumptions of considerable scientific
debate are required. Most notably, an equivalence between relatively
1-6
-------
I
I
I
.
this approach is conservative (JI > ^^ that' While not ,
of leukemia to the general population ^^ °ver"timate the risk
benzene exposure). population resulting from chronic, low-level
water
ao/
case of cancer per million population exposed .
£xP°Sure <=° an ambient
"' * * ™ additio-l
.
Benzene levels for various exposure
mean exposures. Exposure to benzene
occur on a limited basis across the
fraction of the water
routes because
' f°°d' md air*
?r;.8nalyzed C° devel°P
drinkinS wate^ nay
BeCauSS
e
^
could contribute 001 m}d c"Cf.°r Ubor nea
of uncontrolled benzene emissions have rZ staclons. o'tai the si
day. Cigarette smoking has bee^ H potential to add 0.01 me/
source of benzene, addi'ng 1.4 mg/day^r " ' PMSlbl7 3i8nificant
fr
occurring sporadically. in an
sures could add as much as ™
. 3uch
«ting, percutaneous expc-
to
category, Scenario B, is rural *ei
e.osure of about 0.3
i^entio,
1-7
-------
TABLE 1-1. COMPREHENSIVE EXPOSURE SCENARIOS FOR BENZENE
Route
Exposure by Scenario in irig/day
ABC
% of 1970 population 74
26
Ingestion
Water
Food
0.004
0.25
0.004
0.25
0.004
0.25
Inhalation
Baseline
Gas Stations
Cigarettes3
0.1 (urban)
0.01
0.03 (rural) 0.5 (near sources)
0.01 0.01
1.4b i.4&
Percutaneous
Residential
:1.0b
:1.0b
Total Typical Exposure C0.4
Potential Maximum*1 2.8
0.3
2.7
0.8
3.2
A 1978, population of 54 million individuals who smoked cigarettes.
This amount not included in total exposure.
•*
"Excludes percutaneous exposure and that due to cigarette smoking.
These amounts include all possible routes of exposure but not
possible percutaneous absorption.
Source: This report.
1-8
-------
I
I
C would add exposure due to user site emissions for a total of up to
or hofi I! ?6S? t0tal CyplCal exP°sure* -y be exacerbated by smoking
or home use of solvents or other benzene-contaminated substances.
1.4.2 Biotic Effects and Exposure
The lowest concentration of benzene at which effects have been
observed in aquatic organisms is 0.001 mg/1, which affected growth in
several algae species. Acute and sublethal effects to adult fish
including trout, bass and herring, were observed at levels <20 mg/1
Between 20 and 36 mg/1, several freshwater fish exhibited acute toxic
effects. Algal growth was usually inhibited by benzene concentrations
exhibSn H n 36 f ' 10° m§/1- SeVSral m°re Distant *Pecies
exhibited chronic and acute toxic effects in the 100-400 mg/1 range
f reducL^h^f ant J18^ SP6CieS (Chlorella> ^owed inhibited growth and
a reduced photosynthesis: respiration ratio in the 400-1755 mg/1 range.
The levels of benzene that cause deleterious effects in aquatic
lethal""^ n^t "^f ^ raOnitored ™« levels; thus so^e sub-
lethal but not serious effects may be expected. Benzene concentrations
in refinery and chemical plant effluents were in the 0.08-1.0 me/1
aSSflrWfi ^^ TbiSnt l6VelS WerS <0'01 m§/1' The available data
are far from comprehensive; therefore, it is difficult to accurately
represent the total picture of aquatic contamination. However nese
to be^SL8611 Y 10W6r ^ 3 faCt°r °f 2°°° than those determined
a-|0rt ?o6 h*Jhe* <;once"trations associated with chemical plants are
oa^r'L r ^ ^n--f ^r^o-piSc^
of exposures of concern for acute or chronic effects for Aquatic organise.
1-9
-------
I
I
1
2.0 INTRODUCTION'
stances. The results are
these sub-
with
of comprehensive revies of p
effects and exposure to benzenl a^d
into an analysis of risk
°f "" 6XP°SUreS and ^ associated
" lnclud" S
, ' distribution, fate,
integration of this material
serf
of petroleum and petroleum nroducts (i e
in environmental releases of benzene as it
is used predominantly as a c
the to many chemical
^
K
WSl1 3S de^vation
solvents> result
C°ntarainant • Benzene
p.
lowed by a compilation^o
The results of media-specific f
to predict concentration levels
close proximity to significant
trjtion. resulting fro^ free e.
and sediment are presented nex? A
-ne and a summary of criticaffate^
Ascribed in
St "ctlon"fol-
environmental media.
transfer -^els used
air and wate* within
x Squilibri- concen^
betW6en air' soil. water
eu
exposed to documented or predicted esf
risk comprise the later chapters of this report6
concentration of 6.6 ug/i
cancer (U.S. EPA 1930)
the
* Stateme^ of
for benzene:
u Crit!?ia' In water, a
with a 10'* risk of
2-1
-------
The Occupational Safety and Health Administration has established
permanent standards for the regulation of benzene in the workplace.
The time-weighted average concentration for 8 hours should not exceed
32 mg/m3 (10 ppm), with a peak concentration of 160 mg/m3 (50 ppm) for
any 15-minute period during the 8-hour day (RTECS 1980).
Benzene concentrations in air were converted from ppm to mg/m by
using the following relationship: 1 mg/m3 = 3.192 ppm. This factor
was derived assuming 1 atm and 25aC, conditions, which were not absolute
for all atmospheric measurements. However, monitoring data are seldom
reported with the concurrent temperature and pressure; therefore, in
the absence of these data, the conversion factor was used for all
values of benzene in air.
2-2
-------
I
I
REFERENCES
Health Service, Center foJ
Occupational Safety and
(RTECS)> »«
Cont ?™U1 Services-
' Natlonal Institute for
Standards, o.s,
,ualit7
2-3
-------
I
I
3.0 MATERIALS BALANCE
3'-
. of
April 1980, JRB Associates Inc preoreH C° the enviro™*nt. In
exposure assessment. Much of the I«V ^^ f°r USe in this
report, with some reorganization of S ^ *" draWn fr°m that
inc., has not conductef f^er^
industry6 "tfo^pSdulSon'^ c? ^^ 3CqUlri^ the «« recent
rates had been publishe I *™' ^ Pr°CeSS' If
tta« refine Ught...n"--"' °f •»'«!«. pnt.
k
sources of benzene. The remainin, M ! and =oke Pl™ts are direct
may also be s<,urces becLJ Tot thlif ™ '!' th°Ugh i"di™*c "uroes,
or products and process emissioS Thus ™, °f bMZene in the «
because of the production of gasoiinf is an H U1° reflni"S. sP^la
as well as coal coking operations Without " ltldlrect so^" of benzene,
and nuoing and resource processing! 6 recovery, oil spills,
ln Table 3-
r.
ns. eparate data bases were used for the two
3-1
-------
TABLE 3-1. MATERIALS BALANCE FOR BENZENE, 1978
OJ
I
ro
Direct Sources
Refining Production
from Crude
Refinery Production
from Light Oil, etc.
Coke Plant Production
Inventory Withdrawals
Imports
Subtotal
Indirect Sources
Gasoline Refining
Gasoline Imports
Other Fuels
Coal Coking
Contaminated Solvents
Oil Spills
Resource Mining/Processing
TOTALS
kkg
Amount
4,709,900
65, 400 1
178,786 f
272,0001
225,000
5,451,086
1,400,000
3,288,000
959,410
?
22,600
30
148
11,121,274
Balance: Sources - Releases ?
11,094,282
Discrepancy
I 11
34,902
Releases Uses
.3,900
) ?
J 786
^ 26
4,712
20,230*}
1
1,872
30
148
26,992
Uses
,059,380
+ 33,
Chemical Feedstock 5,
Solvent Use
Exports
Transport & Storage
5,
jGasoline Consumption 4,
^Transport £. Storage
Fuel Use
Other Solvents
Amount
251,000
9,600
151,000
„
411,600
665,770
-
959,410
22,600
11,059,380
.? Releases + Carryover
? 11,025,839
541 = 68,443 = 0.6%
Releases
10,916
10,865b
2,510
17
7,272
31,580
130,059
21 ,000
40,213e
7,100f
219,087
kkg
Destruction3
5,107,300
6,590
150,983
0
5,264,873
4,481,670
919,197e
15,520f
10,681,240
Unaccounted
121,919
0
0
-7 272
114,647
0
0
0
114,647
+ Destroyed + Unaccounted for
of total
sources.
bAmount destroyed includes amounts transformed, transferred or otherwise chemically altered
^Carryover into products ; not included in column total.
dlncludes 2,000 kkg destroyed during refining (not described as a release elsewhere)
These releases occur from all sources and users, save gasoline and fuels.and required a negative entry to
avoid double accounting. ' r
^Estimate based on percent released and percent destroyed for gasoline.
Estimate based on percent released and percent destroyed for solvent use.
Source: JRB (1980).
-------
I
I
3-2 PRODUCTION_OF__BENZENE
material
ates from gas wells. Although o?iginlul ±? Production; and condens-
er benzene, petroleum is the§pri^fy so^rc S T ^ C0mmeri^ source
1976) According to the USITC (1976) 178 000 kJ J"! tOday -
directly from coal and 65,400 kkg from lliht n^8 J60""
coklng, vhile 4,710>000 kkg wereSpfro:c light
3'2'1
n W£re
.
the
• Dealkylation of toluene;
• Disproportionate of toluene, and
by-product of ethylene
- ~- -
«- 3ites Of ben2ene proJ^n-^-pT^SS: ^'^ ^°
.
1978. Tabl ?T Jisl "f "ere es"««ed to be
process A vide range exists b««e e"^/"" Pr°duction ^om each
m available release factors: 30-50 000 ?/" presen"d bX JRB based
wnn^f ^leaSeS frcim P^roleum prodi«Ln 171' ™ «"^ted overall
3900 kkg/yr fisure than to the more extreme I?""11' t0 "e Closar « t
conclusion on the judgment that for f"™3 values • JM based this
trol methods would be taple^te I L "On°mlC reas°"=. all feasible con-
Several industrial contacPtsmc^f1PeentUd1°S "' *
fact°rs for »«»!.» refinery production of ben-
Mstes corectl
3-3
-------
TABLE 3-2. PRODUCEIIS AND PRODUCTION OF BENZENE, 1975-79
Estimated Production
U>
Company
Allied Chemical
Aiui-rada llese Corp.
American Petrofliu, IDC.
(Cobdcn Oil i> Chemical Co.)
Ahlilaud Oil. Inc.
Atlantic RlchfU'ld Co.
Charier Internal tonal till Co.
Cltlca Setvluu Co., Inc.
Cuaiial Slaiu& Prud. Co.
Cuitu«onw£al III Oil Refilling Co.
(Commonwealth 1'iU nu l.i ml tali)
Cruuu Central Petroleum Corp.
liuu Chemical Co.
tat t man- Kodak Co.
(Tex, 13 tlatitman Dlv.)
lixxon Corp.
(Icily Oil
uiill Oil Coiporutlon
Kerr-McCee Coip.
(•Joutliucdtern ltd i Kef. Co.)
Marathon 01 1 Co.
Mobil Oil Corp.
Moilu.into Co.
lY-mnol 1 Dulled, Inc.
(Mlau ProcetitilnK)
"lillllpu fun,)). Co.
' (u 1 ill ana-llukfe 1 1
too ul Ion
Winnie. TX
St. Crolx, Virgin Island*
Part Arthur. IX
Bit Spring, TX
Ashland. KY
North Tonauanda. MY
Houston, IX
Wllmlnctoii, CA
Cliannul view, TX
llouuton. TX
l.aku Cliaileti, I.A
Corpus Clirlbtl, TX
1'uiiuu J«is, I'tiiirio HI co
I'aiiadena, TX
Uay Ciiy, hi
Freepori, TX
I'l jijuc'iiilne , \Jt
Longvlew, TX
Halon Rouge, 1A
Baytuun, TX
i:l Dorado, KS
Alliance, LA
I'hl ladclplila, 1'A
Port Artliur, TX
Coi|>ut> Chi lull, TX
lexaa City, TX
Beanmunt , IX
Cliocolate Uay on, TX
slif fv<_-|)iir t , LA
bwcL-ny. TX
t.uayamu, Puurtu Rico
Curpuu ClirlHll, TX
1979
162,000
144.000
159.000
i?,200
139.000
29,800
162.000
12.400
62,100
174.000
460,000
57,200
1 4.1.00
124,000
149,000
?
174.000
149.000
32.300
167.000
92,000
186,000
39.800
17.400
149,000
211.000
87,000
24.900
271,000
224,000
1976
146.000
130,000
144,000
51,700
126,000
27.000
146,000
1 1 , 200
56,200
157.000
416.000
51,700
67,500
112,000
7
157,000
135.000
29.200
151.000
83.200
169.000
36.000
15.700
135.000
191.000
78.700
22.500
247.000
202.000
1977
159
142
156
56
103
29
7U
12
61
171
452
56
73
122
171
147
31
164
90
97
17
147
208
36
24
269
17
.000
.000
,000
,200
.000
.300
.200
.200
,100
,000
,000
,200
,300
.000
f
.000
.000
,800
.000
,400
, /OO
,100
,000
.000
.600
.400
.000
,100
19/6
8,520
71,000
42,600
128,000
142.000
42.600
125.000
34.100
14.200
71.000
199,000
525.000
05.300
85.200
142.000
?
185.000
176,000
37.000
199 ,000
9 3 , 700
108,000
17.000
170.000
213,000
42,600
62.500
312,000
1975
5
47
28
85
95
28
83
22
9
47
1 J3
350
41
56
94
123
117
24
133
62
72
11
114
142
28
41
208
.680
.400
.400
.300
.000
.400
.400
.700
.470
.400
,000
.000
,600
,900
,700
?
.000
.000
.600
,000
.500
,000
.400
.000
.000
.400
.700
.000
Production Procejsea
and Uae
CK
C
CR.
CR.
CR.
CR.
CK
PC
CK
CR
251
PC.
CR.
c.
C.
CR.
67Z
C.
C.
C.
c.
c,
CR,
c.
PC
C.
PC.
CR
TO
TO. I JO
LO
TP
C, CR.
CR. Tl).
1U
TO. PC,
Tl). PC
PC
C. CR
CR
CR. TD
CR. Tl)
CR. PC
CR
PI:
CK. Tl).
CR
CR, Tl)
•11)
PC
1.0
PC
Sources: Arthur D. Little, Inc. (1977), SRI (1977), Versaf, Inc. (1979), Neufeld £t _aK (1978)
-------
TABLE 3-2. PRODUCERS AND PRODUCTION OF BENZENE, 1975-79 (Continued)
I
Cn
estimated Production0 (kkg)
Company
Shell Oil Co.
Standard Oil Co. of Calif.
Standard Oil Co. ( In.! .) (AMOCO)
Standard Oil Co. (Ohio)
(B.P. Oil Co.)
Sun Oil Co.
lY-nncco, Inc.
'Icxaco, Inc.
Union Carbide Corp.
Union Oil Co. ot Calif.
Unlun Oil- American I'ctroflua
Union 1' .let fie Corp.
(Chauip)ln fat roltmm Co.)
TOTAL USITC
Local Ion
Deer Park, TX
Odessa. TX
Wood Klver. IL
tl SegnnJo. CA
Texas City, TX
Mjrcua Hook, HA
Mjrcub (look, PA
Lor ptiti Cliristl, TX
luls,a, OK
lolcdo. Oil
I lialuiullfc. I.A
Port Arthur, TX
U'cbtvlliii. NJ
Taft, LA
l.emont , 11.
lie.lumulll , TX
Corpus Cliristl. TX
riMHiiiCTioN
1979
29 B. 000
29,800
112,000
57.200
211,000
72,100
94.500
59 , 700
184,000
24.900
112,000
87,000
1 7'. ,000
42,300
54,700
24,900
5,430,000C
1978
270,000
27.000
101 .000
51.700
19 1,000
65.200
85.400
54 ,000
166,000
22.500
101,000
78,700
157,000
38,200
49 , 500
22.500
4. 780.000
1977
220.000
29 , 300
110.000
56,200
208 ,000
70,800
92.800
58.600
120,000
24.400
110.000
85.500
171,000
4 1 , 500
53,700
24.400
4,570,000
1976
213,000
17,000
114.000
65.300
22.700
42.600
99.400
63.200
28,400
128.000
90 . 400
19V. 000
54 .000
54.000
J8.400
4.540.01)0
1975
142.000
11 .400
76,000
43,600
161 ,000
1 5 , 200
2U.400
6b. JOO
45.500
18,900
B5.300
66 , 300
131,000
36.000
36.000
18.900
3.1'JO.OOO
Production Processes'1
2nd Use
C, CK, PC
CR, ID
CR, LO
C, CR
c. OR
CK. IT
C. CK. Ill
CR, TP
CK, 11)
CK , l.rt
7U C, CH
PC. CR
C PC
1 • "
CR. 1 O
SO* C. TU
C, CK
BDerlved from plant capacities and UbllC product Ion totala.
Key: C. c.iptlue nac; PC. p,trliully captive; CH, catalytic rutonn.il Ion; TO, tolit.^nu
aUyl.ulun; TP. lolu.-nc Jlupoi port lonai Jon; I'O, pyiolyala gaaollno; 1.0, light
oil; CS , ga^wcll condcnuate.
CEsclmaced ^V «-'»l i apol jt lug IISII'C dal a for tlie inonili.-, lanu«ry
July 197'1.
-------
• N. DAKOTA "f~"
1 \ MINNESOTA
f inufA i
Unplotted - St. Croix, VI; Penuelas, PR; Guayama, PR.
Sources: Arthur D. Little, Inc. (1977), SRI (1978), Versar, Inc. (1977), Neufeld jet jQ. (1978).
FIGURE 3-1 PRODUCERS OF BENZENE FROM PETROLEUM AND COAL, 1978
-------
I
I
TABLE 3-3. BENZENE RELEASES FROM DIRECT PETROLEUM PRODUCTION, 1978
Benzene Produced Estimated
General3
Releases
Catalytic reformation 2,360,000 2,360
Toluene dealkylation 1,300,000 1,300
Toluene disproportionation 121,000 60
Pyrolysis gasoline 925,000 180
Total 4,706,000 3,900
Total Production based on
USITC data 4,775,300
Release factors are given by process for total releases. In the text,
specific release factors are given only for benzene production from
petroleum as a whole.
3-7
-------
thesis processes are acid and alkali sludges (Saxton and Narkus-Kramer
1975). The quantity of solid waste generated from benzene production
was calculated using data of Saxton and Narkus-Kramer, who calculated
the amount of solid waste generated from benzene production in 1972.
These figures include benzene production for all processes. Benzene
releases in solid wastes from petroleum-based production were 141 kkg.
It was assumed that these wastes would be handled as are refining
wastes, which are landfilled. Because benzene represents only l%°of
the total amount of waste generated, it must be realized that the
actual quantities (volumes) of the wastes described above are 100
times larger.
Air releases were estimated by the difference between the total
releases (3900 kkg) and those attributed to land (141 kkg) and water
(620 kkg). Thus, air releases would be about 3140 kkg.
Releases from refining of gas well condensates were not estimated
because of the lack of release factors specific to the process."
3.2.2 Direct Production from Coal
Benzene is obtained from coal by extraction from the light oil
formed during coking. Crude light oil consists of 55-70% benzene by
volume (Arthur D. Little, Inc. 1977). The yield of light oil from
coke ovens producing blast furnace coke is 11.4-15.1 1/kkg of coal
carbonized (PEDCo 1977). The light oil is refined by various processes
that result in separation into benzene, toluene, xylene, and residue
fractions.
The treatment of coal tar may also be used to obtain light oil.
The tar can be distilled to yield a light oil fraction, which is
usually combined with the light oil from coal gas before it is refined
to produce benzene (PEDCo 1977). Light oil is either refined on site
or it is sold. Several petroleum producers refine this coal-derived
light oil (SRI 1978, Arthur D. Little, Inc. 1977).
In 1978, 254,000 kkg of coal-derived benzene were produced (USITC
1978). This represented 4% of total benzene production. Ten plants
refined their own light oil and produced 178,000 kkg of benzene in
1978. An unspecified number of coke plants sell their light oil to
refineries for benzene extraction. This quantity, 65,400 kkg, was
previously accounted for in the section covering petroleum refinery
production of benzene with respect to emissions and total production.
Table 3-4 is a list of producers who derive benzene from coking
operation oils or those who generate the light oil and sell it to
refineries.
Benzene releases from coal coking operations, refining of coal-
derived light oil operations (for which no release factors were found)
are mostly gaseous and some liquid. The amount of benzene released
3-8
-------
1
I
TABLE 3-4. PRODUCERS OF BENZENE FROM COKE
Company
Armco Steel Corp.
Bethlehem Steel Corp,
Mead Corporation
C.F. & I. Steel Corp.
Interlake, Inc.
Jones & Laughlin Steel
Corp. (LTV Corp)
Northwest Industries, Inc.
(Lone Star Steel Corp)
U.S. Steel Corp.
Total Production
Location
Middletown, OH
Bethlehem, PA
Lackawanna, NY
Sparrows Point, MD
Chattanooga, TN
Woodward, AL
Pueblo, CO
Toledo, OH
Aliquippa, PA
Lone Star, TX
Clairton, PA
Geneva, UT
Production in IQ/a
(kkg)
5,700
7,700
0
29,000
0
3,800
5,700
1,900
19,000
1,900
96,000
7,700
178,062
Source: Adapted from JRB (1980).
3-9
-------
to the air during coking operations was estimated using three factors
from the literature. When the factor developed by Walker (1976) was
used to estimate the release of 59,000 kkg benzene, it was assumed
that coking production was at full capacity, requiring consumption of
88,000,000 kkg of coal (derived from Table C-l in Mara and Lee 1978),
and that the yield of coke from coal is 68.4%. The value 88,000,000
kkg of coal was used in calculations with the other release factors.
With the PEDCo (1977) factor, benzene releases to air from all coking
operations were calculated as 6900 kkg based on U.S. EPA (1977) data
for atmospheric emissions. JRB judged the Mara and Lee factor to be
most accurate and estimated releases of 2640 kkg.
Based on data contained in the JRB report, a maximum air release
was estimated for coking operations that derive benzene from the light
oils produced during coking. This calculation does not include air
releases, which may occur during refining of light oil for benzene, nor
releases attributed to coking operations that do not produce benzene.
The ten coking facilities producing benzene have the capacity for
25,600,000 tons of coal. Using the emission factor of Mara and Lee
(1978), for every ton of coal coked, the potential release of benzene
to the air if all ten facilities operate at full capacity is:
2.56 x 107 kkg coal x 3 x 105 benzene
COelX.
In the absence of emission factors for the refining process of
either light oil or coal tar refining for light oil, 768 kkg will be
used as a minimum air release for coal-derived benzene production,
even though the assumption of full capacity is incorrect. Versar, Inc.
(1980) estimates benzene discharges to water for coking operations to
be <10 kkg. JRB also accepted this figure.
Possible sources of release during production of benzene from light
oils are predominantly liquids: shock liquors, aqueous effluents, oil,
wash oil, light oil, etc., and solids in the forms of tars.
No release factors were given for air or water for benzene extrac-
tion from coal tars. Land releases, however, were estimated to be 8 kkg.
3.3 IMPORTS AND EXPORTS OF BENZENE
Benzene imports amounted to 225,000 kkg in 1978. The estimated
releases attributed to importing were 13 kkg to air and 13 kkg to water.
Releases due to imports are the result of unloading operations and
transport to points of consumption. Using release factors developed
by PEDCo (1977) and assuming 95% emission control at dockside and a
50/50 split between air emissions and water discharges, the estimated
benzene release is 13 kkg to each of the two media. No solid wastes
are generated during importation .
3-10
-------
I
I
Exports accounted
used for exports and
ass
(or
Thus>
3'4 IKDIRECT SOURCES OF REM7cmr
Benzene ^y be released from
• Coal coking,
• Petroleum refining for gasoline,
• Use of products (mostly solvents) contaminated with benzene,
• Natural gas well condensates,
• Resource mining and processing,
• Oil well drilling,
• Oil spills, and
• Combustion.
3-4-l Coal Coking
-lvHfr-F- -
Based on the release factor of Mara ^ Je Ifwv™ ^^ P
3-2.1.2, the amount of benzene released tTrl ?} f 6<1 ln Section
these plants is: released to the air during coking at
62, 4 x IQ6 kkg coal x 3 x 10"5 kkg benzene _
kkg coal ~ 1872
that all Plants condense their SSr "M63363 t0 3lr' which
them to the air in the gaseous state § °llS and d° nOt
3-11
-------
Release factors were not available for either land or water
releases from coking operations.
3.4.2 Petroleum Refining for Gasoline
It is estimated that crude oil contains an average of 0.2% benzene
(Walker 1976). Therefore, petroleum refining operations are expected
to be a source of benzene releases. The amount of crude refined in
the United States was 5 x 109 bbls (2.1 x 1011 gal) in 1978. This
amount contains 4.2 x 10° gal of benzene or 1.4 x 10° kkg (one liter of
benzene weighs 0.878 kg).
The literature revealed several release factors for benzene of air
(Mara and Lee 1978, PEDCo 1971, Versar, Inc. 1977). Of these, JRB has used
the data based on Mara and Lee's factor to provide a maximum. Air
releases are estimated to be 20,000 kkg/yr.
One factor for releases to water from petroleum refining wa~s calcu-
lated from data presented by Versar, Inc. (1977). Sampling data for six
refineries were collected by Versar for the Effluent Guidelines Division
of EPA. Of these, one had a benzene concentration of 7 ug/1 in its
effluent, while no benzene was detected in effluents of the other five.
JRB assumed full-capacity production and direct discharge of all efflu-
ents, combined vith a release factor derived from the PEDCo figure to
estimate water releases of 1 kkg for the industry in 1978.
The amount of benzene in solid waste resulting from petroleum
refining was between 71 and 230 kkg (Table 3-5) for 1978. In 1976,
the American Petroleum Institute's survey of the industry revealed
a waste amount of 357,000 kkg for the year. In the United States,
4897 x 106 bbl (6.666 x 108) of crude were processed; 39% of which was
not domestic oil. Using these two figures, a waste generation factor
of 0.54 kg/kkg was derived. Using the conversion factors of JRB (75%
recovery; 16% of waste is oil; benzene content averages 0.5%), the
amount of benzene in refinery wastes was 71.4 kkg.
The waste generation factor used by JRB results in yields of more
waste than crude (1.64 kkg/kkg). Assuming that this factor is off by
10" , the amount of benzene in refinery wastes was recalculated to be
229.8 kkg.
The total amount of benzene released to the environment during
refining operations is 20,230 kkg in 1978. Of the initial amount
available in crude (1,400,000 kkg), 1,379,770 remains in the refined
gasoline product.
3.4.3 Use of Products Contaminated with Benzene
The three solvents co-produced with benzene are toluene, xylene,
and hexane. Their estimated benzene contamination is 0.001-0.04% by
weight. One order of magnitude estimate of the quantity of benzene
3-12
-------
I
1
°— - SOLID PASTES
Disposal Method*
Adapted from Jacobs (1978) by JRB.
J'°°x ^ 116
8'4 0,97 x 108. 19
L'agooning oo •? «
§ 39'7 4.57 x 108 91
Incineration n a 8
°'8 0.09 x 10b 2
TOTAL
228
3-13
-------
in these products is given as 22,600 kkg (see Table 3-6). Actual
releases are unknown. However, if the proportions of destroyed and
released benzene developed for pure benzene solvent are applied to
contaminated solvents (see Section 3.5.2.1), it can be estimated that
15,500 kkg (68.6%) are destroyed and 7100 kkg (31.4%) are released to
the environment.
Other petroleum products that may contain from trace to 3% benzene
(by volume) are solvent naphthas (aromatic petroleum, Stoddard, VM&P,
etc.), coke-oven tar, and lubricating oils. Production figures were
not available for these products. Because of their nature, any con-
taminating benzene could come in direct contact with consumers.
Losses would be evaporative, aqueous (washing), and solid (municipal
wastes).
3.4.4 Natural Gas Well Condensates
Benzene is a component of gas well condensates. Atlas Processing,
a subsidiary of Pennzoil, was reported to produce small quantities of
benzene (SRI 1978). The company's benzene-producing wells are located
in the East Texas gas fields. JRB postulated that other gas wells in
the region also contain benzene. However, attempts were unsuccessful
in obtaining information on the fate of these condensates or well-head
release rates. Further study is needed to determine the number of
gas wells that have condensates containing benzene, the quantity of
benzene contained in the condensates, and the types and quantities
of releases to the environment. These sources are of potential
significance.
3.4.5 Resource Mining and Processing Operations
The mining and processing of mineral, timber, and fiber resources
produced some benzene releases to water. Table 3-7 shows estimates
of benzene releases to water totaling 148 kkg from these resources.
