EPA-540/1-86-024
Agency
Office of Emergency and
Remedial Response
Washington DC 20460
Off'ce of Research and Development
Office of Health and Environmental
-Assessment
Environmental Criteria and
Assessment Office
Cincinnati OH 45268
Superfund
oEPA
HEALTH EFFECTS ASSESSMENT
FOR COAL TARS
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EPA/540/1-86-024
September 1984
HEALTH EFFECTS ASSESSMENT
FOR COAL TARS
U.S. Environmental Protection Agency
Office of Research and Development
Office of Health and Environmental Assessment
Environmental Criteria and Assessment Office
Cincinnati, OH 45268
U.S. Environmental Protection Agency
Office of Emergency and Remedial Response
Office of Solid Waste and Emergency Response
Washington, DC 20460
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DISCLAIMER
This report has been funded wholly or 1n part by the United States
Environmental Protection Agency under Contract No. 68-03-3112 to Syracuse
Research Corporation. It has been subject to the Agency's peer and adminis-
trative review, and 1t has been approved for publication as an EPA document.
Mention of trade names or commercial products does not constitute endorse-
ment or recommendation for use.
11
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PREFACE
This report summarizes and evaluates Information relevant to a prelimi-
nary Interim assessment of adverse health effects associated with coal tars.
All estimates of acceptable Intakes and carcinogenic potency presented 1n
this document should be considered as preliminary and reflect limited re-
sources allocated to this project. Pertinent toxlcologlc and environmental
data were located through on-Hne literature searches of the Chemical
Abstracts, TOXLINE, CANCERLINE and the CHEMFATE/DATALOG data bases. The
basic literature searched supporting this document 1s current up to
September, 1984. Secondary sources of Information have also been relied
upon In the preparation of this report and represent large-scale health
assessment efforts that entail extensive peer and Agency review. The
following Office of Health and Environmental Assessment (OHEA) sources have
been extensively utilized:
U.S. EPA. 1982a. Carcinogen Assessment of Coke Oven Emissions.
Office of Health and Environmental Assessment, Office of Research
and Development, Washington, DC. EPA 600/6-82-003. NTIS PB
83-129551.
U.S. EPA. 1982b. Coal Tars Health Effects Assessment. Environ-
mental Criteria and Assessment Office, Cincinnati, OH. p. 10.
Internal draft.
The Intent 1n these assessments 1s to suggest acceptable exposure levels
whenever sufficient data were available. Values were not derived or larger
uncertainty factors were employed when the variable data were limited 1n
scope tending to generate conservative (I.e., protective) estimates. Never-
theless, the Interim values presented reflect the relative degree of hazard
associated with exposure or risk to the chemical{s) addressed.
Whenever possible, two categories of values have been estimated for sys-
temic toxicants (toxicants for which cancer 1s not the endpolnt of concern).
The first, the AIS or acceptable Intake subchronlc, 1s an estimate of an
exposure level that would not be expected to cause adverse effects when
exposure occurs during a limited time Interval (I.e., for an Interval that
does not constitute a significant portion of the llfespan). This type of
exposure estimate has not been extensively used or rigorously defined, as
previous risk assessment efforts have been primarily directed towards
exposures from toxicants 1n ambient air or water where lifetime exposure 1s
assumed. Animal data used for AIS estimates generally Include exposures
with durations of 30-90 days. Subchronlc human data are rarely available.
Reported exposures are usually from chronic occupational exposure situations
or from reports of acute accidental exposure.
111
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The AIC, acceptable Intake chronic, Is similar 1n concept to the ADI
(acceptable dally Intake). It 1s an estimate of an exposure level that
would not be expected to cause adverse effects when exposure occurs for a
significant portion of the Hfespan [see U.S. EPA (1980) for a discussion of
this concept]. The AIC Is route specific and estimates acceptable exposure
for a given route with the Implicit assumption that exposure by other routes
Is Insignificant.
Composite scores (CSs) for noncardnogens have also been calculated
where data permitted. These values are used for ranking reportable quanti-
ties; the methodology for their development 1s explained 1n U.S. EPA (1983).
For compounds for which there 1s sufficient evidence of cardnogenlcHy,
AIS and AIC values are not derived. For a discussion of risk assessment
methodology for carcinogens refer to U.S. EPA (1980). Since cancer 1s a
process that 1s not characterized by a threshold, any exposure contributes
an Increment of risk. Consequently, derivation of AIS and AIC values would
be Inappropriate. For carcinogens, q-|*s have been computed based on oral
and Inhalation data If available.
1v
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ABSTRACT
In order to place the risk assessment 1n proper context, the reader Is
referred to the preface of this document. The preface outlines limitations
applicable to all documents of this serves as well as the appropriate Inter-
pretation and use of the quantitative numbers.
There are extensive data which Indicated that coal tars and coal tar
components are carcinogenic 1n experimental animals. Human data Indicate
that Industrial exposure mixtures containing coal tar volatHes are asso-
ciated with excess cancer risk.
U.S. EPA (1982a) has used ep1dem1olog1cal data to develop a quantitative
risk assessment for coke oven workers, expressed as an Incremental risk of
3.2 (mg/kg/day)"1. Although coal tar volatHes are present as major
constituents 1n coke oven emissions 1t 1s probable that differences exist
between the composition of the oven emissions and potential exposure
mixtures from coal tar products following the distillation process. It 1s
felt that despite these reservations, exposures should be substantially
similar and that the coke oven data can be used to estimate risk associated
with coal tar exposure.
