Health Effects Assessment For Creosote

TECHNICAL REPORT DATA
(Pttae read Instructions on the reverse before completing]
1. REPORT NO.
EPA/600/8-88/025
2.
3. RECIPIENT'S ACCESSION NO
PB88-179395/AS
4, TITLE ANO SUBTITLE
5. REPORT DATE
Health Effects Assessment for Creosote
6. PERFORMING ORGANIZATION COOE
7. AUTHOH
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EPA/600/8-88/025
July, 1987
HEALTH EFFECTS ASSESSMENT
FOR CREOSOTE
ENVIRONMENTAL CRITERIA AND ASSESSMENT OFFICE
OFFICE OF HEALTH AND ENVIRONMENTAL ASSESSMENT
OFFICE OF RESEARCH AND DEVELOPMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
CINCINNATI, OH 45268
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DISCLAIMER

This document has been reviewed 1n accordance with the U.S.
Environmental Protection Agency's peer and administrative review policies
and approved for publication. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
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PREFACE
This report summarizes and evaluates Information relevant to a prelimi-
nary Interim assessment of adverse health effects associated with creosote
and compounds. All estimates of acceptable Intakes and carcinogenic potency
presented 1n this document should be considered preliminary and reflect
limited resources allocated to this project. Pertinent toxlcologlc and
environmental data were located through on-Hne literature searches of the
TOXLINE and the CHEMFATE/OATALOQ data bases, The basic literature
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DISCLAIMER

This document has been reviewed In accordance with the U.S.
Environmental Protection Agency's peer and administrative review policies
and approved for publication. Mention of trade names or commercial products
does not constitute endorsement 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 creosote
and compounds. All estimates of acceptable Intakes and carcinogenic potency
presented In this document should be considered preliminary and reflect
limited resources allocated to this project. Pertinent toxlcologlc and
environmental data were located through on-Hne literature searches of the
TOXLINE and the CHEMFATE/DATALOG data bases. The bask literature searched
supporting this document Is current up to May, 1986. Secondary sources of
Information have also been relied upon 1n 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 Assess-
ment (OHEA) sources have been extensively utilized:

U.S. EPA. 1980a. Hazard Profile for Creosote. Prepared by the
Office of Health and Environmental Assessment, Environmental
Criteria and Assessment Office, Cincinnati, OH for the Office of
Solid Waste, Washington, DC.

U.S. EPA. 1980b. Ambient Water Quality Criteria Document for
Polynuclear Aromatic Hydrocarbons. Prepared by the Office of
Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH for the Office of Water Regu-
lations and Standards, Washington, DC. EPA 440/5-80-069. NTIS PB
81-117806.

The Intent In these assessments 1s to suggest acceptable exposure levels
for noncarclnogens and risk cancer potency estimates for carcinogens
whenever sufficient data were available. Values were not derived or larger
uncertainty factors were employed when the variable data were limited In
scope tending to generate conservative (I.e., protective) estimates.
Nevertheless, the interim values presented reflect the relative degree of
hazard or risk associated with exposure to the chemlcal(s) addressed.

Whenever possible, two categories of values have been estimated for
systemic toxicants (toxicants for which cancer Is not the endpolnt of
concern). The first, RfD$ (formerly AIS) or subchronic reference dose, Is
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 lifespan).
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 is assumed. Animal data used for RFD$ estimates generally
Include exposures with durations of 30-90 days. Subchronic human data -are
rarely available. Reported exposures are usually from chronic occupational
exposure situations or from reports of acute accidental exposure. These
values are developed for both inhalation (RfD^j) and oral (RfD$Q)
exposures.
111
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The RfD (formerly AIC) Is similar In concept and addresses chronic
exposure. It is an estimate of an exposure level that would not be expected
to cause adverse effects when exposure occurs for a significant portion of
the llfespan [see U.S. EPA (1980) for a discussion of this concept]. The
RfD Is route-specific and estimates acceptable exposure for either oral
(RfDg) or Inhalation (RfOj) with the Implicit assumption that exposure
by other routes Is Insignificant.

Composite scores (CSs) for noncarcinogens have also been calculated
where data permitted. These values are used for Identifying reportable
quantities and the methodology for their development is explained in U.S.
EPA (1983).

