**UNITED STATES ENVIRONMENTAL PROTECTION AGENCY**

**WASHINGTON, D.C. 20460**

![](media/image1.wmf){width="6.0in" height="0.59375in"}

OFFICE OF PREVENTION, PESTICIDES, AND TOXIC SUBSTANCES

DATE: March 31, 2008

**[MEMORANDUM]{.underline}**

SUBJECT: **Creosote**- Preliminary Risk Assessment for the
Reregistration Eligibility

Decision Document (RED). PC Codes 022003, 025003, and 025004.

FROM: Timothy F. McMahon, Ph.D.

Senior Toxicologist, Antimicrobials Division (AD) (7510P)

Norm Cook, Chief

> A. Najm Shamim, Chemist

William Erickson, Ph.D., Biologist

Jonathan Chen, Ph.D., Toxicologist

Risk Assessment and Science Support Branch, AD (7510P)

Timothy Leighton, Environmental Scientist

Regulatory Management Branch II

Antimicrobials Division (7510P)

TO: Jacqueline Campbell- McFarlane, Chemical Review Manager

Regulatory Management Branch I

Antimicrobials Division (7510P)

Attached to this cover memorandum is the Preliminary Risk Assessment for
the creosote RED document in support of the reregistration of creosote.
The supporting disciplinary science chapters are included as attachments
and are listed on the following page.

Updated Ecological Risk Assessment for Creosote. From William Erickson,
Ph.D. Biologist to Timothy F. McMahon, Ph.D. Senior Toxicologist and
Risk Assessor, March 7, 2008.

Creosote: Occupational and Residential Exposure and Risk Assessment for
the Reregistration Eligibility Decision (RED). From Timothy Leighton,
Environmental Scientist, to Timothy F. McMahon, Ph.D., Senior
Toxicologist and Risk Assessor, March 25, 2008.

Epidemiology and Incident Reports Associated with Creosote. From
Jonathan Chen, Ph.D. to Timothy F. McMahon, Ph.D., Senior Toxicologist
and Risk Assessor, March 25, 2008.

Creosote- Toxicology Disciplinary Chapter for the Reregistration
Eligibility Decision Document (RED). From Timothy F. McMahon, Ph.D.,
Senior Toxicologist and Risk Assessor, to Jacquie McFarlane, Chemical
Review Manager, Marwch 25, 2008

Product Chemistry Science Chapter for Creosote (P1/P13 and P2 Fractions)
Reregistration Eligibility Decision (RED) Process. From A. Najm Shamim,
Ph.D., Chemist, to Tim McMahon, PhD, Senior Toxicologist, and Risk
Assessor, February 14, 2008.

Residue/ Dietary Risk Assessment Science Chapter for Creosote (P1/P13
and P2 Fractions) Reregistration Eligibility Decision (RED) Process.
From A. Najm Shamim, Ph.D., Chemist, to Tim McMahon, PhD, Senior
Toxicologist, and Risk Assessor, February 14, 2008.

Environmental Fate and Transport Assessment of Creosote for the
Reregistration Eligibility

Decision (RED) Process. From A. Najm Shamim, Ph.D., Chemist, to Tim
McMahon, PhD, Senior Toxicologist, and Risk Assessor, February 14, 2008.

**TABLE OF CONTENTS**

**1.0 EXECUTIVE
SUMMARY\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\.....4**

**2.0 PHYSICAL AND
CHEMICALPROPERTIES\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\.....15**

**3.0 HAZARD
PROFILE..................\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...17**

3.1 ACUTE
TOXICITY\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\....
\.....17

3.2 DOSE_RESPONSE
ASSESSMENT\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...18

3.3 DERMAL
ABSORPTION\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\....21

3.4 CARCINOGENICITY
CLASSIFICATION\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\....22

3.5 ENDOCRINE
DISRUPTION...............................................................\...22

**4.0 EXPOSURE ASSESSMENT AND
CHARACTERIZATION\...\...\...\...\...\...\...\...\...\...\...\...\...\...\.....23**

4.1 SUMMARY OF REGISTERED
USES\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\....23

4.2 OCCUPATIONAL EXPOSURE AND
RISK\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\....23

.

**5.0 AGGREGATE RISK ASSESSMENT AND
CHARACTERIZATION\...\...\...\...\...\...\...\...\...\...\....28**

**6.0 CUMULATIVE EXPOSURE AND
RISK\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\.....29**

.

**7.0 ENVIRONMENTAL
RISKS\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...30**

7.1 ENVIRONMENTAL FATE
ASSESSMENT\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\....30

7.2 ENVIRONMENTAL EXPOSURE AND ECOLOGICAL RISK ASSESSMENT...\...35

. 7.3 ENDANGERED
SPECIES.......................................................................49

**8.0 INCIDENT
REPORTS\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\....50**

**9.0
REFERENCES\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\...\.....66**

**1.0 Executive Summary**

Creosote is a fungicide, insecticide, and sporicide used as a wood
preservative for above and below ground wood protection treatments as
well as for treating wood in marine environments. All 16 Creosote
products currently registered are Restricted Use Pesticides; 15 are
End-Use Products and 1 is a Manufacturing-Use Product for formulating
industrial end-use wood preservative products. Creosote wood
preservatives are used primarily to pressure treat railroad
ties/crossties (represents close to 70% of all Creosote use) and utility
poles/crossarms (represents 15 - 20% of all Creosote use). Assorted
Creosote-treated lumber products (e.g., timbers, poles, posts and
groundline-support structures) represent the remaining uses for this
wood preservative. The industry refers to different blends of creosote,
based on the wood treatment standards set by the American
Wood-Preservers' Association (AWPA), as P1/P13 and P2. Typically,
railroad ties/crossties are treated with a P2 blend, which is more
viscous than the P1/P13 blend used for treating utility poles.

A recent voluntary cancellation of all non pressure treatment uses
resricts use of creosote to commercial and industrial settings. Creosote
is applied by occupational handlers only. Since it is a restricted-use
pesticide that can only be applied by certified applicators or someone
under their direct supervision, it is not available for sale to or use
by homeowners.

The acute toxicity of both the P1/P13 and P2 blends of creosote is
moderate by the oral, dermal, and inhalation routes of exposure in
experimental animals (Toxicity Categories III and IV). Median lethal
doses by the oral and dermal routes are above 2000 mg/kg, and median
lethal doses by the inhalation route are above 4mg/L, which are
considered limit doses in acute toxicity tests as set by Agency
guidelines. The P1/P13 blend displays eye and skin irritation potential
in experimental animals (eye irritation clearing in 8-21 days, skin
irritation up to 14 days post-dosing). The P2 blend appears to show
somewhat less potential for skin and eye irritation (eye irritation
clearing within 7 days, skin irritation clearing after 72 hours) but
data are incomplete. It is assumed that both blends are dermal
sensitizers as there are no currently acceptable dermal sensitization
studies for either blend.

Subchronic dermal testing with both the P1/P13 and P2 blends of creosote
show a minimum of toxic effects in experimental animals (rats). Using
the P2 blend, one mortality of questionable significance was observed at
a dose of 400 mg/kg/day, while testing of the P1/P13 blend produced
decreases in body weight gain. Effects on the skin in both studies were
minimal to moderate.

Subchronic inhalation testing with creosote produced a wider spectrum of
effects. At a dose of 0.049 mg/L, exposure to the P1/P13 blend produced
myocardial pathology (degeneration, hemorrhage, cardiomyopathy) in males
and females. Altered hematological parameters (decreased hemoglobin,
hematocrit, erythrocytes; increased reticulocytes, polychromasia,
poikilocytosis, anisocytosis) were also observed in males and females.
Testing of the P2 blend by the inhalation route also produced altered
hematological parameters, and resulted in increased absolute and
relative liver and thyroid weights. Follicular cell hypertrophy was
observed. Lesions of the nasal cavity were also observed with the P2
blend.

Developmental and reproductive testing of creosote showed potential
sensitivity of offspring to the P1/P13 blend. Decreased body weight gain
and decreased food consumption were observed in maternal animals at a
dose of 175 mg/kg/day, and at this same dose, increased
post-implantation loss, increased mean resorptions, and decreased live
fetuses per litter were also observed. An overall significant increase
in incidence of developmental malformations was also observed at the 175
mg/kg/day dose. Testing of the P2 blend did not show any apparent
susceptibility of developing offspring to creosote, and reproductive
testing of P1/P13 creosote did not show any apparent susceptibility, but
the reproductive toxicity study contained several deficiencies that
compromised interpretation of the data, such as a low fertility and
pregnancy index for F1 female parental rats. Thus, there is some
uncertainty associated with concluding that creosote is devoid of any
reproductive effects. In this light, the additional 10-fold safety
factor mandated by FQPA was employed to account for this uncertainty as
well as for the effects observed from developmental toxicity testing of
P1/P13 creosote.

In consideration of the available evidence that creosote is a positive
mutagen, the Agency waived the requirement for the standard mutagenicity
battery, and instead required dominant lethal testing of both the P1/P13
and P2 blends. The results of testing of both the P1/P13 blend and P2
blend of creosote showed that, at doses toxic to the dosed animals
(330.5 mg/kg for the P1/P13 blend, and 194 mg/kg for the P2 blend),
there was no evidence of a dominant lethal effect of either creosote
blend.

There are no reliable metabolism data on creosote, as the chemical is a
complex mixture of several classes of polycyclic aromatic chemicals.
Assays are in development to identify marker compounds to determine
exposure to creosote.

A large body of experimental evidence exists which shows a positive
relationship between exposure to creosote and development of tumors in
experimental animals. In addition to its tumor-promoting potential, the
ability of creosote to induce lung tumors after dermal application was
examined. Dermally applied creosote (0.25ml undiluted, twice weekly for
8 months) induced 5.8 lung adenomas per mouse in mice housed in
stainless steel cages, while untreated controls showed 0.5 lung
adenomas/mouse (Roe et al, Cancer Res. 18: 1176-1178, 1958).
Carcinogenicity of two high-temperature derived creosote oils was
studied by Poel and Kammer (JNCI 18: 41-55, 1957). The light creosote
fraction is composed mainly of benzene, toluene, xylene, and solvent
naphtha, while the blended oil is composed of creosote oil, anthracene
oil, and oil drained from recovery of naphthalene. Oils were applied by
drops to the skin of mice at concentrations of 20%, 50%, or 80% three
times a week for life. By weeks 21-26, both oils had induced skin
tumors. Several mice exhibited metastases to the lungs or regional lymph
nodes.

In an oral carcinogenicity study conducted by Culp et al. (1996), the
carcinogenicity of two coal tar mixtures and pure benzo\[a\]pyrene (BaP)
was studied. Coal tar mixture 1 (CTM-1) was a composite of coal tar
samples from seven coal gasification plant waste sites and was dosed at
0.0, 0.01, 0.03, 0.1, 0.3, 0.6, and 1.0% of diet. Coal tar mixture 2
(CTM-2) was a composite of coal tars from three waste sites with high
BaP content and was dosed at 0.0, 0.01, 0.03, 0.1, 0.3% of diet. An
additional group was dosed with pure BaP at 0, 0.0005, 0.0025, and 0.01
% in diet. A control group received solvent control in diet. Each group
consisted of 48 mice.

In mice exposed to coal tar, coal tar acted as a systemic carcinogen and
induced a dose-related increase in hepatocellular adenomas and
carcinomas, alveolar/bronchiolar adenomas and carcinomas, forestomach
squamous epithelial papillomas and carcinomas, small intestine
adenocarcinomas, histiocytic sarcomas, hemangiosarcomas in multiple
organs, and sarcomas in several tissues.

The incidence of forestomach tumors increased sharply between the 0.1
and 0.3% doses. However, there was not a proportional increase in
forestomach tumors above 0.3% because these mice died from
adenocarcinomas of the small intestine. Tumors of the esophagus,
observed in BaP treated mice, were not observed in the CTM1 or CTM-2
treated groups. Lung and hepatocellular tumors observed in the CTM1 and
CTM2 groups were not observed in BaP treated animals.

Multiple neoplasms were noted in liver, lung, forestomach, and the small
intestines of exposed mice. Liver neoplasms occurred in 1, 0, and 4 mice
fed 0.03, 0.1 and 0.3% CTM-1, respectively. Lung neoplasms occurred in
21, 11 and 13 mice fed 0.3% , 0.6% , 1.0% CTM-1, respectively. Eight
mice in the 0.3% CTM-2 group had multiple lung neoplasms. Forestomach
carcinomas were found in 2 and 1 mice fed 0.6% or 1.0% CTM-1,
respectively. Adenocarcinomas were found in the small intestines
(jejunum) of 2 and 12 mice fed 0.6% and 1.0% CTM-1, respectively. Groups
dosed with ≥0.3% CTM-1 or CTM-2 had significantly reduced survival.

In those mice exposed to benzo(a)pyrene, BaP appeared to act as a
point-of-contact carcinogen, causing an increased incidence of
papillomas and/or carcinomas of the forestomach, esophagus and tongue.
The incidence of forestomach tumors increased steeply between 5 and 25
ppm, equivalent to 20.5 and 104 μg BaP/day. Tumors of the esophagus were
not observed in the CTM1 or CTM-2 treated groups. Lung and
hepatocellular tumors, observed in CTM treated mice, were not observed
in mice fed BaP.

Multiple neoplasms of the forestomach occurred in 8 and 21 mice fed 25
and 100 ppm BaP, respectively. Multiple neoplasms of the esophagus and
tongue were noted in 6 and 3 mice, respectively, fed 100 ppm BaP. It
should be noted that all animals in 100 ppm group died before
termination of the study.

In humans, evidence for carcinogenicity of creosote varies. Several
studies have associated occupational exposure to creosote with
development of skin cancer, with a latency period of 20-25 years. These
studies are very old (1920\'s to 1940\'s), when occupational safety
practices were much more lax than today. More recent reports (1980) show
no increase in risk of skin, bladder, or lung cancer in wood treatment
plant workers, or after treatment for 4 years with coal-tar medicinal
therapy for treatment of dermatitis. These reports, however, were
limited in scope. Those reports associated with therapeutic use of coal
tar did not mention the fact that the composition of the coal tar used
therapeutically is different than that used for wood treatment. In the
report on wood treatment workers, the population studied was small, and
the follow-up period was too short to allow a long enough latency for
tumor development.

The Agency in 1988 acknowledged limitations on conducting a quantitative
risk assessment from use of a single component of creosote ([Guidance
for the Reregistration of Pesticide Products Containing Coal
Tar/Creosote As the Active Ingredient]{.underline}, USEPA, 1988), but it
was also observed that creosote mixtures are "complex mixtures with
known synergistic effects" on carcinogenicity.

In conjunction with the Pest Management Regulatory Agency, Health
Canada, a quantitative risk assessment on carcinogenicity of creosote
has been performed using the data of Culp et al. (1998). A dermal
carcinogenicity study by Bushmann et al. (1997) was also available, but
was determined not suitable for quantitative assessment of
carcinogenicity. Ulceration of the skin was significant finding of the
study which potentially affected tumor response. In addition, systemic
toxicity was not examined, and complete histopathology data were not
available. Based upon the analysis of the Culp et al. data, an oral
cancer potency factor of 6.28 x 10^-6^ (µg/kg/day)^-1^ for the coal tar
mixture 1 tested in this study was selected, on the basis of forestomach
tumors observed.

**[Dose-Response Assessment]{.underline}**

On April 1, 1999, the Health Effects Division\'s Hazard Identification
Assessment Review Committee (HIARC) evaluated the toxicological
endpoints selected for occupational and residential (dermal and
inhalation) exposure risk assessments for Creosote. On December 6, 2007,
members of the Antimicrobials Division's Toxicity Endpoint Selection
Committee and members of the Health Effects Division's Carcinogenicity
Assessment Review Committee met to discuss the quantitative
carcinogenicity analysis performed for creosote by the Pest Management
Regulatory Agency, Health Canada and to determine an appropriate potency
factor for creosote.

For creosote, there is no anticipated dietary exposure as there are no
registered food uses for this substance and there is little concern for
potential residues of creosote from trophic transfer (A. Najm Shamim,
Ph.D., Residue/Dietary Risk Assessment.Chapter for Creosote). However,
non-dietary exposures to creosote are expected via the dermal and
inhalation routes of exposure. For these risk assessments, the following
toxicity endpoints were selected: (1) for *short-term dermal risk
assessment,* the NOAEL of 50 mg/kg/day was selected, based on the
observation of decreased body weight gain at 175 mg/kg/day in a
developmental toxicity study in rats (MRID \# 43584201). (2) for
*intermediate-term dermal risk assessment,* the NOAEL of 40 mg/kg/day
was selected, based on the observation of decreased body weight gain at
400 mg/kg/day in a 90-day dermal toxicity study in rats (MRID \#
43616201). (3) for *long-term dermal risk assessment,* the LOAEL of 25
mg/kg/day was selected based on the observation of decreased pre-mating
body weight in parental animals from a 2-generation reproduction
toxicity study ( California EPA review, no MRID). (4) for *inhalation
risk \[short- and intermediate-term\],* the NOAEL of 0.0047 mg/L was
selected , based on decreased body weight gain, altered hematology and
clinical chemistry, and increased absolute and relative weight of the
liver and thyroid observed at 0.048 mg/L in a 90-day inhalation toxicity
study (MRID \# 43600901). For worker risk, naphthalene was selected as
an indicator because 100 percent of the inhalation samples monitored at
the pressure treatment facilities were detectable. For naphthalene, the
Antimicrobials Division used the inhalation reference concentration
(RfC) for naphthalene published in the EPA's IRIS database. The RfC was
derived from a 2 year chronic inhalation study in the mouse in which
exposure was for 6 hours/day, 5 days/week.

A Margin of Exposure of 100 is acceptable for short-term and
intermediate-term dermal and inhalation occupational risk assessments. A
Margin of Exposure of 300 is acceptable for long-term occupational
dermal risk assessments. For long-term occupational inhalation risk
assessment, a Margin of Exposure of 100 is acceptable. Separate Margins
of Exposure should be calculated for dermal and inhalation routes since
oral and dermal NOAELs were selected for dermal risk assessment and an
inhalation NOAEL was selected for this route of exposure.

**Occupational/ Residential Exposure and Risk**

Creosote is used by occupational handlers only. Since it is a
restricted-use pesticide that can only be applied by certified
applicators or someone under their direct supervision, it is not
available for sale to or use by homeowners. Furthermore, the non
pressure treatments of creosote have been voluntarily cancelled by the
registrants. Creosote applications are now restricted to pressure
treatment cylinders.

EPA has determined that there are potential exposures to mixers,
loaders, applicators, and other handlers during typical use-patterns
associated with creosote pressure treatment uses.