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ACKNOWLEDGEMENTS
The Initial draft of this report was prepared by Syracuse Research
Corporation under Contract No. 68-03-3112 for EPA's Environmental Criteria
and Assessment Office, Cincinnati, OH. Or. Christopher DeRosa and Karen
Blackburn were the Technical Project Monitors and Helen Ball was-,the Project
Officer. The final documents 1n this series were prepared for the Office of
Emergency and Remedial Response, Washington, DC.
Scientists from the following U.S. EPA offices provided review comments
for this document series:
Environmental Criteria and Assessment Office, Cincinnati, OH
Carcinogen Assessment Group
Office of A1r Quality Planning and Standards
Office of Solid Haste
Office of Toxic Substances
Office of Drinking Hater
Editorial review for the document series was provided by:
Judith Olsen and Erma Durden
Environmental Criteria and Assessment Office
Cincinnati, OH
Technical support services for the document series was provided by:
Bette Zwayer, Pat Daunt, Karen Mann and Jacky Bohanon
Environmental Criteria and Assessment Office
Cincinnati, OH
v1
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TABLE OF CONTENTS
1.
2.
3.
4.
5.
ENVIRONMENTAL CHEMISTRY AND FATE
ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . .
2.1.
2.2.
ORAL
INHALATION
TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1.
3.2.
3.3.
3.4.
SUBCHRONIC
3.1.1. Oral
3.1.2. Inhalation
CHRONIC
3.2.1. Oral
3.2.2. Inhalation
TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS. . ,
3.3.1. Oral
3.3.2. Inhalation
TOXICANT INTERACTIONS
CARCINOGENICITY
4.1.
4.2.
4.3.
4.4.
HUMAN DATA
4.1.1. Oral
4.1.2. Inhalation ,
BIOASSAYS
4.2.1. Oral
4.2.2. Inhalation ,
OTHER RELEVANT DATA
WEIGHT OF EVIDENCE .
REGULATORY STANDARDS AND CRITERIA
Page
.... 1
.... 3
.... 3
.... 3
.... 4
.... 4
.... 4
. . . . 4
5
5
5
6
6
6
6
7
7
7
7
8
8
8
12
13
14
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TABLE OF CONTENTS (cont.)
Page
6. RISK ASSESSMENT 15
6.1. ACCEPTABLE INTAKE SUBCHRONIC (AIS) 15
6.2. ACCEPTABLE INTAKE CHRONIC (AIC) 15
6.3. CARCINOGENIC POTENCY (q-j*) 15
6.3.1. Oral 15
6.3.2. Inhalation 15
7. REFERENCES 20
APPENDIX: Summary Table for Coal Tars 25
V111
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LIST OF ABBREVIATIONS
AOI Acceptable dally Intake
AIC Acceptable Intake chronic
AIS Acceptable Intake subchronlc
BaP Benzo(a)pyrene
CTPV Coal tar pitch volatHes
CS Composite score
DNA Deoxyrlbonuclelc add
PAH Polycycllc aromatic hydrocarbons
TWA Time-weighted average
1x
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1. ENVIRONMENTAL CHEMISTRY AND FATE
Coal tar is a black, viscous liquid or sem1sol1d substance obtained by
the destructive distillation of bHumlnonus coal as in the production of
coke. Typically, one ton of coal in a coke oven may yield -27.5-34 I of
coal tar (U.S. EPA, 1982a). The physical properties of coal tar vary
substantially. The specific gravity of coal tar may vary from 1.18-1.23
(Hawley, 1981). Coal tar is soluble 1n ether, benzene and chloroform, and
1s partially soluble in ethanol, acetone and methanol and only slightly
soluble in water (Hawley, 1981). The typical constituents of United States
coke oven-derived coal tar are the following: benzene, 0.12%; toluene,
0.25%; o-xylene, 0.04%; m-xylene, 0.07%; p-xylene, 0.03%; ethylbenzene,
0.02%; styrene, 0.02%; phenol, 0.61%; o-cresol, 0.25%; m-cresol, 0.45%;
p-cresol, 0.27%; xylenols, 0.36%; high boiling tar acids, 0.83%; naphtha,
0.97%, naphthalene, 8.8%; 1-methylnaphthalene, 0.65%; 2-methylnaphthalene,
1.23%; acenaphthene, 1.05%; fluorene, 0.64%; anthracene, 0.75%; phenan-
threne, 2.66%; carbazole, 0.6%; tar bases, 2.08%; and medium soft pitch,
63.5% (McNeil, 1983). The pitch contains four, five, six and seven-ring
PAHs and their methylated derivatives (McNeil, 1983). The coal tar obtained
through destructive distillation of coal 1s usually subjected to further
distillation. The distillation of coke oven tar produces the following
fractions: light oil, phenolic oil, naphthalene oil, wash oil, light anthra-
cene oil, heavy anthracene oil and medium soft pitch (McNeil, 1983).
The exposure of undistilled coal tar to the ambient atmosphere is likely
to contaminate the atmosphere primarily with volatile compounds such as
monocyclic and PAHs, phenolic compounds and heterocycllc compounds. The
fate and transport of these compounds in the atmosphere may be determined by
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their chemical and photochemical reactivity and physical removal mechanisms
(dry and wet deposition) 1n the atmosphere. In general, the fate of the
most relevant compounds will be very similar to the fate of PAHs 1n the
atmosphere.