For compounds for which there Is sufficient evidence of carcinogenic!ty
RfD$ and RfD values are not derived. For a discussion of risk assessment
methodology for carcinogens refer to U.S. EPA (1980). Since cancer is a
process that is not characterized by a threshold, any exposure contributes
an Increment of risk. For carcinogens, q-|*s have been computed, if appro-
priate, based on oral and Inhalation data If available.
1v
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ABSTRACT
In order to place the risk assessment evaluation In proper context,
refer to the preface of this document. The preface outlines limitations
applicable to all documents of this series as well as the appropriate
Interpretation and use of the quantitative estimates presented.

Creosote, a coal tar distillate containing a mixture of PAH, 1s
considered to be a carcinogen by IARC (1985) and U.S. EPA (1978). Since
dose-response data sufficient to calculate q-|* values are not available,
no risk assessment values could be derived. Risk estimates for carcinogenic
PAHs, which are a component of creosote, are presented.
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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. Dr. Christopher DeRosa and Karen
Blackburn were the Technical Project Monitors and John Helms (Office of
Toxic Substances) was the Project Officer. The final documents In 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 Waste
Office of Toxic Substances
Office of Drinking Water

Editorial review for the document series was provided by the following:

Judith Olsen and Erma Durden
Environmental Criteria and Assessment Office
Cincinnati, OH

Technical support services for the document series was provided by the
following:

Bette Zwayer, Jacky Bohanon and Kim Davidson
Environmental Criteria and Assessment Office
Cincinnati, OH
v1
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TABLE OF CONTENTS

Page

1. ENVIRONMENTAL CHEMISTRY AND FATE. ... ....... 1

2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS 4

3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS 5

4. CARCINOGENICITY 6

4.1. HUMAN DATA 6

4.1.1. Oral 6
4.1.2. Inhalation 6

4.2. BIOASSAYS 6
4.3. OTHER RELEVANT DATA 6
4.4. WEIGHT OF EVIDENCE . 9

5. REGULATORY STANDARDS AND CRITERIA 10

6. RECOMMENDATIONS 11

7. REFERENCES 13
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LIST OF ABBREVIATIONS

CAS Chemical Abstract Service

PAH Polynuclear aromatic hydrocarbons

PEL Permlssable exposure level

ppm Parts per million

RPAR Rebuttable Presumption Against Registration

SMSA Standard metropolitan statistical area

TLV Threshold limit value

TWA Time-weighted average
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1. ENVIRONMENTAL CHEMISTRY AND FATE

The term creosote has been applied to two complex mixtures of organic

compounds. CAS Registry number 8001-58-9 Is applied to material derived

from the distillation of coal tar. This product has had many uses and

potential exists for the contamination of the environment. Its current use

Is restricted to the preservation of wood. CAS Registry number 8021-39-4 is

applied to a wood-derived product. There are virtually no data available

regarding the toxlcity of the wood-derived product and it is not considered

further In this document.

Creosote is an extremely complex mixture of compounds. The composition

of this mixture varies depending upon the temperature during coal tar pro-

duction and the source of the coal used (U.S. EPA, 1982). Most of the 200

or more compounds in creosote are PAH. The major PAH in creosote listed 1n

Table 1-1 generally constitute at least 75% of creosote (Lorenz and GJovik,

1972). In addition to the aromatic hydrocarbons, creosote also contains

smaller amounts of phenolic constituents as well as nitrogen-, oxygen- and

sulfur-containing heterocyclic ring compounds and aromatic amines (U.S. EPA,

1982). The physical properties of creosote vary depending on the method of

distillation. The physical properties of a typical creosote are as follows:

Moisture content trace
Benzene insoluble content 0.99%
Coke residue content 1.95%
Specific gravity at 38/15.5°C 1.102%
Distillation at 355°C 72.58%
Residue at >355°C 26.67%
Distillation loss at 355°C 0.75%

Creosote is immiscible in water (Hawley, 1981). The half-lives of creo-

sote In air, water and soil could not be located in the available literature.