**Occupational Handler dermal risk estimates**: The results indicate the
short-term (ST) non cancer dermal MOEs do not trigger a risk concern
except for the treatment operator at site C where the dermal MOE is 68
and the target MOE is 100. The intermediate-term (IT) non cancer dermal
MOEs trigger risk concerns for 8 of the 24 scenarios presented. IT MOEs
range from 3 to 2700 and the target MOE is 100. The long-term (LT) non
cancer dermal MOEs trigger risk concerns for 3 of the 24 scenarios. LT
MOEs range from 34 to 34,000 and the target MOE is 300. IT risks being
greater than the LT risks is an anomaly. However, in the case of
creosote it is explainable because the IT toxicity endpoint is based on
a dermal study while the LT endpoint is based on an oral study (i.e.,
there are differences in routes of exposure and dosing levels between
the two studies).

**Occupational Handler Inhalation risk estimates**: The non cancer
inhalation MOEs for worker exposure to naphthalene range from 23 to 1900
with a target MOE of 300. Sixteen of the 19 inhalation MOEs presented
exceed the target MOE of 300, and therefore, are of concern. None of the
average air concentrations for the various job functions exceeded the
TLV of 52 mg/m^3^.

**Cancer risks from dermal and inhalation exposure** : Based on the
selected slope factor of 6.28 x 10^-6^ (µg/kg/day)^-1^ , all of the
cancer risks exceed the Agency's level of concern of 1 x 10^-6^

but only 4 of the risks exceed 1 x 10^-4^ (i.e., risks range from 2.5 x
10^-5^ to 1.6 x 10^-6^).

> **Occupational post-application exposure and risk:** There is the
> potential for post-application exposures to creosote. Potential
> post-application exposure may occur as a result of creosote treated
> wood in commercial, industrial, and residential settings. There is the
> potential for contact with creosote treated wood for occupational
> workers who install railroad ties and poles. Railroad workers may
> become exposed during the mechanical and manual installation of
> pressure treated railroad crossties as well as during inspection
> procedures (ATSDR, 1990). Pole installers may also contact creosote
> treated wood while attaching fittings on telephone poles, installing
> new telephone poles, conducting ground line treatment of telephone
> poles, and maintaining and repairing existing telephone poles (ATSDR,
> 1990). No dermal exposure data were available for these scenarios.
> Mechanical installation and/or the use of appropriate PPE are
> recommended to reduce exposure/contact with creosote treated wood.
>
> Although there are no creosote label registered uses of creosote for
> residential uses, EPA acknowledges that some creosote treated wood
> such as railroad ties are used outdoors in home landscaping. The
> potential dermal and incidental oral exposures to outdoor landscape
> timbers are expected to be episodic in nature.
>
> **[Aggregate Exposure and Risk]{.underline}**
>
> In order for a pesticide registration to continue, it must be shown
> "that there is reasonable certainty that no harm will result from
> aggregate exposure to pesticide chemical residue, including all
> anticipated dietary exposures and other exposures for which there are
> reliable information." Aggregate exposure is the total exposure to a
> single chemical (or its residues) that may occur from dietary (i.e.,
> food and drinking water), residential, and other non-occupational
> sources, and from all known or plausible exposure routes (oral,
> dermal, and inhalation).
>
> **Acute and Chronic Dietary Aggregate Risk**
>
> Under the current policy of the Office of Pesticide Programs, acute
> aggregate risk assessment determines the acute risk from combined
> dietary consumption of pesticide residues, separate from residential
> exposures (Health Effects Division, Standard Operating Procedure 97.2,
> April 1998). In the case of creosote, an acute aggregate (food +
> water) risk estimate was not performed for Creosote. Creosote is not
> registered for any food use, and it has also been determined that
> creosote is not likely to impact the diet or drinking water.
>
> **Short- and Intermediate-Term Aggregate Risks**
>
> Aggregate short and intermediate term risk assessments are designed to
> provide estimates of risk likely to result from exposures to the
> pesticide or pesticide residues in food, water, and from residential
> (or other non-occupational) pesticide uses. Due to the lack of
> exposure through food or water, short and intermediate term aggregate
> risks were not performed. Residential exposures to Creosote residues
> may occur, but data are not available to assess these risks.
>
> **Chronic (Non-Cancer) Aggregate Risk**
>
> Based on the lack of potential for chronic exposure to Creosote
> through food and water, a chronic (non-cancer) aggregate risk
> assessment was not performed.
>
> **Environmental Hazard and Risk**
>
> Process wastewater, dumpsite leachate, storage tank leaks, and spills
> are the major creosote sources to the environment (Merril and Wade,
> 1985). In addition, leachates from pressure treated wood can migrate
> out into soils, and water. The environmental fate and transport of
> creosote focuses primarily on the likely exposure of PAHs into three
> environmental compartments: 1) leaching of creosote mixture into
> surface and ground waters from the railroad ties and utility poles; 2)
> migration into soil/sediments from the railroad ties and utility
> poles, and 3) bioaccumulation into the aqueous and benthic organisms.

Recent studies conducted by Ken Brooke ( Sooke Basin, 2001 and Railroad
ties, 2004) illustrate some important trends: 1) Creosote treated wood
does leach out its constituents; 2) leaching process is acute at the
start of the and tapers off with time; 3) leachate in water soil
consists of a mixture the PAHs ranging from low molecular weight to high
molecular weight; 4) migration of PAHs from the pole or railroad ties is
limited to a short distance: maximum up to 10 meters away from the line
of origin and not more than 60 cm vertically down; 5) initial mixture
ratio for low to high molecular weight PAHs is 1:1 while with the
passage of time (385 days),in favor of high molecular weight PAHs.; 6)
there is possibly an acute impact at short distances away from utility
poles or railroad ties. 7) some high molecular weight PAH s like benzo
(e)pyrene are persistent in soils.

> Data on the migration into soils and water are contradictory, but the
> majority of data indicate that the migration process into these
> environmental compartments is not remarkable. Biodegradation processes
> of PAHs under aqueous aerobic conditions is rapid, and except for a
> few large sized PAHs like benz\[a\]pyrene, fluoranthene,
> benzo\[k\]fluoranthene, most PAHs show a tendency to biodegrade. Under
> anaerobic conditions, biodegradation is not commonly observed and the
> PAHs may become persistent, stable in soils/sediments and lose the
> migration capability.
>
> **Ecological Hazard and Risk**
>
> Because guideline toxicity studies are not available for the major
> component PAHs of creosote expected in the aquatic environment, the
> best available information from the open literature and from existing
> evaluations was used in this assessment. However, data gaps are
> extensive, especially for the complexes of PAHs likely to occur in the
> water column and in aquatic sediments. Therefore, much of the risk
> presumptions are based on a qualitative assessment of the available
> information.
>
> Based on the existing laboratory and field data and modeling of PAH
> aquatic concentrations from use of creosote-treated railroad ties and
> aquatic structures, the following conclusions for risks to freshwater
> and saltwater fish and invertebrates exposed in the water column
> and/or in aquatic sediment are made:
>
> **Aquatic structures:**
>
> · the level of concern (LOC) is exceeded for acute risk to listed
> (i.e., endangered and threatened) freshwater and saltwater
> (estuarine/marine) fish and aquatic invertebrates exposed to PAHs in
> the water column
>
> · the LOC is exceeded for acute risk to non-listed saltwater
> invertebrates exposed to PAHs in the water column
>
> · chronic RQs can not be calculated due to lack of chronic toxicity
> data, but available evidence indicates that chronic risk (survival,
> growth, reproduction, immunotoxicity) is possible to aquatic organisms
> inhabiting the water column
>
> · based on findings from the Sooke Basin field study, PAH accumulation
> in sediments is sufficiently high to pose a risk to benthic organisms
> in the immediate vicinity of creosote-treated pilings for at least a
> year
>
> · although survival and spawning were not affected, short-term adverse
> affects on growth of mussels was reported immediately around pilings
> at Sooke Basin
>
> · one year after pilings were installed in Sooke Basin, an assemblage
> of invertebrate organisms inhabited the creosote-treated pilings,
> suggesting minimal long-term impacts to some non-listed species
>
> · laboratory and field investigation found a major detrimental impact
> on hatching and development of fish (herring) eggs attached to aquatic
> pilings, even pilings that were 40 years old, suggesting that some
> sensitive species may be adversely affected by creosote-treated
> pilings
>
> · creosote had a significant and rapid adverse impact on total
> abundance, number of taxa, and population dynamics of zooplankton in
> microcosms
>
> · impacts of creosote-treated aquatic pilings are likely to vary
> locally, depending on abiotic and biotic factors such as current
> speed, amount of structure per unit area, air and water temperature,
> salinity, and the aquatic species occurring in the immediate area of
> the structures; thus, a site evaluation is essential prior to
> installation of new structures
>
> · potential impacts to aquatic organisms, especially less mobile
> species, may be exacerbated in the vicinity of treatment plants and
> loading docks in aquatic areas
>
> **Railroad structures:**
>
> · the level of concern (LOC) is exceeded for acute risk to listed
> freshwater and saltwater fish and aquatic invertebrates exposed to
> PAHs expected to reaching the water column; in wetter areas, PAHs may
> possibly remain at levels of concern to listed species for many weeks
>
> · in wetter areas with more potential for movement of PAHs into the
> aquatic environment, the LOC also is exceeded for acute risk to
> non-listed fish (freshwater) and aquatic invertebrates exposed to PAHs
> in the water column
>
> · chronic RQs can not be calculated due to lack of chronic toxicity
> data, but available evidence indicates that chronic risk is possible
> to aquatic organisms inhabiting the water column
>
> · based on a mesocosm study, sediment PAH levels around railroad ties
> appear to be lower than those around aquatic pilings
>
> **Endangered Species**
>
> The Endangered Species Act (ESA) requires that federal agencies
> consult with the National Marine Fisheries Service and/or the United
> States Fish and Wildlife Services (FWS) for listed organisms if a
> proposed \"action\" may affect listed species or their designated
> habitat. Because the ecological risk assessment for creosote indicates
> a potential for exposure of listed fish and aquatic invertebrate
> species, a refined assessment is needed that includes delineation of
> the action area and species at risk and evaluation of direct,
> indirect, and habitat effects. A refined listed-species assessment has
> not been conducted for the current risk assessment but is deferred to
> Registration Review.
>
> **Incident Reports**
>
> Creosote and creosote-containing substances are widely used in
> industry and by certain subgroups of individuals, resulting in a large
> population of persons with potential exposure. According to California
> data, the majority of poisoning incident cases occurred as a result of
> handling creosote and applying it to wood without proper protection
> for the skin and eyes. The number of these cases has dropped quite
> markedly in the 1990s. Substantial contact with treated wood appears
> to be a risk factor for skin and eye burns, even years after the wood
> was treated. Symptoms experienced were burns and rashes on the exposed
> body areas, chemical conjunctivitis, headaches, nausea, and eye
> irritation.
>
> While a number of human health studies are available that include
> creosote as a possible, or even likely, target exposure, few studies
> are available with enough information for a rigorous assessment of
> chronic health effects attributable to creosote specifically. By far,
> the most common limitation of studies aimed at evaluating effects of
> creosote exposure is the almost total absence of objective exposure
> measurements for the study participants. For most of the studies,
> assessment of exposure is based on information about past occupational
> activities provided by the participants or assigned by health studies
> professionals such as industrial hygienists with general knowledge of
> occupations and materials. In almost all cases, possible exposure to
> other materials, either separately or concomitantly, cannot be
> excluded. A second important limitation often seen in studies on
> effects of creosote is the lack of statistical significance calculated
> for many of the apparent associations between assigned creosote
> exposure and development of disease.
>
> These limitations notwithstanding, among the epidemiological studies
> on effects of creosote exposure, increased risks for development of a
> number of diseases have been observed. Diseases typically found to be
> in excess include skin cancer and nonmalignant skin disorders, bladder
> cancer, lung cancer and nonmalignant respiratory diseases. Considering
> the information presently available, conclusions regarding chronic
> health effects from exposure to creosote alone should be considered
> tentative.
>
> **2.0 PHYSICAL/CHEMICAL PROPERTIES**
>
> Creosote ,as defined by the American Wood Preservers Association, is a
> distillate derived from coal tar, derived by the high temperature
> carbonization of bituminous coal. Creosote consists primarily of
> liquid and solid polyaromatic hydrocarbons (PAH's) and contains some
> tar acids and tar bases. The two major types of creosote in use are
> P1/P13 creosote (a straight creosote distillate used for ground
> contact, land, and fresh and marine water applications) and P2
> creosote, used in treatment of railroad crossties. A detailed
> assessment of the physical/chemical properties of creosote can be
> found in the product chemistry chapter for the creosote RED (A. Najm
> Shamim, Ph.D.). A summary is shown here.
>
> **P1/P13 Fraction**
>
> Chemical Name: Coal Tar Creosote
>
> Molecular Wt.: No Applicable
>
> Color: 2.5Y2/2 to 2.5Y4/2 ( Based on Munsell color scheme)
>
> Odor: Sharp, aromatic, wood-like
>
> Solubility: 313 μg/ml
>
> Vapor Pressure: 11.1 mm Hg at 24.4 ^o^C
>
> Log P: 3.247
>
> Stability: Short term( accelerated )stability was performed on four
> constituents of the mixture: naphthalene, phenanthrene pyrene and
> chrysene for a period of 30 days at 60 ^o^ C. At the end of thirty day
> period, naphthalene remaining was : 96.5%, phenanthrene: 87.2%,
> pyrene: 86.9% and chrysene: 92.4%
>
> Viscosity; 14.60 mm/s
>
> Storage Stability: Not determined.
>
> Notes:
>
> 1.The P1/P13 samples, provided by the Industry to Research Triangle
> Institute, were distilled, within 95% confidence limit, residues
> remaining were less than 1.1% as required by the AWPA Standard A1-91 (
> This test is similar to the EPA's Certified Limit Test required for
> other pesticides).
>
> 2.Insoluble mass in Xylenes: Duplicate determinations showed that this
> fraction contained between 0.21 to 0.23% insoluble materials.
>
> 3\. Specific gravity of the fraction, for the industry sample ( single
> determination) is 1.0934 ( corrected to 38^o^C)
>
> 4\. Moisture ( water) content for the industry sample ( single
> determination) is 0.4%.
>
> All these results were obtained by using the AWPA Method A1-91 Series.
>
> **P2 Fraction**

Chemical Name: Coal Tar Creosote

Color: 10YR2/1 to 2.5Y5/5 ( Munsell color scheme)

Odor: Strong aromatic, Petroleum-like

Solubility: 306 μg/ml

Vapor Pressure: 8.6 mm Hg at 24.4 to 24.5 ^o^C

Log P 3.311

Stability:

Viscosity: 15.5 mm/s at 25 ^o^C

**3.0** **Hazard Characterization**

**3.1 Acute Toxicity**

The acute toxicity profile for the P1/P13 blend is shown below.

+-------------------+-----+----------------------------+-----+--------+
| **Study Type**    | *   | **Results**                | **  | **MRID |
|                   | *An |                            | Tox | No**   |
|                   | ima |                            | Ca  |        |
|                   | l** |                            | t** |        |
+-------------------+-----+----------------------------+-----+--------+
| 81-1: Acute Oral  | Rat | LD~50~ Male 2451 mg/kg     | III | 43     |
|                   |     |                            |     | 032101 |
|                   |     | Female 1893 mg/kg          |     |        |
+-------------------+-----+----------------------------+-----+--------+
| 81‑2: Acute       | Rab | LD~50~ Male \> 2000 mg/kg  | III | 43     |
| Dermal            | bit |                            |     | 032102 |
|                   |     | Female \> 2000 mg/kg       |     |        |
+-------------------+-----+----------------------------+-----+--------+
| 81‑3: Acute       | Rat | LC~50~ \> 5 mg/L           | IV  | 43     |
| Inhalation        |     |                            |     | 032103 |
+-------------------+-----+----------------------------+-----+--------+
| 81‑4: Primary Eye | Rab | Irritation clearing in     | II  | 43     |
| Irritation        | bit | 8-21 days                  |     | 032104 |
+-------------------+-----+----------------------------+-----+--------+
| 81‑5: Primary     | Rab | erythema to day 14         | III | 43     |
| Dermal Irritation | bit |                            |     | 032105 |
+-------------------+-----+----------------------------+-----+--------+
| 81‑6: Dermal      | Gui | study unacceptable         | N/A | 43     |
| Sensitization     | nea |                            |     | 032106 |
|                   | Pig |                            |     |        |
+-------------------+-----+----------------------------+-----+--------+

The acute toxicity profile for the P2 blend is shown below.

+-------------------+------+--------------------------+-----+--------+
| **Study Type**    | **   | **Results**              | **  | **MRID |
|                   | Anim |                          | Tox | No**   |
|                   | al** |                          | Ca  |        |
|                   |      |                          | t** |        |
+-------------------+------+--------------------------+-----+--------+
| 81-1: Acute Oral  | Rat  | LD~50~ Male 2524 mg/kg   | III | 43     |
|                   |      |                          |     | 032301 |
|                   |      | Female 1993 mg/kg        |     |        |
+-------------------+------+--------------------------+-----+--------+
| 81‑2: Acute       | Ra   | LD~50~ Male \> 2000      | III | 43     |
| Dermal            | bbit | mg/kg                    |     | 032302 |
|                   |      |                          |     |        |
|                   |      | Female \> 2000 mg/kg     |     |        |
+-------------------+------+--------------------------+-----+--------+
| 81‑3: Acute       | Rat  | LC~50~ \> 5.3 mg/L       | IV  | 43     |
| Inhalation        |      |                          |     | 032303 |
+-------------------+------+--------------------------+-----+--------+
| 81‑4: Primary Eye | Ra   | Irritation clearing      | III | 43     |
| Irritation        | bbit | within 7 days            |     | 032304 |
+-------------------+------+--------------------------+-----+--------+
| 81‑5: Primary     | Ra   | no irritation after 7    | III | 43     |
| Dermal Irritation | bbit | days                     |     | 032305 |
+-------------------+------+--------------------------+-----+--------+
| 81‑6: Dermal      | Gu   | study unacceptable       | N/A | 43     |
| Sensitization     | inea |                          |     | 032306 |
|                   | Pig  |                          |     |        |
+-------------------+------+--------------------------+-----+--------+

**3.2 Dose-Response Assessment**

On April 1, 1999, the Health Effects Division\'s Hazard Identification
Assessment Review Committee (HIARC) evaluated the toxicological
endpoints selected for occupational and residential (dermal and
inhalation) exposure risk assessments for Creosote. On September 3,
2003, the Antimicrobials Division Toxicity Endpoint Selection Committee
(ADTC) met to verify the selected endpoints for long-term dermal risk
assessments for creosote and inhalation risk assessment, and also
discussed whether dermal and inhalation Margins of Exposure should be
combined for creosote risk assessment. The toxicological endpoints
selected for various exposure scenarios are summarized in the table
below.