In aquatic systems, coal tar constituents will partition Into two frac-
tions: one very small fraction will be solublUzed 1n the water and stay as
the mobile phase, and the other very large fraction will precipitate as
sediment 1n water. The solublUzed fraction containing different chemical
constituents may undergo chemical and microbiological reactions, and evapo-
rative and sorptlve processes 1n aquatic media. The Insoluble part In the
sediment 1s expected to have a very long lifetime.
In soils, coal tar may partition Itself Into three fractions. Volatile
constituents In coal tar may enter the atmosphere as a vapor or partially 1n
the partlculate phase. A second fraction of coal tar constituents may be
solublUzed by rainwater. This solublUzed part, consisting of several
chemicals, may undergo physical and chemical processes In soil. The third
and very large fraction that may consist of the nonvolatile and Insoluble
part of coal tar may persist In soil for a long period of time.
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2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL MAMMALS
2.1. ORAL
Pertinent data regarding the quantitative absorption of coal tars
following exposure by the oral route were not located 1n the available
literature.
2.2. INHALATION
Pertinent data regarding the quantitative absorption of coal tars
following exposure by the Inhalation route were not located 1n the available
literature.
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3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1. SUBCHRONIC
3.1.1. Oral. Pertinent data regarding the subchronlc oral toxldty of
coal tars were not located In the available literature.
3.1.2. Inhalation. Klnkead (1973) prepared an aerosol of coal tar In
which the solids previously had been removed by centrlfugatlon. He exposed
female Sprague-Dawley yearling rats (64), male (32) and female (32) Sprague-
Dawley weanling rats, male ICR mice (50), and male CAF-1 mice (50) continu-
ously for 90 days at concentrations of 0.2, 2.0 and 10 mg/m3. In addi-
tion, 80 yearling female Sprague-Dawley rats, 9 weanling rats of each sex,
25 male CAF-1 mice, 25 male ICR mice, 24 female New Zealand white rabbits
and 100 male Syrian golden hamsters were exposed continuously for 90 days at
20 mg/m3. Greater than 95% of the aerosol droplets were <5 ym in
diameter.
Considerable mortality among exposed animals was encountered in this
study, which the authors attributed to debilitation causing greater suscep-
tibility to infections. However, cumulative animal mortality was propor-
tional to exposure concentration. In all species tested, there was a marked
effect of exposure on body weight growth curves. Animals either lost weight
(mice, hamsters, rabbits) or grew at a slower rate than nonexposed controls
(rats). Even the lowest exposure concentration, 0.2 mg/m3, produced some
adverse effects on body weight gain, with the most striking effect observed
in male CAF-1 mice whose body weight decreased from 30 g to 25 g during the
90 days in the 0.2 mg/m3 group. Following the termination of exposure,
the inhibitory effect of coal tar aerosol on growth was still evident for at
least 7 months in most species.
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Klnkead (1973) conducted a subsequent study, described by McConnell and
Specht (1973), employing a coal tar 1n which the solid particles and light
oil fractions were retained In the experimental aerosol. Sprague-Oawley
rats, New Zealand white rabbits, JAX mice, and Syrian golden hamsters
(numbers not specified) were exposed continuously for 90 days to the coal
tar aerosol at a concentration of 10 mg/m3. In addition, 150 CF-1 mice
were exposed to the aerosol and serially sacrificed for hlstopathologlc
analysis. Among exposed rats and hamsters, McConnell and Specht (1973) de-
scribed three significant lesions occurring at the termination of exposure.
These were phagocytlzed coal tar pigment In alveolar macrophages and 1n the
peMbronchlal lymphold tissue; hepatic and renal hemoslderosls, which dis-
appeared by 100 days postexposure; and mild central lobular necrosis In the
liver. Among mice sacrificed 99 days postexposure, moderate pigmentation of
alveolar macrophages was observed 1n 14/15 CF-1 mice, but 1n only 1/13
exposed JAX mice.
3.2. CHRONIC
3.2.1. Oral. Pertinent data regarding the chronic oral toxldty of coal
tars were not located 1n the available literature.
3.2.2. Inhalation. MacEwen et al. (1976) prepared a composite coal tar
mixture from multiple coking ovens around the greater PHtsburg area. Coal
tar samples were blended together with a 20% by volume amount of BTX
(benzene, toluene, xylene) fraction of coke oven distillate. This material
was believed to be more representative of that Inhaled by workers on top of
coke ovens. Female (75) ICR-KF-1 mice, female (50) CAF-1-JAX mice, male
(40) and female (40) weanling Sprague-Oawley rats, New Zealand white rabbits
(18), and male (5) and female (9) Macaca mulatta monkeys were exposed to a
coal tar aerosol at 10 mg/m3, 6 hours dally, 5 days/week, for 18 months.
-5-
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Animals were held for an additional 6-month observation period following
termination of exposure. Development of skin tumors 1n mice precluded
assessment of other systemic effects. A significant Inhibition of body
growth rate was observed for both male and female rats after 4 months and
for rabbits by the end of the 1st month. Monkeys showed no significant
Inhibition of growth rate. In this study, 16/18 test rabbits and 6 control
rabbits died during the test period.
3.3. TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS
3.3.1. Oral. Pertinent data regarding the teratogenldty of coal tars
following oral exposure were not located In the available literature.
3.3.2. Inhalation. Pertinent data regarding the teratogenldty of coal
tars following Inhalation exposure were not located 1n the available
literature.
3.4. TOXICANT INTERACTIONS
Pertinent quantatlve data regarding the Interactions of coal tars with
other compounds were not located 1n the available literature.
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4. CARCINOGENICITY
4.1. HUMAN DATA
4.1.1. Oral. Pertinent data regarding the cardnogenldty of orally
administered coal tars were not located 1n the available literature.