0107h ' -1- 02/06/87
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TABLE 1-1

Major Components In Creosote*
Component
Percentage of Whole Creosote
(±0.07%)
Phenanthrene + anthracene

Fluoranthene

Fluorene

Acenaphthene

Pyrene

Olbenzofuran

Methyl anthracenes and methyl phenanthrenes

Naphthalene

Methyl fluorenes

Chrysene

Dlmethylnaphthalenes

Carbazole

Benzof luorenes

2-Methylnaphthalene

1-Methlynaphthalene

Biphenyl
17.4-23.0

7.6-10.0

7.3-10.0

9.0-14.7

7.0-8.5

5.0-7.5

3.9-7.0

1.3-3.0

2.3-3.0

2.6-3.0

2.0-2.3

1.2-2.0

1.0-2.0

1.2-2.8

0.9-1.7

0.8-1.6
*Source: Lorenz and Gjovik, 1972
0107h
-2-
10/27/86
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It has been suggested that decomposition by mlcrofaunal metabolism is a

major factor in the degradation of creosote compounds In aquatic systems

(Borthwick and Patrick, 1982). In addition, the high molecular weight PAH

and azoarene constituents of creosote are expected to bioaccumulate 1n

aquatic organisms and adsorb to suspended solids and sediments in water. In

soil, these components are expected to be relatively immobile. In both

water and soil, some of the high molecular weight components of creosote are

expected to persist for a long time. The possibility of inhalation and

dermal exposure to creosote for applicators of creosote and creosote/coal

tar wood preservatives has been evaluated by U.S. EPA (1982). U.S. EPA

(1982) concluded that there are no adequate quantitative Inhalation or

dermal exposure data available for the general population or those occupa-

tional^ exposed to creosote.
0107h -3- 10/27/86
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2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS

Pertinent data regarding the quantitative absorption of creosote could

not be located in the available literature. Specific PAH, such as benz(a)-

anthracene, chrysene, 7,12-dimethylbenz(a)anthracene, benz(a)pyrene and

3-methylcholanthrene, that are found in creosote are absorbed by the lungs

(Vainio et al., 1976) and from the gastrointestinal tract (Rees et al.,

1971).
0107h -4- 10/27/86
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3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS

Pertinent data regarding the effects of creosote following subchronic or

chronic exposure by oral or inhalation routes could not be located in the

available literature. In addition, data regarding teratogenic or other

reproductive effects following either route of exposure, or data regarding

toxicant interactions could not be located in the available literature.
0107h -5- 10/27/86
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4. CARCINOGENICTY

4.1. HUMAN DATA

Individuals dermally exposed to creosote 1n occupational settings have

developed cancer (Section 4.3.).

4.1.1. Oral. Duslch et al. (1980) found that the breast cancer rates for

females In a Minneapolis suburb were significantly elevated (p<0.0005) over

those 1n nearby municipalities and in the SMSA. Some of the wells supplying

drinking water for the suburb were known to have been contaminated with

creosote. The available information does not allow evaluation of the

association between breast cancer and creosote exposure.

4.1.2. Inhalation. Pertinent data regarding the carcinogenic potential

of creosote In humans following inhalation exposure could not be located in

the available literature.

4.2. BIOASSAYS

Pertinent data regarding the carcinogenic potential of creosote in

laboratory animals following oral or Inhalation exposure could not be

located 1n the available literature. Studies concerning carclnogenicity

following dermal application of creosote are summarized in Section 4.3.

4.3. OTHER RELEVANT DATA

A number of cases of skin carcinoma in humans exposed chronically to

creosote have been reported. These reports were summarized by NCI (1985) as

follows:
Mackenzie (1898) reported papillomas, which were "likely to become
epHheliomatous," on the forearms and scrotum of a man who was
employed for 30 years treating railway ties with creosote.
O'Donovan (1920) described the cases of three men who treated wood
with creosote and had subsequently developed skin cancer. Cookson
(1924) reported a case of squamous cell carcinoma of the right hand
in a 66-year-old man who had worked 1n a creosote factory handling
treated lumber for 33 years. A post-mortem examination revealed
apparent metastases In the lungs, liver, kidney, heart and axillary
0107h -6- 04/06/87
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lymph glands. A similar case of squamous paplllomas on the hands,
forearms, arms and thighs was reported 1n a man exposed to creosote
during log Impregnation (Hald1n-Dav1s, 1935). Lenson (1956)
reported carcinoma of the face and paplllomas of the hands and neck
In a man exposed to creosote while painting planks and scows 1n a
shipyard. Exposure was for about 3 years and carcinoma developed
about 5 years after exposure was terminated. This man was a
painter for 41 years and was exposed to lead-based paints and paint
solvents. Henry (1947) reported that 37 of 753 cases of dermal
eplthelloma could be linked to occupational creosote exposure.
Fourteen cases occurred among lumber treaters, 9 among creosote
storage workers, 10 among brick workers where creosote was used as
a releasing agent, and one case each in workers exposed to creosote
1n a crucible furnace, disinfectant manufacture, a railway worker
and a tar distillery chemist. Recent analytical epidemlologic data
relating exposure levels and duration of exposure to creosote with
skin or lung cancers are not available.