**Toxicology Endpoints for Creosote**

+----------------+----------------+---------------+-------------------+
| **EXPOSURE**   | **DOSE**       | **ENDPOINT**  | **STUDY**         |
|                |                |               |                   |
| **SCENARIO**   | *              |               |                   |
|                | *(mg/kg/day)** |               |                   |
+----------------+----------------+---------------+-------------------+
| Acute and      | **These risk   |               |                   |
| Chronic        | assessments    |               |                   |
| Dietary        | not            |               |                   |
|                | required.**    |               |                   |
+----------------+----------------+---------------+-------------------+
| C              | Creosote has   |               |                   |
| arcinogenicity | been shown to  |               |                   |
|                | exert positive |               |                   |
| (dermal)       | miutagenic     |               |                   |
|                | effects in     |               |                   |
|                | vitro, and has |               |                   |
|                | been shown to  |               |                   |
|                | be positive    |               |                   |
|                | for            |               |                   |
|                | c              |               |                   |
|                | arcinogenicity |               |                   |
|                | in an          |               |                   |
|                | initia         |               |                   |
|                | tion/promotion |               |                   |
|                | study.         |               |                   |
|                | Creosote has   |               |                   |
|                | been           |               |                   |
|                | classified as  |               |                   |
|                | a B1           |               |                   |
|                | carcinogen in  |               |                   |
|                | IRIS. An oral  |               |                   |
|                | cancer slope   |               |                   |
|                | factor of 6.28 |               |                   |
|                | x 10^-6^ (µg   |               |                   |
|                | CT             |               |                   |
|                | M1/kg/day)^-1^ |               |                   |
|                | was selected   |               |                   |
|                | for creosote   |               |                   |
|                | using the data |               |                   |
|                | of Culp et al  |               |                   |
|                | (1998) for the |               |                   |
|                | coal tar       |               |                   |
|                | mixture 1      |               |                   |
|                | (CTM1) on the  |               |                   |
|                | basis of       |               |                   |
|                | forestomach    |               |                   |
|                | tumors.        |               |                   |
+----------------+----------------+---------------+-------------------+
| Short-Term     | Oral NOAEL=50  | decreased     | Developmental     |
| Dermal         |                | body weight   | Toxicity - Rat    |
|                |                | gain at 175   |                   |
| (1-30 days)    |                | mg/kg/day     |                   |
+----------------+----------------+---------------+-------------------+
|                | MOE = 100 (5%  |               |                   |
|                | dermal         |               |                   |
|                | absorption)    |               |                   |
+----------------+----------------+---------------+-------------------+
| Int            | Dermal NOAEL = | Decreased     | 90-Day Dermal     |
| ermediate-term | 40             | body weight   | Toxicity Study in |
|                |                | gain at 400   | the Rat           |
| Dermal         |                | mg/kg/day     |                   |
|                |                |               |                   |
| (1-6 months)   |                |               |                   |
+----------------+----------------+---------------+-------------------+
|                | MOE = 100      |               |                   |
+----------------+----------------+---------------+-------------------+
| Long-Term      | Oral LOAEL =   | decreased     | 2-generation      |
| Dermal^a^      | 25 mg/kg/day   | pre-mating    | reproduction      |
|                |                | body weight   | study - Rat       |
| (\>6 months)   |                |               |                   |
+----------------+----------------+---------------+-------------------+
|                | MOE = 300      |               |                   |
|                | (10x, 10x, 3x  |               |                   |
|                | for use of a   |               |                   |
|                | LOAEL)         |               |                   |
+----------------+----------------+---------------+-------------------+
| Inhalati       | NOAEL =        | decreased     | 90-day Inhalation |
| on-creosote^b^ | 0.0047mg/L     | body weight   | Study in the Rat  |
|                |                | gain, altered | with P2 creosote  |
| (any time      | MOE = 100      | hematology    | (MRID             |
| period)        |                |               | **43600901**)     |
+----------------+----------------+---------------+-------------------+
| Inhalation     | LOAEL = 52     | nasal         | Two year          |
| --naphthalene  | mg/m^3^        | effects:      | inhalation        |
| (any time      |                | hyperplasia   | toxicity study -  |
| period)        | MOE = 300      | and           | mouse (USEPA,     |
|                |                | metaplasia in | IRIS)             |
|                |                | respiratory   |                   |
|                |                | and olfactory |                   |
|                |                | epithelium    |                   |
|                |                | respectively  |                   |
+----------------+----------------+---------------+-------------------+
| Dermal         | 5%, determined |               |                   |
| absorption ^c^ | from the       |               |                   |
|                | results of in  |               |                   |
|                | vivo / in      |               |                   |
|                | vitro testing  |               |                   |
|                | in rats and in |               |                   |
|                | vitro testing  |               |                   |
|                | using human    |               |                   |
|                | skin.          |               |                   |
+----------------+----------------+---------------+-------------------+

  -----------------------------------------------------------------------

  -----------------------------------------------------------------------

^a^after re-examination of the toxicology data, the ADTC concluded that
the 2-generation reproduction toxicity study was appropriate for
long-term dermal risk assessment for the following reasons**:** the
duration of the 2-generation reproduction study is more representative
of the time frame (i.e. long-term) than the 90-day dermal study, and is
consistent with OPP policy regarding duration of the study vs. route of
exposure; body weight gain decreases in the 2-generation reproduction
toxicity study were observed in the F2 generation, supporting the time
frame for the long-term endpoint (i.e. \> 6 months). The 90-day dermal
study effects are not as representative of the time frame for the
long-term dermal risk assessment**.** However, the two studies can be
considered co-critical studies for this endpoint. Correction of the
LOAEL from the 2-generation reproduction toxicity study for dermal
absorption (50%) and use of a LOAEL (3x extra UF) yields a MOE and
endpoint (300 and 50 mg/kg/day) similar to the 90-day dermal toxicity
study (40 mg/kg/day and MOE of 300 \[extra 3x to extrapolate to
long-term endpoint\]).

^b^the ADTC re-examined the use of the inhalation toxicity study
selected for inhalation risk assessment for creosote and concluded that
a developmental toxicity study, as used for the oral and dermal risk
assessments of creosote, is not appropriate for inhalation risk
assessment because: (1) the inhalation toxicity study showed significant
effects on body weight gain early in the study (one week) and is
therefore relevant for short-term assessment (2) it is also a
route-specific study; and (3) the inhalation NOAEL is more sensitive
than the developmental NOAEL. Therefore, the inhalation study will
remain as the study for the short-term inhalation endpoint.

^c^dermal absorption of creosote was determined from submitted in vivo
and in vitro studies on creosote (MRIDs 47179501 and 47179502).

**FQPA Considerations**

As there are no existing food uses for creosote, an FQPA assessment is
not necessary. Potential post-application exposures to residents,
including children (e.g., from use of railroad ties by homeowners),
could not be assessed due to lack of exposure data. The available
evidence on developmental and reproductive effects of creosote was
assessed by the Health Effects Division (HED) Hazard Identification
Assessment Review Committee on April 1, 1999 The committee expressed
concern for potential infants and children's susceptibility of creosote,
based on the severity of offspring vs. maternal effects observed with
testing of creosote in the P1/P13 blend developmental toxicity study in
rats at the 175 mg/kg/day dose level as well as deficiencies observed in
the 2-generation reproduction toxicity study in rats.

**3.3 Dermal Absorption**

In 2003, the Toxicology disciplinary chapter for the reregistration
eligibility decision (RED) document for creosote included toxicity
endpoints of concern, among them an estimation of the magnitude of
dermal absorption for creosote. As there were no data at that time
specifically examining dermal absorption of creosote, a factor of 50%
was estimated, based on comparison of the oral and dermal LOAELs from
the developmental toxicity study in rats (MRID \# 43584201) and the
90-day dermal toxicity study in rats (MRID \# 43616101) using the P1/P13
blend. The oral LOAEL of 175 mg/kg/day observed in the developmental
toxicity study, when compared to the dermal LOAEL of 400 mg/kg/day
observed in the dermal toxicity study, yields an absorption factor of
44%, which was rounded up to 50% by the Committee. The rounding to 50%
took into account the significant dermal irritation which occurs from
dermal exposure to creosote.

Beginning in 2005, a series of meetings were held involving scientific
and regulatory staff of the Antimicrobials Division and the Health
Effects Division, Office of Pesticide Programs, U.S. Environmental
Protection Agency, the Pest Management Regulatory Agency, Health Canada,
and the Creosote Council III as the Creosote Couincil did not agree with
the 50% dermal absorption factor determination. Over the next two years,
a study protocol was discussed to examine dermal absorption of the
creosote mixture. The study protocol was approved in 2007 and the dermal
absorption study was submitted for review by the Office of Pesticide
Programs in 2007. The studies submitted consisted of an in vivo dermal
absorption study in the rat as well as an in vitro dermal absorption
study using both rat and human skin (MRIDs 47179501 and 47179502).

The in vitro study was determined to be unacceptable for regulatory
purposes from initial review, based on the lack of data demonstrating
that the concentration of the creosote solution did not exceed
solubility limits and therefore did not have an artefactual influence on
the magnitude of absorption in the in vitro test system.

The Office of Pesticide Programs further determined that from the in
vivo data, a value of 33.9 (34%) was appropriate for the magnitude of
dermal absorption in the in vivo test system. This was concluded on the
basis of data demonstrating continued absorption of the creosote mixture
after 8 hours as evidenced by urinary and fecal excretion of radiolabel.
The registrant presented an argument that the O-ring used in the initial
study may have acted as a depot for creosote-derived readioactivity and
should therefore be considered artefactual, based on a supplemental
study conducted where the O-ring was not glued to the skin of the
animal. However, significant radioactivity was recovered from the body
wrap used in this supplemental study, compromising interpretation of the
supplemental study results.

In January of 2008, the Creosote Council met again with scientific and
regulatory staff of the Office of Pesticide Programs to discuss their
interpretation of the dermal absorption data. The main point of their
presentation was that the Office of Pesticide Programs should consider
the ratio of absorption of creosote in rat skin vs. human skin based on
the submitted data. These data show an approximate 8-fold difference in
absorption through rat skin vs. human skin (34% in rat skin in vivo and
in vitro vs. 4.2% in human skin in vitro).

Based on the available data, the 8-fold factor for rat skin vs. human
skin with respect to absorption of creosote is supported by the
submitted data. However, uncertainties still exist with these data:

1\) The registrant submitted data on solubility limits of the 8 marker
components used in the in vivo dermal absorption protocol as
representative of creosote. The registrant did not submit solubility
limits for the actual creosote mixture itself. While the solubility data
submitted by the registrant indicated that the solubility limits were
not exceeded for any of the 8 marker compounds used as radiolabelled
tracers, there is uncertainty as to how the mixture behaves.

2\) There is uncertainty regarding absorption after 8 hours exposure.
The O-ring data are not conclusive of an effect of the O-ring acting as
a depot, as absorption is still seen after 8 hours of exposure and
washing of the skin surface contained by the O-ring.

Based on the uncertainties, 8-fold factor describing the difference in
dermal absorption between rat and human skin is acceptable, but the
dermal absorption value for creosote is concluded to be 5% (34% value
from the rat study divided by 8 and rounded upward).

**3.4 Classification of Carcinogenic Potential**

In conjunction with the Pest Management Regulatory Agency, Health
Canada, a quantitative risk assessment on carcinogenicity of creosote
has been performed using the data of Culp et al. (1998). A dermal
carcinogenicity study by Bushmann et al. (1997) was also available, but
was determined not suitable for quantitative assessment of
carcinogenicity. Ulceration of the skin was significant finding of the
study which potentially affected tumor response. In addition, systemic
toxicity was not examined, and complete histopathology data were not
available. Based upon the analysis of the Culp et al. data, an oral
cancer potency factor of 6.28 x 10^-6^ (µg/kg/day)^-1^ for the coal tar
mixture 1 tested in this study was selected, on the basis of forestomach
tumors observed

**3.5 Endocrine Disruption**

EPA is required under the Federal Food, Drug and Cosmetic Act (FFDCA),
as amended by the Food Quality Protection Act (FQPA), to develop a
screening program to determine whether certain substances (including all
pesticide active and other ingredients) "may have an effect in humans
that is similar to an effect produced by a naturally occurring estrogen,
or other endocrine effects as the Administrator may designate."
Following recommendations of its Endocrine Disruptor Screening and
Testing Advisory Committee (EDSTAC), EPA determined that there was a
scientific basis for including, as part of the program, the androgen and
thyroid hormone systems, in addition to the estrogen hormone system. EPA
also adopted EDSTAC's recommendation that EPA include evaluations of
potential effects in wildlife. For pesticides, EPA will use FIFRA and,
to the extent that effects in wildlife may help determine whether a
substance may have an effect in humans, FFDCA authority to require the
wildlife evaluations. As the science develops and resources allow,
screening of additional hormone systems may be added to the Endocrine
Disruptor Screening Program (EDSP).

**4.0 EXPOSURE ASSESSMENT AND CHARACTERIZATION**

**4.1 Summary of Registered Uses**

> Creosote applications are limited to occupational handlers at pressure
> treatment facilities. Since it is a restricted-use pesticide that can
> only be applied by certified applicators or someone under their direct
> supervision, it is not available for sale to or use by homeowners. A
> recent voluntary cancellation of all non pressure treatment uses
> restricts creosote to commercial and industrial settings.

**Dietary Exposure**

Based upon its classification as a restricted use pesticide and
restrictions on use sites since 1984, dietary exposure to creosote is
not expected through food. In drinking water, the Agency has determined
that the use pattern of Creosote is not expected to impact water
resources through labeled uses. In light of this finding, EPA believes
that Creosote\'s use will not impact ground or surface water and
therefore is not expected to lead to exposure to humans through drinking
water.

**4.2 Occupational Exposure and Risk**

> Creosote is used by occupational handlers only. Since it is a
> restricted-use pesticide that can only be applied by certified
> applicators or someone under their direct supervision, it is not
> available for sale to or use by homeowners. Furthermore, the non
> pressure treatments of creosote have been voluntarily cancelled by the
> registrants. Creosote applications are now restricted to pressure
> treatment cylinders. The specific job functions and their descriptions
> for
>
> creosote workers are detailed in the occupational and residential
> chapter for the creosote RED.

The worker exposure study on pressure treatment applications submitted
by the Creosote Council II provided chemical-specific handler dermal and
inhalation exposure data in support of the re-registration of pressure
treatments of creosote (Creosote Council II, 2001).

Because of the overall variability in the composition of creosote (e.g.,
over 100 known chemicals are components of creosote), it is difficult to
characterize its exact nature. Since neither the characterization of
airborne creosote nor the development of inhalation sampling methods is
specific for creosote, there exists a high variability in the creosote
inhalation data presented in the literature. Most of the studies
presented in the literature were conducted by industrial hygienists
using methods approved by the National Institute for Occupational Safety
and Health (NIOSH) and Occupational Safety and Health Administration
(OSHA) for polycyclic aromatic hydrocarbons (PAHs), phenols/creosols,
and the individual constituents of the PAHs (i.e., naphthalene,
phenanthrene, anthracene, etc). The Creosote Council study is the most
recent study presented on creosote exposure and presents both dermal and
inhalation exposure. This study provides the best available data on
worker exposure estimates and encompasses all of the worker activities
contributing to exposure.

**[Estimated Non Cancer and Cancer Risks:]{.underline}** The
calculations of the daily dermal dose of creosote received by workers
were used to calculate the non cancer MOEs for the short-term,
intermediate-term, and long-term durations. The dermal MOEs were
calculated using (1) a NOAEL of 50 mg/kg/day for short-term exposure
with a target MOE of 100: (2) a NOAEL of 40 mg/kg/day for
intermediate-term exposures with a target MOE of 100; and, (3) a LOAEL
of 25 mg/kg/day for the long-term duration with a target MOE of 300.
Note: The intermediate-term dermal endpoint was selected from a dermal
toxicity study, and therefore, a dermal absorption factor was not
necessary to calculate the potential dose. The dermal and inhalation non
cancer MOE equations are as follows:

MOE ~\[dermal\]~ = NOAEL or LOAEL / Potential and/or Absorbed Dermal
Dose

MOE ~\[inhalation\]~ = Human Equivalent Concentration (HEC) / Worker's
air concentration

The cancer risk for creosote is based on the estimated absorbed dermal
lifetime average daily dose (LADD) multiplied by the cancer slope factor
for creosote dose as follows:

Cancer Risk = absorbed LADD (mg/kg/day) x CSF of 6.28 x 10^-3^
(mg/kg/day)^-1^

Using these equations, the worker exposure and risk estimates from the
Creosote Council's exposure study are presented in Table 4 (dermal
MOEs), Table 5 (inhalation MOEs), and Table 6 (dermal cancer risk).

**[Dermal MOEs :]{.underline}** The results indicate the short-term (ST)
non cancer dermal MOEs do not trigger a risk concern except for the
treatment operator at site C where the dermal MOE is 68 and the target
MOE is 100. The intermediate-term (IT) non cancer dermal MOEs trigger
risk concerns for 8 of the 24 scenarios presented. IT MOEs range from 3
to 2700 and the target MOE is 100. The long-term (LT) non cancer dermal
MOEs trigger risk concerns for 3 of the 24 scenarios. LT MOEs range from
34 to 34,000 and the target MOE is 300. IT risks being greater than the
LT risks is an anomaly. However, in the case of creosote it is
explainable because the IT toxicity endpoint is based on a dermal study
while the LT endpoint is based on an oral study (i.e., there are
differences in routes of exposure and dosing levels between the two
studies).