No additional information or process descriptions could be obtained
from Versar, Inc. (1977) who originated these estimates.
3.4.6 Benzene Releases from Oil Well Drilling
The drilling of oil wells produces environmental releases of ben-
zene from drilling fluids, muds, and uncontrolled flow of crude oil
above or below the surface. The quantity of benzene releases depends
on the percentage of benzene in the crude and the extent of uncontrolled
crude flow, which may contain drilling muds and fluid. No information
was obtained on the quantity of benzene involved in this potential
source of environmental release. JRB estimates that oil drilling
sites are a potentially significant source of benzene releases.
3-14
-------
I
TABLE 3-6. BENZENE I;, CKfTAMDiAIED SOLVENTS
Estimated
abUSITC (1978).
Arthur D. Little, Inc. (1977).
3-15
Toluene
Xylene
Hexane
.
-••" A:?/ o
390,000d
2,915,000
200,000
*
(% by Weight- )b
0.04
0.001
0.02
(kkg)
15,600
3,000
4,000
-------
TABLE 3-7. GROSS ANNUAL DISCHARGES OF BENZENE TO WATER FROM
RESOURCE MINING AND PROCESSING, 1976
Process
Nonferrous metals manufacturing
(Al, Cu)
Ore mining (Pb, Zn)
Wood processing
Coal mining
Textile industry (SIC subcategories
40 and 60)
Total
Source: Versar, Inc. (1977).
Estimated Discharge of
Benzene to Water
(kkg/yr)
2.85
1.1
0.4
141.1
2.51
148
3-16
-------
I
3'4'7 Benzene Releases from n-n sp^T,
3'4'8 C°SbHStion of Petroleum-baaed Fuel.
-3'4-8-1 Benzene in Gasoline
,
domestic use (U.S. DOE 1979) TM °f • C1Ot°r gasoline were supplied for
releases from inventories and ^llrll^l^^5 U'S' Production,
estimated the total amount of benz^ e?Ports. ln 1978, JRB
based on the average benzene co^'ratiofn ^ *? 4'4 X 1Q6 kk^'
amount of benzene used annually in mot nr f } ^ ln Sasolirie. The
or is withdrawn from inventories is 3 2«« nnn,,^" °riSinat^ Abroad
originated within the United States in 1978 "' ^ ^^^O kkg
of benzene in the gasolinf in ^ * *° increase ^he concen-
Therefore, gasoline production i^addit^ T "parated ^om the BTX.
significantly contributes to the Lou^ ? \ benZene ProduCtion,
environment. A materials bal«ce^™the b^nZ6ne.relea8ed C° the
fore, may be considered independently frotn , T is §asolin^ there-
zene in general. penaentl/ from a materials balance for ben-
be included in releases
total 248,000 kkg, were detailS
not be described further.
' which
Section 3.4.2) and will
3-17
-------
A flow diagram of gasoline from production center to its ultimate
combustion in a motor vehicle engine is represented in Figure 3-2. The
distribution system, which transports gasoline from the petroleum
refineries to the consumer with intermediate storage stops, is a
source of atmospheric benzene (21,100 kkg). Gasoline is shipped from
refinery storage areas to bulk terminals (regional distribution centers)
by ship, barge, railcar, and pipeline. Then it is transported from the
terminal by tank truck to service stations and commercial and rural
users, either directly or via bulk plants (local distribution centers)
(Burklin _e£ al._ 1975, PEDCo 1977, Mara and Lee 1978). Benzene releases
to air associated with particular segments of this flow are the maximum
estimates given by JRB in each case (see Figure 3-2).
The benzene concentration in gasoline depends on several factors,
including the source of the crude oil from which the gasoline was made,
the location of the crude oil source and the refiner, the grade of gaso-
line, refinery operations, and the seasonal blends produced by each
refinery (PEDCo 1977).
The lowest reported benzene concentration in the surveys referred
to above was 0.25% by volume (premium, summer, district 2). The highest
benzene level was 3.91% (unleaded, winter, district 4). National averages
from the reports (in percent by volume) were as follows:
Unleaded Regular Premium
Summer 1.20 1.19 1.10
Winter 1.26 1.12 1.15
Because the differences in benzene concentration between fuels of
different grades and seasonal blends were smaller than the variation
within each blend or grade, JRB chose the average of the above values,
1.17%, to represent the benzene concentration in all gasolines for
calculating releases and total amount of benzene in gasoline. There-
fore, the total amount of benzene in gasoline was 4.4 x 106 kkg in
1978. Of this amount, 21,000 kkg are the estimated air releases due
to evaporation, venting, etc., during storage, transfer and transpor-
tation operations, which convey the gasoline to the final consumer.
Emissions attributed to vehicular use are from engine exhausts, and
evaporation from the carburetor, etc. JRB calculated these releases
as totaling between 53,894 and 165,521 kkg. At maximum releases, 52%
is attributed to autos, 12% to motorcycles, and 36% to trucks and
buses. Auto exhaust releases were recalculated on the basis of in-
house data (unpublished), which indicated that the emission rates
used by JRB were high and possibly the results from outdated, less
accurate analyses than are possible today. The new figures result in
a total air release between 45,989 and 130,059 kkg. At maximum
releases, 39% is attributed to autos, 14% to motorcycles, and 47% to
trucks and buses. These calculations are given in Appendix A.
3-18
-------
I
I
Imports — Exports
and Inventory Use
of Gasoline
U.S. Gasoline
Production
Rail, Marine, Pipelines
Gasoline Bulk
Terminals
Tank Truck
Transport
Tank Truck
Transport
Service Stations
Commercial, Rural
Users, etc.
Motor Vehicles
Air/Land
~
206,330
Combustion Destruction
and Generation
Environmental Releases
F.GURE 3-2 MATER.ALS BALANCE FOR BENZENE ,N GASOUNE ,N KKG
3-19
-------
3.4.8.2 Benzene in Other Petroleum-based Fuels
The benzene concentrations of eight fuels were estimated by Arthur
D. Little, Inc., (1977) and are presented in Table 3-8. The estimated
benzene content calculated from these concentrations is 959,410 kkg.
These calculations indicate that a significant quantity of benzene is
present in aviation turbine fuel, which consists of naptha and kerosene
types of jet fuel. Because of the magnitude of this estimate, JRB
recommends further investigation to determine the quantity of benzene
released from this fuel.
For the purpose of this materials balance, it has been assumed that
the total 1978 production of these fuels was used and that a similar
fraction (95.8%) of the benzene therein would be destroyed during com-
bustion as it is in gasoline. Thus, 919,197 kkg would have been des-
troyed during the use of nongasoline fuels, and 40,213 kkg would be
released to the air.
3.5 USE OF BENZENE
3.5.1 Consumptive Use
Benzene is predominantly used as a starting material for the
synthesis of other organic compounds. In 1978, 5,230,000 kkg of ben-
zene were consumed by production of these eight compounds: ethylben-
zene, cumene, cyclohexane, nitrobenzene, chlorobenzene, chlorobenzenes,
alkyl benzenes, maleic anhydride, and biphenyl. The eight major direct
derivatives of benzene and their contributors to total benzene con-
sumption are listed in Table 3-9.
The materials balance for benzene use as a chemical feedstock,
showing carryover, destruction and environmental releases totaling
10,916 kkg is given in Table 3-10 for each production process. JRB
used several references to estimate the release factors shown in the
footnotes. The values given represent JRB's best judgment of actual
releases, when several release factor estimates were available for a
specific process.
Although the release rates were not available to estimate benzene
in solid wastes from consumptive use processes, its presence in these
wastes cannot be overlooked during fate and exposure analyses.
The possibility of product contamination by benzene was- examined
for the eight products and their major derivatives. In all cases, test
estimates indicated that benzene carryover was <1% and usually <0.1%.
The maximum carryover was estimated for each process and the total
amount was 10,866 kkg, or 0.2% of benzene use as feedstock. To com-
plete the materials balance for these processes, it was necessary to
base calculations on theoretical process efficiencies in order to
obtain quantity of benzene chemically transformed (or destroyed) during
the eight processes.
3-20
-------
OJ
TABLE 3-8. ESTIMATED BENZENE CONTENT OF FUELS
Benzene-Containing Fuels'
Fuel Produced in 1978
(gallons)
Aviation Gasolines
Farm Tractor Fuels
Diesel Fuel Oils
Aviation Turbine FuelsC
Gas Turbine Fuel Oils
Liquefied Petroleum Gases
Fuel Oils
Kerosene
Total Estimated Benzene Content
^Arthur D. Little, Inc. (1977).
U.S. DOE 1979 tha. A^t.
of „ 'aUons/baar«T
fuel !. the total of
b Estimated Benzene
Concentration
(% by Volume)
lhet trace
5.85 x 10
5.26 x 10
1.62 x 10'
1.5 x 107
4.63 x 10
2.7 x 106
' »«»
0.4 - 3(
0 - trace'
- trace
0
0 - trace
0 - trace
Benzene Produced as
a Component of Fuel
(kkg)
38,000
0 - trace
0 - 3d
200
• 921,000
0
200
10
959,410
'» Aliens using the conver,Jon
»tr.ce.. meant. JRB_
-------
TABLE 3-9. SUMMARY OF CONSUMPTIVE USES OF BENZENE, 1978
N)
to
Product
Ethylbenzene
Cumene
Cyclohexane
Nitrobenzene0
Chlorobenzenes
Alkylbenzenes
Maleic anhydride
Biphenyl
TOTALS
Secondary Products
or Uses
Styrene; polystyrene
Phenol
Cyclohexanone; nylon 66
Aniline
Chemical intermediates
Detergents
Chemical intermediates
PCBs; dyes
Production3
7,340,000
aUSITC figures except where noted. /in,ox
Conversion factors from Neufeld et al. (1978) .
includes nitrobenzene destined for aniline synthesis (96/)
plus nonaniline usage (4%).
d85% was derived from hydrogenation of benzene (Blackford
eUerived from USITC (1978) production figure for linear to
derived fron oxidation of
(Gerry et al._
847 was derived tron oxiuauiuu u*. n.-..~-..~ v j —
830Z was derived from thermal dehydrogenation o£ benzene,
Benzene Required
(kkg)
Consumptive Use
(% of Total)
v.»^&/
3,803,000
1,533,000
l,057,000d
261,000
172,000
330.0006
155,000f
29,0008
•V tJ r
2,810,000
1,030,000
836,000
170,000
134,000
132,000
132,000
_7,000
53.
19.
15.
3.
2.
2.
2.
0,
5
6
9
2
6
5
,5
.1
5,251,000
99.9
-------
TA.L. 3-10.
,OR
Benzene Concentration (kkg)
Co
INJ
CO
Product
Synthesized
Ethylbenzene
Cum en e
Cyclohexane
Nitrobenzene
Maleic Anhydride
Chlorobenzene
Alkybenzenes
Biphenyl
' • — — — — _
TOTALS
Yield Air
99 1 Qnn
96
99
97
70
85
99C
99C
— • ••-.. .,— .
•-* } -f \J\J
2,000
9QA
f- ,7U
340
3 6on
•** y V\/\J
340
170
41
"— • — .,
10,681
to
"*• '- •• — _
Water
— i.
1 OA
L2.0
40
16
j. \j
16
35
NK
235
Total Amount
Land Releases Used
NK
NK
VTTT
NK
0
NK
NK
"•*
NK
)
4,020
2,040
290
356
3,608
356
205
/ «
41
1
10.916
2,810,000
1,030,000
836,000
170,000
132,000
134,000
132,000
7,000
•
'i 9";i rtnn
Amount
Destroyed
2,782,000
988,830
827,640
164,900
92,400
113,915
130f685
6,930
r* - „
Max imum
Carryover
160
15
5,300
4,730
170
330
0.09
Amount
Unaccounted
23,820
39,115
2,770
14
35,832
19,559
780
28.9
jAs shown in JRB from nlne references>
Not known.
^Estimated by Arthur D. Little, Inc.
Based on % yleid and lncludlng
10,865 121,919
-------
When the amounts of benzene released, carried over and destroyed,
were summed and subtracted from the amount used as feedstock, the
difference was 121,904 kkg. This amount, an artifact of inexact
release rates, etc., is the amount unaccounted for and will include
the small fraction of benzene disposed onto land in solid wastes
resulting from these processes. The land releases are not expected
to be significant.
3.5,2 Nonconsumptive Use
In 1978, <5% benzene production was used nonconsumptively; i.e.,
benzene was not converted to another compound before use. The categories
of nonconsumptive use and the estimated amounts used are as follows:
Use Benzene Used
Solvent (kkg)
Pesticide Unknown
3.5.2.1 Solvent Use
Solvent use of benzene has decreased since the 1977 OSHA Emergency
Benzene Standard and the 1977 ban on the use of benzene in consumer
goods by the Consumer Products Safety Commission (Neufeld j2£ al. 1978).
Neufeld et al. (1978) reported on the-use of benzene as a solvent
(9600 kkg in 1978) and the releases associated with this use. They
estimated that benzene solvent was either released or destroyed by
industrial emission control processes. The fraction released was
estimated from information on control systems obtained during inter-
views with representatives of companies using benzene as a solvent.
JRB used data from Hillman et al. (1978) to estimate releases due to
benzene in consumer products. It was assumed that all of this benzene
was released to air except benzene in the "home fuels" category, which
was destroyed (see Table 3-11). These authors also documented the
effect of the 1977 OSHA and CPSC actions on benzene use: estimated
losses of benzene due to solvent use were 600-700 kkg in 1976 and only
2500 kkg in 1978. Cyclohexane is replacing benzene in many solvent
uses.
When used as a solvent in industrial processes, benzene may be
released through evaporation or in effluent discharges. In general,
each of these processes has a characteristic ratio of air to water
releases. However, because of the range of ratios possible — from
50:50 to 100% of air emissions — it x^as not possible to quantify the
total amount of benzene released to each medium as a result of solvent
use. This rationale was also used in Section 3.4.3 for contaminated
solvents.
Releases of benzene due to disposal of solid residues were not
quantifiable; however, these releases are considered small. The rate
' 3-24
-------
I
I
TABLE 3-11. ESTIMATED AIR RELEASES OF BENZENE FROM USE AS A SOLVENT, 1978
Solvent Use
General organic
synthesis
Pharmaceutical
synthesis
Small volume
chemicals
Aluminum aIkyIs
Alcohols
Consumer products
Amount Used
(kkg)
7,400
730
1,000
330
130a
Amount Destroyed
(kkg)
6,400
510
0
150
20
Releases
(kkg)
1,000
220
1,000
180
110
Total 9,590 7,080 2,510
Estimate applies to 1977.
Sources: Neufeld et al. (1978), Hillman et al. (1978)
3-25
-------
of production of benzene-containing residues, the percentage of benzene
(by weight) in the residues, and the method of residue disposal are
required to evaluate land releases of benzene from solid wastes.
3.5.2.2 Pesticide Use
The U.S. EPA Pesticide Product Information File lists seven pro-
ducts (mostly screw worm pesticides) containing benzene. The percentage
of benzene in each product is also given; however, the amount of each
product formulated per year was not available. Thus, total benzene used
for this purpose could not be quantified. Screw worm killers are not a
major part of pesticide sales.
3.6 TRANSPORTATION AND STORAGE OF BENZENE
Releases occur when benzene is moved from producers to users.
The releases described in this section are distinct from those described
in the section related to gasoline, which also includes losses due to
storage and transportation, loading, and storage. Ninety-nine percent
of environmental releases of benzene are to air, with the remainder to
water as a result of barge transportation of benzene. JRB did not
mention leaks or spills onto land. A small amount of benzene is prob-
ably released to land from transfer or other operations.
Benzene releases due to storage are classified as standing and
withdrawal losses. The factors mentioned previously, as well as the
length of storage time cause storage standing losses. Withdrawing
benzene from the tank increases the amount lost; usually, this is
from the evaporation of benzene retained on the sides of the tank as
the roof sinks (PEDCo 1977). Based on release factors of PEDCo (1977)
and SRI (1978), the amount of benzene estimated as air losses during
storage is between 105 and 4900 kkg.
Benzene is transported by railroad tank car, tank trucks, barges
on inland waterways, and pipelines. Generally, before benzene is
transported, it is first collected and temporarily stored in a "rundown
tank", where it is inspected for product quality. Then, it may be
transferred to two sets of shipping tanks, one for railcar and truck
loading and the other for barge loading. The rail and truck loading
tank is also used to feed pipelines. Benzene losses from these tanks
may be characterized as standing losses (caused by evaporation around
perimeter roof seals) and withdrawal losses (caused by emptying the
tank). Based on the release factors of Dunavent (1978), the air
release caused by loading to transport vehicles is 1300 kkg, assuming
all stored benzene is passed through rundown tanks.
To estimate transportation-associated releases, JRB assumed that
50% of the transport takes place by rail or truck, and the rest occurs
by barge. Based on the release rates of SRI (1978), total releases
to air are 980 kkg.
3-26
-------
I
3.7 SUMMARY
the
land-destined wastes, while fuel
source of the
Physically removed 0,
use), and 2.« is release
the
ls destroyed (or
'^ °f
3-27
-------
TABLE 3-12. SUMMARY OF ANNUAL ENVIRONMENTAL RELEASES OF BENZENE
Source
Direct Sources
Refining Production
Coke Plant Production3
Exports
Imports
Transport and Storage
Indirect Sources
Coal Coking
Petroleum Refining
Gasoline Combustion
Gasoline Transport
and Storage
Use of Other Fuels
Oil Well Drilling
Oil Spills
Use of Contaminated
solvents
Resource Mining and
Processing
Uses
Chemical Feedstock
Solvent
Pesticide
TOTAL
Maximum
Air
3,139
768
?
13
7,200
1,872
20,000
130,059
21,000
40 213
7
0
?
0
10,681
?
?
23A,945b
Estimated
Water
620
10
2
13
72
7
1
0
0
1
7
30
?
148
235
?
7
I,i31b
Releases (kkg)
Land
141
8
15
0
7
7
230
0
7
0
7
Total
3,900
786
17
26
7,272
1,872
20,230
130,059
21,000
40,213
7
0 30
? 7,100
0
7
0
7
394
148
10,916
2,510
?
246,080
aReleased from coking operations only. Releases due to light oil refining
not estimated.
"Subtotal does not include releases due to solvent use because the ratio
between air and water was not quantified.
3-28
-------
Inventory
Withdrawal
_-
Co
I
NJ
v£>
Gasoline
Imports
Production
-^
Petroleum
^ Petroleum
Refining
ar Gasoline
Gasoline
Transportation
and
Storage
Transportation
and
Storage
7,272
Contaminated
Solvents
Chemical
Feedstock
(97% Destroyed)
Benzene Destroyed
in Combustion
Product
Carryover
10,865
Air/Land/Water
Environmental Releases
V^3^ Coke Production from Coal
Ore/Mineral Mining/Processing
Oil Spills
FIGURE 3-3 MATERIALS BALANCE FOR BENZENE
(Areas are approximately to scale)
-------
In the balance for benzene used as feedstock alone, 121,191 kkg
were unaccounted for. Some portion of this amount is the volume dis-
posed onto land. Thus, environmental releases are slightly under-
estimated. Consequently, in 1978, the total amount of unaccounted
for benzene in the materials balance is 1.1% of the amount used
(11,059,380).
3-30
-------
I
I
REFERENCES
H»dbook.
and eco^ic impact
s
cited in JRB ASSOC.
1980)
r
International; 1979. (As
on
n .
Hillman, M. ; Jenkins, D. • ra n . vr
J. Final report on inal^ oeSlii^/' J Reddy' T« • m,
a ban on consumer products containing i economl= feasibility of
Washington, DC: Consumer Product £? ? P^cent or mor, henzenef
cited in JRB Assoc. 1980) r°duct Safet^ Commission; 1978. (AS
\f jj T* ra O •
Research '
(As cited in JRB Assoc. 1980)
t0 ^-P^Ic benzene.
Protection Agency; 1978.
3-31
-------
Neufeld, L.; Sittenjuld, M.; Henry, R.; Hunsicker, S. Market input/
output studies task: Benzene consumption as a solvent. Washington,
DC: U.S. Environmental Protection Agency, 1978. (As cited in JRB
Assoc. 1978)
PEDCo Environmental, Inc. Atmospheric benzene emissions. Research
Triangle Park, NC: U.S. Environmental Protection Agency; 1977. (As
cited in JRB Assoc. 1980)
Saxton, J.; Narkus-Kramer, M. EPA findings of solid wastes from industrial
chemicals. Chemical Engineering, pp:107-112; April 28, 1975. (As cited
in JRB Assoc. 1978)
Stanford Research Institute (SRI). Assessment of human exposures to
atmospheric benzene. Menlo Park, CA: Stanford Research Institute-
1978.
Stanford Research Institute (SRI). Chemical economics handbook. Menlo
Park, CA: Stanford Research Institute; 1979.
U.S. Department of Energy (U.S. DOE) Crude petroleum, petroleum pro-
ducts, and natural gas liquids: 1978 (final summary). Energy data
reports. Washington, D.C.: U.S. Department of Energy; 1979. (As
cited in JRB Assoc.)
U.S. Environmental Protection Agency (U.S. EPA). Compilation of air
pollutant emission factors. 3rd ed. Research Triangle Park: U.S.
Environmental Protection Agency; 1977. (As cited in JRB Assoc. 1980)
U.S. International Trade Commission (USITC) 1978. Synthetic organic
chemicals, U.S. production and sales; 1975-1979.
Versar, Inc. Determination of sources of selected chemicals in waters
and amounts from these sources: Estimated GAD's for 57 priority pol-
lutants. Springfield, VA: Versar, Inc. 1977. (As cited in JRB
Assoc. 1980)
Walker, P. Air pollution assessment of benzene. McLean, VA: The
Mitre Corporation; 1976.
3-32
-------
I
I
4.0
^ DISTRIBUTION OF BEM»v. n, ^ m,IRON?E?rr
INTRODUCTION
estimated, where possible
environment is described?'
fate °f
th^-f ^ concent rat ions were
distribution of benzene in the
r
human and biotic receptors First ',°Ugh ^e environment to the
and biological characteristics 0?h'/ ^ ** ph^sical> chemical,
and processes that result JntrL sfeToTbf * ^^ ^ pathw
another are analyzed. This \nCTudls °L T&™ ^°m °ne medium to
supplemented by consideration of tJf ! i ??le Partiti°ning" model,
processes. The next stln i* \ ? relative rates of the transfer
as chemical transformation tha°t "a^f6 ^Or fatS P««—-. such
in which benzene is most likejj to residT "L ""^ °f interest
include chemical transformations and MnJl ^ Processes considered
of interest. Cations and biodegradation within the media
to
ns and intramedia
ranges of concentration of benzene in the ^-^ tO estimate Probable
done by calculations involving "sin^/ environmental media. This is
U.S. EPA's EXAMS (Exposure ^alvll^L^^^ m°dels and b? the
step is to summarize^ crUicirL±'lng SySt6m) m0de1' The fin
of the pollutant in environmental ^T7'/^^ °f COncentrations
available monitoring data. ' COI^Pare these with the
ass
of on
not assigned to any mdia
nL^^^ and chemicai
data that are directly re^evt to thV summari"s the physico-
of benzene in the environment /and alStionaf b/3""^111^ and movement
ties of the bulk chemical that may be usi?ul tbaS1C1lnforms^°n on proper-
situations (e.g., spills). X ln eval"atin? particular
4-1
-------
TABLE 4-1. PROPERTIES OF BENZENE RELATED
TO ENVIRONMENTAL DISTRIBUTION
Property
Molecular Formula
Molecular Weight
Melting Point, °C
Boiling Point, °C
Water Solubility, mg/1
Vapor Pressure, Torr
Saturated Vapor -
Concentration, g/ra
Octanol: Water
Partition Coefficient
Sediment: Water
Partition Coefficient (K )
oc
Bioconcentration
Factor (K )
P
Value
C6H6
78.12
5.5
80.1
1800 at 25°C
1780 at 25°C
1750 at 10°C
820 at 22°C
1 at -36.7°C
10 at -11.5°C
40 at 7.6°C
100 at 26.1°C
400 at 60.6°C
760 at 80.1°C
45 at 10°C
95 at 25°C
193 (5.9) at 10°C
407 (12.5) at 25°C
135 at 25°C
74 at 25°C
22 at 25°C
Reference
Weast (1979)
Weast (1979)
Howard and Durkin (1974)
Mackav and Eeinonen (1975)
Mackav and Leinonen (1975)
Chiou et_ al. (1977)
Weast (1979)
Mackay and Leinonen (1975)
Calculated from vapor
pressure
SRI (1980)
SRI (1980)
SRI (1930)
4-2
-------
I
I
f
factor in Table 4-1 SUg", C?!ff"lents,and ""concentration
i" soil, sediment, »r biottc environ™^ ? "^ " Cumulate
or water. environmental compartments than In air
the uuf >. P— ily because of
It al.. 1970). several author! £L noted ^ "^ SyStem : \alr; Traffic count^ were
Ca hlghway). These counts
J«centration8 fall in
69) for ambient
plants, cars)
2 C°ntaillS air
Batta1^ (1979)
°H' Which indi
levels
4-3
-------
TABLE 4-2. LEVELS OF BENZENE IN AIR
Site Description
Mean
Benzene
-o
Urban Locations
Denver, CO 9.6
Houston, TX
Los Angeles Basin, CA 122
Columbus, OH 118
Midtown Intersection 12.3
Highway:
Eastbound (15,769 cars/21* hr) 9.6
Westbound (20,963 cars/24 hr) 23
Residential—24-hour average 5.1
Nighttime (background) 4.5
Gasoline Station Vicinities3
Within 300 m of 4 Stations 3.1
Within 300 m of 2 Stations 2.3
Within 200 m of 1 Station 2.4
Within 200 m (general)
Other Locations
Within 200 m of Rural Gasoline Stations
N.I
CA 21.7
Background - Remote Areas in U.S. 2.2
Edison, NJ, Landfill Site 900,000
Downwind from Landfill
Upwind from Landfill
Range
95.8 max
4-48
64-192
7-412
5.9-21.3
5.6-14.2
13.8-35.9
3.2- 8.1
0.5-13.7
0.9- 4.5
0.6- 5.0
9.6-32
1.3-11.8
trace-300
18 -34
1.0- 3.5
10 -1550
trace- 200
Reference
Ferman et al. (1977)
Bertsch £t al. (1975)
Altshuller and Bellar (J973)
Battelle (1979)
API (1977)
API (1977)
RTI (1977)
RT1 (1977)
Washington State Univ. (1973)
RTI (1976)
RTI (1976)
RTI (1976)
aData from up to seven monitors were included in the average for each site.
-------
I
I
with benzene concentration measurements taken concurrently; the high-
est levels were recorded during morning and evening rush-hour traffic,
and the lowest levels were recorded late at night, during periods of
lox*- traffic density. The eastbound traffic had a lower overall traffic
density (15,769 vehicles/24 hr) and an average benzene level of 9.6
yg/m3. The westbound traffic, with a higher vehicle count (20,963/
24 hr) had a higher average benzene level of 23 yg/m3. Further research
is required to estimate emission rates from traffic of various vehicle
mixtures, road conditions, street grid patterns, and other sources.
Battelle (1979) did not sample the air directly at gasoline ser-
vice stations; however, monitors were placed within 300 m of such sources.
Higher levels were recorded at the intersection with 4 stations (3.1
yg/m ) as compared with intersections with only one or two stations
(2.3-2.4 yg/m3) . This difference is small and cannot be interpreted
without accompanying traffic data. Levels near rural gasoline stations
fall within the same range (1.3-11.8 ug/m3) as does the air in urban
service station vicinities (
-------
TABLE 4-3. LEVELS OF BENZENE IN AIR NEAR CHEMICAL PLANTS AND PETROLEUM REFINERIES
Description
Chemical Plants
Nitrobenzene Plant, WV
N.I, Nitrobenzene
LA, Nitrobenzene
Cumene Plant, PA
Maleic Anhydride Plant, TN
Maleic Anhydride Plant, WVa
N.I, Maleic Anhydride
Detergent Alky late Plant, CA
WV, Detergent Alkylate
Benzene Plant, LA
TX, Ethyl Benzene Styrene
Coke Ovens, PA
LA, Phenol
TX, (Unknown)
Petroleum Refineries'3
Mid-Atlantic
Pacific N.W.
Midwest
Gulf Coast
Missouri
Texas
California
Q
Mean
8.78
8.9
1.9
40.0
23.16
12.5
2.9
6.4
108.6
20.1
44.7
9.3
2.9
2.6
9.6
6.4
<3.2
16.0
230.0
10.9
824.1
Benzene (ug/m-^)
Range Source
1-3-22.4 Battelle (1979)
RTI (1977)
RTI (1977)
3.8-111.2 Battelle (1979)
8.3-52.4 Battelle (1979)
1.0-94.9 Battelle (1979)
RTI (1977)
3.2-9.6 Battelle (1979)
RTI (1977)
1.9-43.1 Battelle (1979)
RTI (1977)
1.3-39.3 Battelle (1979)
RTI (1977)
RTI (1977)
API (1977)
API (1.977)
API (1977)
API (1977)
RTI (1977)
RTI (1977)
RTI (1977)
Near a coking facility and a refinery.