4.1.2. Inhalation. Studies of workers exposed to "tarry fumes" 1n the
coal gas (Doll et al. 1972, Kawai et al., 1967), steel (Redmond et al.,
1972) and aluminum reduction Industries (G1bbs and Horowitz, 1979; Mllham,
1979) have supported an occupational association with lung, skin and hemato-
poletlc cancers. Tarry fumes, however, were not coal tar per se. Only 1n
the studies of roofers (Hammond et al., 1976) and coke oven workers (Redmond
et al., 1979) was exposure specifically to coal tars or coal tar volatlles.
Hammond et al. (1976) observed Increases In both lung and skin cancer 1n
roofers with >20 years of work experience, and Increases 1n skin cancer 1n a
group with 9-19 years of work experience. A single measurement reported
that workers Inhaled BaP, a polyaromatlc hydrocarbon 1n coal tar, at levels
ranging from undetectable to 153 yg during a 7-hour work shift. The
corresponding levels of coal tar were not reported.
Redmond et al. (1979), in a final report of an extensive epidemlologlc
study of coke oven workers, summarized the results of interim reports by
Lloyd (1971), Redmond et al. (1972, 1976) and Mazumdar et al. (1975). Coke
oven workers (2552 employed 1n Allegheny County) with >5 years of exposure
had an increased relative risk of lung cancer (2.63) and kidney cancer
(3.55). Mazumdar et al. (1975) calculated cumulative exposures to CTPV for
the subgroups of the cohort and suggested that exposures <200 mg/mVmonth
would not result 1n an Increased risk of cancer. Using CTPV estimates,
there was a dose-related Increase 1n lung cancer among nonwhlte workers,
while for white workers, the Increased risk appeared not to be related to
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CTPV. The Increased rate/1000 of lung cancer 1n nonwhHe males was 4.0,
12.9, 24.9 and 54.6 for groups exposed to <199, 200-499, 500-699 and >700
mg/m3-month. In addition, Redmond et al. (1976) reported that side oven
workers also had an Increase In risk of cancer, although these workers are
exposed to much lower levels of CTPV. In 10 plants studied outside
Allegheny county, there was no difference between the races, although
similar excesses 1n risk of lung cancer were reported. The excess risk of
kidney cancer was not apparent 1n the non-Allegheny county plants.
4.2. BIOASSAYS
4.2.1. Oral. Pertinent data regarding the cardnogenldty of orally
administered coal tar to experimental animals were not located 1n the avail-
able literature.
4.2.2. Inhalation. The first experimental demonstration of cancer
produced by Inhalation of coke oven-derived material was by Morton et al.
(1963). They used the same coal tar sample, taken from a coke oven, that
had previously been reported to produce tumors on the skin of mice (Morton,
1961). The tar was characterized as having a BaP content of 0.71%, a high
"tar add" content (5.1%), and a low content of benzene Insolubles (2.74%)
1n comparison with other coal tars. Among 33 C3H mice Inhaling a coal tar
aerosol at 300 mg/m3 for a total of 40-100 hours over a 13- to 35-week
period, 5 developed squamous cell tumors In the periphery of the lung during
the 36-week postexposure observation period. One of the tumors was an
Invasive squamous cell carcinoma. The control mice were killed at 82 weeks
of age and none of the 30 animals had tumors of the lung.
Since the development of cancers by the Inhalation of xenoblotlcs was,
at that time, a rarely observed phenomenon 1n experimental animals, further
Inhalation studies were pursued. Tye and Stemmer (1967) employed two coke
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oven-derived tars 1n their study. The first was a tar sample of the same
composition as that used In previous studies, as described by Horton et al.
(1963). The second coal tar was high In toluene-Insoluble material (17.8%),
low 1n tar adds (1.4%) and had a BaP content of 1.1%. Both tars were
separated Into phenolic and nonphenollc fractions, and various combinations
were used to produce aerosols for Inhalation exposure to male C3H/HeJ mice.
Groups of 50 mice were exposed for 2 hours, three times weekly, for 55
weeks. The concentration of coal tar aerosol was 200 mg/m3 for the first
8 weeks and 120 mg/m3 for the remaining 47 weeks. Animals were examined
after spontaneous death or after scheduled intervals. During the study,
three mice from each group were killed at 4 weeks, five mice from each group
were killed at 31 weeks and all surviving animals were killed at 55 weeks.
Their findings Included the observation of increases in squamous metaplasia,
intrabronchial and alveolar adenomas, and adenocardnomas. The most promi-
nent lesions 1n exposed animals were Intrabronchial adenoma and adenocarci-
noma. None of the control animals developed lung tumors. The authors con-
cluded that the presence of phenols in the coal tar exerted a cocardnogenic
effect together with polynuclear aromatic hydrocarbons, possibly caused by
an irritant effect. No direct evidence was provided, however, to explain
the role of the phenolic fraction in tumor development, and the tumorigenlc
potential of the phenolic fraction alone was not assessed.
In later studies, Kinkead (1973) exposed mice, rats, hamsters and
rabbits to a coke oven-derived coal tar aerosol at 20, 10, 2 and 0.2 mg/m3
continuously for 90 days and observed them until death. The aerosol con-
sisted of a benzene extract of coal tar from which the solids were removed
by centrlfugatlon, and before generating the aerosol, the added benzene and
the light oil fractions were also removed. Several types of tumors devel-
oped in the exposed animals, as described by McDonnell and Specht (1973).