+-----+---+---+-----------------+---------+----------+-----+----+-----+
| *   |   |   |                 |         |          |     |    |     |
| *Ta |   |   |                 |         |          |     |    |     |
| ble |   |   |                 |         |          |     |    |     |
| 4.  |   |   |                 |         |          |     |    |     |
| Cr  |   |   |                 |         |          |     |    |     |
| eos |   |   |                 |         |          |     |    |     |
| ote |   |   |                 |         |          |     |    |     |
| Der |   |   |                 |         |          |     |    |     |
| mal |   |   |                 |         |          |     |    |     |
| M   |   |   |                 |         |          |     |    |     |
| OEs |   |   |                 |         |          |     |    |     |
| .** |   |   |                 |         |          |     |    |     |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     |   |   |                 | Po      | Absorbed | Der |    |     |
|     |   |   |                 | tential |          | mal |    |     |
| Job | S | n | Site            |         | Dermal   | M   |    |     |
|     | i | = | Description     | dermal  | Dose     | OEs |    |     |
|     | t |   |                 | dose    |          |     |    |     |
|     | e |   |                 |         | (mg      |     |    |     |
|     |   |   |                 | (mg/    | /kg/day) |     |    |     |
|     |   |   |                 | kg/day) |          |     |    |     |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     |   |   |                 |         |          | ST  | IT |     |
|     |   |   |                 |         |          |     |    |     |
|     |   |   |                 |         |          |     |    | LT  |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
| TO  | A | 4 | 1940s; manual   | 0.414   | 0.021    | 2   | 97 | 1   |
|     |   |   |                 |         |          | 415 |    | 208 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     | B | 4 | 1983; Eng.      | 0.015   | 0.001    | 67  | 27 | 33  |
|     |   |   | Controls        |         |          | 568 | 03 | 784 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     | C | 5 | 1940s           | 14.800  | 0.740    | 68  | 3  | 34  |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     | D | 5 | 1970s;          | 0.132   | 0.007    | 7   | 3  | 3   |
|     |   |   | Automated       |         |          | 576 | 03 | 788 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
| TA  | B | 4 | 1983; Eng.      | 0.025   | 0.001    | 40  | 16 | 20  |
|     |   |   | Controls        |         |          | 323 | 13 | 161 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
| OU  | A | 4 | 1940s; manual   | 0.887   | 0.044    | 1   | 45 | 564 |
|     |   |   |                 |         |          | 127 |    |     |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     | D | 5 | 1970s;          | 0.938   | 0.047    | 1   | 43 | 533 |
|     |   |   | Automated       |         |          | 066 |    |     |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
| CLO | A | 4 | 1940s; manual   | 0.212   | 0.011    | 4   | 1  | 2   |
|     |   |   |                 |         |          | 717 | 89 | 358 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     | B | 4 | 1983; Eng.      | 0.089   | 0.004    | 11  | 4  | 5   |
|     |   |   | Controls        |         |          | 299 | 52 | 650 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     | C | 5 | 1940s           | 2.120   | 0.106    | 472 | 19 | 236 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     | D | 5 | 1970s;          | 0.117   | 0.006    | 8   | 3  | 4   |
|     |   |   | Automated       |         |          | 547 | 42 | 274 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
| LLO | B | 4 | 1983; Eng.      | 0.018   | 0.001    | 55  | 22 | 27  |
|     |   |   | Controls        |         |          | 249 | 10 | 624 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     | C | 5 | 1940s           | 0.203   | 0.010    | 4   | 1  | 2   |
|     |   |   |                 |         |          | 926 | 97 | 463 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     | D | 1 | 1970s;          | 0.077   | 0.004    | 12  | 5  | 6   |
|     |   | 0 | Automated       |         |          | 953 | 18 | 477 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
| LLO | D |   | 1970s;          | 0.244   | 0.012    | 4   | 1  | 2   |
| (F) |   |   | Automated       |         |          | 098 | 64 | 049 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
| LH  | B | 4 | 1983; Eng.      | 0.023   | 0.001    | 43  | 17 | 21  |
|     |   |   | Controls        |         |          | 860 | 54 | 930 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     | C | 5 | 1940s           | 1.810   | 0.091    | 552 | 22 | 276 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     | D | 5 | 1970s;          | 0.383   | 0.019    | 2   | 1  | 1   |
|     |   |   | Automated       |         |          | 611 | 04 | 305 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
| CK  | C | 5 | 1940s           | 0.822   | 0.041    | 1   | 49 | 608 |
|     |   |   |                 |         |          | 217 |    |     |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
| TB  | A | 4 | 1940s; manual   | 0.112   | 0.006    | 8   | 3  | 4   |
|     |   |   |                 |         |          | 929 | 57 | 464 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     | C | 5 | 1940s           | 1.060   | 0.053    | 943 | 38 | 472 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
| WO  | A | 4 | 1940s; manual   | 0.204   | 0.010    | 4   | 1  | 2   |
|     |   |   |                 |         |          | 902 | 96 | 451 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
|     | B | 4 | 1983; Eng.      | 0.047   | 0.002    | 21  | 8  | 10  |
|     |   |   | Controls        |         |          | 322 | 53 | 661 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
| DP  | C | 4 | 1940s           | 0.150   | 0.008    | 6   | 2  | 3   |
|     |   |   |                 |         |          | 667 | 67 | 333 |
+-----+---+---+-----------------+---------+----------+-----+----+-----+
| S   |   |   |                 |         |          |     |    |     |
| ite |   |   |                 |         |          |     |    |     |
| A   |   |   |                 |         |          |     |    |     |
| ,B, |   |   |                 |         |          |     |    |     |
| C,D |   |   |                 |         |          |     |    |     |
| in  |   |   |                 |         |          |     |    |     |
| dic |   |   |                 |         |          |     |    |     |
| ate |   |   |                 |         |          |     |    |     |
| di  |   |   |                 |         |          |     |    |     |
| ffe |   |   |                 |         |          |     |    |     |
| ren |   |   |                 |         |          |     |    |     |
| ces |   |   |                 |         |          |     |    |     |
| in  |   |   |                 |         |          |     |    |     |
| s   |   |   |                 |         |          |     |    |     |
| ite |   |   |                 |         |          |     |    |     |
| se  |   |   |                 |         |          |     |    |     |
| tup |   |   |                 |         |          |     |    |     |
| (e. |   |   |                 |         |          |     |    |     |
| g., |   |   |                 |         |          |     |    |     |
| eng |   |   |                 |         |          |     |    |     |
| c   |   |   |                 |         |          |     |    |     |
| ont |   |   |                 |         |          |     |    |     |
| rol |   |   |                 |         |          |     |    |     |
| s). |   |   |                 |         |          |     |    |     |
|     |   |   |                 |         |          |     |    |     |
| Der |   |   |                 |         |          |     |    |     |
| mal |   |   |                 |         |          |     |    |     |
| exp |   |   |                 |         |          |     |    |     |
| osu |   |   |                 |         |          |     |    |     |
| res |   |   |                 |         |          |     |    |     |
| are |   |   |                 |         |          |     |    |     |
| not |   |   |                 |         |          |     |    |     |
| n   |   |   |                 |         |          |     |    |     |
| orm |   |   |                 |         |          |     |    |     |
| ali |   |   |                 |         |          |     |    |     |
| zed |   |   |                 |         |          |     |    |     |
| to  |   |   |                 |         |          |     |    |     |
| the |   |   |                 |         |          |     |    |     |
| v   |   |   |                 |         |          |     |    |     |
| ari |   |   |                 |         |          |     |    |     |
| ous |   |   |                 |         |          |     |    |     |
| amo |   |   |                 |         |          |     |    |     |
| unt |   |   |                 |         |          |     |    |     |
| of  |   |   |                 |         |          |     |    |     |
| w   |   |   |                 |         |          |     |    |     |
| ood |   |   |                 |         |          |     |    |     |
| tr  |   |   |                 |         |          |     |    |     |
| eat |   |   |                 |         |          |     |    |     |
| ed. |   |   |                 |         |          |     |    |     |
|     |   |   |                 |         |          |     |    |     |
| A   |   |   |                 |         |          |     |    |     |
| rit |   |   |                 |         |          |     |    |     |
| hme |   |   |                 |         |          |     |    |     |
| tic |   |   |                 |         |          |     |    |     |
| m   |   |   |                 |         |          |     |    |     |
| ean |   |   |                 |         |          |     |    |     |
| of  |   |   |                 |         |          |     |    |     |
| the |   |   |                 |         |          |     |    |     |
| der |   |   |                 |         |          |     |    |     |
| mal |   |   |                 |         |          |     |    |     |
| d   |   |   |                 |         |          |     |    |     |
| ose |   |   |                 |         |          |     |    |     |
| f   |   |   |                 |         |          |     |    |     |
| rom |   |   |                 |         |          |     |    |     |
| Ta  |   |   |                 |         |          |     |    |     |
| ble |   |   |                 |         |          |     |    |     |
| 9   |   |   |                 |         |          |     |    |     |
| of  |   |   |                 |         |          |     |    |     |
| the |   |   |                 |         |          |     |    |     |
| P   |   |   |                 |         |          |     |    |     |
| MRA |   |   |                 |         |          |     |    |     |
| wor |   |   |                 |         |          |     |    |     |
| ker |   |   |                 |         |          |     |    |     |
| st  |   |   |                 |         |          |     |    |     |
| udy |   |   |                 |         |          |     |    |     |
| r   |   |   |                 |         |          |     |    |     |
| evi |   |   |                 |         |          |     |    |     |
| ew. |   |   |                 |         |          |     |    |     |
|     |   |   |                 |         |          |     |    |     |
| Abs |   |   |                 |         |          |     |    |     |
| Der |   |   |                 |         |          |     |    |     |
| mal |   |   |                 |         |          |     |    |     |
| D   |   |   |                 |         |          |     |    |     |
| ose |   |   |                 |         |          |     |    |     |
| (m  |   |   |                 |         |          |     |    |     |
| g/k |   |   |                 |         |          |     |    |     |
| g/d |   |   |                 |         |          |     |    |     |
| ay) |   |   |                 |         |          |     |    |     |
| =   |   |   |                 |         |          |     |    |     |
| der |   |   |                 |         |          |     |    |     |
| mal |   |   |                 |         |          |     |    |     |
| d   |   |   |                 |         |          |     |    |     |
| ose |   |   |                 |         |          |     |    |     |
| (m  |   |   |                 |         |          |     |    |     |
| g/k |   |   |                 |         |          |     |    |     |
| g/d |   |   |                 |         |          |     |    |     |
| ay) |   |   |                 |         |          |     |    |     |
| x   |   |   |                 |         |          |     |    |     |
| 5%  |   |   |                 |         |          |     |    |     |
| der |   |   |                 |         |          |     |    |     |
| mal |   |   |                 |         |          |     |    |     |
| a   |   |   |                 |         |          |     |    |     |
| bso |   |   |                 |         |          |     |    |     |
| rpt |   |   |                 |         |          |     |    |     |
| ion |   |   |                 |         |          |     |    |     |
|     |   |   |                 |         |          |     |    |     |
| Wh  |   |   |                 |         |          |     |    |     |
| ere |   |   |                 |         |          |     |    |     |
| ST  |   |   |                 |         |          |     |    |     |
| NO  |   |   |                 |         |          |     |    |     |
| AEL |   |   |                 |         |          |     |    |     |
| is  |   |   |                 |         |          |     |    |     |
| 50  |   |   |                 |         |          |     |    |     |
| mg/ |   |   |                 |         |          |     |    |     |
| kg/ |   |   |                 |         |          |     |    |     |
| day |   |   |                 |         |          |     |    |     |
| (   |   |   |                 |         |          |     |    |     |
| Tar |   |   |                 |         |          |     |    |     |
| get |   |   |                 |         |          |     |    |     |
| MOE |   |   |                 |         |          |     |    |     |
| =   |   |   |                 |         |          |     |    |     |
| 1   |   |   |                 |         |          |     |    |     |
| 00) |   |   |                 |         |          |     |    |     |
| and |   |   |                 |         |          |     |    |     |
| LT  |   |   |                 |         |          |     |    |     |
| LO  |   |   |                 |         |          |     |    |     |
| AEL |   |   |                 |         |          |     |    |     |
| is  |   |   |                 |         |          |     |    |     |
| 25  |   |   |                 |         |          |     |    |     |
| mg/ |   |   |                 |         |          |     |    |     |
| kg/ |   |   |                 |         |          |     |    |     |
| day |   |   |                 |         |          |     |    |     |
| (   |   |   |                 |         |          |     |    |     |
| Tar |   |   |                 |         |          |     |    |     |
| get |   |   |                 |         |          |     |    |     |
| MOE |   |   |                 |         |          |     |    |     |
| =   |   |   |                 |         |          |     |    |     |
| 30  |   |   |                 |         |          |     |    |     |
| 0). |   |   |                 |         |          |     |    |     |
|     |   |   |                 |         |          |     |    |     |
| Wh  |   |   |                 |         |          |     |    |     |
| ere |   |   |                 |         |          |     |    |     |
| IT  |   |   |                 |         |          |     |    |     |
| NO  |   |   |                 |         |          |     |    |     |
| AEL |   |   |                 |         |          |     |    |     |
| is  |   |   |                 |         |          |     |    |     |
| 40  |   |   |                 |         |          |     |    |     |
| mg/ |   |   |                 |         |          |     |    |     |
| kg/ |   |   |                 |         |          |     |    |     |
| day |   |   |                 |         |          |     |    |     |
| (   |   |   |                 |         |          |     |    |     |
| Tar |   |   |                 |         |          |     |    |     |
| get |   |   |                 |         |          |     |    |     |
| MOE |   |   |                 |         |          |     |    |     |
| =   |   |   |                 |         |          |     |    |     |
| 1   |   |   |                 |         |          |     |    |     |
| 00) |   |   |                 |         |          |     |    |     |
| f   |   |   |                 |         |          |     |    |     |
| rom |   |   |                 |         |          |     |    |     |
| a   |   |   |                 |         |          |     |    |     |
| der |   |   |                 |         |          |     |    |     |
| mal |   |   |                 |         |          |     |    |     |
| stu |   |   |                 |         |          |     |    |     |
| dy. |   |   |                 |         |          |     |    |     |
+-----+---+---+-----------------+---------+----------+-----+----+-----+

**[Inhalation MOEs:]{.underline}** The non cancer inhalation MOEs for
worker exposure to naphthalene range from 23 to 1900 with a target MOE
of 300. Sixteen of the 19 inhalation MOEs presented exceed the target
MOE of 300, and therefore, are of concern. None of the average air
concentrations for the various job functions exceeded the TLV of 52
mg/m^3^.

+-----+---+---+----------------+---------+----------+-------+-------+
| *   |   |   |                |         |          |       |       |
| *Ta |   |   |                |         |          |       |       |
| ble |   |   |                |         |          |       |       |
| 5.  |   |   |                |         |          |       |       |
| I   |   |   |                |         |          |       |       |
| nha |   |   |                |         |          |       |       |
| lat |   |   |                |         |          |       |       |
| ion |   |   |                |         |          |       |       |
| M   |   |   |                |         |          |       |       |
| OEs |   |   |                |         |          |       |       |
| for |   |   |                |         |          |       |       |
| Na  |   |   |                |         |          |       |       |
| pht |   |   |                |         |          |       |       |
| hal |   |   |                |         |          |       |       |
| ene |   |   |                |         |          |       |       |
| **. |   |   |                |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
|     |   |   |                | Average | Average  |       | MOE   |
|     |   |   |                |         |          |       |       |
| Job | S | n | Site           | Naphth  | Naphth   | \% of | (T    |
|     | i | = | Description    | (u      | (        | TLV   | arget |
|     | t |   |                | g/m^3^) | mg/m^3^) |       | 300)  |
|     | e |   |                |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
| TO  | A | 4 | 1940s; manual  | NA      | NA       | NA    | NA    |
+-----+---+---+----------------+---------+----------+-------+-------+
|     | B | 4 | 1983; Eng.     | 221     | 0.221    | 0.4   | 235   |
|     |   |   | Controls       |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
|     | C | 5 | 1940s          | 1320    | 1.32     | 2.5   | 39    |
+-----+---+---+----------------+---------+----------+-------+-------+
|     | D | 5 | 1970s;         | 802     | 0.802    | 1.5   | 65    |
|     |   |   | Automated      |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
| TA  | B | 4 | 1983; Eng.     | 406     | 0.406    | 0.8   | 128   |
|     |   |   | Controls       |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
| OU  | A | 4 | 1940s; manual  | NA      | NA       | NA    | NA    |
+-----+---+---+----------------+---------+----------+-------+-------+
|     | D | 5 | 1970s;         | 925     | 0.925    | 1.8   | 56    |
|     |   |   | Automated      |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
| CLO | A | 4 | 1940s; manual  | NA      | NA       | NA    | NA    |
+-----+---+---+----------------+---------+----------+-------+-------+
|     | B | 4 | 1983; Eng.     | 227     | 0.227    | 0.4   | 229   |
|     |   |   | Controls       |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
|     | C | 5 | 1940s          | 2033    | 2.033    | 3.9   | 26    |
+-----+---+---+----------------+---------+----------+-------+-------+
|     | D | 5 | 1970s;         | 574     | 0.574    | 1.1   | 91    |
|     |   |   | Automated      |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
| LLO | B | 4 | 1983; Eng.     | 27      | 0.027    | 0.1   | 1926  |
|     |   |   | Controls       |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
|     | C | 5 | 1940s          | 694     | 0.694    | 1.3   | 75    |
+-----+---+---+----------------+---------+----------+-------+-------+
|     | D | 1 | 1970s;         | 195     | 0.195    | 0.4   | 267   |
|     |   | 0 | Automated      |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
| LLO | D |   | 1970s;         | 679     | 0.679    | 1.3   | 77    |
| (F) |   |   | Automated      |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
| LH  | B | 4 | 1983; Eng.     | 43      | 0.043    | 0.1   | 1209  |
|     |   |   | Controls       |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
|     | C | 5 | 1940s          | 1870    | 1.87     | 3.6   | 28    |
+-----+---+---+----------------+---------+----------+-------+-------+
|     | D | 5 | 1970s;         | 2251    | 2.251    | 4.3   | 23    |
|     |   |   | Automated      |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
| CK  | C | 5 | 1940s          | 117     | 0.117    | 0.2   | 444   |
+-----+---+---+----------------+---------+----------+-------+-------+
| TB  | A | 4 | 1940s; manual  | NA      | NA       | NA    | NA    |
+-----+---+---+----------------+---------+----------+-------+-------+
|     | C | 5 | 1940s          | 853     | 0.853    | 1.6   | 61    |
+-----+---+---+----------------+---------+----------+-------+-------+
| WO  | A | 4 | 1940s; manual  | NA      | NA       | NA    | NA    |
+-----+---+---+----------------+---------+----------+-------+-------+
|     | B | 4 | 1983; Eng.     | 917     | 0.917    | 1.8   | 57    |
|     |   |   | Controls       |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+
| DP  | C | 4 | 1940s          | 347     | 0.347    | 0.7   | 150   |
+-----+---+---+----------------+---------+----------+-------+-------+
| TLV |   |   |                |         |          |       |       |
| =   |   |   |                |         |          |       |       |
| 10  |   |   |                |         |          |       |       |
| ppm |   |   |                |         |          |       |       |
| (52 |   |   |                |         |          |       |       |
| mg  |   |   |                |         |          |       |       |
| /m^ |   |   |                |         |          |       |       |
| 3^) |   |   |                |         |          |       |       |
| S   |   |   |                |         |          |       |       |
| TEL |   |   |                |         |          |       |       |
| 15  |   |   |                |         |          |       |       |
| ppm |   |   |                |         |          |       |       |
| (79 |   |   |                |         |          |       |       |
| mg  |   |   |                |         |          |       |       |
| /m^ |   |   |                |         |          |       |       |
| 3^) |   |   |                |         |          |       |       |
|     |   |   |                |         |          |       |       |
| m   |   |   |                |         |          |       |       |
| g/m |   |   |                |         |          |       |       |
| ^3^ |   |   |                |         |          |       |       |
| =   |   |   |                |         |          |       |       |
| ug  |   |   |                |         |          |       |       |
| /m3 |   |   |                |         |          |       |       |
| /   |   |   |                |         |          |       |       |
| 1   |   |   |                |         |          |       |       |
| 000 |   |   |                |         |          |       |       |
|     |   |   |                |         |          |       |       |
| \%  |   |   |                |         |          |       |       |
| of  |   |   |                |         |          |       |       |
| TLV |   |   |                |         |          |       |       |
| =   |   |   |                |         |          |       |       |
| (m  |   |   |                |         |          |       |       |
| g/m |   |   |                |         |          |       |       |
| ^3^ |   |   |                |         |          |       |       |
| /   |   |   |                |         |          |       |       |
| 52) |   |   |                |         |          |       |       |
| x   |   |   |                |         |          |       |       |
| 100 |   |   |                |         |          |       |       |
|     |   |   |                |         |          |       |       |
| MOE |   |   |                |         |          |       |       |
| =   |   |   |                |         |          |       |       |
| HEC |   |   |                |         |          |       |       |
| /   |   |   |                |         |          |       |       |
| air |   |   |                |         |          |       |       |
| co  |   |   |                |         |          |       |       |
| nc; |   |   |                |         |          |       |       |
| Wh  |   |   |                |         |          |       |       |
| ere |   |   |                |         |          |       |       |
| HEC |   |   |                |         |          |       |       |
| =   |   |   |                |         |          |       |       |
| 52  |   |   |                |         |          |       |       |
| mg  |   |   |                |         |          |       |       |
| /m^ |   |   |                |         |          |       |       |
| 3^. |   |   |                |         |          |       |       |
+-----+---+---+----------------+---------+----------+-------+-------+

**[Cancer Risks:]{.underline}** All of the cancer risks exceed the
Agency's level of concern of 1 x 10^-6^ but only 4 of the risks exceed 1
x 10^-4^ (i.e., risks range from 2.5 x 10^-5^ to 1.6 x 10^-6^).