All samples within 1 kilometer of plants.
-------
I
I
TABLE 4-4. LEVELS OF BENZENE IN AIS FOR HIM4N ACTIVITI£S
Type of Industrial Plant
• • ___
Coke Plant with Benzene
Refining
Ethylbenzene Plant
Benzene Recovery Plant
Cumene Plant
— Caustic Addition
Aniline Production
— Benzene Unit
Chlorobenzene Production
Alkyl Benzene Production
Benzene Light Oil Plant
Benzol Plant Operator
Service Stations
Customer Areas
Attendant Areas
Attendant Areas
Attendants - charcoal tube
samples
General Air
Mean
——_—.
Benzene dng/m3>)
2.9
4.2
0.86
0.26
0.26
1.02
0.44
Range
^^~™^ ' —w^Hnw
1.6-96
2.7-10.7
2.7-10.7
0-21.5
5.4-32.2
0.32-1.1
0-483.3
0.54-33.3
1.6 -78.9
2.7-268.5
18-64^
Reference
. —
NIOSH (1974)
NIOSH (1974)
NIOSH (1974)
NIOSH (1974)
NIOSH (1974)
NIOSH (1974)
NIOSH (1974)
NIOSH (1974)
NIOSH (1974)
NIOSH (1974)
NIOSH (1974)
0.38-5.4
0.11-0.39
0.29-0.58
0-5.4
Battelle (1979)
Hartle and Young (1976)
Runion (1977)
0.17-0.66 NIOSH (1974)
aTen minute time-weighted
averages.
4-7
-------
4.3.2.1 Drinking Water
Few data are available on benzene levels in drinking water. It
was identified by the U.S. EPA (1977) in 21.6% of finished drinking
water supplies taken from surface water and in 60% of all supplies
tested (Coniglio et al. 1980). Median benzene concentrations for
all NOMS data were <2 yg/1. A study of priority pollutants in tap
water from St. Louis, Atlanta, Cincinnati, and Hartford revealed no
benzene at detection limits of 1 yg/1 and an estimated recovery factor
of 89% (Levins et al. 1979). The U.S. EPA (1972) found trace amounts
of benzene in finished tap water taken from the Mississippi River.
4.3.2.2 Ambient Water
The U.S. EPA's STORET system includes data from 185 ambient water
quality monitoring stations. As of September 1981, the total number of
samples on record was 889, of which 156 were unremarked. Unremarked data
are those for which an accurate (within the testing equipment limitations)
reading of the concentration is given. These are generally accepted at
face value, while remarked data are regarded as upper limits.
Less than 20% of the samples for ambient benzene fall into the un-
remarked category. The distribution shown in Figure 4-1, is flat up to
100 ug/1, with approximately one-third of the data in each of the concen-
tration ranges: 0-1, 1-10, and 10-100 yg/1. Only 4% of the samples were
above 100 ug/1 and <1% were above 1000 ug/1. The distribution of the
remarked samples is shown in Figure 4-2. Ninety percent of these values
were below 100 yg/1, a result similar to the unremarked data. The skew
in the histogram towards the 1-100 yg/1 range is probably due to a pre-
dominance of benzene tests with detection limits of 10 yg/1 and 100 yg/1.
Table 4-5 records the ambient benzene levels by major water basin.
The median (50% level) values were 10 yg/1 or lower for 15 of the 18
basins, and was 5 yg/1 for the country as a whole. The highest maximum
level recorded was 1260 yg/1, an unremarked value from the California
Basin. Levels above 100 yg/1 were shown in the Ohio River Basin (140
yg/1), the Lake Michigan Basin (310 yg/1) and the Lower Mississippi
Basin (210 yg/1).
This data set offers evidence that levels of benzene in ambient water
is <10 yg/1 -v50% of the time and <100 yg/1 ^95% of the time. Rarely have
levels above 100 yg/1 been documented. The Lake Michigan and Lower
Mississippi Basins are the two showing the highest levels, probably due
to the quantity and type of industrial activity prevalent in these
areas.
Levels of benzene documented for POTW systems in six cities in
Table 4-7 ranged from <1 to 143 yg/1 in influent water. The average
percent removal of benzene during treatment was 90% with 3 of 5 plants
achieving ^100% removal. These data also show that benzene is concen-
4-8
-------
I
I
.2
a
Total Number of Unremarked
Samples » 156
0-0.99
1.0-9.99 10.0-99.99
Concentration Ranges (/ug/£)
100-999.99 > 1000
Total Number of Remarked
Samples = 733
0-0.99
1.0-9.99 10.0-99.99
Concentration Ranges
100-999.99 > 1000
•4-9
-------
TABLE 4-5. CONCENTRATIONS OF BENZENE BY MAJOR BASIN IN 1980
Basin Name
I.
2.
3.
4.
5.
6.
7.
8.
9.
.0.
Northeast
REMa
UNREMb
North Atlantic
REM
UNREM
South East
REM
UNREM
Tennessee River
REM
UNREM
Ohio River
REM
UNREM
Lake Erie
REM
UNREM
Upper Mississippi
REM
UNREM
Lake Michigan
REM
UNREM
Missouri River
REM
UNREM
Lower Mississippi
REM
UNREM
No. of
Samples
1
0
36
6
13
10
49
4
27
7
9
0
11
0
9
5
32
0
16
16
Mean
Concentration
(ug/1)
10.0
0.0
0.9
6.5
0.0
6.5
12.5
9.4
51.0
10.0
46.4
5.9
187.2
50.0
4.0
67.7
Median Maximum
Concentration Concentration
(ug/1)
10.0
0.0
0.7
7.5
0.0
5.0
13.0
10.0
15.0
10.0
50.0
5.0
220.0
50.0
5.0
60.0
(ug/1)
10.0
0.0
2.5
10.0
0.0
1 10.0
17.0
10.0
140.0
10.0
50.0
10.0
310.0
50.0
5.0
210.0
REM = Remarked Samples
3UNREM = Unremarked Samples
4-10
-------
1
1
TABLE 4-5. CONCENTRATIONS OF BENZENE BY MAJOR BASIN IN 1980 (Continued)
No. of Mean
Basin Name Samples Concentration
11.
12.
13.
14.
15.
16.
17.
18.
19.
Colorado River
REM
UNREM
Western Gulf
REM
UNREM
Pacific Northwest
REM
UNREM
California
REM
UNREM
Great Basin
REM
UNREM
Lake Huron
REM
UNREM
Lake Superior
REM
UNREM
Hudson Bay
REM
UNREM
United States0
REM
UNREM
(ug/1)
43 8.8
0
18 10.0
0
13 0.0
0
34 5.1
49 57.8
4 10.0
0
11 10.0
0
5 10.0
0
4 0.0
0
677 18.9
129 46.1
Median Maximum
Concentration Concentration
(ug/D (ug/1)
10.0 10.0
10.0 10.0
o.o _ o.o
5.0 10.0
6.0 1260.0
10.0 10.0
10.0 10.0
10.0 10.0
o.o o.o
5.0 100.0
6.8 1260.0
"All samples, 1978-1981
4-11
-------
TABLE 4-6. LEVELS OF BENZENE IN WATER NEAR AND IN EFFLUENTS FROM CHEMICAL PLANTS
I
M
NJ
.Sample Site Description Heau
Water Near Discharges
Ohio R. - Nitrobenzene Plant -downstream 4.1
Nitrobenzene Plant - upstream 12
Cumene Plant - PA 1.4
Maleic Anhydride Plant, TX - upstream <1
Anhydride Plant, TX - downstream 2
Detergent Alkylate Plant, CA
-------
I
I
TABLE 4-7. LEVELS OF BENZENE IN
POTW SAMPLING DATA
Cities
Indianapolis, IN
Cincinnati, OH
Atlanta, GA
St. Louis, MQ
Pottstown, PA
Grand Rapids, MI
Benzene (yg/1)
Primary Secondary Final
fluent .. Sludge _Sludge Effluent;
143
10
Source: Burns and Roe (1979).
Digested sludge.
171
1
10
(1)3
(1)3
33 c
(20)
40 c
Removal
98
70
4-13
-------
Crated in sludge. The levels in secondary or biologically active
sludge are somewhat lower than in the primary (physically settled)
and combined sludges, which may indicate removal of benzene by volatil-
ization during aeration or by acclimated bacteria (biodegradation).
The Versar, Inc. (1978) data in Table 4-6 also show this pattern.
In Table 4-8, the results of an Arthur D. Little, Inc., (Levins
et_ al. 1979) study of wastewaters from various socioeconomic sectors
of four cities are shown. Sewage from commercial neighborhoods
averaged to 2.7 yg/1, industrial sewage was about 1.3 ug/1, while
residential sewage contained close to no benzene at all. In all
four cities tested, no benzene was detected in the tap water.
4.3.3 Soil
Very few data were available on benzene levels in soils. Levels
ranging from 13 to 115 ug/kg were reported in soil samples taken in
the vicinity of chemical plants (see Table 4-9) that produce or use
benzene (Battelle 1979). No background data have been found.
4.3.4 Food
Benzene has been detected in fruits, nuts, vegetables, dairy pro-
ducts, meat, poultry, eggs, fish, and several beverages (see Table 4-
10). It is theorized that it occurs naturally, possibly as a flavor
component in all of these foods. Only a small number of these foods
has been analyzed quantitatively. Eggs have the highest concentrations
(500-1900 ug/kg), followed by haddock (100-200 ug/kg) and Jamaican
rum (120 ug/kg). Butter, beef, lamb, mutton, veal, and chicken have
<10 ug/kg benzene levels (when the meats are cooked). It is postulated
that the increase in benzene levels observed following cooking meats
is due to the breakdown of aromatic amino acids.
Total dietary intake is estimated conservatively at about 250 ug ben-
zene/day (NCI 1977) (as used, conservative implies a high value).
4.3.5 Summary
Concentrations of benzene in the air, water, and soil are higher
in close proximity to sources. Occupational levels of benzene in air
are the highest observed for that medium, while chemical plant and
refinery discharges contain the highest recorded aqueous benzene
levels. As the distance increases from the benzene source, concen-
trations decrease to levels <1 yg/1 in water and 1.0 ug/m in air;
"clean" soil levels have not yet been documented.
4.4 ENVIRONMENTAL FATE MODELING
4.4.1 Equilibrium Partitioning
As an initial step in hazard or risk assessments for toxic chem-
icals, in the planning of laboratory and field tests, and in the inter-
4-14
-------
I
I
TABLE 4-8. LEVELS OF BENZENE IN INFLUENTS TO SEWAGE TREATMENT PLANTS
Benzene (ug/1)
Cities
Cincinnati, OH
St. Louis, MO
Atlanta, GA
Hartford, CT
Tap Type of Neighborhood
Water Residential Commercial Industrial Influent
0 .15
0 .8
0 0
0 0
5.4
2.8
0.43
2.1
a
1.3
1.2
a
3.
7.
0
0
7
0
Source: Levins et al. (1979).
iflot sampled for this city.
4-15
-------
TABLE 4-9. LEVELS OF BENZENE IN SOIL NEAR CHEMICAL PLANTS
Description
Benzene (pg/kg)
Mean
Range
Reference
Nitrobenzene Plant, WV
Cumene Plant, PA
Maleic Anhydride Plant, TX
Detergent Alkylate Plant, CA
Benzene Plant
37.3
22
115
13
2-51
18-73
51-191
12-14
Battelle (1979)
Battelle (1979)
Battelle (1979)
Battelle (1979)
Battelle (1979)
-------
I
I
TABLE 4-10. FOODS REPORTED TO CONTAIN BENZENE
Fruits
Apple
Citrus Fruits
Cranberry and Bilberry
Currants
Guava
Pineapple
Strawberry
Tomato
Nuts
Filbert (roasted)
Peanut (roasted)
Macademia Nut
Vegetables
Beans
Leek
Mushroom
Onion (roasted)
Parsley
Potato
Soya Bean
Trassi (cooked)
Dairy Products
Butter (0.5)D
!?-eu Cheese
Cheddar Cheese
Other Cheese
Meat, Fish and
Bfief (cooked) (2 to 19) c
Chicken (<10)d
EgS (hard boiled) (500 to
1900) e
Haddock (100 to 200) f "
Lamb (heated) (<10)d
Mutton (heated) (<10)d
Veal (heated) (<10)d
Beverages
Cocoa
Coffee
Jamaican Rum (120) s
Tea
Whiskey
Siek and Lindsay (1970).
Rational Cancer Institute (1977).
Merrit (1972).
"MacLeod (1977); MacLeod and Cave (1976).
glrradiated and nonirradiated haddock, respectively.
Liebich et al. 1970.
4-17
-------
pretation of monitoring data, rough estimates of the pollutant's
environmental distribution can often be made by simple inspection
of the chemical's properties. Mackay (1979) proposed a simple
approach based on the fact that the fugacity of the pollutant must
be the same in all phases when the system is in equilibrium.
The approach proposed by Mackay (1979) is a three-tiered approach.
In Level I (the approach used here), all environmental compartments
(phases) are assumed to be directly or indirectly connected and at
equilibrium. The compartments considered are air, surface water,
suspended sediments, bottom sediments, soil and aquatic biota. The
Level I calculations require that these compartments be roughly des-
cribed (volumes, temperature, sediment and biota "concentrations,"
etc.). It is clear that the model output depends on the nature of the
"environment" selected. The compartment-specific parameters chosen
here (somewhat arbitrarily) are listed in Table 4-11. A schematic
diagram of the selected environment is shown in Figure 4-3. The Level
I calculations do not consider degradation, or transport into ar out
of the selected environment. A relatively small number of chemical-
specific parameters (see Table 4-11) are required for equilibrium
partitioning. To obtain an absolute estimate of the equilibrium con-
centrations in each phase, it is necessary to estimate the total
amount of the chemical that is likely to be in the selected environ-
ment.1 The amount here is 30 mole/km , or 30 moles-in the environ-
mental compartment here with a surface area of 1 km. This amount
is equivalent to the U.S. environmental losses over a 15-day period,
divided by the area of the 48 contiguous states. Implicit in the
selection of this quantity is an assumed atmospheric half-life (re-
sulting from oxidative destruction) of about 2 days in urban environ-
ments or 20.days in rural areas. Thus, a value of 15 day's loading
was selected as a reasonable estimate of the environmental burden.
Mackay (1979) provides details of the calculation methods; thus,
they are not repeated here. The results are presented in Table 4-12.
When the percentage distribution of the benzene across compartments
is considered, it is obvious that the high volatility of benzene domi-
nates the environmental partitioning for the Mackay model. More than
99.9% of the chemical is predicted to be in the air medium at equili-
brium. Water and soil account for 0.02 and 0.03%, respectively, of
the benzene loading at equilibrium. The Mackay approach predicts that
only very small fractions of the total mass of benzene will be distri-
buted in the sediments or the biota.
A slightly different perspective is obtained by considering the
concentrations, rather than the total mass loadings, in the environ-
mental media. For the arbitrary but not unreasonable, compartment-
":Jote that predicted ratios of concentrations between two phases will
not be affected by the number selected.
4-18
-------
I
I
TABLE 4-11.
VALUES OF THE PARAMETERS USED FOR TFVFT T
Solubility (mg/L):
Vapor pressure (torr)
Adsorption coefficient (K ) for-
p
Suspended sediments
Sediments
Soils
1800
95
3.0
3.0
0
. ,
.7 I
Assuming 4% organic carbon
in sediments and 1% organic
carbon in soils
Octanol/water partition coefficient 135
(Used for estimating a bioconcentration factor for aquatic biota.)
Total amount of chemical in compartment: 30 moles/km2
(Equivalent to total U.S. environmental losses over a 15-dav period
divxded by the area of 48 contiguous states ) '
Temperature: 25°
Concentrations (S) of suspended sediments: 10g/m3
Concentrations (S) of soils and sediments: 2 x 106 g/m3
Volume fraction (B) of aquatic biota: 50 x 10'6 m3/m3
Fraction (y) of aquatic biota equivalent to octanol: 0 2
Accessible volume for each subcompartment:
Alr Ikmxlkmx3km (high)
Surface Water 1 km x 0.05 km x 3m (deep) =
Sediments 1 km x 0.05 km x 10 cm (deep)
Soils
Note;
3 x 109 m3
1.5 x 105 m3
5 x 103 m3
1 km x 0.95 km x 14 cm (deep) = 1.3 x 105 m3
as the surface »ater
vollme"
to
4-19
-------
Atmosphere
'Soil
. Surface Water
Aquatic Biota and
Suspended Solids
"Bottom Sediments
Note: Diagram is not to scale. Dimensions and accessible volumes
of each subcompartment given in Table 4—11.
Source: Based on Mackay (1979).
FIGURE 4-3 SCHEMATIC OF ENVIRONMENTAL COMPARTMENT SELECTED
FOR ESTIMATION OF EQUILIBRIUM PARTITIONING OF BENZENE
4-20
-------
TABLE 4-12. EQUILIBRIUM PARTITIONING OF BENZENE CALCULATED USING MACKAY'S FUGACITY METHOD
I
NJ
Compartments
Air
.
40
185
3 x 109 ra3
1.5 x 105 m3
2.5 x 10
2.5 x 10
Suspended Sediment 5.5 x 10~3 1.5 x 105 m3 2.5 x 10~10
Sediment
Aquatic Biota
Soil
Assumptions
1.1 x 10
5 x 10
2.5 x 10"1 1.5 x 105
2.7 x 102 1.3 x 105
K
2.5 x 10
2.5 x 10
2.5 x 10
-10
(moles)
30
7 x 10" 3
2 x 10~7
1.3 x 10"
8 x 10~6
8 x 10~3
oc
0.78 ug/m
0.0036 ug/1
0.010 ug/kg
0.010 ug/kg
0.083 ug/kg
0.0024 ug/kg
= 78
% of Total
Loading
99.94
0.02
0.004
0.03
3
H - 229 (ug/m )/(ug/l) KQW = 135 (ug/1) /(ug/1) total benzene loading = 30 mol/km2
Suspended solids at 4% organic carbon content; concentration, 10 g/m3
Sediments
Soil
Biota
Definitions
at 4% organic carbon content; concentration, 2 x 106 g/m3
at 1% organic carbon content; concentration, 2 x 106 g/m3
20% equivalent to octanol; volume fraction 50 x 10~6 m3/m3
Z± - fugacJty capacity constant for benzene in compartment i.
V^^ = effective accessible volume of compartment i.
fi - fugacity of benzene in compartment i. At equilibrium, fugacify in all compartments must be equal.
MI - moles of benzene in compartment i.
C^ = concentration of benzene in compartment i.
-------
specific parameters selected for this calculation, the water medium
has an estimated concentration of 0.0036 ug/1. The equilibrium con-
centration in the air is calculated to be 0.7 yg/m3 of benzene. Con-
centrations in the suspended and bottom sediments are calculated to
be 0.01 yg/kg, about three times higher than those in the water.
The calculated soil concentration is 0.0024 yg/kg; this is lower than
for sediments because of the lower assumed carbon content of soil in
this model. The concentration in aquatic biota was calculated to be
0.083 ug/kg of biomass, which illustrates benzene's moderate tendency
to bioaccumulate.
4.4.2 EXAMS Modelling
The U.S. EPA's Exposure Analysis Modelling System (EXAMS) program
is one approach to the integration of various intermedia transfer and
intramedium transformation processes. The EXAMS model considers
physical constants and reaction rate data for the chemical and the
properties of typical and/or highly specific environments.
The environmental fate of benzene was modeled using four EXAMS
scenarios: a "clean" river, a turbid river, an oligotrophic lake,
and a eutrophic lake. Three loading rates were selected as inputs to
EXAMS. The highest was 3.5 kg/hr based on a maximum effluent level
measured for benzene at a petroleum refinery. The lowest rate was
0.002 kg/hr, which is also an effluent concentration for a refinery.
The third rate, 0.03 kg/hr, was representative of benzene concentra-
tions in both the textile industry and a small-scale coal-derived
benzene production plant. This latter rate only was applied to all
four scenarios. The extreme rates were only used for the riverine
scenarios as the likely receiving water bodies. The results of the
extreme inputs are given in Appendix B. (The results will scale
directly with the loading rate until/unless the water solubility is
exceeded or some other environmental compartment saturates.) The
fundamental difference between the river and lake scenarios is that
the former are flowing systems so that downstream transport/dispersal
appears as a major fate process. The turbid river has a fivefold
higher level of suspended sediment than the "clean" river.
The eutrophic lake differs from its "clean" counterpart in that it
has much higher (three orders of magnitude) bacterial populations, as
well as somewhat higher levels of sediment.
Schematic summaries of the results using EXAMS for these four
scenarios are presented in Figures 4-4 through 4-7. In the river
systems, downstream export appears as the dominant fate process and
as 95.2% of the load. Volatilization is also a significant transport
process, accounting for loss of 1.7% of the load within the ^ 20-
minute residence time of the river "slice" (see Figures 4-4 through
4-7). In the oligotrophic lake system, the relative importance of
export and volatilization are reversed; volatilization accounts for
95% of the load and export for approximately 4%. In the eutrophic
4-22
-------
I
I
FIGUK 4-4'
Ecosystem: Turbid
EXPORT TO AIR
Volatilization Rate:
Percent of Load:
INPUT
••—•«_
Mass Flux 0.03 |
-------
'3-
Ecosystem: River; Benzene
EXPORT TO AIR
Volatilization Rate: j ' 0.519 q/hr
Percent of Loac
INPUT
Mass Flux 0.03 kg/hr
WATER COLUMN
Average Concentration: ug/l
Maximum Concentration: ug/l
Steady-state Accumulation:
Persistence3:
BOTTOM SEDIMENTS
Average Concentration :yg/kg
Maximum Concentration:ug/kg
Steady- state Accumulation:
Persistence2:
1: 1.73 %
0.029
0.0295
99.4 %
0 %
:•':•':•:•:•:•: o.oos :/>:•:•:•:
vXvX 0.016 VA::V:
:::-:-x-> 0.6 %:•>:•>:•:•
yviw 92.7 %;:-:-v:v
X'1'X'I'X'l'X'X'X'X'X'X'.'v'''"'''''''"
System Self Purification Time: 3.326 hour
EXPORT: DOWNSTREAM ADVECTION
Mass Flux 0.028
Percent of Load:
BIODEGRADATION BY
BACTERIA
Mass Flux 0.00092
Percent of Load:
BIODEGRADATION BY
BACTERIA
Mass Flux 0
Percent of Load:
kg/hr
95.2 %
WATER COLUMN
kg/hr
3.07 *
BOTTOM SEDIMEM
kg/hr
0 %
Bioabsorbtion: Plankton; 6.6 x 10"A ug/g; Benthos: 6.8 x 1Q~5
aThe percent of the pollutant remaining in that medium 12 hours
after loading ceases.
4-24
-------
I
I
EXPORT TO AIR
Volatilization Rate:
Percent of Load:
INPUT
•—
Mass Flux 0.03 kg/hr
WATER COLUMN
Average Concentration: g
Maximum Concentration-ug/l
Steady-state Accumulation:
Persistence3:
BOTTOM SEDIMENTS
Average Concentration:pg/kg
Maximum Concentration: ug/kg
Steady-state Accumulation-
Persistence*:
0.0286
95.32
kg/hr
%
DOWNSTREAM ADVECTION
• -^
Mass Flux 0.0013 kg/hr
Percent of Load: 4.33 %
Mass Flux O.OQQl
99.98
28.21
Percent of Load: 0.35
BY BOTTOM SEDIMENT
Percent of Load: 0
System Self Purification Time:_ 65.7 days
8,9 x 10-2 yg/g; Benthos:
12 hours
4-25
-------
FIGURE 4-7. RESULTS OF EXAMS MODELING OF THE ENVIRONMENTAL F^TE
OF BENZENE IN A EUTROPHIC LAKE
Ecosystem: Eutrophic Lake: Benzene
EXPORT TO AIR
Volatilization Rate: J l 6.6 x 10~5 kq/hr
Percent of Load: 5.31 %
INPUT
Mass Flux 0.03 kg/hr
WATER COLUMN
Average Concentration: ug/l
Maximum Concentration: us/1
Steady-state Accumulation:
Persistence3:
BOTTOM SEDIMENTS
Average Concentration: ^g/kg
Maximum Concentration: ug/kg
Steady-state Accumulation:
Persistence3:
0.22
0.82
99.92 %
63.3 %
.v.v.v. 0 . 02 v.v.v.
XvIvX 0.05 vXvX
•XvXv 0.08 ZXvXv
XvXv 7.8 %vXvX
X;XyXyXvX':vlvXv:X;X;Xv:v:;
System Self Purification Time: 41.9 hours
EXPORT: DOWNSTREAM ADVECTION
Mass Flux 3.lxlo~7kq/hr
Percent of Load:.
BIODEGRADATION BY
BACTERIA
Mass Flux .0012
Percent of Load:
BIODEGRADATION BY
BACTERIA
Mass Flux 0
Percent of Load:
0.02 %
WATER COLUMN
kg/hr
94.66 %
BOTTOM S EDI MEN'
kg/hr
0 %
Bioabsorbtion: Plankton: 1.8 x 10"2 ug/g; Benthos: 3.6 x 10~4 ug/%
aThe percent of the pollutant remaining in that medium 12 hours
after loading ceases.
4-26
-------
I
I
C5.
„.
cally, one might exp to fd the r
tnan the 10-7 biodegradation rate esti^^ ;°r °f 10 to 10
calculation. If the biolysis «* "*»«« "=ed in the basic EXAMS
then EMS would predict tha? 8lf JT ^ 1S °n the ord« ^ W9.
and. 15X will biodegrade ta a eue^onhif ? J°CalTben2me »«! volatilLe
be determined prtafrily b^ environment all!'f In ^ rlver' rei»oval
and voUtilization thedoLant r™o^l process's."""
betwer^te ^tdi^nts^is^JucTt'h^^
water column and < u in the bott^ sedL^ts
and
ls in the
vdatili.ati
to about 27 days' total loadSg fato I!?S" 3^ *" e
ether aquatic compartments for all scInLiof rt V°lume' In a11
benzene concentration is <1 Ug/l scana"os, the maximum calculated
<••<>. 3 Intermedia Transfers
F"" Air Medium to Surface ».,.... -
sure of benzene is
chemical will have a strong
a vapor. Dry deposition 2 not
F"r^ermore. ^ vapor pre-
" S° that thls
atI°OSPhere as
out asrraem:v2^:nrisS:1m1yilb1r.e1sur
benzene removed by this process is small
woarlt °f
transfer0
-
rain and
rainout of benzene
"
, benzene
aan
4-27
-------
TABLE 4-13. HALF-LIVES FOR TRANSFORMATION AND TRANSPORT OF
BENZENE FOR SEVERAL EXAMS SCENARIOS
Half-life (hr)
River Lake
Clean Turbid Oligotrophic Eutrophic
Bacterial Degradation
Water column 20 20 66,000 7.9
Bottom sediments 280 91 109,000 140
Volatilization 35 35 240 140
Uaterfaorne 0,6 0.6 5,400 30,000
Total Transformation
and Transport 0.6 0.6 230 7.5
Source: Arthur D. Little, Inc.
4-28
-------
I
I
FOR
iMaximum ConcentraM™..
in Water Column, g/i
in Plankton, g/i
in Benthic Organisms, g/g
in Bottom Sediments, g/fcg
Total Steady State Accum-
Benzene 0.03 kg/hr Input
0-03 0.03
0.0007 0.0007
0.00007 0.00007
0-016 0.006
Eutrophic
4
.09
.001
0.21
0.8
0.02
0.0004
0.05
kg
% in Water Column
% in Bottom Sediments
Persistence
Recovery Period , hra
* of Initial Benzene
Burden Lost from:
Water Column
Bottom Sediments
0-026 0.026
99.39 99.80
0-61 0.20
12
12
10
99.98
0.02
0.32
99.92
0.08
576
12
100
7.3
100
17
72
61
63
7.8
Time after loading
of persist^.
£or
Source: Arthur D. Little, Inc.
E™'
cn
4-29
-------
These calculations do not determine a rate for benzene rainout,
rather, they determine the percentage of benzene in the atmosphere that
could reach the surface as a result of rainout during a specific
rainfall event. Thus, monitoring data for atmospheric benzene at a
given location were used along with rainfall data for that same loca-
tion. Although the concentration of benzene in the atmosphere as well
as the amount of rainfall in each event may fluctuate, this approach
will indicate the significance of rainout as a removal mechanism.
No data are available on the concentration of benzene in rain, so
the equilibrium partitioning cannot be determined from actual concen-
tration data. However, the concentration of benzene in the rain can
be estimated if the concentration in the air is known and if the Henry's
Law constant is either known or calculable. Unless the benzene con-
taminated air is confined to a low altitude, the droplets and the
contaminated air can be expected to reach equilibrium. In the case of
a confined "dirty" air mass, raindrops falling through the mass would
have insufficient time to reach equilibrium; thus, they could not contribute
to rainout. Assuming that equilibrium may be attained, the concentration
of benzene in rain can be estimated by the following expression:
C a HC
air rain Eq. 4.4-1
where H is the Henry's Law constant, Cair is the concentration of ben-
zene in the air, and Crain is the concentration of benzene in rain.