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An Independent analysis of the pathologic data from this study was conducted
by the National Institute for Occupational Safety and Health (NIOSH, 1978),
and the findings are summarized in Table 4-1. No data were available for
the 20 mg/m3 concentration. From the NIOSH (1978) analysis of the Kinkead
(1973) data, it was concluded that the coal tar aerosol produced a dose-
related incidence of lung tumors 1n mice. In addition, the Increased Inci-
dence of splenic lymphosarcomas 1n mice and lung tumors in rats was also
felt to be related to the coal tar exposure. There is some disagreement
between the exposure data of Kinkead (1973) and the pathologic report in
NIOSH (1978). Kinkead (1973) stated that rabbits and hamsters were exposed
only at 20 mg/m3, while the NIOSH (1978) report gives data for these
species at lower exposure concentrations. These conflicting points make it
unclear as to whether the animals examined in NIOSH (1978) were the same
animals exposed by Kinkead (1973) and examined by McConnell and Specht
(1973).
A follow-up long-term study reported by MacEwen and Vernot (1976) and
MacEwen et al. (1976) involved the exposure of female ICR CF-1 (75) and
CAF-1 JAX (50) mice, male (40) and female (40) weanling Sprague-Oawley rats,
18 New Zealand albino female rabbits, and male (5) and female (9) Macaca
mulatta monkeys to a coke oven-derived coal tar aerosol. Animals were
exposed to a chamber concentration of 10 mg/m3, 6 hours dally, for up to
18 months. Hlstopathologic data for mice and rats have been reported. The
rabbits and monkeys were not sacrificed and examined 1n this study, but were
maintained for long-term, postexposure observation.
Various tumors were found In mice, although principally alveolargenic
carcinomas of the lung were observed (26/61 in ICR CF-1 mice and 27/50 1n
CAF-1 JAX mice as compared with 3/68 and 8/48 1n the respective controls).
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TABLE 4-1
Tumors from Exposure to Airborne Coal Tar 1n Four Animal Species3
Tumor Incidence (%)
Spec1esb
Mice
Rats
Hamsters
Rabbits
Tumor
skin
lung
spleen
kidney
liver
urocyst
skin
lung
spleen
kidney
liver
skin
lung
spleen
kidney
liver
adrenals
skin
lung
spleen
kidney
liver
urocyst
0.00 mg/m3
3
30
5
1
9
0
10
4
8
1
1
0.7
0.6
0.7
2
0.6
27
0
0
0
0
0
0
0.20 mg/m3
1
39
20
3
4
0
6
3
4
0
0
0
3
0
1
0
0
0
0
0
0
0
0
2.00 mg/m3
1
58
5
0
11
3
3
10
4
0
0
0
0
0
0
0
57
0
0
0
0
0
0
10.00 mg/m3
6
77
14
0
0
0
0
18
8
6
3
4
4
4
0
2
17
12
0
0
0
0
0
aSource: NIOSH, 1978
bResults are based on data from a total of 63 rabbits, 376 hamsters, 498
rats and 563 mice.
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The Incidence of squamous cell carcinomas 1n the lungs of exposed rats was
100% 1n males and 82% 1n females. None of the control rats developed lung
tumors.
4.3. OTHER RELEVANT DATA
Horton (1961) demonstrated that twice weekly dermal application of coal
tar to the shaved skin of mice resulted 1n Increases In dermal tumors. The
latency period ranged from 7-15 months depending on the source of the tar.
Human case reports dating back to 1885 (NIOSH, 1978) have also supported an
association between occupational exposure to coal tars and the development
of skin cancer.
Although coal tar contains Individual components, primarily PAHs, which
have been extensively evaluated and found to be mutagenic (F1shbe1n, 1976;
U.S. EPA, 1982a), few data are available concerning the mutagenlcity of coal
tar mixtures as a whole. Brat et al. (1982) tested roofing tar pot emis-
sions for genotoxicity 1n a number of systems using mammalian cells. No
details were given concerning sample collection methods or sample composi-
tion. The tar emission samples gave positive results in a HPC/DNA repair
assay using primary hepatocyte cultures, but not the ARL/H6PRT mutagenesis
assay. Coke oven emissions were also tested 1n the DNA repair assay and
yielded greater DNA repair activity than the tar sample (106 grains/nucleus
vs. 37.7 grains/nucleus) when both were tested at doses of 10"1 mg/mS,.
More extensive data are available concerning the mutagenlcity of coke
oven emission; these are reviewed 1n U.S. EPA (1982a). Extracts of coke
oven door emissions have been shown to be mutagenic 1n bacteria. Extracts
of samples from coke oven collecting mains have been shown to cause muta-
tions in bacteria and mammalian cells in culture. These studies are
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relevant to coal tars In that a large proportion of the Identified mutagenlc
compounds 1n coke oven emissions are PAHs, presumably from coal tar vola-
tilization.
BaP 1s the marker PAH which has been most extensively monitored. BaP
was detected 1n "air contaminated with coal tar pitch fumes" at a level of
400 ng/1000 m3 (1800 pg/g partlculates) (Sawlckl et al., 1965).
Worker-exposure concentrations of BaP 1n coal and pitch coking plants have
been measured as 0.3-35 mg/1000 m3 (Fishbein, 1976). Emissions from coke
ovens In the USSR have been reported to contain 120-1700 yg BaP/g
partlculates (von Lehmden et al., 1965).