+-----+---+---+----------------+--------+-----------+--------+------+
| *   |   |   |                |        |           |        |      |
| *Ta |   |   |                |        |           |        |      |
| ble |   |   |                |        |           |        |      |
| 6.  |   |   |                |        |           |        |      |
| Cr  |   |   |                |        |           |        |      |
| eos |   |   |                |        |           |        |      |
| ote |   |   |                |        |           |        |      |
| Der |   |   |                |        |           |        |      |
| mal |   |   |                |        |           |        |      |
| Can |   |   |                |        |           |        |      |
| cer |   |   |                |        |           |        |      |
| Ri  |   |   |                |        |           |        |      |
| sks |   |   |                |        |           |        |      |
| .** |   |   |                |        |           |        |      |
+-----+---+---+----------------+--------+-----------+--------+------+
|     |   |   |                | Pot    |           |        |      |
|     |   |   |                | ential |           |        |      |
| Job | S | n | Site           |        | Abs       | Abs    | Creo |
|     | i | = | Description    | dermal | Dermal    | LADD   | sote |
|     | t |   |                | dose   | Dose      |        |      |
|     | e |   |                |        |           | (mg/k  | Risk |
|     |   |   |                | (mg/k  | (m        | g/day) |      |
|     |   |   |                | g/day) | g/kg/day) |        |      |
+-----+---+---+----------------+--------+-----------+--------+------+
| TO  | A | 4 | 1940s; manual  | 0.414  | 0.0207    | 0.0071 | 4.5  |
|     |   |   |                |        |           |        | E-05 |
+-----+---+---+----------------+--------+-----------+--------+------+
|     | B | 4 | 1983; Eng.     | 0.0148 | 0.0007    | 0.0003 | 1.6  |
|     |   |   | Controls       |        |           |        | E-06 |
+-----+---+---+----------------+--------+-----------+--------+------+
|     | C | 5 | 1940s          | 14.8   | 0.7400    | 0.2534 | 1.6  |
|     |   |   |                |        |           |        | E-03 |
+-----+---+---+----------------+--------+-----------+--------+------+
|     | D | 5 | 1970s;         | 0.132  | 0.0066    | 0.0023 | 1.4  |
|     |   |   | Automated      |        |           |        | E-05 |
+-----+---+---+----------------+--------+-----------+--------+------+
| TA  | B | 4 | 1983; Eng.     | 0.0248 | 0.0012    | 0.0004 | 2.7  |
|     |   |   | Controls       |        |           |        | E-06 |
+-----+---+---+----------------+--------+-----------+--------+------+
| OU  | A | 4 | 1940s; manual  | 0.887  | 0.0444    | 0.0152 | 9.5  |
|     |   |   |                |        |           |        | E-05 |
+-----+---+---+----------------+--------+-----------+--------+------+
|     | D | 5 | 1970s;         | 0.938  | 0.0469    | 0.0161 | 1.0  |
|     |   |   | Automated      |        |           |        | E-04 |
+-----+---+---+----------------+--------+-----------+--------+------+
| CLO | A | 4 | 1940s; manual  | 0.212  | 0.0106    | 0.0036 | 2.3  |
|     |   |   |                |        |           |        | E-05 |
+-----+---+---+----------------+--------+-----------+--------+------+
|     | B | 4 | 1983; Eng.     | 0.0885 | 0.0044    | 0.0015 | 9.5  |
|     |   |   | Controls       |        |           |        | E-06 |
+-----+---+---+----------------+--------+-----------+--------+------+
|     | C | 5 | 1940s          | 2.12   | 0.1060    | 0.0363 | 2.3  |
|     |   |   |                |        |           |        | E-04 |
+-----+---+---+----------------+--------+-----------+--------+------+
|     | D | 5 | 1970s;         | 0.117  | 0.0059    | 0.0020 | 1.3  |
|     |   |   | Automated      |        |           |        | E-05 |
+-----+---+---+----------------+--------+-----------+--------+------+
| LLO | B | 4 | 1983; Eng.     | 0.0181 | 0.0009    | 0.0003 | 1.9  |
|     |   |   | Controls       |        |           |        | E-06 |
+-----+---+---+----------------+--------+-----------+--------+------+
|     | C | 5 | 1940s          | 0.203  | 0.0102    | 0.0035 | 2.2  |
|     |   |   |                |        |           |        | E-05 |
+-----+---+---+----------------+--------+-----------+--------+------+
|     | D | 1 | 1970s;         | 0.0772 | 0.0039    | 0.0013 | 8.3  |
|     |   | 0 | Automated      |        |           |        | E-06 |
+-----+---+---+----------------+--------+-----------+--------+------+
| LLO | D |   | 1970s;         | 0.244  | 0.0122    | 0.0042 | 2.6  |
| (F) |   |   | Automated      |        |           |        | E-05 |
+-----+---+---+----------------+--------+-----------+--------+------+
| LH  | B | 4 | 1983; Eng.     | 0.0228 | 0.0011    | 0.0004 | 2.5  |
|     |   |   | Controls       |        |           |        | E-06 |
+-----+---+---+----------------+--------+-----------+--------+------+
|     | C | 5 | 1940s          | 1.81   | 0.0905    | 0.0310 | 1.9  |
|     |   |   |                |        |           |        | E-04 |
+-----+---+---+----------------+--------+-----------+--------+------+
|     | D | 5 | 1970s;         | 0.383  | 0.0192    | 0.0066 | 4.1  |
|     |   |   | Automated      |        |           |        | E-05 |
+-----+---+---+----------------+--------+-----------+--------+------+
| CK  | C | 5 | 1940s          | 0.822  | 0.0411    | 0.0141 | 8.8  |
|     |   |   |                |        |           |        | E-05 |
+-----+---+---+----------------+--------+-----------+--------+------+
| TB  | A | 4 | 1940s; manual  | 0.112  | 0.0056    | 0.0019 | 1.2  |
|     |   |   |                |        |           |        | E-05 |
+-----+---+---+----------------+--------+-----------+--------+------+
|     | C | 5 | 1940s          | 1.06   | 0.0530    | 0.0182 | 1.1  |
|     |   |   |                |        |           |        | E-04 |
+-----+---+---+----------------+--------+-----------+--------+------+
| WO  | A | 4 | 1940s; manual  | 0.204  | 0.0102    | 0.0035 | 2.2  |
|     |   |   |                |        |           |        | E-05 |
+-----+---+---+----------------+--------+-----------+--------+------+
|     | B | 4 | 1983; Eng.     | 0.0469 | 0.0023    | 0.0008 | 5.0  |
|     |   |   | Controls       |        |           |        | E-06 |
+-----+---+---+----------------+--------+-----------+--------+------+
| DP  | C | 4 | 1940s          | 0.15   | 0.0075    | 0.0026 | 1.6  |
|     |   |   |                |        |           |        | E-05 |
+-----+---+---+----------------+--------+-----------+--------+------+
| S   |   |   |                |        |           |        |      |
| ite |   |   |                |        |           |        |      |
| A   |   |   |                |        |           |        |      |
| ,B, |   |   |                |        |           |        |      |
| C,D |   |   |                |        |           |        |      |
| in  |   |   |                |        |           |        |      |
| dic |   |   |                |        |           |        |      |
| ate |   |   |                |        |           |        |      |
| di  |   |   |                |        |           |        |      |
| ffe |   |   |                |        |           |        |      |
| ren |   |   |                |        |           |        |      |
| ces |   |   |                |        |           |        |      |
| in  |   |   |                |        |           |        |      |
| s   |   |   |                |        |           |        |      |
| ite |   |   |                |        |           |        |      |
| se  |   |   |                |        |           |        |      |
| tup |   |   |                |        |           |        |      |
| (e. |   |   |                |        |           |        |      |
| g., |   |   |                |        |           |        |      |
| eng |   |   |                |        |           |        |      |
| con |   |   |                |        |           |        |      |
| tro |   |   |                |        |           |        |      |
| ls) |   |   |                |        |           |        |      |
|     |   |   |                |        |           |        |      |
| Der |   |   |                |        |           |        |      |
| mal |   |   |                |        |           |        |      |
| ex  |   |   |                |        |           |        |      |
| pos |   |   |                |        |           |        |      |
| ure |   |   |                |        |           |        |      |
| not |   |   |                |        |           |        |      |
| n   |   |   |                |        |           |        |      |
| orm |   |   |                |        |           |        |      |
| ali |   |   |                |        |           |        |      |
| zed |   |   |                |        |           |        |      |
| to  |   |   |                |        |           |        |      |
| v   |   |   |                |        |           |        |      |
| ari |   |   |                |        |           |        |      |
| ous |   |   |                |        |           |        |      |
| a   |   |   |                |        |           |        |      |
| mou |   |   |                |        |           |        |      |
| nts |   |   |                |        |           |        |      |
| of  |   |   |                |        |           |        |      |
| w   |   |   |                |        |           |        |      |
| ood |   |   |                |        |           |        |      |
| t   |   |   |                |        |           |        |      |
| rea |   |   |                |        |           |        |      |
| ted |   |   |                |        |           |        |      |
| per |   |   |                |        |           |        |      |
| s   |   |   |                |        |           |        |      |
| ite |   |   |                |        |           |        |      |
|     |   |   |                |        |           |        |      |
| A   |   |   |                |        |           |        |      |
| rit |   |   |                |        |           |        |      |
| hme |   |   |                |        |           |        |      |
| tic |   |   |                |        |           |        |      |
| m   |   |   |                |        |           |        |      |
| ean |   |   |                |        |           |        |      |
| f   |   |   |                |        |           |        |      |
| rom |   |   |                |        |           |        |      |
| Ta  |   |   |                |        |           |        |      |
| ble |   |   |                |        |           |        |      |
| 9   |   |   |                |        |           |        |      |
| of  |   |   |                |        |           |        |      |
| the |   |   |                |        |           |        |      |
| P   |   |   |                |        |           |        |      |
| MRA |   |   |                |        |           |        |      |
| r   |   |   |                |        |           |        |      |
| evi |   |   |                |        |           |        |      |
| ew. |   |   |                |        |           |        |      |
|     |   |   |                |        |           |        |      |
| Abs |   |   |                |        |           |        |      |
| Der |   |   |                |        |           |        |      |
| mal |   |   |                |        |           |        |      |
| D   |   |   |                |        |           |        |      |
| ose |   |   |                |        |           |        |      |
| (m  |   |   |                |        |           |        |      |
| g/k |   |   |                |        |           |        |      |
| g/d |   |   |                |        |           |        |      |
| ay) |   |   |                |        |           |        |      |
| =   |   |   |                |        |           |        |      |
| der |   |   |                |        |           |        |      |
| mal |   |   |                |        |           |        |      |
| d   |   |   |                |        |           |        |      |
| ose |   |   |                |        |           |        |      |
| (m  |   |   |                |        |           |        |      |
| g/k |   |   |                |        |           |        |      |
| g/d |   |   |                |        |           |        |      |
| ay) |   |   |                |        |           |        |      |
| x   |   |   |                |        |           |        |      |
| 5%  |   |   |                |        |           |        |      |
| der |   |   |                |        |           |        |      |
| mal |   |   |                |        |           |        |      |
| abs |   |   |                |        |           |        |      |
|     |   |   |                |        |           |        |      |
| Cr  |   |   |                |        |           |        |      |
| eos |   |   |                |        |           |        |      |
| ote |   |   |                |        |           |        |      |
| R   |   |   |                |        |           |        |      |
| isk |   |   |                |        |           |        |      |
| =   |   |   |                |        |           |        |      |
| L   |   |   |                |        |           |        |      |
| ADD |   |   |                |        |           |        |      |
| (m  |   |   |                |        |           |        |      |
| g/k |   |   |                |        |           |        |      |
| g/d |   |   |                |        |           |        |      |
| ay) |   |   |                |        |           |        |      |
| x   |   |   |                |        |           |        |      |
| cr  |   |   |                |        |           |        |      |
| eos |   |   |                |        |           |        |      |
| ote |   |   |                |        |           |        |      |
| o   |   |   |                |        |           |        |      |
| ral |   |   |                |        |           |        |      |
| CSF |   |   |                |        |           |        |      |
| of  |   |   |                |        |           |        |      |
| 6   |   |   |                |        |           |        |      |
| .28 |   |   |                |        |           |        |      |
| E-3 |   |   |                |        |           |        |      |
| (mg |   |   |                |        |           |        |      |
| /kg |   |   |                |        |           |        |      |
| /da |   |   |                |        |           |        |      |
| y)^ |   |   |                |        |           |        |      |
| -1^ |   |   |                |        |           |        |      |
+-----+---+---+----------------+--------+-----------+--------+------+

**OccupationalOccupational Post-application Exposures and Risks**

There is the potential for post-application exposures to creosote.
Potential post-application exposure may occur as a result of creosote
treated wood in commercial, industrial, and residential settings. There
is the potential for contact with creosote treated wood for occupational
workers who install railroad ties and poles. Railroad workers may become
exposed during the mechanical and manual installation of pressure
treated railroad crossties as well as during inspection procedures
(ATSDR, 1990). Pole installers may also contact creosote treated wood
while attaching fittings on telephone poles, installing new telephone
poles, conducting ground line treatment of telephone poles, and
maintaining and repairing existing telephone poles (ATSDR, 1990). No
dermal exposure data were available for these scenarios. Mechanical
installation and/or the use of appropriate PPE are recommended to reduce
exposure/contact with creosote treated wood.

There is no creosote product registered for residential uses; however,
EPA recognizes that some creosote-treated wood such as railroad ties are
used outdoors in home landscaping. Based on the label directions of
creosote products, EPA considers such uses of creosote-treated wood to
be illegal under FIFRA 12(a) (2) (G). For creosote-treated wood that is
misused in residential landscaping, the potential dermal and incidental
oral exposures to outdoor landscape timbers are expected to be episodic
in nature. During the public comment period on this risk assessment, EPA
received comments recommending wipe studies to assess dermal and
incidental oral exposure to children contacting creosote treated
landscape ties. EPA has considered the need for surface residue data on
recycled, creosote-treated railroad ties once they are removed from
service. A similar type of assessment was conducted for CCA-treated
lumber using the SHEDS model. The CCA SHEDS assessment was developed for
arsenic exposure to treated dimensional lumber. The CCA SHEDS model
assesses children that are exposed to play sets and decks specifically
built for contact by children. Compared to play sets EPA expects there
would be considerably less contact and less frequent contact by children
with landscape ties and on wood not used for specific children's play
structures. Based on this type of comparison, the fact that creosote
used in residential settings is a misuse of the product, and creosote is
less potent of a carcinogen then arsenic, EPA does not believe a
SHEDS-type of an assessment for creosote treated ties used as landscape
timbers is warranted at this time.

> **5.0 [Aggregate risk assessment]{.underline}**
>
> Under the current policy of the Office of Pesticide Programs, acute
> aggregate risk assessment determines the acute risk from combined
> dietary consumption of pesticide residues, separate from residential
> exposures (Health Effects Division, Standard Operating Procedure 97.2,
> April 1998). In the case of creosote, an acute aggregate (food +
> water) risk estimate was not performed for Creosote. Creosote is not
> registered for any food use, and it has also been determined that
> creosote is not likely to impact the diet or drinking water.