H may be written in a nondimensional form:
H - /PA /M \ /Pair\ » 0.24 for benzene Eq. 4.4-2
where: Pr = vapor pressure of benzene = 0.125 atm
Pt = partial pressure of air = 1 atm
M = molecular weight of benzene = 78.1 (g/mole)
29 = "molecular weight" of air (g/mole)
Pair = density of air 1.29 g/1 (1.29 kg/m3)
Xg = solubility of benzene = 1.78 g/1
Using this estimate of the Henry's Law constant, the rainfall concentra-
tion of benzene can be estimated for any given air concentration of
benzene.
Riverside, California was selected for this example. Because of
benzene producing petroleum plants nearby in El Segundo and a high
4-30
-------
I
I
volume of vehicles on the road in this portion of California (see
Chapter 3.0) , a detectable concentration of benzene will exist in the
air. Monitoring data have shown ambient air concentrations of benzene
of 25.5 yg/nr3. Using Equation 4.4-1, the corresponding rain concentra-
tion of benzene is calculated to be 0.1 ug/i. Assuming an annual
precipitation in Riverside of 0.51 m with an annual average of 65 rain-
fall events (days), then the average rainfall event is 7.85 x 10~3 m.
Using the above variables, the quantity of benzene lost from the atmos-
phere via rain can be calculated.
Let Tr = quantity of benzene lost from the atmosphere (yg/m2)
crain ~ concentration of benzene in the rain (ug/m3)
Mpa = quantity of average rainfall event (m)
such that Tr = Crain Mpa Eq. 4.4-3
For this example, Tr = 0.83 yg/m2. To place rainout in perspective,
the percentage of atmospheric benzene released during rainout was
determined. i
Monitoring data show the benzene concentration to be 25.5 yg/m3 in
air. If the mixing depth is 1 kilometer, then the amount of benzene in
the air is about 25.5xl03 yg/m2. Rainout decreases the amount of ben-
zene in the air by 0.83 yg/m2, which is much less than 1% of the total.
Therefore, the role of rainout in reducing atmospheric benzene is slight
Most atmospheric benzene remains in the air where its ultimate fate is
determined by intramedia processes.
4-4.3.2 Intermedia Transfers from Water Medium
Water to Air
Volatilization is an important process in the depletion of benzene
from water. Benzene emitted to the water compartment either by direct
entry or by chemical process is decreased because of benzene's hi^h
volatility. °
The half-life for volatilization of benzene in water depends on
both physical and chemical parameters. Physical parameters describe
the physical properties of the given scenario, such as the depth of the
water body (D), the wind speed (Vw), and the current speed (Vc). The
chemical parameters are the liquid-phase exchange coefficient (k^) , the
gas phase exchange coefficient (k ) , the. liquid phase mass transfer
(KL), the molecular weight (M), and the nondimensional Henry's Law
constant (H).
If values are assumed for the physical parameters such as,
4-31
-------
Vw - 2 m/s
Vc - 1 m/s
D « 1 m
(values for Vw are from Battelle 1979, V is from Mackay and Leinonen
1975, Vc is assumed) then the chemical parameters can be estimated
using the following equations from Southworth (1979);
.. 0.969 n „. .
fcl " 23-51 (Ic ) V327M e°'526 (V* ' 1-9) = 16 CTn/hr
D0.673
kg = 1137.5 (Vw + vc) VIsTM - 1639 cm/hr
H k k.
Using the value of the liquid phase mass transfers, kT , the half-life
is estimated to be: L
t1/2 - 0.693 D/kL = 4.6 hr.
Given that the half-life is 4.6 hours and the current velocity, Vc, is
1 m/s, then the distance downstream the water would flow before 50% of
the benzene had volatilized would be:
Distance Downstream = t1/2 (hr) x Vc(m/s) x 3600 (s/hr)
= 16,560 m.
In addition to volatilization, benzene in the water segment will
be diffused throughout the water column and will be adsorbed by the
sediment and aquatic organisms. The EXAMS model accounts for the
benzene that will be both volatilized and diffused. Therefore, from
the output of the EXAMS model, downstream distances can be calculated
that estimate the distance the benzene in the water segment would flow
until some percentage of the load has either evaporated or been adsorbed
by sediments and organisms.
For all the scenarios used in the EXAMS model, the current velocity
is 0.93 m/sec, the depth of the water column is 3 meters, the width and
length of the water column are 100 and 1000 meters, respectively, and the
water flow rate is 2.41 x 107 m3/day. In both turbid and clean rivers, 95.2%
of the benzene in the original flux into the river segment analyzed is'
passed onto the next segment, 1.73% volatilizes, and 3.07% is biodegraded.
The physical representation of an EXAMS river allows the use of an
exponential decay function to solve for the number of river segments
4-32
-------
I
The calculation is:
(mass flux % to next river segment)"
0.01
n log (0.952) = log 0.01
n = 93.62.
M™« I lsunecess*ry for this 99% r
tions show that a reduction of 50% of
over a river stretch of '' ~
distances downstream at
Water to Soil
y Of 0.93 m/sec,
tJ°i°?CUJ- Slniilar Cal
76 > °3d °CCUrs ln" 4'2
to the
on the organic content d the porsi
adsorption for additions! inforSn o
°n
ntermedia Transfers fro^ Soil Medim
Soil to Water
The
suggests
v-ffl iaa i,-""~" —- uj. oenzene from the
via leaching or to surface water via runoff
mental fate process. °"
for benzene
C° gr°und wate-
important environ
4-33
-------
I
l*J
-C-
tt
o
100
90
80
70
60
50
-------
I
I
The partition coefficient is given by:
'r -ben2ene in soil \ /
benzene in water/ X If
~~~"™*v^u W J. t d^J
tratiorls are given in ug/kg of
tent were equilibrated'wirt ™~S ** SOXl With 1% °rganic carbon con-
and the act^a! ben^e* ^ oadinVS b*' """""-^ of be^ane
higher in the an«e«,« ^u.__ ., s would be approximatelv 1.1 +-;^~
ss oaing woud
higher in the aqueous phase than 2 the soil ^pro^a^y 1-3 times
°f
dominant fate
ol
reasons. First, it is not powlblJ% -f enera11^ feasible for two
(runoff or leachate) th* ^ ^ d reJli^L^llfbf ! ^T °f Wat"Sr
any given quantity of soil in thlf • assumed to contact
mass loading of bLzene in the two ^iT"6"' I""' ^ ^"""rium
though the ratios of concentration. t* 1™°* b& calculated, even
Second, this intermedia tracer in th°e ^ 6stimated from Koc.
across the solid-liquid pha^e xnt efface ^^f inV°1VeS t?ansP°«
as well as equilibrium phenomena Sf% ? affe^ed by kinetic
of equilibrium steady sSte^So^ve? i^rC^ulat:lon ±S m ^icatlon
possible rate of transfer procH! I ? V " n0 information on the
significance of soil-to-w P^g estimates of the
°
^ ^^oSs1;^^^." > « — »^
a mBinal amount of benzena sorted to soUrt ?j ^° reSiSt des°'P"
They found soil benzene to b. "M.J? ? 7Uld be losc to "ater."
their »ork covers M."tJ^ ^j*^ ^^.r"*1- alth°U8h
their work covers
Soil to Air
-
stant as follows: constant and the soil adsorption con-
4-35
-------
H
Csoil
^ - = Koc X fraction o.c. in soil
water
Csoil Koc X fraction °'c- in soil "Vol.
For benzene, assuming a typical soil organic carbon content of 1%,
an H value of 229 (see Table 4-12) and a KQC value of 74 (see Table 4-1)
K , is numerically equal to:
K - 229 _ o mg/m3 in air
vol 74 X 0.01 " mg/kg in soil.
This indicates a strong driving force for volatilization of benzene
from surface soil.
A soil concentration of 25 mg/kg in soil, which is within the
range observed in the vicinity of chemical plants (see Section 3.2),
corresponds to a calculated equilibrium air concentration of 7800
mg/m3 or about 8 g/m3. This value is considerably higher than the
1-100 ug/m3 benzene concentrations reported for air samples in the
vicinity of chemical plants (see Table 4-3). It is, however, greater
than the maximum air level recorded above a landfill site of 900 mg/m3.
Because the levels of benzene within the wastes or soils at this land-
fill were not documented, the 900 mg/m3 may be representative of the
local equilibrium conditions. Downwind levels from this site were
between 0.01 and 1.55 mg/m3 demonstrating dispersion effects while
upwind levels (possibly indicative of diffusion effects) were measured
at trace to 0.2 mg/m3. These results are consistent with the expecta-
tion that "equilibrium" concentrations would not be typical except in a
shallow layer of air near the soil surface. Dispersion and diffusion
would rapidly reduce benzene concentrations by several orders of magni-
tude.
4.4.4 Intramedia Fate Processes
4.4.4.1 Air
The predominant fate process within the air medium are dispersion
and reaction with hydroxyl radical.
Dispersion
A model for the atmospheric dispersion of benzene by Youngblood of
the U.S. EPA has been reported in a recent U.S. EPA document on human
exposure to benzene (Mara and Lee 1978). Youngblood's modeling effort
was based on D. B. Turner's (1970) modeling techniques from which ground-
4-36
-------
I
to 20 kilometers from the Source were derived h sances «P
rate (100 g/s) and by assuming a fm/s wlnTf Y^"8 a fixed emission
class. Excerpts of the resultVof
Chemical Manufacturin
as
uton ch
of benzene consumption in the che™v ? chemlcals- To assess the impact
concentrations in'th atmosphere a SiT**"™** ±ndust^ on ^nzene
used. Because the height of the'source TJ*" m°del (Turner 1970) was
representative heigfats^er chosen The ^ v««* . ""ong plants, three
were: A, ground-level (effective st Jk h! ^ «"«aion source heights
(effective stack height = 10 m) a^d C ^§ \ T ° m)' B' bui^g level
stack height = 20 m) For cafcil^ i 1 "T" ^ (effective
source, the results from fuSir's^SSo^lJSf bU,ildlng hSight
'' ^
population denstta (ara «PWw"r™r ^ leaSt " haVe lw
annual average would bTSo n»/3 W°"ld.be twice a« great while the
°
plants show concentrations of benzene wit-h-r -i i
from 1.6 to 186.4 ,g/m3 (RT? 1977) TH , °f the Plant to ran§e
using Turner's point ^n,,^ V annual average concentration
concentration actu^Lrobserve1^"31011 m°de1' ^ Within ™ <* *•
Coke Ovens and Petroleum Refineries
and
area of the emissTonnourc^^Unlikrthe chf aC^ts for the la^ge
emissions from coke ovens and petr 1 £hemical Pla*t example above,
to a single point source, but rather^Ln!^^63 3r6 n0t restricted
cx°oala"o^%:n;rLo«-~ SmPeT:Lt,s^ng
used the Point, Area and Line So r ^Sr ? release» Youngblood (1977)
Peterson 1975). For coke rt,«nc I ,. U Dispersion Model (Turner and
model inlcude: operations, the assumptions used for this
• Benzene emissions occur mostly from oven leaks,
• The plant site is square,
-------
.e-
oo
TABLE 4-15. ROUGH ESTIMATES OF AMBIENT CROUND-LEVEL BENZENE CONCENTRATIONS (8-HOUR)
AVERAGE3 PER 100 g/s EMISSION RATE FROM A CHEMICAL MANUFACTURING PLANT
Source
Category
0.15
km
A 51,000
B . 11,000
C 510
3
Benzene (pg/m )
0.3
km
14,000
6,100
3,500
0.45
km
7,000
3,800
3,500
0.6
km
4,500
2,800
2,800
0.75
km
3,000
2,100
2,100
1.6
km
900
740
800
2.5
km
440
370
410
4.0
km
220
220
220
6.0
km
120
120
120
9.0
km
62
62
62
14.0
km
34
34
34
20.0
km
20
20
20
To give rough estimates of annual average concentrations, multiply by 0.04,
Source: Youngblood (1977).
-------
I
I
A - Ground-Level Source
B — Building Source
C - Elevated Source
M - Average of Curves A, 8. and C
0.1
Distance from Source — km
Source: Youngblood (1977)./
Based on an emission rate of 100 grams
FIGURE 4-9 DISPERSION MODELING RESULTS FOR EACH
TYPE OF SOURCE CATEGORY3
4-39
-------
• The emissions are uniformly distributed throughout the
specified area,
• Effective stack height = 10 meters,
• Wind speed = 4 m/s,
• Stability class = neutral, and
• Emissions rate = 100 g/s. (This is an unusually high rate.
Most coke-oven operations and petroleum refineries have
emission rates less than 10 g/s.)
The concentration of benzene at gradual distances from plants of
varying areas is shown in Table 4-16. For the smallest plant, the con-
centration ranges from 20 yg/m3 at 20 km from the source to 5000 yg/m3
at only 0.3 km from the source. The larger plants show smaller concen-
trations at corresponding distances outside their boundaries, which
would be expected because the plant size has increased while the emis-
sion rate has remained constant. Note that the benzene concentrations
from the smallest plant (0.01 km2) at each distance from the source
fall within the range of the concentrations of benzene at the corres-
ponding distances from the chemical manufacturing plant. For a coke
oven or petroleum refineries facility with a larger area (Mara and Lee
1978 choose 0.25 km^ as a "typical plant area" for a coke-oven plant),
the concentration is much less than the 0.01 km2 plant. Furthermore,
the emission rate used in this calculation (100 g/s) is significantly
greater than the usual coke-oven or petroleum refineries emission rate
(10 g/s) of Mara and Lee (1978). The anticipated benzene concentration
in the vicinity of these facilities can then be expected to be much
smaller than those reported here and, consequently, much smaller than
those found in the vicinity of a chemical manufacturing plant.
Atmospheric Oxidation
The rate of benzene depletion due to free radical oxidation directly
depends on the reaction rate of benzene with hydroxyl radicals and with
ozone. The reaction rate of benzene x^ith hydroxyl radicals is consider-
ably faster than the reaction rate with ozone, and, therefore, is the
rate limiting reaction. The product of the benzene/hydroxyl radical
reaction is phenol (Hendry 1978).
+ OH
Benzene
Phenol
The rate of benzene depletion due to free radical oxidation also
depends on the concentration of hydroxyl radicals and ozone in the
atmosphere. Table 4-17 illustrates that the concentration varies
depending on the environmental setting. Rate constants for the ben-
zene-hydroxyl radical reaction, kOH, and the benzene-ozone reaction,
kQo, have been estimated to be 8.4 x 1011 cm3/mole-sec and 28 cm3/
mole-sec, respectively (Hendry 1978).
4-40
-------
TABLE 4-16.
JN
I
IH stance
From
Source
Area
(km)
0.3
0.45
0.60
0.75
1.6
2.5
4.0
6.0
9.0
14.0
20.0
~
0.01 km2
5,000
3,850
2,850
2,150
800
405
205
110
60
33
20
Benzem
- —
^06 J
-------
TABLE 4-17. CONCENTRATIONS OF HYDROXYL RADICALS AND OZONE
IN ATMOSPHERE OF DIFFERENT ENVIRONMENTAL
SETTINGS
Urban
Rural
Concentration
of OH
(mole/cm^)
5 x 1(T18
5 x ID'19
Concentration
of 03
(mole/cm-^)
1 x 1CT12
1.6 x 10~12
Source: Arthur D. Little, Inc.
TABLE 4-18. OXIDATION RATE CONSTANTS AND HALF-LIVES OF
BENZENE IN DIFFERENT ENVIRONMENTAL
SETTINGS
Urban
k (sec )
ox
tl/2 ^nrs)
4.2 x 10
46
-6
Rural
4.2 x 10"7
458
Source: Arthur D. Little, Inc.
4-42
-------
kox
where kox = rate of oxidation (sec'l)
KOH
rate constant of benzene with hydroxyl radical (—SiL_)
fnui mole-sec
[OHJ concentration of OH radical in troposphere (**£>
rn i cm
103J - concentration of 03 radical in troposphere (SS^S.)
k03 = rate constant of benzene with ozone (- CI"3 )
mole-sec
^ lu ° sec while for a rural * clon rate of benzene
Pheric oxidation is slighter lower 4 2 x^n-T*™-I**? rate °f atmos-
slightly smaller hydroxyl radical concent^t • "^ I' 6CaUSe °f the
reaction rate constant k theh ?J ? f n* Knowin§ the oXidat
can be calculated using fe-fS^-SSM0^"- ^ ^
cacu
evaluated the concentration If hydroxyfrJl ^ ~ ^ (1977) who
tudes for different hours of the if^rS. b± ^^ * ^^ °f lati-
months. The reaction of benzene with § Wlnter and Summer
work because the rate of reaction is "^ ^ ^ add™ss*« in their
on the rate of oxidation. ?able 4-?9 11"^" H' \' ? h3S mininial effe"
tration (measured here in mole/cU) and the f^?1^1 radic^ concen-
culated on the basis of kOH = ( 59 \ "o'S ^ff",1^8 °f benzene cal-
half-life of benzene in the lower aLnL cmJ/™ole-Sec. The average
which is in the same range as The haS I *?* ^^ ^°m U t0 ^ 'ours,
hydroxyl radical concentration Therffnrf °bserved usin§ an average
specific concentration or an "ierSe cSHV"8"8 3 1OCati°n and
result - a half-life of ^
days H
ysis), it is expected tt tranport ^h"11"117 (such as via
significant factor in the dlTSSiS T£anisms wil1 be^n:e a more
isms. Thus, atmospheric dispersion ° l^^ ^ Chemical mech
a great distance from the source of eTi* ^ C° C^y benzene
a regional problem and less of a "
Photochemistry
Howard and Durkin (1974), Walker
previous wlw. on the
4-43
-------
I
.£-
Concentration
of Oil
(in millions of
moles/cm^)
Tj/2 (hr)
TABLE 4-19. HALF-LIFE OF BENZENE IN THE LOWER TROPOSPHERE*
Latltutte, Time of Day, and Season for Various Model Conditions _
30°N
8 AM
Summer
30°N
12 Noon
Summer
30°N
Diurnal
Summer
30°N
12 Noon
Winter
30°N
Diurnal
Winter
70°N
12 Noon
Summer
70°N
Diurnal
Summer
37°N
12 Noon
Summer
6
20
10
12
4
30
2
61
1
121
3
40
2
61
9
13
3 KQH = 1.59 x 10~12 cm3/mole-sec
.693
"1/2 K
0
x
Source: Davis e_t al. (1977).
-------
I
ws a:
:»
«=.
yields on the order of 0.01-0.
0.22) for Photochemically excited ban,.7 ?f hS (*uant™ 7^" about
less decay to the ground state thus ^n F1uuor^cence and radiation-
benzene excited stftes elen whJn h- hP6ar t0 ^ dominant Processes for
employed. Neither procesrresSts.'f /^^ (" <254 nm) ra<^<:ion is
Phase. Process results in depletion of benzene from the gas
4.4.4.2 Water
in aquatic environments. Its aromatif i? ^Pically occur with-
density that impedes nucleophiLc attack (Lrr^ a "e«atlw ch^e-
fusion is an important physical in?ra^dium f It^ **? 1973)' Dif-
because it leads to a major interned^ n ^ Pr°cess for benzene
water to air. BiodearaStion «JT Pathway: volatilization from
Biodegradation
unsubstlS -
tlfied species) or specie! hav^been is'oilte! ?°P atl°nS (°f ™ide»
domestic sewage, petroleum walL !!!/ °m actlvated sludge,
ment (Howard and lu^n^lir^l^^ ^ rlV6r Water and «dl-
of potential benzene degradew AlLt alfh"5 * WidesPread Distribution
lated from different habita?^ becfus^of their^^-degraders we^e iso-
zene, toluene or aromatics in general ThJ « 7 C° gr°W on ben~
exposed to benzene alone. senera1' ^^se organisms were subsequently
4-45
-------
Degradation Pathways
Two major pathways are commonly followed in the microbial degrada-
tion of benzene (Swisher 1970); the first step in both reactions is oxi-
dation to catechol and then splitting the ring either betx^een or adjacent
to the two hydroxyl groups. The two pathways and their metabolic pro-
ducts are depicted in Figure 4-10. A third pathway has been reported
for phenol-acclimated sludge. Both reactions produce compounds that
are commonly found in cell metabolites or components.
Several hypotheses have been suggested concerning the first step
of the reaction between benzene and catechol (Gibson et al. 1968). The
first theory (see 1, Figure 4-10) is that the benzene nucleus under-
goes expoxidation, then hydrolysis to produce transbenzene glycol, which
is dehydrogenated to catechol (Taniuchi et_ al. 1964). A second hypothesis
is that benzene goes through a monohydroxylation reaction to phenol, then
hydroxylation to catechol (see 2, Figure 4-10). The third is that a
hydroperoxide is formed and undergoes hydroxylation to catechol (see
3, Figure 4-10). The third hypothesis has been tested using Pseudomonas
Putida and the results, though tentative, are supportive (Gibson et al.
1968, 1970). Because the first step is probably ratelimiting (Marr"and
Stone 1961), it should be examined, if it has not been, for a variety
of microbial species.
Degradation Rates
It is difficult to compare the results of different experiments
because biodegradation tests, in general, are variable and observations
are rarely quantified as rate constant. Consequently, it is impossible
to estimate a benzene biodegradation rate and the extent to which con-
trolling variables influence it. Using the oxygen consumption measure-
ments presented in Table 4-20, however, an examination of the rates
measured will give an idea of the variability in rates. Slower rates
may be due to the lack of acclimation and/or a short experimental
period. Other factors that may have influenced the rates include the
presence of alternative carbon sources or oxygen consumption by activ-
ities not involving benzene (e.g., endogenous respiration). Extrapo-
lating these results to environmental conditions is difficult; however,
in most cases, controlled laboratory conditions are more conducive
to degradation (using adapted populations, providing optimum temperature
and benzene concentration, controlling volatilization) than are natural
conditions. Consequently, the results reported in Table 4-20 can gen-
erally be considered as upper limit rates. Reported rates ranged from
45% in 10 hours to 0.6% in 1 week.
Biodegradation During Wastewater Treatment
Biodegradation of benzene appears to occur during wastewater treat-
ment. In a survey of the susceptibility of numerous substances to bio-
logical wastewater treatment, Thorn and Ag (1975) classified benzene as
biodegradable following acclimation. In contrast, Helfgott et al.
4-46
-------
H
H
OH
BENZENE EPOXIDE
OH
trans BENZENEGLVCOL
BENZENE
\
PHENOL
OH
CATECHOL
H
OH
:O
BENZENEHYDROPEROXIDE
OH
H
HC COjH
H
,HCO,H
H
\
CO,H
H
HaC
HOCH
H2
.c"!
HC
H2C
0=CH C =
H,
Acataldehydn
Pyruvic acid
Jl
H
O-C'
c2
:=o
coan
: acid
Source: Gibson etal. (1968), Howard and Durkin (1974).
t
F,GURE4.,0 DEORADAT.ON PATHWAYS FOR BEN2ENE
-------
TABLE 4-20. BENZENE BIODEGRADATION RATES3
% Degraded
3.2
45 b
33
132
20
0 - 0.6
36
46
49; 100
Extremely slow0
Time
6 hr; 5 days
10 hr
12 hr
8 days
1 day
7 days
8 days
5 day
7 days; 14 days
Reference
Bogan and Sawyer (1955)
Okey and Bogan (1965)
McKlnney et al. (1956)
Malancy (1960)
Winter (1962)
Marion (1966)
Malancy (1960)
Marion (1966)
Tabak et_ al. (1980)
Chambers et al. (1975)
All studies used mixed species microbial populations and measured
oxygen uptake.
'Culture isolated fron adapted activated sludge.
•%
"Culture isolated from petroleum waste lagoon.
4-48
-------
I
usually less than 10 yg/l although i If'
one plant in Indianapolis. Inhibfto^ le
considerably higher, reported at 100?™ /Tf
EPA 1977). The fractiofof direct loss §0f
bial activity cannot be determined fro™
However, the combined effect^f all
appears to be successful '
concentrations were
"* " ^ Ug/1 at
W3ge treatment are
digestion CU.S.
a£tributable to micro-
(19?9)
population acclimation
'or or the rate of
concentration,
Mitchell 1973)
Pseudomona?. (Walsh and
(Marr and Stone 96l)
of lag periods
statlc conditions compared with 0 24
ture. No studies
.
-------
• Presence of Other Nutrients. The biodegradation of benzene,
which only provides a carbon source, may be limited by low
concentrations of other nutrients required for microbial
growth, such as nitrogen and phosphorus (Howard and Durkin
1974) .
• Presence of Other Hydrocarbons. Benzene in the presence
of dodecane and/or napthalene in a culture study was
degradable, while benzene alone was not (Walker and
Colwell 1975). The authors suggested that co-oxidation
was necessary for degradation and/or that the benzene con-
centration was too high in the single hydrocarbon culture.
Glaus and Walker (1964) suggest that enzymes with similar
activities are involved in the metabolism of benzene and
toluene. In this laboratory study, toluene-acclimated
microorganisms had an advantage, consequently, they were
able to immediately degrade benzene while glucose-raised
organisms could not.
• Competing Reactions. Other processes controlling benzene
concentrations, particularly volatilization, may operate
at rates much faster than biodegradation. Faster pro-
cesses may reduce toxic concentrations to levels supporting
metabolism or, in other cases, to levels too low to support
metabolism.•
4.4.4.3 Soil
Little data are available on chemical or biological fate processes
that affect benzene in the soil environment. It is unlikely that any
purely chemical transformations of the chemical will occur: benzene'
is resistant to hydrolysis, to oxidation, and to other chemical
reactions except under extreme conditions (e.g., concentrated nitric
or sulfuric acid, high temperature).
Versar, Inc. (1975) asserted that benzene in solid waste leachate from
landfills "can be degraded during soil migration. Although specific
documentation of this degradation has not been found, at least five
microbial species, which proved capable of surviving with benzene as
their sole carbon source (i.e., they biodegraded the benzene), have
been isolated from various soils (see Table 4-21). The biodegradation
process has been described in detail in Section 4.4.4.2 and will not
be repeated here. Although the other factors cited are important,
oxygen is the critical limiting factor for soil degraders. Benzene
will volatilize from surface soils faster than organisms can degrade
it. Submerged soils, deep subsurface layers of water and soil, cold
regions, and other colder seasons in temperate climates are environments
where volatilization is slow and, therefore, support persistent benzene
levels. Microbial activity, however, would also be reduced under these
conditions. No evidence exists for anaerobic degradation of benzene;
thus, the compound may persist in low oxygen habitats, such as saturated
soil, groundwater aquifers, or lake and estuarine sediments.
4-50
-------
I
TABLE 4-21. }
OP
Species
Cladosperium resinae
Pseudomonas
S£.
Used
Benzene
as Sole C
yes
yes
Achromobacter sp.
Pseudomonas putida
Nocardia sp.
Pseudomonas aeruginosa
yes
yes
Mycobacterium rhodochrous
yes
Note
Growth began
>22 days
Benzene-accli-
mated organisms
showed no lag
but organisms
raised on glucose
did not achieve
a maximum rate of
oxidation until
190 min.
Benzene-accli-
mated organisms
showed no lag;
glucose-grown
organisms
exhibited lag
Reference
Cofone et al.
(1973)
Claus and
Walker (1964)
Claus and
Walker (1964)
Gibson et al.
(1968)
Wieland _et al.
(1958)
Marr and Stone
(1961)
Marr and Stone
(1961)
4-51
-------
Rogers et al. (1980) performed laboratory analyses of benzene
behavior in montmorillonite clay and two silty clay loams. Absorption
and desorption of benzene from three solutions of 10, 100, and 1000 ug/I
were measured. It was found that "Montmorillonite clay saturated with
Ca sorbed less benzene than the soils: however, Al-saturated clay .
was able to sorb and retain much more benzene than could the soils."
These researchers concluded that "sorption of benzene is not the major
effect of soil on benzene."
4.4.4.4 Plants
Uptake and metabolism of benzene have been reported for numerous
terrestrial plant species (Cross et al. 1979, Howard and Durkin 1974).
Degradation pathways more closely resemble those observed in animals
than in microorganisms with conversion of benzene to phenol, muconic,
fumaric, succinic acids, and phenylalanine. Jansen and Olson (1969)
provide the only study that observed the metabolism of benzene for a
sufficient length of time. In that study, only a small fraction (0.004 -
0.007%) of benzene was degraded to C02; most of it was converted to
simple compounds that could be used by plants in metabolic processes.