4.4. WEIGHT OF EVIDENCE
Studies 1n rats and mice Indicate that Inhalation exposure to coal tars
results 1n Increased Incidence of lung tumors (Tye and Stemmer, 1967;
Klnkead, 1973; McConnell and Specht, 1973; MacEwen et al., 1976). In epi-
demic! ogle studies of roofers exposed to coal tars, there was an elevated
risk of both skin and lung cancer (Hammond et al., 1976), while coke oven
workers exposed to coal tars had an elevated risk of lung and kidney cancers
(Redmond et al., 1979). The evidence for carclnogenldty for coal tars In
animals Is "sufficient," and the evidence for carclnogenldty 1n humans 1s
"limited," bordering on "sufficient," using the criteria for weight of evi-
dence proposed by the Carcinogen Assessment Group of the U.S. EPA (Federal
Register, 1984). Coal tars as a chemical class are, therefore, most appro-
priately classified as a Group 81 chemical.
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5. REGULATORY STANDARDS AND CRITERIA
NIOSH (1978) has recommended a 10-hour TWA concentration for coal tars
(cyclohexane-extractable fraction) of 0.1 mg/m3. The ACGIH (1980) con-
siders coal tar pitch volatHes to be a recognized carcinogen and suggests a
TWA of 0.2 mg/m3.
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6. RISK ASSESSMENT
6.1. ACCEPTABLE INTAKE SUBCHRONIC (AIS)
Coal tars are a class of chemicals that are known to be animal carcino-
gens and for which a carcinogenic potency factor has been estimated by the
Carcinogen Assessment Group from human ep1dem1olog1c data. It 1s, there-
fore, Inappropriate to calculate an oral or Inhalation AIS for coal tars.
6.2. ACCEPTABLE INTAKE CHRONIC (AIC)
Coal tars are a class of chemicals that are known to be animal carcino-
gens and for which a carcinogenic potency factor has been estimated by the
Carcinogen Assessment Group from human ep1dem1olog1c data. It 1s, there-
fore, Inappropriate to calculate an oral or Inhalation AIC for coal tars.
6.3. CARCINOGENIC POTENCY (q^)
6.3.1. Oral. Pertinent data regarding the cardnogenldty of coal tars
following oral exposure were not available for calculating a cardnogenldty
potency factor, q,*.
6.3.2. Inhalation. The animal studies available also do not provide
sufficient data to derive a q,* using the linearized multistage model.
The subchronlc study by Klnkead (1973) reports dose-related Increases 1n
lung tumors In mice exposed to coal tar aerosols of between 0.2 and 10
mg/m3. The number of animals per group and number of tumor-bearing
animals were not provided In this report, which precludes the derivation of
a q,*. The chronic study of MacEwen et al. (1976) employed only one
exposure level and male rats at this level had 100% tumor Incidence. Since
male rats appear to be the most sensitive spedes, this group should be used
1n risk assessment; however, a q,* cannot be derived from data when only a
single exposure 1s used and 100% tumor Incidence 1s reported.
-15-
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The U.S. EPA (1982a) Cancer Assessment Group (CAG) has used the eplde-
mlologic data from the study of Redmond et al. (1979) along with the expo-
sure data developed by Mazumdar et al. (1975) to calculate a carcinogenic
potency factor for coke oven emissions. In the analysis of the study of
Redmond et al. (1979), the CAG grouped the nonwhHe coke oven workers Into
four age and exposure groups as summarized in Table 6-1. Using these data,
CAG calculated a unit risk of 0.9xlO~3 for lifetime exposure to 1
yg/m3 of coal tars. This incremental risk can also be expressed as 3.2
(mg/kg/day)"1 by assuming a 70 kg man breathes 20 m3 of air per day and
that complete absorption occurs.
Coal tar is a by-product of bituminous coal distillation in coke produc-
tion. Many components of coke oven emissions are present in coal tar, espe-
cially a wide variety of PAHs and their methylated derivatives. However, it
might be suspected that the exposure mixture would be somewhat different
during exposure to oven emissions as compared to exposure to the coal tar
product after the coke oven distillation process 1s completed.
Good epidemiological data for exposure to coal tars per ^e_ are not
available for risk assessment purposes. Despite uncertainties concerning
potential differences In exposure mixture composition, it 1s felt that
exposures should be substantially similar and that the coke oven data can be
used to estimate risk associated with coal tar exposure.
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TABLE 6-1
Average Dose Levels, Lung Cancer Deaths, Person-Years
Observation for Risk, and Rates Used to Estimate Dose-Response
Relationships, by Model Used to Define Dose and by Age
at Entry to Study3
NonwhHe Workers Only
Dose Model Age at Dose
Entry Range'5
Zero lag 25-34 nonoven
0-99
100-199
200-299
300+
35-44 nonoven
0-149
150-299
300-499
450+
45.-S4 nonoven
0-249
250-449
450-699
700+
55-69 nonoven
0-249
250-449
450-749
750+
5-year lag 25-34 nonoven
0-49
50-149
150-199
200+
35-44 nonoven
0-99
100-199
200-349
350+
Average
Dose6
0
36.6
149.0
249.5
386.8
0
67.8
226.8
366.4
590.9
0
147.7
353.2
564.5
885.5
0
153.3
333.4
600.9
972.4
0
19.0
102.3
172.2
265.0
0
44.6
149.0
259.3
462.1
Lung Cancer
Deaths
3
1
0
3
4
4
0
2
3
5
17
1
4
4
8
4
1
1
4
10
3
1
0
4
3
4
0
2
4
4
Person-
Years
22,405
3,202
2,685
3,030
3,062
16,227
2,388
2,976
2,727
2,027
11,306
1,527
1,706
1,545
1,330
5,820
491
596
716
450
22,405
2,567
3,985
2,822
2,605
16,227
2,254
2,952
3,072
1,840
Yearly Rate
per 100,000
13.4
31.2
0
99.0
130.6
34.7
0
67.2
110.0
246.7
150.4
65.5
234.5
258.9
601.5
68.7
203.7
167.8
558.7
2222.2
13.4
39.0
0
141.7
115.2
24.7
0
67.8
130.2
217.4
-17-
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TABLE 6-1 (cont.)