Creosote has also been shown to be carcinogenic In mice following

repeated skin exposure. These studies are summarized 1n Table 4-1.

The NCI (1985) summary of mutagenlclty studies of creosote Is presented

below:
Creosote was mutagenlc 1n the Salmonella typhlmurlum assay In
tester strains TA100, TA98, TA1538 and TA1537 (Bos et al., 1983).
Strain TA1535 showed no Increase 1n the number of revertants per
plate. Creosote was an effective mutagen only when a rat liver
mlcrosomal preparation was supplied, thus Indicating the require-
ment for metabolism to occur prior to expression of mutagenlc
activity. Creosote was also reported to be mutagenic 1n £. typhl-
murium strains TA1537, TA98 and TA100 and EscheMchia coli WP2
strain (Simmon and Poole, 1978). Mitchell and Tajiri (1978)
reported creosote to be mutagenlc to mouse lymphoma cells (L5178Y)
with increasing activity following metabolic activation. Bos et
al. (1984) demonstrated the presence of mutagenlc substances in the
work environment of a creosote-wood treating facility. Despite the
presence of creosote, the urine of workers showed no mutagenlc
activity during a 10-day test period. Environmental samples of
creosote residues, liquid creosote, and the urine from rats exposed
to creosote by IntrapeMtoneal Injection showed mutagenlc activity
in S. typhimurium strains TA98 and TA100 when a metabolic activa-
tion system was provided.
0107h -7- 04/06/87
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4.4. WEIGHT OF EVIDENCE

Adequate studies examining the carcinogenic potential of creosote by the

oral or Inhalation routes of exposure could not be located In the available

literature. One study Involving exposure of humans to creosote-contaminated

well water was considered Inadequate (Dusich et a!., 1980). The only animal

carcinogeniclty studies on creosote available are dermal studies using mice;

these studies indicate that creosote is a carcinogen. Also case reports of

humans occupationally exposed to creosote also indicate that creosote is

carcinogenic. In addition, some of the PAH components of creosote _(e.g.,

benz(a)anthracene and benzo(a)pyrene) are known to be carcinogenic.

From this information, IARC (1985) stated that there is sufficient

evidence for the carcinogeniclty of creosote in laboratory animals and

limited evidence for the carcinogeniclty In humans. The evidence is suffi-

cient to place creosote in Group Bl, probable human carcinogen, according to

the EPA (U.S. EPA, 1986) classification scheme.
0107h -9- 04/06/87
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5. REGULATORY STANDARDS AND CRITERIA

As a result of RPAR proceedings, U.S. EPA (1984a) published a proposed

Intent to cancel registration of creosote for all uses except as a wood

preservative. Under this proposal, creosote cannot be used as a herbicide,

fungicide (on canvas and rope), disinfectant, larvacide, insecticide or

repellent. As stated in U.S. EPA (1984b), creosote can be used only by

certified applicators, and a consumer awareness program recommends against

the use of treated wood in contact with food, feed and drinking water.

Creosote-coated products are also not to be used Indoors.

No standards or criteria have been instituted for creosote. OSHA (1985)

lists 0.2 mg/m3 as the PEL for coal tar pitch volatHes (benzene soluble

fraction), anthracene, benzo(a)pyrene, phenanthrene, acrldlne, chrysene and

pyrene. These compounds are also found in creosote. ACGIH (1986) lists 0.2

mg/m3 as the TLV-TWA for the benzene soluble fraction of coal tar pitch

volatlles and lists the class as a recognized human carcinogen.

An ambient water quality criteria of 28 ng/i for the 10~5 risk level

for PAH compounds, based on the carcinogenic potential of benzo(a)pyrene,

has been derived (U.S. EPA, 1980b). Because creosote contains a mixture of

PAH compounds, this value could be applied to creosote contaminated water.
0107h -10- 02/06/87
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6. RECOMMENDATIONS

U.S. EPA (1984b) reported that creosote poses a significant risk of

oncogenlclty to humans and developed regulations to limit exposure. The

dermal studies In mice and the human case reports that are available do not

provide quantitative data by a relevant route of exposure Because of the

lack of quantitative data, q * values for oral and inhalation exposure

cannot be calculated.