Uptake of benzene from the atmosphere has been observed for water
hyacinths, Swiss chard, sugar beet, avocados, potatoes, apples, peppers,
and other fruits (Cross et al. 1979, Jansen and Olson 1969); root
absorption by tea, laurel, grape and corn plants has also been reported
(Howard and Durkin 1974). In the most detailed uptake study, Cross
et_ al. (1979) found an initial lag period before significant degrada-
tion occurred, an absorption rate proportional to benzene concentration,
and complete transformation of benzene to other compounds (unidentified).
Initial atmospheric benzene concentrations were approximately 300 yg/1.
It is difficult to interpolate the results of these experiments to
environmental conditions. Certain conditions that are possibly essen-
tial to plant degradation of benzene may not occur in the field. For
example, atmospheric concentrations high enough and long enough will
induce the appropriate plant enzyme systems or support acclimation of
an associated microflora.
4.5 SUMMARY
This chapter has described the environmental fate of benzene from
the perspective of the three major environmental compartments. The pro-
cesses that may transfer benzene from one to the other have been analyzed
for their significance and reaction rate. The processes that have poten-
tial to alter chemically or degrade benzene within a given compartment
have been similarly considered.
4-52
-------
I
The major fate processes, both inter- and intramedium, are shown
in Figure 4-11 and summarized below.
4.5.1 Intermedium Transfer Processes
4.5.1.1 Air
• Rainout to Water and Land. A process limited first, by benzene's
low solubility in water and, second, by the small volume and
surface area of precipitation nucleii and droplets.
Conclusion. Limited overall importance.
4.5.1.2 Water
• Volatilization to Air. Occurs quite quickly; controlled
by diffusion within water bodies.
Conclusion. A major pathway.
• Adsorption to Soils. Occurs on a limited basis; highly
dependent on soil type, i.e., organic content, relative
concentrations, etc.
Conclusion. Limited overall importance.
4.5.1.3 Soil
• Volatilization to Air. Occurs quite quickly; controlled by
aeration within soil, i.e., enclosed soils will not encourage
benzene loss.
Conclusion. A major pathway.
• Solution into Water. Soil benzene is tightly bound,-
unbound benzene will dissolve in soil water as determined
by its solubility.
Conclusion. Limited overall importance.
• Runoff to Water. Surficial benzene would be preferentially
volatilized. Any benzene bound to surface particles could
be carried off physically.
Conclusion. Limited overall importance.
4-53
-------
Air
Oxidative Destruction
(Very Fast)
Water
Inert; small losses
from Biodegradation
o
Soil
Inert; small losses
from Biodegradation
FIGURE 4-11 MAJOR FATE PROCESSES FOR BENZENE
4-54
-------
I
I
4'5'2 Intranedlum Fate Processes
4.5.2.1 Air
*
4.5.2.2 Water
'-<
taportant in so,e habitats, but not universal^
4.5.2.3 Soil
n. Important in so»e habitats, but not universally
4'5'3 Critical Pathw^c for
"critical" because they defthe oj Pfh"a''s «e "lied
total environments! load o"bLene * *"" 3Ct to reduce
'h.
«uctlon, an, 3, land sources
Ss 2S.-2S--S;
pathway occurs.
It may be concluded that the bulk nf x
one medium in which they are most speedifv ST* f16"68 °CCUrs in the
small remainder will eventuallv frt?? • n down and that the
ultimate fate; a very small ^unt oft o'talh"1 ^^ C° the Same
degrade and a similarly smalfaTunt WJ? * T releases will bio-
onto sediments, or airborne remain diss°lved, adsorbed
4-55
-------
Use as
Chemical
Feedstock
Resource
Mining and
Processing
4>-
Cn
Use as
Chemical
Feedstock
21%
Benzene\petroleum
reduction
36% ' 58%
ATMOSPHERIC SOURCES
234.945 kkg
Rainout
Soil
Water
OXIDATIVE
DESTRUCTION
AQUATIC SOURCES
1.131 kkg
VOLATILIZATION
Biodegradation
" Adsorption to Sediments and Soils
. Soil
LAND SOURCES
394 kkg
VOLATILIZATION
Biodegradation
• Leaching and Runoff
Notes: Processes in boxes and bold type are major fate pathways
for any benzene in that particular medium.
Processes that lead to other media are indicated by an
arrow, which leads to that medium and implies that all
fate processes for that medium apply.
Water
FIGURE 4-12
CRITICAL PATHWAYS FOR BENZENE
(Released Amounts for 1978 Materials Balance)
-------
I
I
REFERENCES
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Glaus, D.; Walker, N. The deomposition of toluene by soil bacteria
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Cofone L. Jr.; Walker, J.D.; Cooney, J.j. Utilization of hydrocarbons
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Coniglio, W.A.; Miller, K.; MacKeever, D. The occurrence of volatile
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Davis, L.N.; Santodonato, T.; Howard, P.M.; Sayena, J. Investigations
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i
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Plants,
»: rtnur "it""^".
„„. (AS
Thomas 1978)
Durkin 1974)
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Chinn>
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to
and Waste
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Southworth, G.R. The role of volatilization in removing polycyclic
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Walker, P. Air pollution assessment of benzene. McLean, VA; Mitre
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4-62
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5.0 HUMAN EFFECTS AND EXPOSURE
5.1 HUMAN EFFECTS
5.1.1 Pharmacokinetics
For an assessment of chronic toxicity, it is useful to compare
and contrast the pharmacokinetics of benzene with that of toluene.
These solvents have similar physicochemical characteristics, and
where they have been directly compared, they appear to be similar
with respect to absorption and distribution"in the body. Significant
differences do occur in metabolism and this probably accounts for the
differences in chronic toxicity.
5.1.1.1 Absorption
Benzene has volatile and highly lipid-soluble chemical character-
istics that permit absorption by all exposure routes: dermal, oral and
inhalation. The concentration of benzene and the permeability to ben-
zene of the intervening membranes are the principal determinants of the
rate of absorption.
Dermal absorption of benzene vapor is presumed to be slow, compared
with inhalation at the same air concentration, even though, apparently
no one has studied the rate of benzene vapor uptake via the exposed '
skin surface. Riihimaki and Pfaffli (1978) did study the absorption
°* ??inene/aSrOSS the body surface of human volunteers at a concentration
of ZZbO mg/m-3. The subjects were exposed for 3.5 hours and their faces
were covered with an inhalation mask under slight positive pressure to
prevent inhalation uptake. They were clothed only in lightweight pajamas
and socks. These researchers calculated total uptake as approximately
26 milligrams, based on a 16% recovery of absorbed dose in the expired
air. It is estimated that the same total uptake in 3.5 hours via inhala-
tion would occur at an air concentration of only 38 mg/m3. (This estimate
assumes a respiratory rate of 7 1/min at rest and'a respiratory retention
factor of 47% for toluene; see the discussion below.) In their experiments
on the percutaneous absorption of xylene, Riihimaki and Pfaffli show that
uptake is proportional to air concentration. Based on these data and
the similarities between xylene, toluene, and benzene, the approximate
average skin permeability of the human body to benzene is calculated to
be 0.002 mj/(nrx hr). z
2Uptake
8 mg/hr - permeability x 2260 mg/m3 x 1.8 m2, where
2260
- - „. -- ,- ---j •<>• *-<-vv tug/m- A j..o m-, wnere zzou
mg/mj was the exposure concentration and 1.8 m3 is the approximate
body surface area.
5-1
-------
Dermal absorption of liquid (neat) benzene is much faster than that
of vapor, because of the higher concentration and a defatting action on
skin that would significantly increase the permeability. Skin absorption
of neat benzene was estimated using the data of Sato and Nakajima
(1978). In their experiments, human volunteers soaked one hand in neat
toluene for 30 minutes. Blood levels after the 1/2-hour exposure reached
approximately 25% of the blood levels measured after 1/2-hour inhalation
exposure at 376 mg/m3. It can be shown that blood level is directly
proportional to uptake rate, when rate is constant. If it is assumed
that the skin absorption rate was constant (an oversimplification, but
useful for a demonstration), it is estimated that the uptake rate via
the skin of the hand was ^20 mg/hr.3 The surface area of the hand is
about 2% of the body surface area of 1.8 m2, or .036 m2 (Diem and Lentner
1971); therefore, an estimate of absorption rate through skin of liquid
benzene is 550 mg/m2/hr.
Absorption of benzene via inhalation is the most important.exposure
route in the occupational setting, because benzene is highly volatile
and absorption into the body via the lungs is rapid. A useful parameter
of inhalation absorption is the retention factor, which may be defined
as the fraction (or percent) of the inhaled solvent that is absorbed from
the inspired air. Most reports indicate that the respiratory retention
factor is between 40-50% (U.S. EPA 1978c). Toluene absorption has been
more carefully investigated, because of its much lower toxicity, and
findings from these studies are extrapolated to benzene exposures.
Veuletnans and Masschelein (1978a) found that the respiratory uptake
rate of toluene was directly proportional to minute volume and concen-
tration. The range of experimental minute volume was varied from a rest
rate of 7 1/min to >50 1/min with heavy work, and concentration ranged
from 190 to 750 mg/m-5. The retention factor for toluene was 47%. Be-
cause of the similar chemical properties of toluene and benzene and the
comparable retention factors, the total respiratory uptake of benzene
into the body may be estimated by the following equation :
uptake (mg) = concentration (mg/m3) x minute volume (m3/min) x
time (min) x retention factor (.5).
5.1.1.2 Distribution
In discussing the distribution in the body of a lipid-soluble,
water insoluble compound, it is appropriate to view the body as a multi-
compartmental system. Although each organ may be considered a compartment,
it is more usual to treat the body as containing 2-4 compartments, with
A
376 4g/m x .47 x 0.45 m3/hr = 20 mg/hr, where 376 m^/m3 was the air
concentration for equivalent blood levels via inhalation, 0.47 was the
respiratory retention factor and 0.45 m3/hr was the respiratory rate
at rest.
5-2
-------
I
6
each compartment made up of organs and tissues having similar pharmaco-
kinetic characteristics. For benzene, a 3-compartment model has generally
been adequate to characterize the pharmacokinetics. The first compart-
ment is generally considered to be composed of the blood and hishly
perfused organs, such as the heart, kidneys, liver, Intestines,"endo-
crine glands and brain. This central compartment is the one from which
the other compartments, called peripheral compartments, receive drugs
and chemicals and from which the chemicals are eliminated from the body.
The second compartment is composed of tissues and organs with moderate
blood perfusion, such as muscle and skin. The third compartment, espec-
ially important in the case of lipid-soluble organics, is composed of
slowly perfused tissues, such as fat. Fat differs from most other
tissues in having a much higher tissue/blood partition coefficient for
organic solvents; i.e., it can accumulate benzene to a greater extent
than might be expected on the basis of volume alone. A useful index of
the time it takes for the various tissues (or compartments) to reach
equilibrium with the central compartment (i.e., the blood, since it can
be assumed that rapid mixing occurs within the central compartment) is
the saturation half-life, t1/2. The saturation half-life depends
directly on the volume of the compartment (VT) and the tissue/blood
partition coefficient (X); and inversely on the blood flow (Q) for the
compartment as follows:
= (X • VT/Q) x .693.
Rough estimates of saturation half-lives for several tissues and
the three composite compartments are presented in Table 5-1. Clearly,
the distribution to the brain and the central compartment is very
rapid. It is so rapid that often it is difficult to delineate this
compartment in pharmacokinetic analysis. The third compartment equili-
brates so slowly that it usually does not reach saturation equilibrium
with the blood during continuous exposure, such as an 8-hour occupational
exposure. For the same reason, a tendency for "baseline" blood levels
to build up over continuous day-to-day exposure could occur as a result
of this third compartment being similarly slow.
Blood levels usually cannot be used to quantitate absorption
unless exposure conditions in terms of both concentration and time are
known.^ During inhalation exposure, blood levels rise rapidly to a
quasi"-steady state, reflecting rapid absorption and slow metabolism
and distribution to other tissues. When exposure is terminated, blood
levels fall rapidly at first, reflecting continued distribution to the
rest of the body as well as metabolism and elimination. After an
initial rapid decline, slower phases of decline are noted, because
elimination is rate limited by the transfer of the chemical from the
peripheral compartments into the central compartment.
Sato _e_t al._ (1974) studied and compared the pharmacokinetics of
benzene and toluene in human volunteers. The decline in blood levels
5-3
-------
TABLE 5-1. ESTIMATES OF THE SATURATION HALF-LIFE OF TOLUENE
AND BENZENE BETWEDI BLOOD AND TISSUE
Compartment 1
Liver
Kidney
Brain
Compartment 2
Compartment 3
Fat
Marrow
a A =
xa
Benzene Toluene
1.5 2
1.6 2.6
1.1 1.5
1.9 3.0
1.1 1.2
50 100
58 113
16 35
lood partition coefficients
al. (1974).
VT/Q°
1.5
2.5
.24
1.3
17
(resting)
47
50
25
obtained
t
Benzene
1.5
2.8
0.2
1.7
13
1630
2000
390
from data of
t;
1/2
Toluene
2
4.5
0.2
2.7
13
3200
3900
850
Volume of tissue/blood flow (ml/ml/min) from Papper and
Kitz (1963).
°ts/2 = Saturation half-life = . 693 x VT/Q x X (minutes).
5-4
-------
I
I
after a 2-hour exposure to either benzene (at 80 mg/m3) or toluene
(at 377 mg/m3) was followed for 5 hours. The equations that describe
the decline in blood levels are sums of three exponentials as follows:
benzene,
y = 0.0593e
toluene,
-0.418t
0.
0.355e-°-355t + 0.352e-°-0197t + 0.129e-°'00339t
where t is the time in minutes and y is blood concentration in mg/1.
These model equations together with other data indicate that ben-
zene and toluene are absorbed and distributed into the body quite
similarly. The exponents of the equations are similar to a striking
degree. Also, the coefficients of the toluene equation are about 4-6
times higher than the respective coefficients in the benzene equation,
which follows from the fact that the toluene exposure concentration
was 4.7 times the benzene exposure concentration.
In an important respect, the equations are probably misleading for
both^ toluene and benzene, because they suggest no appreciable accumulation
of either solvent from day to day. Data reported by Konietzko et_ al.
(1980) and theoretical considerations indicate that accumulate on~carT~
occur on a day-to-day basis. Konietzko monitored exposure concentrations
and blood concentration levels at the beginning and end of each 8-hour
work day over a 2-week period in workers occupationally exposed to
toluene. These data are reported in Table 5-2. An apparent upward
trend in the toluene blood concentration values occurs each morning
before exposure over the 5-day work week. The lowest levels were
measured on Monday mornings. The half-life of the terminal phase of
elimination would have to be on the order of 2000 minutes (30 hours)
for baseline blood levels to build up as they appeared to do in the
exposed workers. This half-life is comparable with the theoretical
saturation half-life for fat given in Table 5-1. The terminal phase
half-life calculated from the equations of Sato et_ al. (1974) are on
the order of 200 minutes. This finding of Sato and coworkers is under-
standable because the exposure was only for 2 hours in their experiments
and the blood concentration data were only determined for 5 hours after
the exposure. These time periods are too brief to delineate a very slow
elimination phase.
In summary, benzene is absorbed into the body regardless of the
route; the major difference among routes is the rate of absorption.
Once benzene is into the blood, it is distributed widely to all tissues.
The relative rate of uptake into each tissue is determined by the rela-
tive perfusion of the tissue by blood. Accumulation in fat 'is slow
because of low perfusion; however, the potential uptake is high because
of the lipid solubility of benzene.
5-5
-------
TABLE 5-2. TOLUENE CONCENTRATIONS IN AIR AND BLOOD
I
o\
Toluene in air (ppm)
First Week Toluene in blood
before exposure (yg/ml)
after exposure
Toluene in air (ppm)
Second Week Toluene in blood
before exposure (pg/ml)
after exposure
Monday Tuesday
225 233
(95-303) (153-383)
0.12
(0.09-0.24)
3.63
(2.3-4.75)
285 304
(145-473) (190-521)
0.27
(0.07-0.57)
11.60
(6.99-17.10)
Wednesday Thursday
209 212
(107-341) (92-314)
0.51
(0.28-0.82)
6.69
(4.21-10.36)
309 232
(213-413) (125-451)
1.00
(0.35-1.51)
10.29
(3.24-20.31)
Friday
203
(124-309)
0.77
(0.29-1.
6.70
(3.39-30
191
(305-432)
1.21
(0.44-2.
5.85
(1.94-9.
67)
.67)
29)
78)
Range in parenthesis and means of data for eight persons.
Source: Konietzko et al. (1980).
-------
I
I
5.1.1.3 Metabolism and Excretion
The metabolism of benzene has been studied in several mammalian
species. Figure 5-1 indicates the pathways that have been identified.
A large fraction of absorbed benzene is excreted unchanged in the expired
air. The actual proportion excreted unchanged varies among species and
also depends on the dose. Andrews and coworkers (1977) reported that
70-85% of a subcutaneously administered dose (880 mg/kg) was expired
in mice. Parke and Williams (1953a, b) found 40-50% of an oral dose
(150-500 mg/kg) in the expired air of rabbits. Estimates of the
fraction excreted in the expired air of humans range between 12 and
50% (Teisinger et al. 1952, Srbova et al. 1950, Nomiyama and Nomiyama
1974).
Alternatively, a mixed function oxidase system, which is associated
with the microsomal fraction of tissue homogenates, oxidizes benzene.
This system is a group of enzymes; the specificity and activity of which
varies considerably with the species and tissue. Gonasun and coworkers
(1973) described this mixed-function oxidase system from mouse, rat, and
rabbit liver microsomes. It required a NADPH generating system and
oxygen for activity and contained cytochrome P-450. Pretreatment of
the animals with benzene increased the jLn vitro activity of the system
about 80%. The mouse derived system was about 10 times as active for
oxidizing benzene on a per milligram of protein basis as that from rat
and rabbit. Generally, the liver contains a highly active mixed-function
oxidase system that is easy to prepare in useable quantities; however,
other tissues also contain active systems that contribute to benzene
metabolism and may figure prominently in understanding mechanisms of
toxicity.
The product of the initial reaction of benzene with the mixed-
function oxidase is the intermediate, benzene epoxide— an unstable,
reactive metabolite,which may undergo a variety of interactions with
cellular constituents. Only three pathways for which there is evidence
are shown in Figure 5-1. The major route is to phenol, which occurs
by a nonenzymatic reaction (Jerina et al. 1968, Snyder and Kocsis 1975).
The fraction of benzene that is metabolized to phenol also shows species
and dose dependent variation. Parke and Williams (1953a, b) found that
about 20% of an oral dose (150-500 mg/kg) was excreted in the urine of
rabbits as conjugates of phenol. The much lower ratio of catechol/phenol
metabolites when rabbits were dosed with phenol compared with the ratio
when rabbits were dosed with benzene (i.e., 'v.Ol and .08, respectively)
suggests that catechol was derived primarily from phenol.
A second route of degradation of the epoxide is catalyzed by the
enzyme epoxide hydrase, which oxidizes the intermediate to trans-1,2-
dihydro-l,2-dihydroxybenzene (benzene glycol). Jerina and coworkers
(1968) identified this enzyme in both microsomal and soluble fractions
of rabbit liver homogenates. The soluble fraction of liver homogenates
dehydrogenated the 1,2 glycol to catechol. Previously, Parke and
5-7
-------
B«nan«{100%>
oeJd05%) Olid*
ghrtothioM
NHAc
I ttwsfwosi
Eipirtd «fldwn$«d (40%)
Gt-CIt irwcofltt ocid
bwniw alycoi (02%) mucame odd COOH
,H
iooH
hrdroqwfld (5%)
|10H.
HO^
PAPS,
*-x'^
wlpto-eoniuqutn
pototsrun phenol lutratt
(SO-100%)
'OH
tpoxid* *«yX5H
hydras*
tpontoneou*
(23-50%) catKhol (3-2S%)
OH ?
i • P I II
OH
JJOPG
Witt
in urin«
0-CHj!CHOH|,CHCO,K
f lucuronid*
(0-50%)
COOH
\O.J '«/
Percentages are approximate values and do not
necessarily apply to humans.
NOTES:
AHH = arv' hydrocarbon hydroxylase
UDPG = uridine diphosphate glucuronyl transferase
PAPS - 3'-phospho-adenosin-5'-phosphosulfate
Source: U.S. EPA (1978b)
FIGURE 5-1 METABOLIC PATHWAY OF BENZENE IN LIVER3
*5-8
-------
Williams (1953a, b) had shown that the muconic acids were only found
in rabbits dosed with benzene but not in those dosed with phenol.
The third route of metabolism via the benzene epoxide is conjugation
of the intermediate with glutathione, presumably via the glutathione-S-
transferase system. A phenyl mercapturic acid is the eventual product
after the elimination of glycine (Jerina et_ al._ 1968, Goldstein 1974).
In contrast to benzene metabolism, toluene is preferentialy oxidized
at the methyl group of benzyl alcohol. Approximately 80% is metabolized
via benzyl alcohol, while another 16% is excreted unchanged in expired
air (Veulemans and Masschelein 1978a, b, 1979). A small percentage of
toluene is metabolized via a reactive intermediate, i.e., toluene epoxide
to cresols and methylphenyl mercapturic acid (Dean 1978, Van Doom et al.
1980). —
Several compounds have been shown to inhibit benzene metabolism,
presumably by competitive inhibition of the mixed function oxidise
system. Benzene metabolism was inhibited fay compounds known to inter-
act with the mixed function oxidase system, such as aniline, metyrapone,
aminopyrine, SKF-525A, and cytochrome c (Gonasun _et al. 1973). Toluene
inhibited benzene metabolism in vitro of the 10,000 G supernatant
fraction, which contains the microsomal enzymes (Sato and Nakajima 1979).
These researchers demonstrated in rats a dose-dependency of the fraction'
of benzene excreted as total phenol, from 41% of dose at 0.3 mmol/ka
(24 mg/kg) to 8% of dose at 5 mmol/kg (390 mg/kg). Coadministration
of toluene at 5 mmol/kg reduced the percent of benzene (at 5 mmol/kg)
excreted as phenol to about 1% of the dose. Their work indicates a
reciprocal competitive inhibition between benzene and toluene in which
toluene is a far more effective inhibitor of benzene than benzene of
toluene. Inhibition was most apparent at high dose levels. Human
volunteers showed no inhibition of benzene by toluene or toluene by
benzene following coexposure to 376 mg/m3 toluene and 80 mg/m3" benzene.
Results of the studies of Andrews et al. (1977) and Irons et al.
(1980) show that metabolism of benzene occurs in other tissues as well
as in the liver, especially in the bone marrow. Using various extrac-
tion procedures to differentiate benzene from benzene metabolites in
bone marrow, Andrews showed that metabolites were nine times higher in
marrow than in blood and six times higher than in the liver after
benzene was injected (880 mg/kg s.c.) in mice. They showed that the
bone marrow was unable to concentrate phenol, phenyl glucuronide
or phenyl sulfate to this extent when these metabolites of benzene
were injected. The simultaneous injection of toluene x*ith benzene
markedly reduced the concentration of benzene metabolites in the tissues
including marrow, fat, spleen, liver, and blood. However, tissue levels'
of nonmetabolized benzene were not as markedly altered by simultaneous
injection of toluene.
5-9
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5.1.2 Acute Effects
Benzene is a general central nervous depressant in acute doses.
The nature and extent of specific acute symptoms have shown marked
variations between individuals. This probably reflects, for the most
part, differences in the rate of uptake (exposure concentration) and
the extent of uptake (exposure duration).
Death has resulted from single exposures to benzene in air at con-
centrations of 20,000 ppm (64,000 mg/m3) within 5 to 10 minutes. Symp-
toms proceeded through headache, nausea, staggering gait, paralysis,
convulsions, unconsciousness and death. Death may result from respira-
tory arrest or cardiovascular collapse. Severe but nonfatal acute'
exposures have produced similar symptoms. Less severe exposures may
produce giddiness and euphoria (U.S. EPA 1980).
Death may be due to cardiac arrhythmias resulting from sensitization
by benzene of the heart muscle to catecholamines . Thus, the danger of
fatality from benzene exposure may be increased during periods of physi-
cal activity and stress (Snyder and Kocsis 1975).
5.1.3 Chronic Effects
The most important effect resulting from chronic benzene exposure
is hematotoxicity. Extensive discussions of the literature on hemato-
toxicity of benzene have been presented in recent reviews (U.S. EPA
1978a, b, c; 1980, Snyder and Kocsis 1975, and others listed in U.S.
EPA 1980). This discussion is limited to a brief review of the hema-
tological disorders considered to represent the most significant hazards
associated with chronic benzene exposure and for which risk estimates
might be calculated. These disorders are pancytopenia (and closely
related phenomena) and leukemia.
5,,!.3.1 Pancytopenia
Pancytopenia is a deficiency of all cellular elements of the blood.
In benzene poisoning, the deficiency results from an inadequate produc-
tion of the several blood cell types, i.e., cytopenia associated with
hypoplasia of the bone marrow or occasionally with a hypercellular
marrow exhibiting ineffective hematopoiesis. In its less severe forms,
specific deficiencies may occur in blood elements (e.g., anemia, leuco-
penias, or thromfaocytopenia). Deficiencies in each element lead to
certain symptoms, such as hemorrhagic conditions resulting from thrombo-
cytopenia or susceptibility to infection because of leucopenias. In its
severe form,a pancytopenia caused by benzene poisoning is usually asso-
ciated with aplastic anemia.
Systematic studies of occupationally-exposed workers where deter-
minations of benzene levels were also performed are summarized in Table
5-3. The causal relationship between benzene and pancytopenia in
humans is strongly supported by several studies (Greenburg e_t £l. 1939,
5-10
-------
TABLE 5-3. SUMMARY
Industry
Rotogravure Printing
Rubber Factory
Raincoat Factory
Rubber Coating Plant
Shoe Manufacturing
Shoe Manufacturing
Chemical Factory
Incidence of Level of
Number of Hewtological Exposure
EH?l2*Ses Toxicitv ^E/.n3)
332 exposed g5a
82 controls
1104 10fib
mrnC
60
32 5d
217 51e
100 controls
NR 32f
3o5 *\/nvR
35-3380
420 median
1595 peak
319 ave.
437-695
80-3 19
96-670
478-1914
32-130
Duration of
Exposure
3-5 yr
NK
NR
NK
3 mos-17 yr
4 mos-15 yr
< 1 yr
rinding »,re .ne.u,
of
ob,,r,.d
Reference
Creenburg et al. 1939
Coldwater 1941
Goldwater and Tevkubury 1941
Wilson 1942
llelmer 1944
Pagnotto e^ al. 1961
Aksoy e£ a). 1971
Aksoy et^ aj_. 3972
Ooskin 1971
NK - not reported.
-------
Goldwater 1941, Goldwater and Tewksbury 1941, Helmer 1944), which showed
that the hematological effects essentially ended when benzene was replaced
with another solvent.
These studies strongly implicated benzene as a major cause of
hematological disorders. A more definite interpretation, however
especially with regard to a dose-effect relationship is difficult.
One reason is that in the occupational setting, workers have had
widespread exposure to other solvents. Though these solvents may not
be hematotoxic themselves, they could interact with benzene in the
body and perhaps alter its metabolism and thereby affect its toxicity.
The most important issue is that it cannot necessarily be assumed
that the average concentrations of benzene measured in a workplace
actually indicate the average exposure dose to each worker. It is
much more likely that there is a wide variation in absorbed doses
among workers because of variations in work habits and tasks.
Furthermore, it is likely that most incidences of hematological-dis-
orders are associated with the higher exposures to benzene. The essen-
tial data for estimating a dose-effect relationship are missing, unless
the individual's exposure dose can be compared with the occurrence of
disease in that individual. Thus, while the epidemiological data tend
to indicate that benzene can cause hematological disorders, they cannot
be applied to describe the dose-effect relationship.
The hematotoxicity of benzene has been extensively studied in
experimental animals. Frequently, it has been reported that benzene
causes leucopenia (i.e., decreased white blood cell counts) in experi-
mental animals. The U.S. EPA notes problems in the interpretation of
studies reporting depression of white blood cell counts (U.S. EPA
1978b). White blood cell counts vary considerably among species, with
stress, age, and among individual animals of the same species. The
U.S. EPA's report points out that many studies have inappropriate con-
trols. Furthermore, it is unclear whether depressed white blood cell
counts truly reflect bone-marrow damage. Though leucopenia may be
difficult to specify and, in general, is a nonspecific index of disease,
in the case of benzene, leucopenia has generally been shown to be an
early indicator of toxicity reflecting depression of hematopoietic
tissue. A dose-response relationship has been demonstrated (Wolf £t al.
1956, Deichmann et _al. 1963). Table 5-4 summarizes results from a
number of studies on the leucopenic effect of benzene. For comparative
purposes, the exposure doses have been recalculated in some cases on a
mg/kg/day, 5 day/week basis. To recalculate from inhalation exposure,
appropriate minute volumes for the species, body weights, and an
assumed retention factor of 50% were used as shown in the two examples.