NonwhHe Workers Only
Dose Model Age at
Entry
5-year lag 45-54
(cont.)
55-69
10-year lag 25-34
35-44
45-54
55-69
Dose
Rangeb
nonoven
0-199
200-349
350-599
600+
nonoven
0-199
200-399
400-649
650+
nonoven
0-49
50-99
100-149
150+
nonoven
0-99
100-149
150-249
250+
nonoven
0-149
150-249
250-499
500+
nonoven
0-149
150-299
300-549
550+
Average
Dose6
0
112.4
268.9
460.3
763.0
0
115.4'
293.0
535.5
851.7
0
18.8
76.8
120.6
193.1
0
46.7
123.5
191.5
353.0
0
76.4
193.0
362.4
641.8
0
95.3
299.8
439.4
729.7
Lung Cancer
Deaths
17
1
4
2
10
4
1
2
4
9
3
1
3
1
3
4
1
1
4
4
17
2
3
2
10
4
1
1
5
9
Person-
Years
11,306
1.828
1,397
1,573
1,310
5,820
516
665
567
503
22,405
3,964
3,371
3,226
1,418
16,227
3,956
2,283
2,360
1,519
11,306
2,308
1,308
1,607
1,162
5,820
660
576
505
512
Yearly Rate
per 100,000
150.4
54.7
286.3
127.2
763.4
68.7
193.8
300.8
705.5
1789.3
13.4
25.2
89.0
31.0
211.6
24.7
25.3
43.8
169.5
263.3
150.4
98.5
229.4
124.5
860.6
68.7
151.5
173.6
990.1
1757.8
-18-
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TABLE 6-1 (cont.)
NonwhHe Workers Only
Dose Model Age at Dose
Entry Rangeb
15-year lag 25-34 nonoven
0-9
10-39
40-69
70+
35-44 nonoven
0-9
10-69
70-129
130+
45-54 nonoven
0-69
70-149
150-349
350+
55-69 nonoven
0-69
90-199
200-429
430+
Average
Dose6
0
1.5
27.1
55.3
100.3
0
1.6
43.3
97.1
197.7
0
24.4
104.7
222.7
486.6
0
48.7
141.3
331.4
604.9
Lung Cancer
Deaths
3
2
2
0
4
4
1
2
2
5
17
2
3
2
10
4
1
2
6
7
Person-
Years
22,405
4,457
2,303
3,098
2,121
16,227
2,374
3,014
2,601
2,129
11,306
1,623
1,612
1,512
1,361
5,820
602
609
579
461
Yearly Rate
per 100,000
13.4
44.9
86.8
0
188.6
24.7
42.1
66.4
76.9
234.9
150.4
123.2
186.1
132.3
734.8
68.7 .
166.1
328.4
1036.3
1518.4
aSource: U.S. EPA, 1982a
-months exposure to CTPV
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7. REFERENCES
ACGIH (American Conference of Governmental Industrial Hyglenlsts). 1980.
Documentation of the Threshold Limit Values, 4th ed. (Includes Supplemental
Documentation, 1981, 1982, 1983). Cincinnati, OH. p. 102.
Brat, S.V., C. long and G.M. Williams. 1982. Detection of genotoxlc
airborne chemicals 1n rat liver culture systems. In: Genotoxlc Effects of
Airborne Agents, R.R. T1ce, D.L. Costa and K.M. Schalch, Ed. Plenum Press,
NY. p. 619-632.
Doll, R., M.P. Vessey, R.W.R. Beasley, et al. 1972. Mortality of gas-
workers — Final report of a prospective study. Br. J. Ind. Med. 29:
394-406. (Cited In NIOSH, 1978)
Federal Register. 1984.- Environmental Protection Agency Proposed Guide-
lines for Carcinogenic Risk Assessment. 49 FR 46294-46299.
•
F1shbe1n, L. 1976. Atmospheric mutagens. In: Chemical Mutagens, Princi-
ples and Methods for Their Detection, A. Hollaender, Ed. Plenum Press, NY.
Vol. 4, p. 219-320.
G1bbs, G.W. and I. Horowitz. 1979. Lung cancer mortality 1n aluminum re-
duction plant workers. J. Occup. Med. 21: 347-353. (Cited In U.S. EPA,
1982b)
-20-
-------
Hammond, E.G., I.J. Sellkoff, P.L. Lawther and H. Seldman. 1976. Inhala-
tion of benzpyrene and cancer 1n man. Ann. NY Acad. Sd. 271: 116-124.
(Cited 1n U.S. EPA, 1982b)
Hawley, G.G. 1981. The Condensed Chemical Dictionary, 10th ed. Van
Nostrand Reinhold Company, New York. p. 257-258.
Norton, W.S. 1961. An investigation of the carcinogenic properties of
various coal tars or commercial fractions thereof. Report of the Kettering
Laboratory, Department of Preventive Medicine and Industrial Health, Univer-
sity of Cincinnati. 32 p. (Cited in NIOSH, 1978)
Horton, A.M., R. Tye and K.L. Stemmer. 1963. Experimental carcinogenesis
of the lung. Inhalation of gaseous formaldehyde or an aerosol of coal tar
by C3H mice. J. Natl. Cancer Inst. 30: 31-43. (Cited in NIOSH, 1978)
Kawai, M., H. Amamoto and K. Harada. 1967. Epidemiologic study of occupa-
tional lung cancer. Arch. Environ. Health. 14: 859-864. (Cited in U.S.