**Short- and Intermediate-Term Aggregate Risks**

> Aggregate short and intermediate term risk assessments are designed to
> provide estimates of risk likely to result from exposures to the
> pesticide or pesticide residues in food, water, and from residential
> (or other non-occupational) pesticide uses. Due to the lack of
> exposure through food or water, short and intermediate term aggregate
> risks were not performed. Residential exposures to Creosote residues
> may occur, but data are not available to assess these risks.
>
> **Chronic (Non-Cancer) Aggregate Risk**
>
> Based on the lack of potential for chronic exposure to Creosote
> through food and water, a chronic
>
> (non-cancer) aggregate risk assessment was not performed.
>
> **6.0 CUMULATIVE RISK**
>
> FQPA (1996) stipulates that when determining the safety of a pesticide
> chemical, EPA shall base
>
> its assessment of the risk posed by the chemical on, among other
> things, available information
>
> concerning the cumulative effects to human health that may result from
> dietary, residential, or other non-occupational exposure to other
> substances that have a common mechanism of toxicity. The reason for
> consideration of other substances is due to the possibility that
> low-level exposures to multiple chemical substances that cause a
> common toxic effect by a common mechanism could lead to the same
> adverse health effect as would a higher level of exposure to any of
> the other substances individually. A person exposed to a pesticide at
> a level that is considered safe may in fact experience harm if that
> person is also exposed to other substances that cause a common toxic
> effect by a mechanism common with that of the subject pesticide, even
> if the individual exposure levels to the other substances are also
> considered safe.
>
> AD did not perform a cumulative risk assessment as part of this RED
> for creosote. Creosote is a
>
> complex mixture of chemical substances that may act by various modes
> to produce toxicity. A
>
> review to determine if there are any other chemical substances that
> have a mechanism of toxicity
>
> common with that of creosote has not been initiated, and it is
> unlikely that there are other such
>
> mixtures that approach that of creosote in terms of complexity.
>
> Notwithstanding, the registrant must submit, upon EPA's request and
> according to a schedule
>
> determined by the Agency, such information as the Agency directs to be
> submitted in order to
>
> evaluate issues related to whether creosote shares a common mechanism
> of toxicity with any other
>
> substance. If the Agency identifies other substances that share a
> common mechanism of toxicity
>
> with creosote, the Agency will perform aggregate exposure assessments
> on each chemical, and will
>
> begin to conduct a cumulative risk assessment.
>
> The Health Effects Division, Office of Pesticide Programs, has
> recently developed a framework
>
> proposed for conducting cumulative risk assessments on substances that
> have a common mechanism
>
> of toxicity. This guidance was issued for public comment on January
> 16, 2002 (67 FR 2210-2214)
>
> and is available from the OPP Website at:

http://www.epa.gov/pesticides/trac/science/cumulative_guidance.pdf. In
the guidance, it is

stated that a cumulative risk assessment of substances that cause a
common toxic effect by a common mechanism will not be conducted until an
aggregate exposure assessment of each substance has been completed.

> Before undertaking a cumulative risk assessment, AD will follow
> procedures for identifying
>
> chemicals that have a common mechanism of toxicity as set forth in the
> *YMBOL 65 \\f \"WP*
>
> *TypographicSymbols\" \\s 12* *Guidance for Identifying Pesticide
> Chemicals and Other Substances*
>
> *that Have a Common Mechanism of Toxicity* (64 FR 5795-5796, February
> 5, 1999).
>
> **7.0 ENVIRONMENTAL RISKS**
>
> **7.1 ENVIRONMENTAL FATE ASSESSMENT**

The major uses of creosote since 1988 have been railroad ties,
crossbars, decks on marinas and utility poles. Polyaromatic hydrocarbons
(PAHs) constitute the highest percent

(85%) of coal tar creosote while the phenolic substances are about 10
percent, and N-- and S- containing substances represent the remainder of
the mixture. Most of the PAHs are non-volatile, therefore; creosote
normally does not contaminate the air. The major route of exposure from
creosote is through water and soil, and from these environmental
compartments into the aquatic and benthic organisms (bioaccumulation).

Estimated half-lives of PAHs in water, soil and sediments are presented
in Table 1. The half-lives of the PAHs in these environmental
compartments tends to increase with increasing complexity of the
molecules (Howard et al. 1991). K~ow~ values also increase with the
complexity of the PAH. Half-lives in water (and air) are much lower than
in soils and sediments.

**Table 1. Estimated Half-lives of PAHs in Various Environmental Media**

+-------------+---------+---------+--------+--------+--------+-------+
| **PAH**     | **No.   | **Mol   | **Est. |        |        | **K~  |
|             | aro     | ecular\ | hal    |        |        | ow~** |
|             | matic** | wt**    | f-life |        |        |       |
|             |         |         | (we    |        |        |       |
|             | **      |         | eks)** |        |        |       |
|             | rings** |         |        |        |        |       |
+-------------+---------+---------+--------+--------+--------+-------+
|             |         |         | **w    | **     | **sedi |       |
|             |         |         | ater** | soil** | ment** |       |
+-------------+---------+---------+--------+--------+--------+-------+
| Naphthalene | 2       | 128     | 1      | 8      | 32     | 3.37  |
+-------------+---------+---------+--------+--------+--------+-------+
| Acenapthene | 3       | 152     | 3      | 32     | 104    | 4.03  |
+-------------+---------+---------+--------+--------+--------+-------+
| Fluorene    | 3       | 166     | 3      | 32     | 104    | 4.12  |
+-------------+---------+---------+--------+--------+--------+-------+
| P           | 3       | 178     | 3      | 32     | 104    | 4.57  |
| henanthrene |         |         |        |        |        |       |
+-------------+---------+---------+--------+--------+--------+-------+
| Anthracene  | 3       | 178     | 3      | 32     | 104    | 4.54  |
+-------------+---------+---------+--------+--------+--------+-------+
| F           | 4       | 202     | 8      | 104    | 312    | 5.22  |
| luoranthene |         |         |        |        |        |       |
+-------------+---------+---------+--------+--------+--------+-------+
| Pyrene      | 4       | 202     | 8      | 104    | 312    | 5.18  |
+-------------+---------+---------+--------+--------+--------+-------+
| Chrysene    | 4       | 228     | 8      | 104    | 312    | 5.91  |
+-------------+---------+---------+--------+--------+--------+-------+

Half-lives in tissues of aquatic organisms are discussed in the Updated
Creosote Environmental Fate Chapter. Aquatic organisms remove residues
with half-lives of only a few days for the PAHs addressed in this
assessment (Table 2). Biomagnification apparently is not a concern,
because vertebrates metabolically transform PAHs and excrete them before
they accumulate to higher levels (Brummelen et al. 1998 in Poston 2001).

**Table 2. Half-lives of PAHs in Aquatic Organisms**

  --------------------------------------------------------------------------
  **Species**            **PAH**                        **Half-life (days)**
  ---------------------- ------------------------------ --------------------
  ***Vertebrates:***                                    

  Rainbow trout          fluoranthene                   6

                         fluorene                       7

                         anthracene                     7

                         phenanthrene                   9

  ***Invertebrates:***                                  

  Mussel                 anthracene                     1.9

                         naphthalene                    2

                         phenanthrene                   1.9-2.2

                         fluoranthene                   2.0-11.1

                         pyrene                         4.1-5.5

                         chrysene                       5.0-14.2

                         fluoranthene                   29.8

  Clam                   napthalene                     2.0

                         chrysene                       3.3

                         fluoranthene                   3.3

                         pyrene                         3.6-10.3

                         phenanthrene                   4.5-6.1

                         fluoranthene                   8.4

  Oyster                 phenanthrene                   3.4

                         pyrene                         6.7

                         fluoranthene                   5.9

                         chrysene                       15.1

  Shrimp                 fluoranthene                   0.8

                         pyrene                         0.8

                         phenanthrene                   0.9

  Polychaete             chrysene                       4.3

                         phenanthrene                   4.8

                         pyrene                         4.8

                         fluoranthene                   5.8
  --------------------------------------------------------------------------

***Abiotic Degradation***

The PAHs are fused aromatic polycyclic rings which have no hydrolyzable
hydrogens and the solubility of these compounds are very low in water.
Environmentally, hydrolysis does not appear to be an important pathway
for dissipation of the composite mixture of PAHs in water; however, some
molecules like benzo\[k\]fluoranthene and benz\[a\]pyrene could persist
in water.

Very few studies are reported in the open literature on field
volatilities for PAHs present in creosote. Gevao et al. (1998) showed
that acenaphthene, fluorene, phenanthrene, anthracene, and fluoranthene
volatilized at a faster rate at 30°C than at 4°C. The study also showed
that 85 percent of these components remained in the wood after seven
weeks. The rate of volatilization was slow for acenaphthene (half-life,
one year) and fluoranthene (half-life, one year). In most cases, the
initial rates of dissipation are caused by partitioning between the wood
and air and biodegradation in the presence of microbial populations.
Therefore, exposure to air does not appear to be an important factor in
fate assessment for most PAHs.

Photooxidation is a common phenomenon, and therefore an important
degradation pathway for the creosote PAHs. The photolytic half-lives of
the PAHs in aqueous medium are dependent on the season, geographical
location, surface water measurements, and complexities of the parent
molecules (two fused rings vs. five fused rings). In most cases,
half-lives under the conditions mentioned do not appear very long.
Because of this, and the fact that most of the PAHs are not readily
soluble (except for a few low molecular weight ones), the PAHs may not
be a problem in surface and groundwater runoffs. However, it should be
noted that the photooxidized products of PAHs are stable; therefore, may
persist in air/water and soils and become an environmental concern as
these photooxidized products are also bioaccumulative.

***Mobility***

Once introduced to an aquatic environment, creosote components are
subjected to several fractionation processes. Many PAHs adsorb to
sediments and may persist for long periods of time. Creosote
contaminated sediments usually contain relatively higher levels of
hydrophobic PAHs than whole creosote (Bieri et al., 1986). Eventually,
sediment adsorbed PAHs may dissolve or become re-suspended in the water
by tides, storms, bioturbation, shipping, or dredging. As a result,
local biota may be exposed to low level PAHs over the long term (Fowler
et al., 1993). Therefore, the adsorption/desorption processes in water
involved with creosote-derived PAHs are a significant consideration in
fate assessments of creosote contamination.

Additionally, colloidal matter present in a cresote-contaminated
environment has been found to affect the desorption rates of specific
PAHs. One study found that PAHs partitioned to course (of sizes \>100
nm) colloid fractions and were linearly correlated with the PAH
octanol-water partition coefficient, indicating the partitioning was
hydrophobic (Villholth, 1999).

The PAHs from creosote-treated utility poles and/or railway ties tend to
leach out initially in the first seven days and remain in the sediment
surrounding the poles or railroad ties not migrating far from the wood.
Most of the PAHs, however, tend to stay inside the wood (\~85%). One
study showed that background levels for PAHs leached from wood were
attained within three months and may have been due to photolysis or
biodegradation of the PAHs. A detailed study of 200 U.S. estuaries
showed that PAHs that leached from the treated wood of decks and
bulkheads, 175 had muddy sediments. Higher amounts of PAHs leached into
such soil types. No systematic work has been carried out on all the PAHs
and the representative soil types to show which one would have a higher
tendency of retention for the PAHs.

Migration studies of PAHs into groundwater have shown that migration of
some of the PAHs have been observed. Vertical or lateral migration of
the PAHs from the utility poles indicated that at ground level the
migration was not significant beyond 150 meters from the site of
contamination (base of utility poles). The vertical or downward
migration of the PAHs was even more limited and the existence of the
PAHs were not found below a 12 meter depth.

***Biodegradation***

Most of the PAHs have a tendency to biodegrade under aerobic conditions.
It has been reported that over eighty percent of biodegradation occurs
in the first month after the wood preservative application, with the
exception of benz\[a\]pyrene and benzo\[k\]fluoranthene, which have
shown resistance to biodegradation. A number of aerobic soil metabolism
studies on PAHs conducted at various contaminated sites as well as in
simulated microcosms reported that low molecular weight PAHs generally
metabolized in aerobic conditions and the greater the oxic environment,
the higher the biodegradation level.

Aerobic degradation of PAHs associated with soil and groundwater often
leads to a rapid depletion of dissolved oxygen which eventually
decreases the redox potential. This decrease in the redox potential can
result in favorable environments for denitrifying, sulfate-reducing, or
methanogenic microbes. Therefore, anaerobic transformations may be a
significant factor in oxygen-depleted habitats (Karthikeyan and
Bhandari, 2001). Under these conditions, anoxic or anaerobic degradation
stimulated by denitrifying or sulfate-reducing bacteria can become an
important pathway for the cleanup of contaminated sites.

***Bioaccumulation in Fish***

The major components of the PAHs in creosote have shown the ability to
form neutral to oxidized transformation products under aerobic
soil/aquatic conditions. For example, fluorene forms hydroxy fluorene
and acenaphthene converts into diacetic acid acenaphthene. These
oxidized species are stable and bioaccumulative. Numerous studies have
shown that photooxidized transformation products of these PAHs are
bioaccumulative and result in adverse effects on the aqueous biota as
well as on the organisms in the soils and benthic sediments.

In aquatic habitats, fish, shellfish, and crustaceans readily
bioaccumulate PAHs from the environment and store these at high levels
in the tissues. Seven PAHs: naphthalene, anthracene, phenanthrene,
pyrene, 9-methyl anthracene, benz\[a\]anthracene and perylene were shown
to bioaccumulate in *Daphnia pulex*. PAHs like naphthalene,
biphenyl/acenaphthylene, fluorene, phenanthrene/anthracene/chrysene, and
benzopyrene were found to bioaccumulate in clams (*Rangia cuneate)*. The
most dramatic increases were in cases such as
benz\[a\]anthracene/chrysene which reported a bioaccumulation of 41 ppb
(week zero) and increased to 190 ppb (week 4). Similarly, benzopyrene
bioaccumulated from 8 ppb (week zero) to 600 ppb (week 4). Depuration
was within two weeks. This study was conducted after the creosote spill
into the Bayou Bonfuca at the American Creosote Works Plant Site at
Slidell, Louisiana.

A study on benthic invertebrates showed a bioaccumulation concentration
ranging from 0.10 to 11.00 ppm. A bioconcentration study on zebra
mussels in the Great Lakes found that pre-spawning species (high lipid)
bioaccumulated benzo\[a\] pyrene at a faster rate than the post-
spawning (low lipid) species.

Bioaccumulation data on marine mammals are not readily available, and
only one study on whales and seals has been reported. That study
indicated a bioaccumulation of 0.10 and 1.21 ppm in the muscles of these
mammals, respectively.

Some of the PAHs, particularly those that have a high molecular mass
(higher number of the fused aromatic rings) have a higher tendency to
adsorb to soil organic carbon. Such adsorption coefficients (K~OC~) have
been reported in literature. Some PAHs with a high K~oc~ can bind
strongly with the organic carbon of the soils/sediments and may not be
bioavailable to the aquatic organisms. However, if the octanol/ water
coefficients (K~ow~) is high, and if the PAHs are desorbed from the
soils/sediments to which they are bound, some of these PAHs can become
bioaccumulative to the benthic organisms.

It has been suggested that based on theoretical calculations and
modeling, the half-lives of the PAHs obtained from coal tar creosote can
be estimated in air, water, soils and sediments. From these calculations
and modeling, one can arbitrarily divide the PAHs into 3 distinct
groups: PAHs with two fused rings, PAHs with three fused rings and PAHs
that have 4 to 5 fused rings. The half-lives in the environmental
compartments (air, water, and soils) for PAHs are as follows: the
half-lives of two fused rings PAHs \< three fused rings \< 4/5 fused
rings. The K~ow~ values lie between 3 and 4 for PAHs with two fused
rings, between 4 and 5 for PAHs with 3 fused rings, and at 6 or above
for the third group of the PAHs. In general, the half-lives in air and
water environmental compartments are much lower than in soils/sediments
because the soil adsorption coefficients are higher. The longer the
half-life, the greater the persistence of the PAHs in soils. Some of the
4/5 fused ring PAHs are more persistent in soils and sediments and since
their K~ow~ values are higher, they can bioaccumulate because some of
them adsorb onto soils and they may not be bioavailable for benthic
organisms.

The third group of PAHs show a higher degree of bioaccumulation,
persistence in soils and water, resistance to biodegradation and
photooxidation. Additionally the components of these group have less of
a tendency to leach from the wood structure and have high sorption
constants to soils. On the other hand, these higher members of the PAHs
(4/5 fused ring compounds) are not readily soluble in water and their
percent on a mass basis in the creosote mixture is very low compared to
the first group (2 fused rings) of the PAHs, and may not be available
for biomagnification and migration into surface and ground waters.

**7.2 ENVIRONMENTAL EXPOSURE AND ECOLOGICAL RISK ASSESSMENT**

The toxicity endpoints typically used in OPP\'s assessments are obtained
from guideline toxicity studies conducted for wildlife, aquatic
organisms, and plants (40 CFR §158.2060). Guideline studies are required
for all pesticides to provide acute and chronic measures of effect for
one or more test species in several taxonomic groups. As noted in the
2003 preliminary ecological risk assessment, guideline toxicity studies
are not available for creosote. The preliminary assessment relied on the
whole creosote data available in the open literature, but insufficient
data were obtained to assess chronic effects to freshwater invertebrates
or to marine/estuarine aquatic organisms. For the updated assessment,
available acute and chronic toxicity information for the PAHs has been
obtained from the open literature, including relevant laboratory,
microcosm, and field studies obtained through ECOTOX searches and other
sources, including EPA Sediment Quality Criteria documents for
fluoranthene (EPA 1993a), phenanthrene (EPA 1993b), and acenaphthene
(EPA 1993c).

[Acute toxicity]{.underline}

Most PAHs for which data are available are highly to very highly toxic
to freshwater and saltwater fish and invertebrates (Table 8), with
anthracene and fluoranthene being the most toxic PAHs in the water
column.