Based on these data, it is estimated that the threshold for the leucopenic
effect in laboratory animals is between 1 and 10 mg/kg/day, administered
over an extended period of time. Following a nonlethal exposure to ben-
zene in experimental animals, hematological disorders generally return
to normal.
5-12
-------
TABLE 5-4. LEUCOPENIC EFFECTS OF BENZENE
Oi
Species
Rat
Rat
Rat
Dog
Rabbit
Rat
Rat
Guinea
Pig
Dog
Route/Duration
Inhalation/8 hr/d, 5 d/wk,
20 wk
Gavage/132 days
Subcutaneous/14 days
Inhalation/5-8 hr/d, 4-5 d/wk
^ 12 weeksc
Subcutaneous/2 wk
Inhalation/5-6 hr/d, 4 d/wk
31 wk
Inhalation/continuous
for 127 days
Lowest Effect Level
158 mg/m3
OvL2.6 mg/kg/day)a
10 mg/kg/day
440 mg/kg/day
2500 mg/m3
(^ 240 ing/kg/day)1'
0.2 ml/kg/day
145 mg/m3
(^ 8 mg/kg/day)
No Effect Level
1/mg/kg/day
95 mg/m3
(i> 5 mg/kg/day)
56 mg/m3
(^ 16 mg/kg/day)
Reference
Nau et_ a] . 1966
Wolf et al. 1.956
Matsushita 1966
Hougli e£ a_l. 1944
Kissling and Speck 1972
Deichmann et^ al. 1963
Jenkins et al. 1970
a.5 x .0001 m3/min x 60 min/hr x 8 hr x 158 mg/m3 x -
b.5 x .005 m3/min x 60 min/hr x 6.5 hr x 2500 mg/m3 x
cLeucopenia was evident by this time.
12.6 mg/kg/day.
240 mg/kg/day.
-------
Other results, summarized in greater detail in the U.S. EPA (1978b),
are consistent with the evidence that benzene exposure is hematotoxic;
benzene depresses iron incorporation into erythrocytes, granulocyte
precursor activity, and DNA synthesis in bone marrow. Studies by
Lee £t al. (1974), Uyekl et al. (1977), Moeschlin and Speck (1967), and
others have deomonstrated that the toxic effect is on proliferating
cells, i.e., cells undergoing division and differentiation. Nonprolifer-
ative cells (e.g., reticulocytes) or nonproliferating cells (e.g., resting
stem cells) appear to be relatively resistant to benzene toxicity.
5.1.3.2 Leukemia
Leukemia can be defined as a neoplastic proliferation and accumu-
lation of white blood cells in blood and/or bone marrow. The four
main types of leukemia include: acute and chronic myelogenous (also
known as granulocytic) leukemia, and acute and chronic lymphocytic
leukemia. In addition, other types of leukemia are related to these
four major types. There is some disagreement concerning the diagnostic
criteria. Erythroleukemia, acute promyelocytic leukemia, stem cell
leukemia and acute myelomonocytic leukemia, all of which have been
associated with benzene exposure, are generally considered to be
variants of acute myelogenous leukemia (U.S. EPA 1978b).
The concept that benzene could induce leukemia in humans required
considerably more time to develop than the idea that benzene produced
aplastic anemia or pancytopenia. This resulted because of the early
success in demonstrating benzene-induced bone marrow depression, but
a failure to produce leukemia in experimental animals with benzene.
Moreover, there were diagnostic problems in identifying leukemias in
populations of workers subject to bone marrow depression.
It was estimated that the literature contained references to
approximately 150 cases of benzene-associated neoplastic disease; and
the best documented of these occurred in industries where chronic
benzene poisoning has been detected. It was observed that, "Very
often leukemia develops in subjects with benzene-induced hyporegenera-
tive anemia or pancytopenia of more or less longstanding duration and
constitutes the acute terminal stage of the disease. The leukemia
might become clinically apparent only a few weeks before death; in
these cases, the anemia can be considered as being a pre-leukemia
stage." (Vigliani and Forni 1976).
It is generally recognized that severe bone marrow depression may
predispose to leukemia. Vigliani and Forni (1976) cited 83 cases of
benzene hemopathy observed in Italy; 14 of these deaths were due to
aplastic anemia and 18 x^ere due to leukemia. In a recent review of
44 pancytopenia patients, Aksoy and Erdem (1978) noted that six had
developed leukemia. It is significant that these cases of leukemia
5-14
-------
I
I
depression (U.S. EPA 1978b, 1980)
bone marrow
durations
leukemia. Aksoy observed*! patiL? wJth acu^T ** °r
were using benzene solvent during shoe leuke<^- These employees
occupational exposures in the range of
ranging from 1-15 years Amnno. i? il
-re acute myelobla^'leut mfa'l ei '
3 acute lymphoblastic leukemia a^d 1 I!,h' 3CUte ^^heroleuk
acute monocytic leukemia WaS a°Ute Pr°^locytic and
of
1966~73' These
13 Per 100>000>
°f 6
were calculated
which is signif
100,000 for the general
ently derived fro°m the
being specific to Istanbul which Q e°Pe nft!ons, rather than
^^^
(1978a) report estimate!
over a 10-hour day, a
t
UnCertain; however> ^e U.S. EPA
Sadies
of mortality in a 10-year experience of mf?
facturing plants. Their finding's
Out of 5106 deaths, 1014 wereJue
of the lymphatic and hematopoietic yste
and were increased in cohorts of each of
standard mortality
ated with the
*
Ur
Health
investi§ated the causes
" 3t four tire »anu-
in the U.S. EPA
*? C°
than
The
er °f
sarcoma and Hodgkin's disease) 130 for all fo J If cftegory lympho-
lymphatic leukemia; and 291 for Ivmnh \ i , °f leukemia; 158 for
40-64. These studies did not eva^atf ^ Ukem±a in the a§e
and other environmental toxi a^nts Lit'L'o^6 ^/^
to estimate the levels of exposure ^ benzene. °° * "***
Infante and coworkers
5-15
-------
from January 1, 1940 to December 31, 1949. The authors succeeded in
obtaining data on the vital status of 75% of the employees from January
1, 1950 through June 30, 1975. The work is concerned with death due
to malignancy of the heinatopoietic and lymphatic system and leukemia
and clearly demonstrates a significant increase in the SMR for these
diseases among the workers studied compared with two control populations.
Control 1 was U.S. white male general population standardized for age
and time period over which the study cohort lived. Control 2 consisted
of 1447 white men who had been employees in Ohio at a fibrous-glass
construction products factory between January 1, 1940 and December
31, 1949. Using updated data reported in the Carcinogen Assessment
Group's (CAG) report (U.S. EPA 1978a), 9 deaths resulted from all forms
of leukemia in the two occupationally-exposed groups, where the expected
incidence was 1.25, for a standardized mortality ratio of 720. The SMR
was greater when cases of chronic myelogenous leukemia were excluded
from consideration. Some do not consider chronic myelogenous leukemia
to be linked with benzene (U.S. EPA 1978b).
Estimates of the exposure levels to benzene of the study group are
highly debatable and must be regarded as uncertain. Infante et al.
(1977a, b) argue that benzene was the only solvent that could be respons-
ible for the increases in leukemia and that benzene levels averaged
between 32-50 mg/m3, based on a 1946 survey. However, other sources
suggest levels may have been considerably higher.
According to testimony before the Occupational Safety and Health
Administration (OSHA), levels exceeded 700 rng/m3 in certain plant
areas (Harris 1977). Several references cited by Tabershaw and
Lamm (1977) in a letter to the editor in response to the study by
Infante _et .al. (1977a) also indicate that the exposure levels in these
plants were probably greater than the prevailing standards of the times
during the 1940s; i.e., they may have been in the 300-3000 mg/m3 range.
%
The Carcinogen Assessment Group's final report (U.S. EPA
1978a) assumed that the average worker exposure was the same as the
prevailing recommended maximum limits for the years 1940-75. They calcu-
lated a time-weighted average occupational exposure for the 36-year period
of 23.3-39.9 ppm (74-127 mg/m3). Although this estimate is higher
than the estimate of Infante and coworkers, it still may not be high
enough for two reasons. First, benzene levels were not monitored in
one factory from 1940-46. In 1946, new ventilation equipment was
installed after which a survey showed "most areas" in the plant ranged
from 0-15 ppm (0-48 mg/m3) (U.S. EPA 1978a). Prior to 1946, the CAG
estimate of benzene levels is only 15-100 (48-319 mg/m3), which Tabershaw
and Lamm (1977) have already pointed out as appearing unrealistically
low. Second, the estimate of the CAG group includes the years between
1957-75, when maximum permissible limits had been significantly
reduced, but when most workers in this study probably had already
left the plants because of retirement or new jobs (see discussion
below).
5-16
-------
I
I
«»' «» *•»«<» of
disease. The CAG reort U ° rkfi" who later developed
EPA
avaiiabie data 3 study the
workers exposed to benZe-3 di n^ ? & T^ estiniate- Out of 594
kemia, where 0.8 was expected (R=3 75T ^^^"c, nonmonocytic leu-
deaths evaluated, the increase L nf h ' /e?ause of the ±™ number of
'
t™ aa
.55 mg/m3. to ulth the In « ««»«< I""1™ "tlmate of
and the occurrence of
. data - •
. . .
the incidence of LlaJtinLS, ""f /T "^ °f "hlch related '<>
aplastic anemia »2 too lo^ to pemit '?' Th6 Inciden" °«
sons between the vorkirs aid thf^ afurate statistical compari-
leukemia in the g^er.rD»ulSl 8r°UP' The ill<:««« of
Overall, 18 cases of "Luke™, ' "*S reported c° "== 3-8/100,000.
-er, eiact diagnoses ^^lnlT^:^^ ^ ^ «»•»! "
It could not be demonstrated that rll }eukf la "*™ not available.
Plants exceeded the ™™
5-17
-------
Benzene is also produced in the steel industry as a by-product
of the coking process. The health status of coke-oven workers has been
of continuing interest and Redmond et al. (1976) pursued a longitudinal
study of the mortality among 58,828 workers in steel plants in western
Pennsylvania. Data include records of 8628 deaths and the results
showed that coke plant workers exhibited a greater risk.of respiratory
cancer and kidney cancer than the general population of steel workers.
Any indication of cancer of the lymph or hematopoietic organs is
significantly lacking from these data.
Animal experimental results weakly support the view that benzene
is leukemogenic. The best available data in terms of experimental
design, adequacy of reporting, and duration of the study are summarized
in Table 5-5. Statistically significant results were obtained by Snyder
et al- (1980) in C57BL/6J mice — a strain that carries a virus, which
makes these animals much more susceptible to induction of lymphoma
following exposure to radiation, carcinogens, or immuno-suppressive
agents. Of the eight animals that died with hematopoietic neoplasms,
six were from lymphocytic lymphoraa in which there was thymic involvement,
one with plasmacytoma (myeloma) and one with leukemia (predominant
cell type appeared to be hematocytoblast). The two control animals
died of lymphocytic lymphoma without thymic involvement. In contrast,
results with AkR strain mice were negative with respect to increased
incidence of hematopoietic neoplasms, although this strain is also
susceptible to lymphoma. A lower exposure level was necessary because
of very poor survival of this strain at the 950 mg/m3 exposure level.
Maltoni and Scarnato (1979) reported a statistically significant
increase in zymbal gland carcinomas. Zymbal gland carcinomas are
reported to be rare in untreated rats; however, they are readily induced
by systemically administered carcinogenic agents (Baker et al. 1979).
A nonstatistically significant, increased incidence of leukemias,
apparently more pronounced in male rats, was also reported.
5.1.4 Summary of Effects on Humans
5.1.4.1 Ambient Water Quality Criteria — Human Health
Because benzene is suspected as being a human carcinogen and no
recognized safe concentration exists for a human carcinogen, the recom-
mended concentration of benzene in water is zero (U.S. EPA 1980).
This water quality criterion is based on the human epidemiological
data (Askoy 1977, Infante et al. 1977a, b, Ott et al. 1978), and is
supported by the animal experimental data in Sprague-Dawley rats
(Maltoni and Scarnato 1979). These epidemiological studies were used
by the U.S. EPA to recommend a target water level of 8 yg/1 to
keep any additional lifetime cancer risk below 10~5. The 8 yg/1
level is based on an equivalence in response to an absorbed dose of
16.2 yg/day for a human lifetime, regardless of the route. This
target-water level was predicted to give an incremental lifetime risk
of leukemia of 10~5. Further details of the derivation are given in
the Appendices to the criteria document for benzene (U.S. EPA 1980) and
the CAG report (U.S. EPA 1978a), and is also discussed in Section 5.1.6
below.
5-18
-------
BEN2ENE
^oute/dosage
Mlc;; ;57BL/6ja ™««i«/95o »8/m3
65 (f 6 hr/d s j/ . °
AkK;
Rats, Sprague-
Dawley, ?
Mice, C57BL/6N'
*-*-***/ ^~*\j iiii*/r
6 hr/d, 5 d/wk for
lifetime
(^200 mg/kg/day for
lifetime)
Inhalation/300 mg/m3
as above.
Gavage/250 mg/kg
4-5 d/wk, 52 wks
50 mg/kg as above
Subcutaneous/0.9-2 6
8/kg b.w./injection
2x/wk, 54 wk
(the average dose
rate was approx.
»"g/kg b.w./day)
Bone marrow hyperpiasla
noier^ 6VidenCe °f
poietic neoplasm
Spleen hyperplasia without
"ematopoietic neoplasm
No statistically significant
differences in survival and
8/40
13/32»>
16/32b
Mammary Carcinomas
Zymbal Gland Carcinomas
Leukemias
Total Leukemias
Granulocytic Leukemia
Total Tumors
0/38
2/38
Referenice
Snyder et a]
L980 — &
IS
-------
TABLE 5-5. CARCINOGENICITY OF BENZENE IN EXPERIMENTAL ANIMALS (Continued)
Species
Mice, C57BL63
AkR, C3H, DBA2
30
O
Subcutaneous/^50 mg/
once/wk. Presumed
for 43 wk
mg/kg b.w./day
for lifetime)
Leukemia incidence:
6/20bbefore 300 days in
test group.
29/212 before 300 days
in untreated controls.
Kirschbaum and
Strong (1942)
These strains of mice are susceptible to induction of lymphomas.
p <0.05; chi-square test, one-tailed, comparison to controls.
-------
I
I
Sufficient evidence demonstrates that benzene is a probable
leukemogen in humans and probably causes other hematological disorders,
especially pancytopenia. The dose-effect relationship between benzene
exposure and the incidence of these diseases in humans is uncertain,
primarily because of the absence of individual exposure data. Most
importantly, mean exposure data for an entire work force may under-
estimate the exposure to individuals who develop the disease.
Further uncertainties are introduced when the occupational exposure
levels are converted to a water concentration at which a lifetime con-
sumption of 2 I/day will give the same total dose. Hattis and coworkers
(1980) briefly discuss two reasons why it may be inappropriate to assume
that all increments of exposure (by increased concentration or by increased
duration) are equivalent. First, high-level occupational exposure could
be far more effective in-producing leukemia than low-level environmental
exposure; thus, the effect of low-level exposure could be overestimated.
Second, workers experienced their exposures as adults, whereas lifetime
exposure means exposure to persons during childhood as well. If leukemia
is a multistaged process and if benzene affects the early stages of
that process, then the longer the time interval of exposure to benzene,
the greater the risk of developing leukemia. Thus, the effect of life-
time exposure could be underestimated, when based on the dose conversion
from the occupational data.
5.1.4.2 Additional Health Effects
Aside from the reported hematological effects of chronic benzene
exposure, most adverse effects associated with benzene exposure are
of an acute nature and occur at considerably higher exposures. High
air concentrations of benzene can result in acute central nervous
system effects ranging from mild euphoria, giddiness, staggering
gait to paralysis, convulsions and potential death from respiratory
arrest and/or cardiovascular collapse. Air concentrations in the
vicinity of 64,000 mg/m3 for 5-10 minutes are generally lethal.
Teratogenic effects have been observed in mice with very high
exposures (3ml/kg on day 13 of gestation). Other toxic effects
noted in pregnant rats and the developing embryo include decreased
body weight in mothers, decreased litter size, embryonic resorptions
and decreased fetal weights. These effects occurred with continuous
inhalation exposure to benzene concentrations between 370 and 1783
mg/m-5. The U.S. EPA (1980) concluded that benzene is unlikely to be
a potential teratogen.
5-21
-------
5.1.5 Estimated Dose/Response Relationship for Cancer
Below, an estimate is derived for the potential lifetime carcino-
genic risk to humans as a result of the ingestion or inhalation of
benzene at a constant daily rate.
Ideally, this problem would be approached in tx^o ways:
• Given human dose/response data (generally from retrospective
studies of past occupational exposure, or of unusually high
ambient exposure levels), various extrapolation models would
be applied to obtain an approximate dose/response relation-
ship (a relationship giving percent excess carcinogenic re-
sponse as a function of daily dose or exposure level).
• Given dose/response data from controlled experiments on lab-
oratory animals, the animal doses would be converted to
estimated equivalent human doses, and again the various
extrapolation models would be applied to obtain an approximate
human dose/response relationship.
The advantage of the first approach is that the results are most
relevant to humans because the "test?1 subjects are humans. Extra-
polation of effect levels obtained from animal studies to "equivalent
human doses" adds a degree (unquantifiable) of uncertainty to the
dose/response relationship derived for man due to possible differences
in susceptibility, pharmacokinetics, repair mechanisms, etc.
On the other hand, in retrospective human studies, the exposure
levels, duration of exposure, and even response rates (carcinogenic
responses per exposed population) are usually "best estimates."
Furthermore, unknown factors (e.g., exposure to carcinogens other than
the one in question) may seriously bias the data. Information on
exposure, response, and general circumstances for the laboratory
animals is accurate, because these are design parameters. Also,
controlled animal experiments can yield a broader range of dose/
response data points, which allows straightforward application of the
extrapolation models. Usually this is not possible from human retro-
spective studies because of the insufficient data.
In addition to the uncertainties inherent in the type of data
used in the analysis, other important and largely unquantifiable sources
of uncertainty exist:
• The main purpose of risk analysis is to use observed response
rates at relatively high exposure levels to extrapolate
expected response rates (risks) at the relatively low levels
that might be found in the environment. However, the extra-
polation models cannot be tested at low exposure levels of
concern (low enough to keep excess lifetime risk per capita
5-22
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I
I
•— I-.
the occupational seti™ h .a" entlre l"«i»e. In
the exposure period is siSSicanti ? *XpOSUre' Slnce
of the test subjects a aSif if" 7 Chan the lifetime
performed to deterge a S?i • f * extraP°la<:ion is
actual dose. Howler rt? J™" d?" ecluival^t: to the
short duratlon^ ^.rttt^t or
analysis ls conservative mst': r«"^3; thus, the
of a
ba!
.
in the aPPlication of thedosl/resnons! T° £?uivalent exposure, and
Even greater uncertainty arises in ^ extrapolation »del themselves.
short-term exposure to equivalent lifet^"6"1011 °f SP°radic °r
present scientific methods Io not PSit ! eXp°SUre' In «* case,
assessment of lifetime human carcinog^nt rSk" aCCUrat£ " definitive
5-23
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5.1.6 Discussion of Available Data
Although not ideal, the available human data for benzene are
relatively good. The inherent validity of extrapolation within species
far outweighs the quantitative uncertainty in the human data. The CAG
(U.S. EPA 1978a) and MIT (Hattis et al. 1980) groups have done risk
analyses based on the studies of Aksoy and coworkers (1977), Infante
and coworkers (1977a, b) and Ott and coworkers (1978). Both CAG and
MIT computed potential risks of lifetime exposure to benzene in air
at low levels. The analysis below computes risk from ingestion of
benzene. The study of Ott et al. (1978) was not used for these risk
calculations. It is believed that their data are inconclusive because
of the relatively few deaths evaluated (only 3 deaths due to leukemia),
which tends to disproportionately affect risk estimates.
Having carefully considered both the CAG (U.S. EPA 1978a) and MIT
(Hattis eit al. 1980) analyses of risk, this discussion is limited to
noteworthy deviations from these two analyses. The interested reader
is urged to review these analyses to appreciate the sources of dis-
crepancies, the uncertainties involved, and the rationale of the risk
calculations. Differences in predicted risks stem from differences in
exposure estimates, response estimates, and model equations. The first
two categories are the input data and are given in Table 5-6 for the
three analyses that were based on the Infante and Aksoy studies.
5.1.6.1 Infante Study
The CAG analysis considered total leukemias, 9 cases, in the
exposed worker group vs. 1.25 in the nonexposed controls for a rela-
tive risk (R) of 7.2. The per capita probability of dying from all
forms of leukemia at zero exposure to benzene [noted here as PL(O)]
was given by the CAG in their Table 2 as Px » 0.0067. This report
concurs with the MIT group's choice to change R and consequently
PL(O) to reflect consideration of only non-lymphatic leukemias. This
makes a comparison with the analysis of the Aksoy data more appropriate
and is consistent with the view that benzene exposure is associated
much more closely with the non-lymphatic leukemias.
The occupational exposure concentration estimate by the CAG group
for the Infante study is considered unrealistically low (see Section
5.1.3.2). Yet, the duration of exposure (25-36 years) may be unreal-
istically high as pointed out by the MIT group. The longer duration
of exposure has been maintained to compensate for the likely under-
estimate in exposure concentration. Finally, the dose (see calculation
Table 5-6) was computed on a mg/day basis assuming, as discussed in
Section 5.1.3.2, that response is dependent on absorbed dose and is
independent of exposure route.
5-24
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Oi
TABLE 5-6. COMPARISON OF
LEUKEMIA FROM
Study
*- .
Infante
Aksoy
Analysis
CAG
MIT
ADL
CAG
MIT
ADL
R
7.2
10.7
10.7
19.9
19.9
19.9
L(0)a
l-i ' "" ——
0.0067
0.0045
0.0045
0.0045
0.0045
0.0045
40-23 ppm x 25-36 yrs
40-23 ppm x 5-15 yrs
345 mg/day x 25-36 yrs
63.6 ppm x 9.7 yrs
(78.8 - 32.4) ppm x 9.7 yrs
3250 mg/day x 9.7 yrs
probability of
(40 + 23) ,
2PPm x 1.2 mj/hr x 8 hr/day x 3.19
d» PP. x X.
, 150
x 10 hr/day + 22.5
x .5 „ 6 day/7 day ,
2.8 ppm
°-84 ppm
150 mg/dayb
4.2 ppm
9.8 ppm
450 mg/dayc
-------
5.1.6.2 Aksoy Study
All three risk analyses agree on the response input data
R and PL(0). Discrepancies do exist in estimating exposure concen-
trations. The reason for the much lower estimate by the CAG begins
with the assumption that average exposure concentration can be
estimated by the geometric mean of the midpoint of two intervals
(15-30 ppm for non-working hours and 150-210 ppm for work hours).
The arithmetic mean would be more accurate since total exposure is
proportional to the sum C^ + C2t2 .... Cntn. Using (150+210)/2 for
10 hours and (15+30)/2 for 14 hours gives -88 ppm/hr compared to
their geometric mean of 63.6 ppm. More importantly, the CAG reduces
the average exposure again by adjusting for the 10-hour work day
(i.e. 63.6 x 10/24 = 26.5 ppm); thus, it appears they adjust for
lower non-work exposure concentrations twice. The MIT estimate is
somewhat lower than the ADL estimate and stems from use of the
geometric mean of a "worst" case and "best " case. MIT "worst" case
is interpreted here as being closer to an average case since 180 ppm
and 22.5 ppm are the arithmetic means of the CAG estimates, respectively,
of the working concentration (150-210 ppm from CAG) and of the non-
working concentration (15-30 ppm from CAG). Furthermore, their use
of the geometric instead of the arithmetic mean results in a smaller
exposure. The estimate given in Table 5-6 is more straightforward
and believed to be more realistic.
In the conversion of occupational exposure data to lifetime
average daily ingestion, the occupational exposure via inhalation
is adjusted for 1.2 m3/hr respiratory rate, 8- or 10-hour work days,
a 3.19 mg/nr3 per ppm conversion factor, 50% inhalation retention, 5
(or 6) days/7-day work week, and average 70-year lifetime. These
factors were utilized in Table 5-6. Tables 5-7 and 5-8 also provide
a rough basis for comparing the predicted risks between studies by
relating ppm to mg/day.
5.1.7 Application of Dose/Response Models to Estimation of Human Risk
The ADL risk predictions utilize two different models, the first
model is the one-hit model (Arthur D. Little, Inc., 1980):
P(x) - 1 - e-(A+Bx)
which is very closely approximated by the so-called linear model,
utilized by CAG and MIT, for small values of P(x); that is for P(x)
<.l,
P(x) ~ A+Bx
where P(x) is the lifetime probability of leukemia at dose x. For
clarity, the notation PL(X) is used. The assumption here, as with
CAG and MIT, is that "R", the relative risk of leukemia for benzene-
5-26
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Ln
I
N>
ADL linear
B s .0003
per mg/day
ADL Log Probit
A a -3.9
GAG Linear
B = .01
per ppm
MIT Linear
B = .05 per ppm
TABLE 5-7.
Ingestion Rate in mg/day
^^lation__cpncen^ration in
2.8
14
8.4
42
30
90
28
140
84
420
300
52
280
1400
a 0.28 ppm x 3.19
ppm
22.4 -x 0.5 . 1 mg/day>
900
350
840
4200
3000
1800
2800
14000
-------
TABLE 5-8. PREDICTED EXCESS LIFETIME LEUKEMIAS PER MILLION
POPULATION DUE TO BENZENE INGESTION (INHALATION),
BASED ON THE STUDY OF AKSOY AND COWORKERS
Ingestion Rate in mg/day
Ui
1
to
CO
•01 .03 .1 .3
(.00028) (.00084) (.0028) (.0084)
ADL Linear
B = 0.0002 per
rog/day 2 6 20 60
ADL Log Probit
A = -4.0 - _ i 3
GAG Linear
B = 0.02
Per PP»" 5.6 17 56 168
MIT Linear
B = 0.009 2.5 7.6 25 76
m /m3 3
a .028 ppm x 3.19 -8^_ x 22.4 ~ x .5 = 1 mg/day.
1 3 10
(.028) (.084) (.28)
200 600 2000
32 300 1400
560 1680 5600
250 760 2500
-------
I
I
exposed workers compared to age or time-matched control population,
was independent of the length or age of exposure; that is,
occupational " p (Q) lifetime
Thus * R - A+B(x)
Thus, R - A+B(Q)
where pi/°) = A+B(0)
so that by algebraic manipulation,
B - PL(0; (R-D/x
where x is lifetime average daily exposure dose equivalent to the
occupational exposure, PL(0) is the lifetime probability of leukemia
with no or negligible benzene exposure, and B is the excess probability
of leukemia per mg/day. Using the input data given in Table 5-6,
BInfante= 0.00029 per mg/day
BAskoy = 0.00019 per mg/day
Log Probit Model
PE (x) = PL(x) = is
the cumulative normal distribution. Using the same assumption about
R as above [such that PL(0)R = PL(x)]; the following relationship is
obtained^
PE(x) - PL(0) (R-l)
and the values of the parameter A are as follows:
AAskoy - -4-02
^ Using the input data given in Table 5-6 and the two models, the
predicted risks at various exposure levels were calculated for the
two studies and are presented in Tables 5-7 and 5-8.
There is moderately good agreement among the eight separate pre-
dictions of risk at the higher levels of exposure (i.e. at >10 mg/day).
An exception is the MIT estimate based on the Infante study, which is
almost an order of magnitude higher than the others, this is because of
5-29
-------
a considerably lower estimated total exposure by the MIT group
for this study. At lower exposure levels, five of the risk estimates
are quite clearly parallel, the MIT/Infante prediction is consistently
high, and the ADL Log Probit predictions for both the Infante and
Aksoy studies are considerably lower because of the mathematical
model employed.
5-30
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I
I
5.2 HUMAN EXPOSURE
5.2.1 Introduction
Monitoring data on benzene in the environment indicate a wide range
of benzene levels in the natural environment and in foodstuffs. The
fate analyses also support the conclusion that benzene may occur in all
environmental media. As discussed in the human effects section, it has
been determined that benzene can be absorbed by all three routes of
exposure-- ingestion, inhalation, and dermal contact. The potential
absorption of benzene by these three routes has been considered in the
following analysis to estimate total daily absorbed doses.
Benzene concentrations in various media were estimated on a conser-
vative basis in order to avoid underestimating the actual exposure that
could occur. These data were combined with data on rates of air, water,
and food intake and/or duration of exposure to estimate the amounts
through each exposure route. Ideally, the absorption of benzene would
be analyzed with respect to subpopulation factors such as age, weight,
sex, breathing rates, food and water consumption, commuting and working
patterns, etc. For benzene, such detailed data are not available and
the variability and scarcity of the monitoring data do not justify
a detailed analysis. Instead, in the analysis below, total daily
absorption of benzene has been approximated for three broad population
groups, based on their location with respect to major benzene sources
of emission.