Ep1dem1olog1cal studies of humans occupatlonally exposed to creosote may

provide Information about the carcinogenic potency of creosote; however, the

exposure route and dose would be difficult to define in these studies.

Long-term cancer studies of creosote in laboratory animals would provide

additional information that may be useful for quantitative risk assessment

and permit promulgation of criteria and regulations. A large variable in

these studies would be the high variability In the components of creosote.

Studies of creosote from one source may not provide accurate risk estimates

for creosote from a different source. The oral route of exposure should be

the primary route investigated, although inhalation exposure also occurs,

particularly in wood-treating facilities.

U.S. EPA (1980a) noted that creosote consists of liquid and solid cyclic

hydrocarbons and "substantial" amounts of naphthalene and anthracene, 12-14%

phenanthrene and 200 ppm benz(a)pyrene. U.S. EPA (1980b) based ambient

water quality criteria for PAH on a q * of 11.53 (mg/kg/day)~1 for benz-

(a)pyrene. Lacking more definitive quantitative data on the carcinogenic

potency of creosote, the q,* of 11.53 (mg/kg/day)'1 for PAH may be

considered for creosote pending further testing v.Mth creosote itself.
0107h -11- 04/06/87
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U.S. EPA (1982) noted that creosote contains several known carcinogens

as well as related chemicals that may act as cocardnogens. Initiators,

promoters, potentlators or Inhibitors of carclnogenesls. U.S. EPA (1982)

concluded that analysis of the carcinogenic potency of Individual components

of creosote is not appropriate for predicting the cardnogenldty of creo-

sote as a whole because of the possibility of synerglsm of the components.
0107h -12- 04/06/87
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7. REFERENCES

ACGIH (American Conference of Industrial Hyglenlsts). 1986. Documentation

of the Threshold Limit Values and Biological Exposure Indices, 5th ed.

Cincinnati, OH. p. 143.

Borthwick, P.W. and J.M. Patrick, Jr. 1982. Use of aquatic toxicology and

quantitative chemistry to estimate evironmental deactivation of marine-grade

creosote in seawater. Environ. Toxicol. Chem. 1: 281-288.

Bos, R.P., C.T.J. Hulshof, J.L.G. Theuws and P.T. Henderson. 1983. Muta-

genlclty of creosote in the Salmonella mlcrosome assay. Mutat. Res. 119:

21-26. (Cited in NCI, 1985)

Bos, R.P., C.T.J. Hulshof, J.L.G. Theuws and P.T. Henderson. 1984. Geno-

toxlc exposure of two workers creosotlng wood. Br. J. Ind. Med. 41:

260-262. (Cited in NCI, 1985)

Boutwell, R.K. and O.K. Bosch. 1958. The carcinogenic!ty of creosote oil

-- Its role in the induction of skin tumors in mice. Cancer Res. 18:

1171-1175. (Cited in U.S. EPA, 1980a; NCI, 1985)

Cookson, H.A. 1924. Eplthelioma of the skin after prolonged exposure to

cresote. Br. Med. J. i: 368. (Cited 1n NCI, 1985)

Dus'ch, K., E. Slgurdson, W.N. Hall and A.G. Dean. 1980. Cancer rates in a

community exposed to low levels of creosote components In municipal water.

Minn. Med. 63: 803-806.

0107h -13- 04/06/87
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Haldin-Davis, H. 1935. Multiple warts 1n a creosote worker. Proc. Roy.

Soc. Med. 29: 89-90. (CHed In NCI,1985)

Hawley, G.G., Ed. 1981. The Condensed Chemical Dictionary, 10th ed. Van

Nostrand Reinhold Co., New York. p. 285.

Henry, S.A. 1947. Occupational cutaneous cancer attributable to certain

chemicals In industry. Br. Med. Bull. 4: 389-401. (CHed in NCI, 1985)

IARC (International Agency for Research on Cancer). 1985. IARC Monographs

on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Poly-

nuclear Aromatic Compound, Part 4, Bitumens, Coal-tars and Derived Products,

Shale-oil and Soots. WHO, IARC, Lyons, France. Vol. 35, p. 137-140.

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