**Table 8. Acute Toxicity of Creosote PAHs to Fish and Invertebrates
Exposed in the Water Column**

+-------+--------------------------+---------+---------+-------------+
| **P   | **Species**              | **Exp   | **LC    | **Source**  |
| AH/** |                          | osure** | 50/EC50 |             |
|       |                          |         | (       |             |
| **    |                          | **d     | µg/L)** |             |
| media |                          | uration |         |             |
| ^a^** |                          | (h)**   |         |             |
+=======+==========================+=========+=========+=============+
| **An  |                          |         |         |             |
| thrac |                          |         |         |             |
| ene** |                          |         |         |             |
+-------+--------------------------+---------+---------+-------------+
| SW    | Fish - no data           |         |         |             |
+-------+--------------------------+---------+---------+-------------+
|       | Mysid shrimp             | 48      | 3.6     | Pelletier   |
|       |                          |         |         | 1997        |
+-------+--------------------------+---------+---------+-------------+
| FW    | Bluegill (*Lepomis       | 96      | 1.27    | McCloskey   |
|       | macrochirus*)            |         |         | 1991        |
+-------+--------------------------+---------+---------+-------------+
|       | Scud (*Hyalella azteca*) | 240     | 5.6     | Hatch 1999  |
+-------+--------------------------+---------+---------+-------------+
| *     |                          |         |         |             |
| *Fluo |                          |         |         |             |
| ranth |                          |         |         |             |
| ene** |                          |         |         |             |
+-------+--------------------------+---------+---------+-------------+
| SW    | Sheepshead minnow        | 96      | 0.8     | EPA 1993b   |
+-------+--------------------------+---------+---------+-------------+
|       | Mysid shrimp             | 96      | 0.58    | Spehar 1999 |
+-------+--------------------------+---------+---------+-------------+
| FW    | Fathead minnow           | 96      | 6.8     | Diamond     |
|       |                          |         |         | 1995        |
+-------+--------------------------+---------+---------+-------------+
|       | Water flea               | 48      | 0.97    | Spehar 1999 |
+-------+--------------------------+---------+---------+-------------+
| *     |                          |         |         |             |
| *Acen |                          |         |         |             |
| aphth |                          |         |         |             |
| ene** |                          |         |         |             |
+-------+--------------------------+---------+---------+-------------+
| SW    | Sheepshead minnow        | 96      | 2200    | Heitmuller  |
|       |                          |         |         | 1981        |
+-------+--------------------------+---------+---------+-------------+
|       | Mysid shrimp             | 96      | 160     | EPA 1993c   |
+-------+--------------------------+---------+---------+-------------+
| FW    | Brown trout (*Salmo      | 96      | 580     | Holcombe    |
|       | trutta*)                 |         |         | 1983        |
+-------+--------------------------+---------+---------+-------------+
|       | Stone fly (*Tallaperla   | 96      | 240     | Horn 1983   |
|       | maria*)                  |         |         |             |
+-------+--------------------------+---------+---------+-------------+
| **    |                          |         |         |             |
| Fluor |                          |         |         |             |
| ene** |                          |         |         |             |
+-------+--------------------------+---------+---------+-------------+
| SW    | Fish - no data           |         |         |             |
+-------+--------------------------+---------+---------+-------------+
|       | Polychaete worm          | 96      | 1000    | Rossi 1978  |
+-------+--------------------------+---------+---------+-------------+
| FW    | Bluegill                 | 96      | 760     | Mayer 1986  |
+-------+--------------------------+---------+---------+-------------+
|       | Water flea               | 48      | 420     |             |
+-------+--------------------------+---------+---------+-------------+
| **Nap |                          |         |         |             |
| hthel |                          |         |         |             |
| ene** |                          |         |         |             |
+-------+--------------------------+---------+---------+-------------+
| SW    | Sheepshead minnow        | 24      | 2400    | Anderson    |
|       |                          |         |         | 1974        |
+-------+--------------------------+---------+---------+-------------+
|       | Humpy shrimp (*Pandalus  | 96      | 971     | Korn 1979   |
|       | goniurus*)               |         |         |             |
+-------+--------------------------+---------+---------+-------------+
| FW    | Pink salmon              | 96      | 890     | Rice 1989   |
|       | (*Oncorhyncus            |         |         |             |
|       | gorbuscha*)              |         |         |             |
+-------+--------------------------+---------+---------+-------------+
|       | Water flea (*Daphnia     | 96      | 1000    | Trucco 1983 |
|       | pulex*)                  |         |         |             |
+-------+--------------------------+---------+---------+-------------+

  ------------------ -------------------------- ---------- ---------- --------------
  **Chrysene**                                                        

  SW                 Fish - no data                                   

                     Polychaete worm (*Neanthes 96         \<1000     Rossi 1978
                     arenaceodentata*)                                

  FW                 Fish - no data                                   

                     Water flea                 20         1900       Kagan et
                                                                      al.1987

  **Pyrene**                                                          

  SW                 Fish - no data                                   

                     Opossum shrimp             48         0.89       Pelletier et
                     (*Americamysis bahia*)                           al. 1997

  FW                 Fathead minnow             3.2        25.6       Oris 1987

                     Water flea                 2          4          Kagan et al.
                                                                      1987

  **Phenanthrene**                                                    

  SW                 Atlantic silverside        96         108        EPA 1993a
                     (*Menidia menidia*)                              

                     Mysid shrimp               96         17.7       

  FW                 Bluegill                   96         234        EPA 1993a

                     Hydra (*Hydra* sp.)        96         96         
  ------------------ -------------------------- ---------- ---------- --------------

^a^ SW = saltwater; FW = freshwater

[Chronic toxicity]{.underline}

No guideline chronic-toxicity studies are available to assess chronic
risks of the PAHs addressed in this assessment. Some data are available
in the EPA Sediment Quality Criteria documents for fluoranthene,
acenaphthene, and phenanthrene (Table 9). Adverse affects on survival,
growth, and reproduction have been reported at concentrations as low as
8 µg/L for phenanthrene and 18.8 µg/L for fluoranthene.

**Table 9. Chronic Toxicity of Creosote PAHs to Fish and Invertebrates
Exposed in the Water Column**

+-----+---------------------+----------+------------+----------------+
| **  | **Species**         | **N      | **Effect** | **Source**     |
| PAH |                     | OEC/LOEC |            |                |
| /** |                     | (µg/L)** |            |                |
|     |                     |          |            |                |
| **m |                     |          |            |                |
| edi |                     |          |            |                |
| a^a |                     |          |            |                |
| ^** |                     |          |            |                |
+=====+=====================+==========+============+================+
| *   |                     |          |            |                |
| *Fl |                     |          |            |                |
| uor |                     |          |            |                |
| ant |                     |          |            |                |
| hen |                     |          |            |                |
| e** |                     |          |            |                |
+-----+---------------------+----------+------------+----------------+
| SW  | Fish - no data      |          |            |                |
+-----+---------------------+----------+------------+----------------+
|     | Mysid               | 11.1 /   | survival,  | Champlin and   |
|     |                     | 18.8     | re         | Poucher 1991   |
|     |                     |          | production |                |
+-----+---------------------+----------+------------+----------------+
| FW  | Fathead minnow      | 10.4 /   | survival,  | Brooke 1991    |
|     |                     | 21.7     | growth     |                |
+-----+---------------------+----------+------------+----------------+
|     | *Daphnia magna*     | 10.6 /   | growth     | Brooke 1992    |
|     |                     | 21.2     |            |                |
+-----+---------------------+----------+------------+----------------+
| *   |                     |          |            |                |
| *Ac |                     |          |            |                |
| ena |                     |          |            |                |
| pht |                     |          |            |                |
| hen |                     |          |            |                |
| e** |                     |          |            |                |
+-----+---------------------+----------+------------+----------------+
| SW  | Fathead minnow      | 332 /    | growth     | Cairns and     |
|     |                     | 495      |            | Nebeker 1982   |
+-----+---------------------+----------+------------+----------------+
|     | Mysid (*M. bahia*)  | 44.6 /   | re         | Thursby et al. |
|     |                     | 91.8     | production | 1989           |
+-----+---------------------+----------+------------+----------------+
| FW  | Sheepshead minnow   | 520 /    | survival   | Ward et al.    |
|     |                     | 970      |            | 1981           |
+-----+---------------------+----------+------------+----------------+
|     | Midge               | 295 /    | egg        | NAS 1982       |
|     | (*Paratanytarsus*   | 575      | hatching   |                |
|     | sp.)                |          |            |                |
+-----+---------------------+----------+------------+----------------+
| *   |                     |          |            |                |
| *Ph |                     |          |            |                |
| ena |                     |          |            |                |
| nth |                     |          |            |                |
| ren |                     |          |            |                |
| e** |                     |          |            |                |
+-----+---------------------+----------+------------+----------------+
| SW  | Fish - no data      |          |            |                |
+-----+---------------------+----------+------------+----------------+
|     | Mysid               | 5.5 /    | survival   | Kuhn and       |
|     |                     | 11.9     |            | Lussier 1987   |
+-----+---------------------+----------+------------+----------------+
| FW  | Rainbow trout       | 5 / 8    | survival   | Call et al.    |
|     |                     |          |            | 1986           |
+-----+---------------------+----------+------------+----------------+
|     | *Daphnia magna*     | 57 / 163 | rep        |                |
|     |                     |          | roduction, |                |
|     |                     |          | survival   |                |
+-----+---------------------+----------+------------+----------------+

^a^ SW = saltwater; FW = freshwater

Some additional but scanty information is available for some PAHs.
Brooks (2000) reviewed the available data and concluded that \"it
appears that sustained water column concentrations of 30 to 50 ppb PAH
can have subtle, but important, chronic impacts on populations of marine
organisms.\" He cites Neff (1979) in reporting that copepod (*Eurytemora
affinis*) exposed to 10 ppb of naphthalene, 2-methylnaphthalene,
2,6-dimethylnaphthalene, or 2,3,5-trimethylnaphthalene displayed
significantly reduced lifespan and brood size. Moore et al. (1989 in
Brooks 2000) reported reduced feeding rates of mollusks at PAH levels of
30 to 40 ppb in seawater.

Poston (2001) cites two developmental studies with salmon and herring
exposed to PAHs from weathered crude oil (Heintz et al. 1999, Carls et
al. 1999). He concluded that developmental affects might occur at about
0.4 to 1.0 µg/L total dissolved PAH in the water column, and that
similar concentrations of PAHs leached from creosote-treated wood could
be expected to exert the same impact on aquatic organisms.

Karrow et al. (1999) evaluated the effects of creosote on immunotoxicity
to female rainbow trout in 12,000-L outdoor microcosms dosed with liquid
creosote. The fish were exposed for 28 days to creosote concentrations
ranging from 0 to 100 µl/L. Stimulatory and suppressive effects were
observed; a concentration-response relationship was evident. The LOEC
was 17 µl/L nominal creosote concentration, which represents 0.61 µg/L
total PAHs in the water. The researchers concluded \". . . that
environmental concentrations of PAHs can impair fish immune parameters,
possibly to a degree where resistance to disease is compromised.\"

**Sediments**

Sediment toxicity studies are not available for most of the PAHs.
However, the EPA Sediment Quality Criteria documents provide some
sediment and pore water LC50s for several species of saltwater and
freshwater organisms, mostly invertebrates, exposed to sediments spiked
with fluoranthene, acenaphthene, or phenanthrene (Table 10).

**Table 10. Toxicity of PAHs to Aquatic Organisms Exposed to Spiked
Sediments (from EPA 1993a,b,c)**

+-----+-----------------+-------+------+-------+-------+---+-----------+
| **  | **Species**     | **Exp | **   | **Sed | **    |   | *         |
| PAH |                 | osure | TOC^ | iment | Pore- |   | *Source** |
| /** |                 | durat | b^** | L     | water |   |           |
|     |                 | ion** |      | C50** | L     |   |           |
| **m |                 |       | **(  |       | C50** |   |           |
| edi |                 |       | %)** | **(µ  |       |   |           |
| a^a |                 |       |      | g/g** | **(µg |   |           |
| ^** |                 |       |      |       | /L)** |   |           |
|     |                 |       |      | **dry |       |   |           |
|     |                 |       |      | wt)** |       |   |           |
+=====+=================+=======+======+=======+=======+===+===========+
| *   |                 |       |      |       |       |   |           |
| *Fl |                 |       |      |       |       |   |           |
| uor |                 |       |      |       |       |   |           |
| ant |                 |       |      |       |       |   |           |
| hen |                 |       |      |       |       |   |           |
| e** |                 |       |      |       |       |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
| SW  | Amphipod        | 10 d  | 0.18 | 3.4   | 22.7  |   | Swartz et |
|     |                 |       |      |       |       |   | al. 1990  |
|     | (*Rhepoxynius   |       |      |       |       |   |           |
|     | abronius*)      |       |      |       |       |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 0.31 | 6.5   | 29.4  |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 0.48 | 10.7  | 24.2  |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     | Amphipod        | 10 d  | 0.34 | 15.0  | 14.1  |   | De Witt   |
|     |                 |       |      |       |       |   | et al.    |
|     | (*R. abronius*) |       |      |       |       |   | 1992      |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 0.40 | 12.6  | 19.2  |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 0.31 | 8.65  | 9.38  |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     | Amphipod        | 10 d  | nm   | 5.1   | nd    |   | De Witt   |
|     |                 |       |      |       |       |   | et al.    |
|     | (*Eohaustorius  |       |      |       |       |   | 1989      |
|     | estuaries*)     |       |      |       |       |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
| FW  | Fathead minnow  | 30 d  | nm   | 0.43  | nd    |   | Gendusa   |
|     |                 |       |      |       |       |   | 1990      |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 | 96 h  |      | 0.97  |       |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     | Channel catfish | 96 h  | 0.70 | 3.68  | nd    |   |           |
|     |                 |       |      |       |       |   |           |
|     | (*Ictalurus     |       |      |       |       |   |           |
|     | punctatus*)     |       |      |       |       |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     | Amphipod        | 10 d  | 0.46 | 2.3   | 45.9  |   | Suedel et |
|     |                 |       |      |       |       |   | al. 1993  |
|     | (*Hyallela      |       |      |       |       |   |           |
|     | azteca*)        |       |      |       |       |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 0.50 | 7.4   | 236.5 |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 0.44 | 5.5   | 97.6  |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     | Midge           | 10 d  | 0.46 | 7.3   | 91.2  |   |           |
|     |                 |       |      |       |       |   |           |
|     | (Chir*onomus    |       |      |       |       |   |           |
|     | tentans*)       |       |      |       |       |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 0.50 | 8.7   | 251.0 |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 0.44 | 3.0   | 75.7  |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     | *Daphnia magna* | nr    | nm   | 4.2   | nd    |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
| *   |                 |       |      |       |       |   |           |
| *Ac |                 |       |      |       |       |   |           |
| ena |                 |       |      |       |       |   |           |
| pht |                 |       |      |       |       |   |           |
| hen |                 |       |      |       |       |   |           |
| e** |                 |       |      |       |       |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
| SW  | Amphipod        | 10 d  | 1.23 | 44.4  | 800   | S |           |
|     |                 |       |      |       |       | w |           |
|     | (*E.            |       |      |       |       | a |           |
|     | estuaries*)     |       |      |       |       | r |           |
|     |                 |       |      |       |       | t |           |
|     |                 |       |      |       |       | r |           |
|     |                 |       |      |       |       | z |           |
|     |                 |       |      |       |       | 1 |           |
|     |                 |       |      |       |       | 9 |           |
|     |                 |       |      |       |       | 9 |           |
|     |                 |       |      |       |       | 1 |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 2.49 | 47.8  | 609   |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 4.21 | 68.4  | 542   |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     | Amphipod        |       | 1.62 | \>193 | \     |   |           |
|     |                 |       |      |       | >1720 |   |           |
|     | (*Leptocheirus  |       |      |       |       |   |           |
|     | lumulosus*)     |       |      |       |       |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 2.52 | 193   | 1410  |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 3.66 | 382   | 1490  |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
| *   |                 |       |      |       |       |   |           |
| *Ph |                 |       |      |       |       |   |           |
| ena |                 |       |      |       |       |   |           |
| nth |                 |       |      |       |       |   |           |
| ren |                 |       |      |       |       |   |           |
| e** |                 |       |      |       |       |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
| SW  | Amphipod        | 10 d  | 1.02 | 39.2  | 138   | S |           |
|     |                 |       |      |       |       | w |           |
|     | (*E.            |       |      |       |       | a |           |
|     | estuaries*)     |       |      |       |       | r |           |
|     |                 |       |      |       |       | t |           |
|     |                 |       |      |       |       | r |           |
|     |                 |       |      |       |       | z |           |
|     |                 |       |      |       |       | 1 |           |
|     |                 |       |      |       |       | 9 |           |
|     |                 |       |      |       |       | 9 |           |
|     |                 |       |      |       |       | 1 |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 2.47 | 97.2  | 139   |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 3.33 | 122   | 146   |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     | Amphipod        |       | 1.96 | 92.4  | 387   |   |           |
|     |                 |       |      |       |       |   |           |
|     | (*L.            |       |      |       |       |   |           |
|     | plumulosus*)    |       |      |       |       |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 2.50 | 162   | 306   |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+
|     |                 |       | 3.60 | 255   | 360   |   |           |
+-----+-----------------+-------+------+-------+-------+---+-----------+

^a^ SW = saltwater; FW = freshwater

^b^ OC = organic carbon; nm = not measured; nd = not determined

Some additional information is available for creosote or creosote
components. Tagatz et al. (1983) evaluated the toxicity of
creosote-contaminated sediment (sand) to field- and laboratory-colonized
estuarine benthic communities exposed for 8 weeks to concentrations of
177, 844, or 4420 µg/g. At the two highest concentrations, the number of
individuals and species were significantly reduced from the control
numbers. Animal abundance also was reduced at 177 µg/g in the field.
Echinoderm, annelid, and arthropod numbers were adversely affected at
the lowest concentration. Mollusks numbers were significantly reduced at
844 µg/g. Changes in indices of species diversity and dominance occurred
at the middle and high concentrations. Creosote sediment concentrations
decreased by 30% in the laboratory and 42% in the field during the 8
weeks of exposure.

Padma et al. (1998) exposed mysid shrimp to creosote-contaminated
sediment and to the water-soluble portion of the sediment. The 24-h LC50
was 700 µg/L for mysid exposed to the whole sediment. The 24-h LC50 was
180 µg/L for mysid exposed to the water-soluble fraction of the
sediment, which contained higher concentrations of the low-molecular
PAHs than did the whole sediment.

**Other Effects Information**

[Zooplankton and phytoplankton communities]{.underline}

Sibley et al. (2001a,b) examined the structure and dynamics of
zooplankton communities (86 spp.) and phytoplankton (200 spp.) for up to
83 days following single applications of liquid creosote directly to
water in 12,000-L outdoor microcosms. Concentrations ranged from 0.06 to
109 mg/L. Results indicate that zooplankton communities may be highly
sensitive to creosote exposure. Creosote had a significant and rapid
adverse impact on total abundance, number of taxa, and population
dynamics of individual taxa at all concentrations. Community-level EC50s
were 44.6 µg/L (NOEC = 13.9 µg/L) at 5 days and 46.6 µg/L (NOEC = 5.6
µg/L) at days. Creosote had no direct adverse affect on the
phytoplankton community based on total abundance and number of taxa.

[Herring]{.underline}

Vines et al. (2000) investigated the effects of creosote-treated wood on
embryonic development in Pacific herring (*Clupea pallasi*) in the
laboratory and in the field. Herring spawn their eggs onto various
substrates, including aquatic pilings, and creosote diffused from
pilings had a detrimental affects on hatching rate and survival of
embryos. In the laboratory, embryos were incubated in glass bowls of
seawater containing either creosote-treated wood (from pilings at least
40 years old), untreated wood (Douglas fir), or only seawater. The LC50
for hatching success was 50 µg/L, with statistically significant
reductions in hatching success at \~9 µg/L. None of the eggs adhering to
treated wood hatched, and only 9% of free-floating eggs hatched in bowls
containing treated wood. Hatching success was 89% for the control and
73% for untreated wood. The effects observed in the laboratory also were
observed in the field, where herring eggs deposited onto aged
creosote-treated pilings (Fort Baker, CA) did not hatch.