To illustrate that exposures to the general population are relatively
low, occupational exposure to benzene has been evaluated for each expo-
sure route (where appropriate) for a comparison with general population
exposure groups.
5.2.1.1 Populations Exposed through Contaminated Drinking Water and
Foodstuffs ~ " ~ "~
The available data on benzene levels in drinking water are summarized
in Section 4.3.2.1. These data indicate that benzene is detectable in
drinking water from surface sources, generally, however at levels <2 ug/1.
Maximum levels cited were <10 pg/1.
inn .
-------
Data on levels of benzene in groundwater sources of drinking water
are extremely sparse. Coniglio et 30
Ug/day and as much as 250 ug/day (NCI 1977).
Results from estimation of exposure to benzene through ingestion are
documented in Table 5-9. Based on a water consumption of 2 I/day, at the
concentrations shown in Table 5-9, the average benzene intake is 4 yg/day
and a maximum of 20 yg/day. In order to avoid an underestimate in the
true mean exposure through food ingestion, the NCI estimate of 250 yg/
day was used to calculate the potential daily absorption of benzene from
food.
5-32
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I
I
TABLE 5-9. ESTIMATED BENZENE EXPOSURE THROUGH INGESTION
Water;
Median
High
foodstuffs
Butter
Beef
Chicken, Lamb, Veal
Eggs
Haddock
Subtotal
NCI Estimate of Total
Foodstuff Exposure0
Concentration3
(Ug/l)
2
10
US/kg
0.5
2-19
<10
500-1900
100-200
Amount
Consumed
Dailyb
(1)
2
2
0.056
0.025
0.055
0.026
Daily
Exposure
(Ug/day)
4
20
0.03
0.004
28-105
2.6-5.2
31-108
250
data are taken from Table 4-10.
Data taken from ICRP (1974).
Q
Data taken from NCI (1977).
5-33
-------
5.2.1.2 Populations Exposed through Inhalation
Sources of direct releases of benzene to the atmosphere include
the plants that isolate benzene, the industrial plants using benzene,
traffic, and gasoline distribution facilities.
Population groups exposed to benzene by inhalation have been
categorized into four groups that are distinguished by atmospheric
levels of benzene: urban (high levels due to traffic congestion) , sub-
urban (lower levels from less dense traffic), rural/remote (low levels—
sparsely distributed vehicular sources), and user/manufacture sites
(high level, point sources). These groups coincide with typically
available monitoring data for atmosphere concentrations resulting from
the broad range of emission categories. Cigarette smoking has been
treated as a separate exposure situation.
The labor force in the vicinity of a source may be exposed 8 hr/day,
while residents in the area of a source may be exposed up to 24Jhr/day.
In the latter case, emissions may be reduced or eliminated at the close
of the working day, as a function of local meteorological conditions;
and nighttime exposure could drop to the local background level. Thus,
pollutant concentrations, which depend on the dispersion of emissions,
will vary over time in any given location, even if the emission rate is
absolutely constant.
Without performing site-specific modeling to determine actual con-
centrations, durations, and hence exposures, the analysis was simplified
to the consideration of average and maximum observed concentrations.
Because of the intermittent nature of point sources, the maximum con-
centrations are unlikely to exist longer than 8 hr/day and are probably
much shorter in duration. The mean concentrations, which were obtained
from monitoring data near sources, were applied to 24 hr/day exposure
scenarios.
Cigarette smoking has also been determined to add to the amount of
benzene inhaled and increase levels in the surrounding air. According
to Drill and Thomas (1978), the average benzene exposure is 90 ug/
cigarette. Based on data from the 1979 report from the U.S. Surgeon
General, the average smoker (1.56 packs/day) would be exposed to 2.8
mg/day and retain 1.4 mg/day (Richmond 1981). The U.S. Surgeon General
also reports a total of 54 million smokers in the United States in 1978
for all age groups.
Young et al. (1978) have stated that "unknowing inhalation" in the
home can occur from the use of paint strippers, carburetor cleaners.
denatured alcohol, rubber cement, and arts and crafts supplies. These
sources have not been documented, and exposures are assumed to be infre-
quent as well as dilute.
It has been assumed that the general population visits gas stations
periodically, although the frequency ranges from perhaps once a day to
5-34
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I
I
once or twice per month. A frequency of one visit per week for a 10-
minute duration was chosen as a representative pattern, which is
equivalent to 0.02 hr/day. The assumption that a 10-minute/week expo-
sure is equivalent to 0.02 hr/day is consistent with the guideline'set bv
the U.S. EPA (U.S. EPA 1979), which states that lifetime carcinogenic '
risk is dependent upon total exposure, and not the frequency or duration
of individual exposures. The units of minutes/week were converted to
hr/day in order to conform to the units of exposures from other sources.
In any event, the exposure due to gas station use by the general popu-
lation is relatively small and does not play a crucial role in the risk
assessment.
Occupational exposures to benzene by inhalation are analyzed at
the OSHA standard and over a range of observed workplace values to pro-
vide contrast with ambient exposure scenarios. The standard established
by OSHA is 10 ppm (32 mg/m3) as a time-weighted-average for the 8-hour
work day. Inhalation of benzene at this concentration would permit an
absorption of 153 mg/day.
The product of the benzene concentration, duration of exposure, and
appropriate respiratory rates were used to estimate potential daily
exposure (see Table 5-10). Exposures were calculated using the average
active adult breathing rate of 1.2 m3/hr (16 hours), which falls to 0.4
nrVhr during sleep (8 hours) (ICRP 1975). The numbers presented in
Table 5-10 represent possible exposures to benzene, and include a
respiratory retention factor of 0.5.
The results of the exposure calculations in mg/day (Table 5-10)
show that nonoccupational inhalation intakes may range from 0.005-10 mg/
day, while exposure at the occupational standard is 153 mg/day. The
average exposure of residents near a refinery, which appears to be the
source of the highest mean exposure (0.5 mg/day), is about 300 times
lower than the exposure of workers at the OSHA standard of 10 ppm
(31,920 yg/m3). Other nonoccupational activities are associated with
even lower relative exposures.
Urban and suburban areas do not differ greatly for typical benzene
concentration values; however, urban areas have a larger and higher
range. Average benzene concentrations in remote areas are only 1/5
and 1/3 the urban and suburban levels, respectively.
5.2.1.3 Percutaneous Exposure
Pure benzene is no longer readily available for residential use.
The majority of solvents, paint removers, paints and other substances
used in the home would contain only small amounts of benzene as a con-
taminant or possibly as a deliberately included component. As described
in Section 5.1, the rate of dermal absorption for benzene is about 550
mg/m /hr. Assuming a situation involving a 5% benzene solution and a
1/2-hour exposure duration, the calculation is:
5-35
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TABLE 5-10. ESTIMATED BENZENE EXPOSURE THROUGH INHALATION
I
to
CT>
Exposure Activity
Nonoccupational Activities in
Urban Areas
Suburban Areas
Rural/Remote Areas
Near Manufacture /User Sites
Chemical
Refinery
Gas Station Use
Cigarette Smoking
Occupational Activities
Outdoor In-traffic Job
In Benzene Recovery Plant
Range of Known Industrial Levels
Gas Station Employees
Exposure at the OSHA Standard
Benzene Concentration
Mean
(Mg/m3)
8.0
5.1
2.2
20
46
860
Range3
0.5-412
3.2-8.1
1.0-3.5
1-111
3-824
100-5400
Exposure
Duration
(hr/day)T>
< 24
<24
I24
8
<24
0.02
Mean
0.09
0.05
0.03
0.01
0.5
0.01
f\
Exposure
Rangea
(mg/day)
0.005-4.6
0.04--0.09
0.01-0.04
0.005-0.55
0.04-10
0.001-0.08
90 ng/cigarette
1.6 packs
12.3
4200
?
260
31,920
5.9-21.3
2700-10,700
0-483,300
110-5400
—
8
8
8
8
8
1.4
0.06
20
1.2
153
0.03-0.1
13-51.5
0-2320
0.5-26
3
The range given represents the spread of available data and is not meant to imply absolute limits.
The symbol <_ indicates that because of the nonconstant character of the emissions, the exposure
at the levels shown probably does not occur over the entire day.
'Exposures were calculated based on a respiratory retention factor of 0.5.
-------
I
I
550 mg/m2/hr x 0.072 in2 x 0.05 x 0.5 hr = 1
mg.
It is not realistic to assume that this level of exposure is typical;
however, for some small populations, it may represent a sporadic expo-
sure.
For comparison, assuming a worst case exposure in an industrial
situation in which an employee had both hands immersed in benzene for
1 hr/day, the resulting exposure would be:
550 mg/m2/hr x 0.072 m2 x 1 hr/day - 40 mg/day
where 0.072 m2 is the surface area of the hands. In Section 5.1.1.1,
a permeability factor was estimated to compute absorption of benzene
vapor through the skin; this factor was 0.002 m3/(m2xhr). At the
OSHA standard of 10 ppm (32 mg/m3), absorption of benzene vapor into
the body via the skin would be ^0.9 mg/8-hour work day.
5.2.2 Comprehensive Exposure Scenarios
The results of the exposure estimates are summarized in Table 5-11.
These data have been used in comprehensive exposure scenarios for all
routes (see Table 5-12). Scenario A involves the potential exposure of
urban dwellers (149,639,720 people or 74% of the 1970 Census population),
and would include exposure by inhalation, ingestion of predominantly
surface water (110 million people drink surface water supplies, which
are usually supplied to urban areas whose size is greater than 60,000
people), food consumption, and the use of gas stations. Percutaneous
exposure was not included in this comprehensive scenario because it
was assumed to be restricted to a small subpopulation using benzene
sporadically. The total typical daily exposure is about 0.4 mg/day.
Cigarette smoking could add 1.4 mg/day to this amount, as well as to
the amounts in the scenarios described below.
Considering the next largest population, rural dwellers (53,572,206
people as of 1970 or 26%), as Scenario B, inhalation exposure was included
as well as foodstuffs, drinking water, and gas station usage. Although
the drinking water supply is nearly 100% from groundwater, average expo-
sure levels are unknown. For the purpose of calculation, therefore, the
same value, i.e., urban value, was used. The total exposure for the rural
scenario is approximately 0.3 mg/day.
Scenario C, involves residents near a user or manufacturing site.
In this case, inhalation dominates the other routes by adding up to
0.5 mg/day for a total of 0.8 mg/day. The number of people involved
in this scenario cannot be accurately determined at this point; however,
it is likely to be small, compared with Scenarios A and B.
5-37
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TABLE 5-11. SUMMARY OF ESTIMATED BENZENE EXPOSURE AND ROUTES
Route and
Activity
Ingestion
Water
Fooda
Mean
Daily Intake
(mg/day)
0.004
0.250
Estimated Exposure
Population
(millions )b.
220
Inhalation — Nonoccupational
Urban 0.1
Suburban 0.05
Rural 0.03
Near Emission Sources 0.01-0.05
Gas Station Use 0.01
Cigarette Smoking 1.4
150
70
unable to estimate
220
54 million (1978)
Inhalation — Occupational
Outdoor In-traffic Jobs
Industrial
Gas Station Employees
At Occupational Standard
Percutaneous
Occupational -
Occupational -
- Liquid
- Vapor
Residential — Liquid
0.05
20
1.5
153
Worst Case
(mg/day)
40
0.9
unable to estimate
unable to estimate
unable to estimate
unable to estimate
an undeterminate sub;
of 0.1 million
subpopulation unknowr
but quite small
inhere are as yet insufficient data to determine truly typical values.
These data are the NCI's (1977) "conservative estimate."
Populations based on 1970 Census Data (U.S. Bureau of the Census 1979).
5-38
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I
I
TABLE 5-12. COMPREHENSIVE EXPOSURE SCENARIOS FOR BENZENE
Route
% of 1970 Population
Exposure by Scenario in mg/day
A B C
74 26 ~7~
Ingestion
Water
Food
0.004
0.25
0.004
0.25
0.004
0.25
Inhalation
Baseline
Gas Stations
Cigarettes3
0.1 (urban) 0.03 (rural) 0.5 (near sources)
0.01 0.01 0.01
1.4 1.4 1.4
Percutaneous
Residential
<1.0b
<1.0£
TOTALS
Potential Maximum0
0.4
1.8
0.3 0.8
1.7 2.2
In 1978, a population of 54 million individuals smoked cigarettes.
This amount not included in total exposure.
«*
"These amounts include smoking.
Source: Arthur D. Little, Inc.
5-39
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To provide a contrast with these three ambient exposure scenarios,
potential industrial exposures of employees producing and utilizing
benzene were calculated. If exposure occurs at the OSHA standard, the
employee can add 153 mg/day to baseline (food and water and nonoccupational
inhalation) exposure. If percutaneous exposure also occurs, an additional
exposure to 40 mg/day is possible. It is possible that a very small number
of individuals in this category (i.e., a most improbable event) will
receive the maximum possible exposures from all routes, about 190 mg/
day. Not only is the level of exposure unlikely, it would only occur
for less than a lifetime duration. Nevertheless, these calculations
indicate that occupational exposures to benzene are potentially much
higher than nonoccupational exposures.
j
5.2.3 Summary
In comparison- to the potential occupational exposure to benzene at
the OSHA standard, the nonoccupational exposures are low. The total
absorbed dose, excluding smoking, is on the order of 0.3-0.8 mg/day.
At the average rate of 1.56 packs/day, smoking was estimated to add
1.4 mg/day to the total absorbed daily dose. In contrast, the con-
tribution of water ingestion to total benzene absorption appears to be
quite low; however, the contribution of food may be one-half the total
for nonsmokers. Although the data on benzene levels in water and food-
stuffs are scarce, the reported levels are considered to be indicative
of the approximate benzene levels commonly found in these sources.
5-40
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REFERENCES
benzene. Blood. 52:285
u,
1974c. (As cited by D.S EPA mfla™ be"Zene- Hun' H«Sd. 24:70-74;
..
(As cited by s. EW 1978^ Haematoiogica 55:65-
l,76b
~
Bureau of Labor Statistics (BLS) n
-------
Dean, B.J. The genetic toxicology of benzene, toluene, xylenes and
phenols. Mut. Res. 47:75-97; 1978.
Deichmann, W.B.; MacDonald, W.E.; Bemal, E. The hemopoietic tissue
toxicity of benzene vapors. Toxicol. Appl. Pharmacol. 5:201-224; 1963.
Diem, K.; Lentner, C., eds. Scientific tables. 7th edition. Ciba-
Geigy Limited, Basle, Switzerland; 1971; 528.
Drill, S.; Thomas, R. Environmental sources of benzene exposure source
contribution factors. U.S. Environmental Protection Agency, Office of
Drinking Water; 1978.
Goldstein, A.; Aronow, L.; Kalman, S.M. Principles of drug action:
The basis of pharmacology. New York, NY: John Wiley & Sons- 1974.
262-264.
Goldwater, L.J. Disturbances in the blood following exposure tcr ben-
zene (benzol). Jour. Lab. Clin. Med. 26:957-973; 1941. (As cited by
U.S. EPA 1978b)
Goldwater, L.J.; Tewksbury, M.P. Recovery following exposure to benzene
(benzol). Jour. Indust. Hyg. 23:217-231; 1941. (As cited by U.S. EPA
1978b)
Gonasun, L.M.; Witmer, C.; Kocsis, J.J.;• Snyder, R. Benzene metabolism
in mouse liver microsomes. Toxicol. Appl. Pharmacol. 26:398-406; 1973.
Greenburg, L.; Magew, M.R.; Goldwater, L.; Smith, A.R. Benzene poisoning
in rotogravure printing. Jour. Industr. Hyg. Toxicol. 21:395-420; 1939.
(As cited by U.S. EPA 1978b)
Harris, R.L. Testimony before occupational safety and health administra-
tion. U.S. Department of Labor. Washington, DC; August 8, 1977. (As
cited by U.S. EPA 1978a)
Hattis, D.; Mendez, W.; Ashford, N.A. Discussion and critique of the
carcinogenicity assessment group's report on population risk due to
atmospheric exposure to benzene. Center for Policy Alternatives,
Massachusetts Institute of Technology, Cambridge, MA; 1980.
Helmer, K.J. Accumulated cases of chronic benzene poisoning in the
rubber industry. Acta Medica Scand. 118:354; 1944. (As cited in U.S.
EPA 1978a).
Hough, V.H.; Bunn, F.D.; Freeman, S. Studies on the toxicity of com-
mercial benzene and of a mixture of benzene, toluene and xylene. J.
Ind. Hyg. 26:296-306; 1944.
5-42
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I
I
Infante, P.F.; Rinsky, R.A.; Wagoner, J.K. ; Young, R.J. Leukemia in
benzene workers. Lancet. 2:76-78; 1977a.
Infante, P.P.; Rinsky, R.A. ; Wagoner, J.K. ; Young, R.J. Benzene and
leukemia. Lancet. 2:867; 1977b.
International Commission on Radiological Protection (ICRP). Report
of the task group on reference man. New York, NY: Pergamon Press-
Adapted 1974.
Irons, R.D. et al. Benzene is metabolized and covalently found in bone
marrow in situ. Chem. Biol. Interact. (In press); 1980". (As cited fav
U.S. EPA 1980)
Jenkins, L.J. et al. Long-term inhalation screening studies of benzene,
toluene, o-xylene and cumene on experimental animals. Toxicol. Appl
Pharmacol. 16:818; 1970. (As cited by U.S. EPA 1980)
Jerina, D. ; Daly, B. ; Witkop, P.; Zaltzman-Nirenberg, P.; Udenfriend, S.
Role of the arene-oxide-oxepin system in the metabolism of aromatic sub-
strates. In vitro conversion of benzene oxide to a premercapturic acid
and a dihydrodiol. Arch. Biochem. Biophys. 128:176-183; 1968.
Kim, N.K.; Stone, D.W. Organic chemicals and drinking water. Albany,
NY: New York State Department of Health; 1979.
Kirschbaum, A.; Strong, L.C. Influence of carcinogens on the age
incidence of leukemia in the high leukemia F strain of mice. Cancer
Res. 2:841-845; 1942.
Kissling, M. ; Speck, B. Chromosomal aberrations in experimental benzene
intoxication. Helv. Med. Acta. 36:59-66; 1972.
Konietzko, H. ; Keilbach, J. ; Drysch, K. Cumulative effects of daily
toluene exposure. Int. Arch. Occup. Environ. Health 46:53-58; 1980.
Lee, E.W. ; Kocsis, J.J.; Snyder, R. Acute effect of benzene on
incorporation into circulating erythrocytes. Toxicol. Appl. Pharmacol.
27:431-436; 1974.
Maltoni, C.; Scarnato, C. First experimental demonstration of the carcin-
ogenic effects of benzene: long-term bioassays on Sprague-Dawly rats
by oral administration. Med. Lav. 70:352; 1979. (As cited by U.S. EPA
1980)
Matsushita, T. Experimental studies on the disturbance of hematopoietic
organs due to benzene intoxication. Nagova Jour. Med. Sci. 28 • ?04-234-
1966.
5-43
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Moeschlin, S.; Speck, B. Experimental studies on the mechanisms of
action of benzene on the bone marrow (radioautographic studies using
3H-thymidine). Acta Haemat. 38:104-111; 1967.
National Academy of Sciences (NAS). Drinking water and health.
Washington, DC: National Academy of Sciences; 1977.
National Cancer Institute (NCI). On the occurrence, metabolism, and
toxicity, including reported carcinogenicity of benzene. Washington,
DC: National Cancer Institute; 1977.
Nau, C.A. ; Neal, J.; Thornton, M. Cg-C12 fractions obtained from
petroleum distillates. Arch. Environ. Health 12:382-393; 1966.
Nomiyama, K. Nomiyama, H. Respiratory elimination of organic solvents
in man. Int. Arch. Arbeitsmed. 32:85-91; 1974.
Ott, M.G. et al. Mortality among individuals occupationally exposed to
benzene. Arch. Environ. Health. 33:3; 1978. (As cited by U.S. EPA
1978as 1978b)
Pagnotto, L.D. et al. Industrial benzene exposure from petroleum
naphtha. I. Rubber coating industry. Am. Ind. Hyg. Assoc. Jour. 22:
417; 1961. (As cited by U.S. EPA 1978b, 1980)
Papper, E.W.; Kitz, E. Uptake and distribution of anesthetic agents.
New York, NY: McGraw-Hill; 1963.
Parke, D.V.; Williams, R.T. Studies in detoxification. LIV. The metabolism
of benzene. Biochem. J. 55:337-340; 1953a.
Parke, D.V.; Williams, R.T. Studies in detoxification. XLIX. The metabolism
of benzene containing [14C] Benzene. Biochem. J. 54:231-238; 1953b.
Redmond, C.K.; Strobino, B.R.; Cypress, R.H. Cancer exposure among
coke by-product workers. Ann. N.Y. Acad. Sci. 271:102; 1976. (As
cited by U.S. EPA 1978b)
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the Surgeon General. Washington, DC: Office of the Surgeon General;
1981.
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in man. SF-00290 Helsinki 29, Scand. J. Work Environ. Health 4(1)73-85;
1978.
Sato, A.; Nakajima, T. Dose-dependent metabolic interaction between
benzene and toluene in vivo and in vitro. Toxicol. Appl. Pharmacol.
48:249-256; 1979.
5-44
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I
I
Sato, A.; Nakajima, T. Differences following skin or inhalation exposure
in the absorption and excretion kinetics of trichloroethylene and toluene.
Br. J. Ind. Med. 35(1):43-49; 1978.
Sato, A.; Nakajima, T.; Fujiwara, Y.; Hirosawa, K. Pharmacokinetics of
benzene and toluene. Int. Arch. Arbeitsmed. 33:169-182; 1974.
Snyder, C.A.; Goldstein, B.D.; Sellakumar, A.R.; Bromberg, I.; Laskin, S.;
Albert, R.E. The inhalation toxicology of benzene: incidence of hema-
topoietic neoplasms and hematoxicity in AkR/J and C57BL/6J mice. Toxicol.
Applied Pharmacol. 54:223-331; 1980.
Snyder, R.; Kocsis, J.J. Current concepts of chronic benzene toxicity.
CRC Grit. Rev. Toxicol. 3:265-288; 1975.
Srbova, J.: Teisinger, J.; Skinnieskg, S. Absorption and elimination
of inhaled benzene in man. Arch. Ind. Hlth. Occupational 2:1-8; 1950.
(As cited by Nomiyama and Nomiyama 1974)
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1977.
Teisinger, J. et al. The metabolism of benzene in man. Procovni Lekarstvi.
4:175; 1952. (As cited by U.S. EPA 1978c)
Thorpe, J.J. Epidemiological survey of leukemia in persons potentially
exposed to benzene. Jour. Occup. Med. 16:375; 1974. (As cited by U.S.
EPA 1978b)
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in the U.S. 1970 and 1960. Washington, DC: U.S. Department of
Commerce, Bureau of the Census; 1979.
U.S. Environmental Protection Agency (U.S. EPA). Estimation of population
cancer risk from ambient benzene exposure. Carcinogen Assessment Group,
U.S. Environ. Prot. Agency, Washington, DC; 1978a.
U.S. Environmental Protection Agency (U.S. EPA). Assessment of health
effects of benzene germane to low-level exposure. Report No. EPA
600/1-78-061. Washington, DC: Office of Research and Development-
1978b.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria. Criteria Document - Benzene. Washington, DC: Criteria
and Standards Division, Office of Water Planning and Standards; PB292-
421; 1978c.
U.S. Environmental Protection Agency (U.S. EPA). Water quality criteria
Appendix C: guidelines and methodology used in the preparation oThealth
effect assessment chapters of the consent decree water criteria documents
reaeral Register 44(52):15980; 1979. aocumencs.
5-45
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U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for benzene. Washington, DC: Office of Water Regulations
and Standards Division. Available from: NTIS, Springfield, VA.
Report No. EPA 440/5-80-018; 1980.
Uyeki, E.M.; Ashkar, A.E.; Shoeman, D.W.; Bisel, T.U. Acute toxicity
of benzene inhalation to hemopoietic precursor cells. Toxicol. Appl
Pharmacol. 40:49-57; 1977.
Van Doom, R.; Bos, R.P.; Brouns, R.M.E.; Leijiekkers, C.M.; Henderson,
P.T. Effect of toluene and xylenes on liver sluthathione and their urinary
excretion as mercapturic acids in the rat. Inst. Pharmaco. and Toxicol.,
University of Nijmesen, Nijmesen, Netherlands. Arch. Toxicol. 43(4) •
293-304; 1980.
Veulemans, H. Masschelein, R. Experimental human exposure to toluene.
I. Factors influencing the individual respiratory uptake and elimination.
Int. Arch. Occup. Environ. Health 42(2):91-103; 1978a.
Veulemans, H.; Masschelein, R. Experimental human exposure to toluene
II. Toluene in venous blood during and after exposure. Int. Arch.
Occup. Environ. Health 42:105-117; 1978b.
Veulemans, H.; Masschelein, R. Experimental human exposure to toluene
III. Urinary hippuric acid excretion as a measure of individual solvent
uptake. Int. Arch. Occup. Environ. Health 43:53-62; 1979.
Ward, J.M.; Weisburger, I.H.; Yamamoto, B.S. Benjamin, T.; Brown, C.A.
Weisburger, E.K. Arch. Environ. Health. 30:22-25; 1975.
Wilson, R.H. Benzene poisoning in industry. Jour. Lab. Clin. Med.
27:1517-1521; 1942. (As cited by U.S. EPA 1978b)
Wolf, M.A.; Rowe, V.K.; McCollister, D.D.; Hollingworth, R.L., Oyen, F.
Toxicological studies of certain alkylated benzenes and benzene. Arch.
Ind. Health. 14:387-398; 1956.
Young, R.J. Benzene in consumer products. Science 199:248; 1978.
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I
6.0 BIOTIC EFFECTS AND EXPOSURE
6.1 EFFECTS ON BIOTA
6.1.1 Introduction
This chapter provides information on the exposure levels of ben-
zene that cause mortality or disrupt physiologic functions and processes
in aquatic organisms. Fairly extensive recent data exist for both marine
and freshwater organisms, including fish (adult, juvenile, larval, and
egg stages) invertebrates, plankton, algae, and microorganisms. The
toxic effects of benzene have been studied on cells, tissues, organisms,
and behavioral functions, such as reproduction, feeding, and locomotion.
Basically, it appears that benzene disrupts the cell membrane permeability,
which changes the ionic content of the blood and tissues, resulting in
internal poisoning.
Primarily, static bioassay techniques have been used to test the
effects of benzene on aquatic organisms. The static bioassay test
utilizes one initial exposure to an appropirate concentration of a
chemical to determine toxicity. In flow-through bioassay tests, a
fresh solution containing the test substance is continuously or period-
ically supplied to the organisms throughout the test period. Benzene
is a highly volatile compound, only slightly soluble in water. The
half-life in water (the time required for the concentration of a com-
pound to drop to one-half of its initial value) is very short for ben-
zene, approximately 4.5 hours because of evaporation (Buikema and Hendricks
1980). The problem of evaporation is inherent to both static and flow-
through bioassay tests where concentrations are determined nominally,
i.e., through introducing a measured amount of the substance other than
direct periodic measurement during the bioassay. As a result, the
validity of the data from toxicity tests for volatile substances where
the test solution is open to the environment is questionable (Buikema
and Hendricks 1980).
No data on the toxicity of benzene to terrestrial biota were
available.
6.1.2 Mechanisms of Toxicity
Several authors note that the basic mode of action of benzene, a
fat-soluble anesthetic, appears to be the disruption of cell membrane
permeability and changes in the ionic content of the blood and tissues.
Though the mechanisms of toxicity are unclear, it has been noted that
benzene causes an increase in cell permeability.
The mode of action may be disruption of the lipo-protein linkages
of the membrane. Based on changes in the blood chemistry of young coho
6-1
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salmon, Morrow et al. (1975) suggest that narcosis resulting from changes
in gill permeability causes ionic imbalance and internal C02 poisoning.
Shifts in ionic balance would interfere with the fish's ability to con-
trol the gas content in the swim bladder, which may account for the
observed loss of equilibrium. It is believed that benzene is absorbed
across the fish gill directly into the blood. From there, it is trans-
ported to tissues, such as liver, muscle, and kidney where it may be
oxidized to phenol (Brocksen and Bailey 1973).
Benzene may accummulate in the lipid-rich nervous tissue and result
in narcosis. In turn, narcosis may cause respiratory depression and
collapse by depressing the central nervous system (CNS). Depression of the
CNS function will occur if the cells cannot maintain their proper ionic
balance for nerve impulse transmission. At high concentrations of ben-
zene, fish pass sequentially through phases of restlessness (rapid,
violent, and erratic swimming), "coughing" or backflushing of water
over the gills, increased irritability, loss of equilibrium, paralysis,
and death (Leibmann 1960, Morrow et al. 1975).