EPA, 1982b)
Kinkead, E.R. 1973. Toxicity of coal tar aerosol. .In.: Proceedings of the
Fourth Annual Conference of Environmental Toxicology, Fairborn, OH: October
16-18, p. 177-188.
Lloyd, J.W. 1971. Long term mortality study of steelworkers. V. Respira-
tory cancer in coke plant workers. J. Occup. Med. 13(2): 53-68. (Cited in
NIOSH, 1978)
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MacEwen, J.D. and E.H. Vernot. 1976. Carcinogenic effects of chronic
Inhalation exposure of animals to coal tar aerosol. Toxic Hazards Research
Unit Annual Technical Report: 1976 Aerospace Medical Research Laboratory.
Wright-Patterson A1r Force Base, OH: AMRL-TR-76-57. (Cited in NIOSH, 1978)
MacEwen, J.D., A. Hall and L.D. Scheel. 1976. Experimental oncogenesls In
rats and mice exposed to coal tar aerosols. Presented before the Seventh
Annual Conference on Environmental Toxicology, Dayton, OH: October 16,
p. 66-81.
Mazumdar, S., C. Redmond, W. Sollecito and N. Sussman. 1975. An epidemlo-
loglcal study of exposure to coal-tar-pitch volatiles among coke oven
workers. APCA J. 25(4): 382-389. (Cited in NIOSH, 1978)
McConnell, E.E. and H.D. Specht. 1973. Lesions found in animals exposed to
coal tar aerosols, in: Proceedings of the Fourth Annual Conference on
Environmental Toxicology, Fairborn, OH: October 16-18, p. 189-198.
McNeil, D. 1983. Tar and pitch. .In: Kirk-Othmer Encyclopedia of Chemical
Toxicology, 3rd ed., Vol. 22, M. Grayson, Ed. John Wiley and Sons, Inc.,
New York. p. 564-600.
Mllham, S. 1979. Mortality in aluminum reduction plant workers. J. Occup.
Med. 21: 475-480. (Cited in U.S. EPA, 1982b)
-22-
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NIOSH (National Institute for Occupational Safety and Health). 1978.
Criteria for a Recommended Standard...Occupational Exposure to Coal Tar
Products. U.S. DHEW, PHS, CDC, Rockvllle, MO. Publ. No. 78-107.
Redmond, C.K., A. Ciocco, J.W. Lloyd and H.W. Rush. 1972. Long term
mortality study of steelworkers. J. Occup. Med. 14(8): 621-629. (CHed 1n
NIOSH, 1978)
Redmond, C.K., B.R. Stroblno and R.H. Cypess. 1976. Cancer experience
among coke by-product workers. Ann. NY Acad. Sc1. p. 102-115. (Cited 1n
NIOSH, 1978)
Redmond, C.K., H.S. Wleand, H.E. Rockette, R. Sass and G. Welnberg. 1979.
Long-term mortality experience of steelworkers. Prepared under Contract No.
HSM-99-71-32. NIOSH, Cincinnati, OH: June 1979. (CHed 1n NIOSH, 1978)
Sawlckl, E., O.E. Meeker and M.J. Morgan. 1965. The quantitative composi-
tion of air pollution source effluents 1n terms of aza heterocycllc and
polynuclear aromatic hydrocarbons. Int. J. A1r Water Pollut. 9: 291-298.
Tye, R., and K.L. Stemmer. 1967. Experimental cardnogenesis of the lung.
II. Influence of phenols 1n the production of carcinoma. J. Natl. Cancer
Inst. 39: 175-186. (CHed in NIOSH, 1978)
U.S. EPA. 1980. Guidelines and Methodology Used in the Preparation of
Health Effects Assessment Chapters of the Consent Decree Water Quality
Criteria. Federal Register. 45:79347-79357.
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U.S. EPA. 1982a. Carcinogen Assessment of Coke Oven Emissions. Office of
Health and Environmental Assessment, Office of Research and Development,
Washington, DC. EPA 600/6-82-003. NTIS PB 83-129551.
U.S. EPA. 1982b. Coal Tars Health Effects Assessment. Environmental
Criteria and Assessment Office, Cincinnati, OH. p. 10. Internal draft.
U.S. EPA. 1983. Methodology and Guidelines for Reportable Quantity Deter-
minations Based on Chronic Toxlclty Data. Prepared by the Environmental
Criteria and Assessment Office, Cincinnati, OH, OHEA for the Office of Solid
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von Lehmden, D.J., R.P. Hangebrauck and J.E. Meeker. 1965. Polynuclear
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Control Assoc. 15: 306-315.
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APPENDIX
Summary Table for Coal Tars3
Species
Experimental
Dose/Exposure
Effect
Inhalation
AIS
AIC
Carcinogenic humans
potency
NO
NO
0-700* mg/m3- lung tumors 3.2b
month (mg/kg/day)"1
Oral
AIS
AIC
Carcinogenic
potency
NO
NO
NO
aSource: U.S. EPA, 1982a
bTh1s value 1s not a q-|*, but Instead an Incremental risk value expressed
1n equivalent units and based on human ep1dem1olog1cal data from coke oven
workers.
NO = Not derived
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