Benzene can also cause acute anemia and decrease the oxygen trans-
port capacity of the blood, which results in anoxia. The actions of
benzene on the cell membrane, however, are rapidly reversible when the
benzene stress is removed (Brocksen and Bailey 1973, Goldacre 1968,
Morrow et al. 1975).
6.1.3 Freshwater Organisms^
Toxicity studies on freshwater biota included tests on algae, three
invertebrate species, and ten fish species (Tables 6-1 through 6-4).
Because of the extreme volatility of benzene and poor static toxicity
methodologies, no meaningful LC50 values for freshwater fish were obtained.
In addition, because benzene solubility decreases as salinitv increases
freshwater toxicity values should not be based on data obtained from
marine organisms (Berry and Brammer 1977)„
Other studies (U.S. EPA 1978a) report LC50 values for freshwater
organisms similar to those reported in Buikema and Hendricks (1980).
The range of LC$Q values for five species of freshwater fish was 20.0
mg/1 for the blue gill (Lepomis macrochirus) to 386.0 mg/1 for the
mosquito fish (Gambusia affinis) (Table 6-3).
Various authors (Buikema and Hendricks 1980) studied five algae
genera under static conditions. Toxic effects varied from 0.001 to >1000
mg/1 benzene, and Dunstan et al. (1975) state that 10 mg/1 benzene
appeared to be the inhibition threshold for all marine algae tested
except for the green alga Dunaliella. This alga was capable of good
growth up to 100 mg/1 benzene. It was concluded that benzene concen-
trations would rarely be as high as 10 mg/1 except for extremely short
periods because of its volatility (Dunstan et al. 1975).
6-2
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TABLE 6-1. EFFECT OF BENZENE ON AQUATIC FLORA
Toxicant
Concentration Length of
I
U)
Species
ALGAE
Amphidinium cartarae
Skeletonema costatum
Dunaliella tertiolecta
Cricosphaera carterae
Skeletonema costatum
Chlorella vulgaris
(mg/1)
0.001 - 100
0.001 - 50
100
0.001
0.01 - 100
0.001 - 20
50 - 100
0.1 - 10
20 - 100
25 - 500
1000 - 1744
Experiment
3 days
3 days
3 days
3 days
3 days
3 days
3 days
10 days
10 days
10 days
10 days
Chlorella sp.
FUNGI
Saccharomyces anomalus
PLANTS
Anacliaris canodensis
(Elodea)
55 - 553
312
625 - 937
1016 - 1250
741
12 hours
1 hour
Effect
inhibited growth
no effect
inhibited growth
stimulated growth
no effect
no effect
inhibited growth
no effect
inhibited growth
no effect
inhibited growth
reduced photosynthesis/
respiration ratio
no effect
toxic
lethal
killed plants
Reference
Dunstan et al. (1975)
Dunstan et al. (1975)
Dunstan et al._ (1975)
Dunstan et^ al. (1975)
Dunstan et al. (1975)
Dunstan et al. (1975)
Dunstan et al. (1975)
Atkinson et^ al. (1977)
Atkinson et al. (1977)
Hutchinson £t _al^ (1972)
Hutchinson et al^ (1972)
Potera (1975)
Levan (1947)
Levan (1947)
Levan (1947)
Currier and Peoples (1954)
-------
TABLE 6-2. ACUTE TOXICITY OF BENZENE TO INVERTEBRATES
Species
Tigriopus californicus
Crassostrea gigas (larvae)
Balanus amphitrite
Aedes aegypti
Brachionus plicatilis
Crago franciscorum
Palaemonetes pugio
Test Test
Habitat Duration Type
EC50
or
(larvae)
(adult)
Artemia salina
Nitrocra spinipes
Daphnia magna
Cancer magister
SW
SW
SW
1
FW
SW
SW
SW
SW
SW
FW
SW
(hour)
168
48
1
24
48
24
48
24
48
96
74
74
24
24
48
48
96
240
1*1 111 •! 1
S
s
s
s
s
s
?
s
s
s
s
s
s
s
s
s
CF
CF
CF
T5I7TT
>0.087
0.38
»1.0
-1.4
H.5
22.0
33.0
43.5
35.0
27.0
74.4-90.8
37.5-38.0
66.0
82-111.5
203.0
"347.0
108.0
<5.5
Reference
Barnett and
Kontogiannis (1975)
LeGore (1974)
Baras'h (1974)
Hubault (1936)
Berry and Brammer
(1977)
Eldridge and
Echeveiria (1977)
Benville and Korn
(1976)
Tatem and Anderson
(1974)
Potera (1975)
Tatem and Anderson
(1974)
Tatem and Anderson
(1974)
Neff et^ al. (1976)
Tatem and Anderson
(1974)
Potera (1975)
Potera (1975)
Price et_ al. (1974)
Potera (1975)
U.S. EPA (1978a)
Caldwell et_ al. (1976)
Caldwell et_ al. (1976)
Caldwell et al. (1976)
6-4
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I
I
I
TABLE 6-3. TOXtCITY OF BENZENE TO FRESHWATER ORGAMISMS*
Species^
Bluegill sunfish (Lepomis macrochirus)
Bluegill sunfish (Lepomis macrochirus)
Fathead minnow (Pimephales promelas)
Goldfish ( Carasslus auratus )
Guppy (Poecilia reticulatu£)
Mosquitofish ( Gambusia affinis )
Daphnia magna
Daphnia
Daphnia pulevb
Daphnia culcullat:a
Daphnia magna
Alga (Chlorella vulgaris)
Concentration
(mg/1)
20.0
22.49
32.0-33.7
34.42
36.6
386.0
203.0
356-620
265-345
356-390
>96.0
Effect
48-hr LC
50
96-hr LC
'50
48-hr LC
50
525.0
Chronic value
48-hr EC5Q
Reduction in cell no.
EPA <1973a>,
Cntrow and Adema (1978).
6-5
-------
TABLE 6-4. TOXICITY OF BENZENE TO SALTWATER ORGANISMS
Species
Striped bass
(Morone saxatilis)
Anchovey
(Engraulis mordax)
Pacific herring
(Clupea pallasi)
Coho salmon
(Oncorhynchus kisutch)
Test
Duration
(hour)
48
48
24
Test
Type LC5Q value Reference
CiigTT)
72, 96
24
96
CF
S
S
S
9.6
15
6.9
5.6
SR
4-55
S(?) 50
Meyeroff (1975)
Brocksen and Bailey (1973)
Benville and Korn (1977)
Benville and Korn (1977)
Struhsaker et al. (1974)
SR 17.6-22 Struhsaker j^t al. (1974)
Morrow et al. (1975)
-------
I
I
I
620 mg/1, both for
'» «.«. "ere
ranges from 203.0 to
6*1-4 Marine Organi
sm*
s
normally measured in the environment
saltwater species are
Buikema and Hendricks (1980)
saltwater fish, i.e., Morons
tained from a continuoI^w
""""trations
toxlcity data for nine
meaful LC50 value for
8)
Pacific herring ad 55
Sublethal Effects
took longer to develop. Ome develon T ? °f 45 mg/1 benzene
larvae exposed to 45 mg/1 benz^ ?h rr abn°rmalitie« occurred in
larvae exposed to benSae ^2^25 2/7 5? f°r 6arly Pacific
than eggs to benzene; ^ Were m°re
recover fro, benzene
wet
sre
have resulted from aired fen
The energy to metabolLebenaene
of energy for growth
decread-
effect may
con"ntrations
- 1 mgbnZene ^"S^-" -posed to 6.7 and
and coworkers (1974) substantiateJthis effect h§ "TT'3' Struh«^er
fzsh larvae with food in their guts Tnt i 7 he lower incidence of
exposed to an average benzene concur J?venile striped bass acutely
locate and consume t'heir food ration lft°er°f 6'°^/l ™™ Unable to
improved, and by the end of 4 wJeks strfnL K ' feedinS SUCCess
consumed 50% of their ration (Korn et al 333 eXP°Sed tO 3'5
6-7
-------
Several studies cited in Buikema and Hendricks (1980) indicate
that fishes exposed to sublethal doses of benzene exhibit significant
changes in oxygen consumption, and that the effects vary with life
stage. Studies on Pacific herring, chinook salmon and striped bass
indicate that oxygen consumption generally increases with exposure to
greater concentrations of benzene. There are several theories on the
mechanism by which oxygen consumption increases. One is that it results
from the oxidation of benzene to phenol by body tissues (Brocksen and
Bailey 1973).
6.1.5 Factors Affecting the Toxicity of Benzene
Certain environmental conditions may affect the results of toxicity
tests, both in the field and the laboratory. One principal parameter
that may affect the toxicity of benzene is salinity. The resistance
of copepods increases as salinity increases. However, a reverse response
has been noted for larval grass shrimp, while the adults were not as
salinity dependent (Potera 1975). These differences in response-may
reflect the lower solubility and thus biological availability of benzene
in saltwater (Lee et al. 1974) and differences in organism size between
the two age classes thus influencing uptake.
Temperature interactions have been studied only for algae, harpact-
icoid copepods, and grass shrimp. Adult grass shrimp were more tolerant
at lower test temperatures. This suggests that benzene enters the
organism more slowly perhaps because of lower metabolic rate (Potera
1975).
The factor of size as an effect on the response of fish to benzene
has been investigated and related to gill surface area. Less area is
related to less accumulation and excretion over time. Brocksen and Bailey
(1973) have also speculated that the different susceptibilities of the
species tested may be related to differences in lipid-rich tissue and the
biochemical pathways associated with fat metabolism. In addition, several
studies in Buikema and Hendricks (1980) indicate that the sensitivity of
an organism varies with the life stage tested. Larger and/or more mature
organisms are generally more resistant to benzene. However, Struhsaker
(1977) found that the eggs of the northern anchovy and the Pacific
herring were more resistant than the early larvae.
6.1.6 Conclusions
According to the literature surveyed, the lowest concentration of
benzene at which effects have been observed in aquatic organisms is
0.001 mg/1. This concentration affected growth in several algae species.
Acute effects on freshwater plants (Elodea) were found at 741 mg/1.
Toxic effects on algae were noted in concentrations ranging from 0.001
to 1000 mg/1 benzene; the alga Chlorella vulgaris was not affected in
concentrations of <500 mg/1 benzene. Acute effects for invertebrates
ranged from >0.087 mg/1 benzene for the copepod Tigriopus californicus
6-8
-------
I
I
ranging from 20.0 mg/1 for the blu'T? % , ^S rep°rt LC50
to 36.6 mg/1 for the SUDDV ?S«J ?? SUnflSh (Lepomis m^ro-
sensxtive fish in'this «Sy las the^ff^ff ^^tus) . The I£ST
with a LC50 of 386.0 mg/1. Mosquito fish ( Gambusia affinis )
The only value
An oervi o t tsu' T* " Strlped bass
important factor in the sensitivitv "Uggests that life cycle is
tests o * SP6CieS tO benZene'
tests on several marine f h «, • * SP6CieS tO benZene' From
be more sensitive than eggs to benLne^86116^1'/^36 W6re f°und t
capacity to recover from Xnzene ^^ever, larvae had a greater
toxicity varies among organisms Oth VK u Se Paramete^ affect
solubility with the LcrlTsl ol'saHnitv T fl decfease of Benzene
can be drawn regarding the effec?so? th^ definitive conclusion
of benzene. streets of these parameters on the toxicit
ranges
not rigidly-del^r^ £""£'""; J^T!: ^ ™^~«
°-001
trout (Salmo gardnerii)
-"• — - <•«-*
6-9
-------
• 36 - 100 mg/1. Concentrations in this range inhibited growth
in several species of freshwater algae; and
in one species, it stimulated growth. These
concentrations were acutely toxic to several
small invertebrates including copepods.
• 100 - 400 mg/1. Concentrations had chronic and acutely toxic
effects on a variety of organisms, including
the resistant mosquito fish, Dungeness crab
(Cancer magister); and several Daphnids.
• 400 - 1744 mg/1. Such concentrations inhibited growth, and
reduced photosynthesis—respiration ratio
in the resistant algae species, Chlorella.
6.2 EXPOSURE OF BIOTA TO BENZENE
Benzene is a fairly common substance in aquatic systems in the
United States, and has been detected in numerous types of waters,
including drinking water, rivers, chemical plant effluents, well water,
and lakes (Buikema and Hendricks 1980).
Industrial operations, which are the nain sources of direct aquatic
contamination, include: chemical production and processing, coating
operations, and storage and transportation. Direct input to the environ-
ment can occur via spills, leaks, and/or effluents from industrial sites.
The losses from production are concentrated primarily along the Texas
Gulf coast and in the Northeast (Buikema and Hendricks 1980).
Aquatic exposures can occur in any water contaminated with benzene
from a discharge, runoff, or as the result of an intermedia transfer
from land (landfill leachate infiltration of ground and the surface
waters) or air (rainout).
Our analysis will discuss probable levels of benzene involved in
aquatic exposures and compare them with the concentrations known to have
acute toxic or sub lethal effects.
6.2.1 Exposure Route
No information addressed the ingestion of benzene by aquatic biota.
The available data suggest that the primary mechanism of toxicity of
benzene to fish is changes in gill permeability, which results in internal
C02 poisoning. In chronic bioassays, benzene was found to impair feeding
in juvenile striped bass (Morone saxatilis); however, this effect was
not necessarily attributed to the ingestion of benzene.
6.2.2 Fish Kills
No data were found in the literature concerning any fish kills
related to benzene in aquatic environments.
6-10
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I
I
6.2.3 Monitoring Dat-a
Water quality data provided bv ^f" timSS greater
ssrs c^iS-i.L-hm-bi^^^
S-ri^rc^-SS^"^ --rr^:-
these effluent concentratio^ner^^r^T01' the length of time
and Missouri, concentrations near several S C°nn?cticut' Florida,
reached 1000 ug/l several chemical companies have
6.2.4 Exposure
not extensive, thus it is
benzene in aquatic sys^em BalL T^' °f exP°su^ levels
where benzene is" detected it is a^t^l^ *f * available' however,
concentrations. These level* f* * always found in 1^ (yg/1)
that have been datarSn.^^™^-^ ^- than conclnfrations
2000 The few incidences of hx.her concen?r\ " ^^ by a factor of
chemical plants are still below (bj loSx) th! ^ ar°Ciated with
'
level of benzene downstre depends pSj"6"' r!SUltS ta a h^a
available for dilution and on ?te str^J r °J the uPst««" flow
and streaB veloclty r"t
p i of many
aJi*,™88 "°del na" ^ ^^SificantTdTjf 3 Sln"ar —= Action
-
6-11
-------
The EXAMS model may underestimate the actual water column concen-
trations because it allows complete mixing throughout the 1000-meter x
100-meter x 3-meter river segment. Many discharges will form effluent
plumes, which will remain distinct from the flow of the river and will
naturally contain higher concentrations than EXAMS would predict for the
entire segment. Although the EXAMS results indicate that only the mildest
effects (inhibited growth to one alga species) may occur from exposure
to the largest aquatic discharge modeled, more serious effects could
be possible.
These considerations, however, when tempered with STORET data for
ambient levels do not give rise to predictions of aquatic exposures at
levels of benzene of concern for acute or serious chronic (sublethal)
effects.
6-12
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I
I
REFERENCES
Atkinson, L. P.; Duhstan. W.M.; Natoli J c Th
volatile hydrocarbon concentrations^ K analys" and control of
Water, Air, Soil Pollut. 8 23?-242 1977' ^^ ^^ oil ^ssavs.
1980) *'"* 242' 1977- (As cited in Buikema and Hendricks
.
Int.. Vodosnabzben, Kana« cS ' , Jh"?™- Nach' -
on
<" .« n-cnocyclic crude
„„. (AS
Brocksen, R.W • Bailev H T D
sahnon and striped bass expose^ tTSnzS/"^086 °f JUV6nile chinook
crude oil. Proceedings of the Joint ?««?' Water-soluble component of
"
e ont ««
of Oil Spills, Washinton DC £ JC2 "pISSJ
1973. (As cited by Buike.a and Hendrick! I 1980)
Buikema, A.L.; Hendrick^
F^^"«:S^ £S£ -ni
systems. New York, N£ ?er^n J °O " marI^{^^^ndJ7cLo-
Hendricks 1980) PergainOn Pr8SS> 1976' (As cited in Buikema and
Cantrow, J.H.•
sensitivity of Daphnia~na7np »^>! ^^"^ ma§na and comparison of the
t y "apunxd magna with Daphn"1" —1 ' - -
^QQn^ " tiyQroDiol. 591
iyo(J J
•S. EPA
6-13
-------
Currier,^H.G.; Peoples, S.A. Phytotoxicity of hydrocarbons. Hilgardia
23(6):115-173; 1954. (As cited by Buikema and Hendricks 1980)
Dunstan, W.M.; Atkinson, L.P.; Natoli, J. Stimulation and inhibition of
phytoplankton by low molecular weight hydrocarbons. Mar. Biol. 31: 305-
310; 1975. (As cited in Buikema and Hendricks 1980)
Eldridge, M.B.; Echeveiria, L. Fate of 14C benzene (an aromatic hydro-
carbon of crude oil) in a sample flood chain of rotifers and Pacific
herring larvae, Cal-Neva Wildlife Transactions, 1977:90-96. (As cited in
Buikema and Hendricks 1980).
Goldacre, R.J.. Effect of detergents and oils on the cell membrane. Carthy,
J.D.; Arthur D.R., eds. Biological effects of oil pollution on littoral
communities. London: Field Studies Council; 1968.
Hubault, E. Nocivite de carbures d'hydrogene vis a vis du poisson de
riviere. C.R. hebd. Seanc. Acad. d'Agric. (France):22:130-133; 1936.
(As cited in Buikema and Hendricks 1980)
i
Hutchinson, T.C.; Kauss, P.; Griffiths, M. The phytotoxicity of crude
oil spills in freshwater. Water Pollut. Res. Can. 7:52-58; 1972. (As
cited in Buikema and Hendricks 1980)
Korn, S.; Struhsaker, J.W.; Benville, P. The uptake, distribution and
14C toluene in Pacific herring, Clupea harengus pallasi. Fish. Bull
75(3):633-636; 1977.
Lee, C.C.; Craig, W.K.; Smith, P.J. Water soluble hydrocarbons from
crude oil. Bull. Environ. Contain. Toxicol. 12(2):212-217; 1974.
LeGore, R.S. The effect of Alaskan crude oil and selected hydrocarbon
compounds on embryonic development of the pacific oyster, Crassostrea
gigas. Diss. Abs. B. 35(7):3168; 1974. (As cited in Buikema and Hendricks
1980)
Levan, A. Studies on the camphor reaction of yeast. Hereditas 33:457-
514; 1947. (As cited in Buikema and Hendricks 1980)
Liebmann, H. Handbuch der Frischwasser-und-Abwasser biologie II. Munich:
R. Oldenburg; 1960.
Meyeroff, R.D. Acute toxicity of benzene, a component of crude oil, to
juvenile striped bass (Morone saxtilis). J. Fish. Res. Board Can. 32(10):1864-
1866; 1975. (As cited in Buikeraa and Hendricks 1980)
Morrow, J.E.; Gynitz, R.L.; Kirton, M.P. Effects of some components to
crude oil on young coho salmon. Copeia 2:326-331; 1975. (As cited in
Buikema and Hendricks 1980)
6-14
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I
I
marin
respiration, and
of
petroleul" °° survival,
76; 1975.
n
; 1977. (A. oiced
Hendricks 1980)
' T-
, 1974.
cited in Buikema and
quality
; 1973a.
U.S. Environmental Protection Agency (Tj S FPA^ *
quality criteria. Draft Document u *• ' )- Benzene. ambient water
1978b. Document. Washington, DC: NTIS No. PB292421;
U.S. Environmental Protection Agency (n S F
health and environmental impact! of selected v
^n, DC: U.S. Environmental Protection Agenc
8' "A)
°n
Washing
Planning and Regulations, s!
6-15
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I
I
7.1 HUMANS
and hematological disorders
chronic
(3°°-1200
levels than
to benzlnTa"
of four risk models that were u
Tables 5-7 and 5-8 for two separate
these results with the exposure
shown in Table 7-1 for the
exposure scenarios, with n
following estimates of risTare
for three very general
^exposure route and assume
f *" ChaPter 5' The results
****** W8re Prese*ted in
^ r6SUltS °f couPlin§
Presented in Table 5-11 are
three c^Prehensive
se?arately- Note thaE the
'^lnt^ tOtal ben26ne lntakes
the or
tion of drinking water (mostly ?ro
and gas station'usage! For Ls p
to benzene was estimated at 0.4 mg/Sav
was applied to the four
°CCUr by inhal"ion,
74, Of
'
hi e average, daily exposure
" t0tal
ana 3..000
The remainder of the 1970
rural dwellers, was considered
occurs by inhalation, ingestion of i t
the use of gas stations?8 §
million
exposure
*"* foodstuf^. and
,
lation. e rura w^lers that comprise this subpopu-
The third scenario developed, Scenario r i i j
a user or manufacturing plant For thl? K ' ^Cludes residents near
-
7-1
-------
TABLE 7-1. POTENTIAL RISK ESTIMATES FOR BENZENE EXPOSURE SCENARIOS USING DIFFERENT MODELS
Predicted Number of Excess Lifetime Leukemlas per Million Population
Scenario and
Data Base
A (0.4 mg/day)
Aksoy
Infante
B (0.3 mg/day)
Aksoy
Infante
C (0.8 mg/day)
Aksoy
Infante
Smoking Factor3
1.4 mg/day)
Aksoy
Infante
ADL Linear
Model
80
120
60
90
160
240
280
420
ADL Log Probit
Model
5
9
3
5
21
32
60
90
GAG
Linear Model
224
112
168
84
448
224
784
392
MIT
Linear Model
m-
560
76
420
202
1119
350
1960
Overal 1
RAH PP
IXQ 1 1 £^ C
5-560
3-420
21-1139
60-1960
''These numbers may be added to the numbers for the scenarios above.
-------
I
existed, benzene in cigaretS Ot
S°Urce of
population exposed.
cases
only occur in a small
a considerable amount
per million
and to
md
tO
Cigarette smoking (1.56 nacks/dav)
to benzene than fli of theloutes
scenarios. The potential exn±r.
similar because LhalSon SpL'r
small compared with food injestion
however, are regarded as incomple";
risk somewhat uncertain
11' nrrical
conclusions can be drawn
'° Pr°dUCe & larger Sx
°f the three exposure
^ ™al livin* a-
C C0ncentr^ions, is
' '
ir contribution to
as
7.2 BIOTA
JS2
monitored ambient levels oes not
Though effluent levels of benzene
the dispersion effect of flowing
fairly quickly. Thus, while «b u
benthic or algal populations might be "s
suffer some loss in numbers or health
highly localized and no SmlfS in
ecological community effects
"«
laborat0^ ""h
SOme ^stances,
T the concentration
" n°C end^
exposure and
ta^enta are
t0 Cause
7-3
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I
I
APPENDIX A. VEHICLE RELEASE OF BENZENE
This appendix contains the results of JRB Associates and Arthur D.
Little, Inc. (ADL) calculations on evaporative and exhaust emission of
benzene from automobiles. The ADL work is based on a set of (SWRI
unpublished) exhaust emission factors significantly lower, and more
recent, then the JRB figures. Thus, these latter were used in the
final materials balance. The reader is referred to the JRB Materials
Balance report for greater detail.
1. Automobiles
A. Evaporative - JRB calculation of 11,000-21,000 kkg/yr
B. Exhaust
1) With catalytic converter
a. JRB emission rate: 0.005-0.020g/mile
Emissions = (8.55 x 10" vehicle miles) (.005-.02g/mile)
= 4275-17,098 kkg
b. ADL data: 0.005-0.007g/mile
Emissions = (8.55 x 10" vehicle miles) (0.005-0.007=r/mile)
= 4275-5984 kkg
2) Without catalytic converter
a. JRB data: 0.05-0.15g/mile
Emissions = (3.16 x 10" vehicle miles) (0.05-0.15^/mile)
= 15,810-47,430 kkg
b. ADL data: 0.025-.073
Emissions - (3.16 x 10" vehicle miles) (0.025-0.073g/mile)
= 7905-23,082 kkg
C. Total auto emissions including evaporative
1) JRB: 31,085-85,528 kkg
2) ADL: 23,180-50,066 kkg
A-l
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2. Motorcycles
A. Crankcase emissions
JRB calculation of 0-73 kkg
B. Evaporative emissions
JRB calculation of 44 kkg
C. Exhaust
1) Two stroke engine
JRB emission rate: 0.27-O.Sg/mile
Emissions - (2.31 x 10" vehicle miles) (0.27-0.8g/mile)
- 6247-18,511 kkg
2) Four stroke engine
JRB emission rate: 0.05-0.15g/mile
Emissions = (2.31 x 10" vehicle miles) (0.05-0.15g/mile)
- 1156-3470 kkg
D. Total motorcycle emissions
JRB estimate: 1200-18,628 kkg
3. Trucks and buses
A. Light duty trucks
1) Evaporative
JRB calculation of 4578 kkg
2) Exhausts
JRB emission rate 0.06-0.2g/mile
Emissions - (2.8 x 10" vehicle miles) (0.06-0.2g/mile)
- 16,835-56,116 kkg
3) Total emissions
JRB: 21,413-60,744
B. Heavy trucks and buses
1) Evaporative
A-2
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I
I
B. Heavy trucks and buses
1) Evaporative
JRB calculation: 26 kkg
2) Exhaust
JRB emission rate: 0.2-0. 7g/mile
Emissions = 170-595 kkg
3) Total heavy truck and bus releases
JRB: 196-621 kkg
*' ehlCle rel6a , buses
A. JRB: 53,894-165,521 kkg
B. ADL- 45,989-130,059 kkg
A-3
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REFERENCES
JRB Associates, Inc. Level II. Materials balance. Benzene. McLean,
VA: JRB Assoc.; 1980.
Southwest Research Institute (SWRI). Unpublished data on automobile
emission concentrations; 1980.
A-4
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I
I
APPENDIX B. EXAMS SCENARIOS
1. Petroleum Refinery
EGD data
flow - 2 MGD
[Benzene] in effluent - 60 ug/1
assume 24 hour day
Loading Rate =1.9 g/hr = 0.002 kg/hr
2. Petroleum Refinery
from EGD data
assume flow = 10 MGD, 24 hour day
[Benzene] = 2 mg/1
Loading Rate =3.15 kg/hr
3. Solvent Use (textiles industry)
from EPA's "GAD to Water" 1976
flow = 3.74 million I/day
[Benzene] » 64 ug/1
assume 8 hour day
Loading Rate = 30 g/hr - 0.03 kg/hr
B-l
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I
APPENDIX C. LIQUID CONSUMPTION FOR EXPOSURE ESTIMATES
was 35.9
-« --"•
per capita consumption of each tvne of K« maret "S^nts,
shown in Table C-l The "aver* ^ beverage was calculated as
of beverages, tocLl^ .oSTTi^'S.? " C°nSUmeS °'85 1/d^
and bottled waters. (Of course actual inA- ^S?/P"lts' soft drinks,
vary widely.) Ctual lndlvidual consumption patterns
has becoercppd £!" ° */d.7> alnost half
111 reduce the ^Jt'of^he ^SnL/llsJ 0Tfe ^ '«
consumed unaltered. ^«niaining 1.154 of tap water that is
p .
ozonation (Westerman 1980) or activlt^ ^ P ?CSSS W3ter by either
processes are excellent striker? of m V S^anular carbon. Both
paration for coffee and tea ?aLo aids in °TSan^S' Boili-g> as in Pre-
evaporation. Therefore const™- / organics removal through
'
Therefore
Percent of total li'uld •lS^^r^8 "
organics consumed, if any are present L ^h V ?" ^he amount of
or occupational wat^F supples individual's domestic
C-l
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TABLE C-l. U.S. BEVERAGE CONSUMPTION IN 1979
Beverage
Soft Drinks
Beers
Fruit Drink
Soft Drink Mixes
Wines
Distilled Spirits
Bottled Waters
TOTAL
Percent3
of Market
43.8
29.2
12.4
7.8
2.5
2,5
1.8
100
Total
Gallons5
Consumed
7,950,287,7001
5,314,400,000
2,256,800,000
1,419,600,000
455,000,000
455,000,000
327,600,000
18,178,687,000
Per Capita
Consumption0
gal/yr £/day
35.9
24
10.2
6.4
2.1
2.1
1.5.
82.2
0.37
0.25
0.11
0.07
0.02
0.02
0.02
0.854
'Data given in Beverage World (1980).
'Total Consumption calcula
gallons and market share.
:Per
of:
Total Consumption calculated from total market figure of 18.2 billion
I
cPer capita consumption based on total consumption and U.S. population
7,950,287,700 gallons 001 ,,, ,Q0 . . , .
35.7 gal/person = 221,456,482 derived from the soft
drink data presented in above cited reference.
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I
I
REFERENCES
Beverage World, 1980 Market index and sales planning guide. Beverage
World, April 1980. p32.
Westerman, M. The argument for non-cheaiical water treatment. Beverage
World, Nov. 1980. p208.
C-3
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