Other effects were observed in the laboratory study. For embryos not
attached to wood but exposed to creosote in the water, 40-50 % exhibited
delayed development. All creosote-exposed embryos that survived to hatch
were abnormal as compared to 20% in the wood-only treatment and 8% in
the control. Abnormalities included fluid retention in the visceral
cavity (ascites), fluid accumulation around the heart (pericardial
edema), and spinal curvature (scoliosis). Embryonic heart rates measured
post-fertilization increased from 92 and 97 beats/min on Day 5 to 127
and 130 beats/min at Day 9 in the control and wood-only treatments,
respectively, but decreased from about 50 beats/min to \<10 beats/min in
the creosote-exposed treatment. Other effects recorded only in the
exposed treatment included severe arrhythmic heart contraction patterns,
erratic and increased body movements within the chorion (egg wall), and
embryo tremors and twitches.

[Mussels]{.underline}

No adverse effects on the survival of mussels (*Mytilus edulis edulis*)
suspended in cages from the Sooke Basin pilings were observed in a two
year *in-situ* bioassay. However, mussels grown in close proximity (15
to 30 cm) to either the WP piling or BMP piling grew more slowly than
did mussels grown farther away (Table 11).

**Table 11. Survival and Growth of Mussels after Dolphin Installation in
the Sooke Basin Field Study**

  ------------------------------------- ---------- -------- --------- ---------
  **Station (distance from pilings)**   **%                           
                                        survival                      
                                        over                          
                                        time**                        

                                        **0 d**    **14 d** **185 d** **384 d**

  BMP treated dolphin (0.5 m)           100        100      97        79

  BMP treated dolphin (2.0 m)           100        100      100       88

  BMP treated dolphin (10.0 m)          100        99       98        81

  WP piling (0.5 m)                     100        100      99        88

  Open control                          100        100      99        80

                                                                      

  **Station and distance from pilings** **Growth                      
                                        (valve                        
                                        length,                       
                                        mm) over                      
                                        time**                        

                                        **0**      **14**   **185**   **384**

  BMP treated dolphin (0.5 m)           29         32.5     46.7      59.3

  BMP treated dolphin (2.0 m)           29.5       32.7     51.6      67.2

  BMP treated dolphin (10.0 m)          31.2       33.3     56.6      68.7

  WP Piling (0.5 m)                     29.1       31.4     49.1      64.2

  Open Control                          30.2       32.4     55.6      69.5
  ------------------------------------- ---------- -------- --------- ---------

Prior to being placed in the water at Sooke Basin, mussel-tissue PAH
concentrations were relatively low (16.15[+]{.underline} 2.19 ng/g).
These levels increased an average of 328% on Day 14 of the study. The
most significant increases were observed in close proximity (within 0.5
m) of either the BMP or WP dolphins. Following that initial increase,
levels returned to normal by Day 185 and were slightly lower than the
baseline levels by Day 384. Higher levels of PAHs were observed in
gonadal tissue than were observed in whole body tissues as shown below
(Table 12). Overall, tissue concentrations were low.

**Table 12. Low and High Molecular Weight PAHs in Gonad and Whole-body
Tissue of Mussels (*Mytilus edulis edulis*) Grown at Varying Distances
from Creosote-treated Dolphins**

  -------------------- ----------------- ---------- ---------- --------- ---------- ----------
  **PAH component**    **concentration                                              
                       (ng/g wet tissue)                                            
                       at each site^1^**                                            

                       **OC^2^**         **BMP      **BMP      **BMP     **WP       **Avg.**
                                         0.5^3^**   2.0^3^**   10^3^**   0.5^4^**   

  LPAH in Gonad        14.8              15.1       18.2       10.0      16.4       15.0

  HPAH in Gonad        22.0              29.2       32.4       15.6      32.4       26.3

  LPAH in Whole Tissue 6.7               6.4        9.8        5.6       6.1        6.9

  HPAH in Whole Tissue 15.0              15.4       26.0       11.5      16.7       16.9

  Total PAH in Gonad   36.7              44.3       50.6       25.5      48.8       41.2

  Total PAH in Whole   21.7              21.9       35.8       17.0      25.5       24.4
  Tissue                                                                            
  -------------------- ----------------- ---------- ---------- --------- ---------- ----------

^1^ tissues were analyzed at Day 185 when the mussels were ripe and
ready to spawn

^2^ OC = open control site located upstream of all structures

^3^ BMP = creosote-treated piling produced using Best Management
Practices at specifed distance (m)

^4^ WP = 8-year-old weathered creosote treated piling

**Aquatic Risk Assessment**

**Water column**

[Acute risks]{.underline}

When a new creosote-treated wood structure is installed in an aquatic
environment, there is an immediate release of creosote components into
the water column. During their study in the Sooke Basin, Goyette and
Brooks (1998) report that creosote leaching from the portions of aquatic
pilings above the water line initially forms a sheen on the water
surface. They speculated that microdoplets from the surface sheen
subsequently move down through the water column and into the sediment,
with little of that creosote dissolving in the water column. However,
they did not measure water-column concentrations until 6 months after
pilings (dolphins) were installed in Sooke Basin. Ingram et al. (1982)
and Bestari et al. (1998) measured PAH concentrations in the water
column in the initial days and weeks and found levels that might be of
concern for exposure of aquatic organisms.

Acute RQs for aquatic organisms exposed to the PAH component expected in
the water column are presented in Table 13. The weighted acute toxicity
values used to calculate RQs for the total PAH component are as follows:

Freshwater fish weighted LC50 = 405 µg/L

Freshwater invertebrate weighted EC50 = 267 µg/L

Saltwater fish weighted LC50 = 1150 µg/L

Saltwater invertebrate weighted EC50 or LC50 = 399 µg/L

**Table 13. Acute RQs for Exposure of Aquatic Organisms to PAHs in the
Water Column**

+-----------------+-----------+---------+---------+---------+--------+
| **Site**        | **Time    | **F     |         | **      |        |
|                 | after     | reshwat |         | Estuari |        |
|                 | initial   | er^a^** |         | ne/Mari |        |
|                 | e         |         |         | ne^a^** |        |
|                 | xposure** |         |         |         |        |
+=================+===========+=========+=========+=========+========+
|                 |           | *       | **In    | *       | **Inv  |
|                 |           | *Fish** | vert.** | *Fish** | ert.** |
+-----------------+-----------+---------+---------+---------+--------+
| 300-gal tanks;  | 72 hr     | n/a     | n/a     | **0     | **1.08 |
| seawater        |           |         |         | .37\*** | \*\*** |
|                 |           |         |         |         |        |
| (Ingram et      |           |         |         |         |        |
| al.1982)        |           |         |         |         |        |
+-----------------+-----------+---------+---------+---------+--------+
|                 | 12 day    | n/a     | n/a     | **0     | **0.   |
|                 |           |         |         | .13\*** | 39\*** |
+-----------------+-----------+---------+---------+---------+--------+
| 1200-L outdoor  | 7 day     | **0     | **0     | n/a     | n/a    |
| microcosms;     |           | .24\*** | .36\*** |         |        |
| freshwater      |           |         |         |         |        |
|                 |           |         |         |         |        |
| (Bestari et     |           |         |         |         |        |
| al.1998)        |           |         |         |         |        |
+-----------------+-----------+---------+---------+---------+--------+
|                 | 3 mo.     | 0.02    | 0.02    | \<0.01  | 0.02   |
+-----------------+-----------+---------+---------+---------+--------+
| Sooke Basin;    | 6 mo.     | n/a     | n/a     | \<0.01  | \<0.01 |
| marine          |           |         |         |         |        |
|                 |           |         |         |         |        |
| (Goyette and    |           |         |         |         |        |
| Brooks 1998)    |           |         |         |         |        |
+-----------------+-----------+---------+---------+---------+--------+
| Railroad        | 0 hr      | **0.7   | **1.1   | **0     | **0.78 |
|                 |           | 7\*\*** | 6\*\*** | .27\*** | \*\*** |
| (wet scenario)  |           |         |         |         |        |
+-----------------+-----------+---------+---------+---------+--------+
|                 | 96 hr     | **0     | **0.6   | **0     | **0.   |
|                 |           | .45\*** | 9\*\*** | .16\*** | 46\*** |
+-----------------+-----------+---------+---------+---------+--------+
|                 | 21-day    | **0     | **0     | **0     | **0.   |
|                 | avg.      | .23\*** | .35\*** | .08\*** | 24\*** |
+-----------------+-----------+---------+---------+---------+--------+
|                 | 60-day    | **0     | **0     | **0     | **0.   |
|                 | avg.      | .15\*** | .22\*** | .05\*** | 15\*** |
+-----------------+-----------+---------+---------+---------+--------+
|                 | 90-day    | **0     | **0     | 0.04    | **0.   |
|                 | avg.      | .13\*** | .20\*** |         | 13\*** |
+-----------------+-----------+---------+---------+---------+--------+
| Railroad        | 0 hr      | **0     | **0     | 0.04    | **0.   |
|                 |           | .12\*** | .18\*** |         | 12\*** |
| (dry scenario)  |           |         |         |         |        |
+-----------------+-----------+---------+---------+---------+--------+
|                 | 96 hr     | **0     | **0     | 0.02    | **0.   |
|                 |           | .07\*** | .11\*** |         | 07\*** |
+-----------------+-----------+---------+---------+---------+--------+
|                 | 21-day    | 0.03    | 0.04    | \<0.01  | 0.03   |
|                 | avg.      |         |         |         |        |
+-----------------+-----------+---------+---------+---------+--------+
|                 | 60-day    | 0.01    | 0.02    | \<0.01  | 0.01   |
|                 | avg.      |         |         |         |        |
+-----------------+-----------+---------+---------+---------+--------+
|                 | 90-day    | \<0.01  | 0.01    | \<0.01  | \<0.01 |
|                 | avg.      |         |         |         |        |
+-----------------+-----------+---------+---------+---------+--------+

**^a^** based on weighted toxicity values: FW fish = 405 ppb; FW
invertebrate = 267 ppb;

SW fish = 1150 ppb; SW invertebrate = 399 ppb

***\*\**** exceeds the acute LOC for non-listed spp. (RQ
[\>]{.underline}0.5) and listed spp. (RQ [\>]{.underline}0.05)

***\**** exceeds the acute LOC for listed spp.

The RQs determined for Sooke Basin do not exceed the Agency\'s acute
LOC; however, those concentrations were measured 6 months after pilings
were installed and may simply represent background PAH concentrations.
Based on the total PAH concentrations reported in seawater by Ingram et
al. (1982) and in freshwater by Bestari et al. (1998) and the weighted
toxicity values, the acute LOC is exceeded for listed fish and aquatic
invertebrates. The acute LOC also is exceeded for non-listed
estuarine/marine invertebrates. Exceedance of an LOC indicates a
potential for adverse effects on nontarget organisms and identifies a
need for regulatory action to mitigate risk (Appendix B).

Based on the EECs modeled for railroad structures, the acute LOC for
listed freshwater and saltwater species is exceeded in wet areas (MS
scenario). Exposure levels of concern potentially exist for several
months. Non-listed species also are at acute, short-term risk. In drier
areas (CA scenario), the acute LOC is only exceeded for listed species
and only in the short-term.

Zooplankton communities also may be at acute risk. Comparing the 5-day
EC50 of 44.6 µg/L for community-level effects to the aquatic EECs
(Tables 3 and 5) indicates that the LOC would be exceeded 1- to 10-fold
for acute risks due to creosote leaching from aquatic structures and
railroad structures.

[Chronic risks]{.underline}

Insufficient data exist to calculate weighted toxicity values for the
PAH component; therefore, chronic RQs are not calculated. However,
comparing EECs to the available data (previously presented in the
Toxicity Data section) indicate that adverse affects on survival,
growth, and/or reproduction could be expected in some situations (Table
14). Chronic risk is presumed in OPP risk assessments when the chronic
EEC (21-day-avg. for invertebrates and 60-day-avg. for fish) exceeds the
NOEC. Chronic exposure in the water column potentially poses risks to
fish and/or aquatic invertebrates around aquatic structures and,
especially in wetter areas, where leachate from railroad structures may
move into the aquatic environment.

**Table 14. EECs and Adverse Effects from Chronic Exposure in the Water
Column**

+-----------------+------------------+---------------------------------+
| **Site**        | **EEC (µg/L)**   | **Reported effect**             |
|                 |                  |                                 |
|                 |                  | **concentrations (µg/L)**       |
+=================+==================+=================================+
| 300-g SW tanks  | 156 (12 d)       | 0.4-1.0 (salmon, herring;       |
|                 |                  | development)                    |
|                 |                  |                                 |
|                 |                  | 0.61 (rainbow trout;            |
|                 |                  | immunotoxicty)                  |
|                 |                  |                                 |
|                 |                  | 9 (herring; hatching sig.       |
|                 |                  | reduced)                        |
|                 |                  |                                 |
|                 |                  | 44.6 (zooplankton; community    |
|                 |                  | EC50)                           |
|                 |                  |                                 |
|                 |                  | 30-50 (invertebrates; survival, |
|                 |                  | brood size)                     |
|                 |                  |                                 |
|                 |                  | 5-57 (phenanthrene NOECs^a^)    |
|                 |                  |                                 |
|                 |                  | 10-11 (fluoranthene NOECs^a^)   |
|                 |                  |                                 |
|                 |                  | 44-520 (acenapthene NOECs^a^)   |
+-----------------+------------------+---------------------------------+
| 12,000-L FW     | 0.8-6.7 (84 d)   |                                 |
| microcosms      |                  |                                 |
+-----------------+------------------+---------------------------------+
| Railroad        | 94.4 (21-d-avg.) |                                 |
|                 |                  |                                 |
| (wet scenario)  | 59.3 (60-d-avg.) |                                 |
+-----------------+------------------+---------------------------------+
| Railroad        | 11.4 (21-d-avg.) |                                 |
|                 |                  |                                 |
| (dry scenario)  | 5.0 (60-d-avg.)  |                                 |
+-----------------+------------------+---------------------------------+

^a^ NOECs based on survival, growth, and reproduction

**Sediments**

Due to lack of sediment-toxicity data for most PAHs and the total PAH
component, RQs cannot be calculated for acute and chronic risks to
benthic organisms potentially exposed to the PAH matrix in sediments.
However, the Sooke Basin study provides information on the potential
adverse affects of creosote-contaminated sediments. Goyette and Brooks
(1998) compared sediment loads (see Table 4) to proposed or interim
sediment quality criteria for Canada and Washington State. Based on
those criteria, several PAHs pose potential risks to benthic organisms
in sediments immediately around aquatic pilings (Table 15).

**Table 15. PAHs Exceeding Canadian and/or Washington State Sediment
Quality Criteria at Various Distanced from the BMP Dolphin in Sooke
Basin After 384 Days (from Goyette and Brooks 1998)**

  ----------------------------------------------------------------------------
  **PAH**            **Distance                                     
                     (m) from                                       
                     pilings**                                      
  ------------------ ------------ ----------- ---------- ---------- ----------
                     **0.5 m**    **1 m**     **1.5 m**  **7.5 M**  **10 m**

  Fluoranthene       ●            ●                                 

  Acenaphthene       ●            ●                                 

  Phenanthrene       ●            \*          \*         \*         

  Chrysene           ●            \*                                

  Fluorene           ●                                              

  Pyrene                                                            

  Anthracene                                                        

  Naphthalene                                                       
  ----------------------------------------------------------------------------

● exceeds Canadian and WA State Sediment Quality Criteria

\* exceeds Canadian Sediment Quality Criteria

Goyette and Brooks (2001**)** also conducted various tests to evaluate
sediment toxicity in proximity to the creosote-treated pilings in Sooke
Basin. Marine amphipods (*Rhepoxynius abronius* and *Eohaustorius
washingtonianus*) were exposed to sediments from the BMP and control
sites. Because these amphipods are not supported in the Sooke Basin,
control reference sediments also were collected from elsewhere for
comparison to the toxicity from exposure to BMP sediments. Sediments
collected within 0.5 m of the BMP dolphin at Days 14 and 185 were toxic
in comparison to the reference sediments. Fluoranthene and phenanthrene
appeared to be the major contributors to this toxicity. At Days 1360 and
1540, toxicity was found in some, but not all, samples within 2 m of the
BMP dolphin. However, by this time elevated hydrogen sulfide levels were
elevated in the sediments (from buildup and decomposition of fouling
organisms and their waste falling from the pilings) and were thought to
have contributed to the observed toxicity. Pore-water toxicity testing
with Microtox™ assays and a marine bioluminescent bacterium demonstrated
toxic conditions in sediments within 2 m of the BMP dolphin and beneath
the WP dolphin, but not at the open control site. Fertilization tests
with sea urchins at Day 535 also indicated toxicity within 0.5 m and
below the BMP, WP, and untreated dolphins.

Regarding the PAH sediment concentrations detected in mesocosm
sediments, Brooks (2004) concluded that newly treated railway ties pose
minimal environmental risk to the endangered dragonfly inhabiting
wetland areas crossed by a rail line. Using benchmark methodology
proposed by Swartz (1999), Brooks (2004) also concludes that no adverse
biological effects can be expected at the observed PAH levels. However,
due to the lack of sediment-toxicity tests and actual field monitoring,
the potential for adverse affects to aquatic organisms exposed to PAH in
sediments from leaching from railroad structures remains uncertain.

One other study deserves mention regarding contaminated river sediments.
Pastorok et al. (1994) investigated the effect of creosote-contaminated
sediments on aquatic organisms nearby a creosote-treatment plant in the
lower Willamette River in Oregon. Endpoints evaluated included amphipod
(*Hyalella azteca*) mortality and Microtox (*Photobacterium
phosphoreum*) bioluminescence. Toxicity occurred within approximately
300 feet of the shoreline, with a highly toxic area near a dock used for
creosote off-loading. A low level of contamination of crayfish and lack
of serious liver lesions in suckers collected near the site suggest that
risk to mobile species from chronic contamination is low. There was no
evidence of adverse effects throughout the rest of the main channel of
the river.

**Risk Characterization**

**Aquatic structures**

Based on the available toxicity and exposure data, acute risk is
presumed for listed freshwater and saltwater fish and aquatic
invertebrates exposed to PAHs in the water column. Acute risk also is
presumed for non-listed saltwater invertebrates. These risk presumptions
are made from LOC exceedances determined from RQs calculated from
water-column EECs generated in outdoor microcosms and large tanks and
from weighted toxicity values for the PAH complex expected in the water
column. Insufficient data are available to determine chronic toxicity of
the PAH complex or even the toxicity of the individual PAHs addressed in
this assessment. Therefore, chronic RQs cannot be determined. Limited
data from the literature indicate that adverse chronic effects
(survival, growth, reproduction, immunotoxicity) are possible from some
PAHs or mixtures of PAHs at exposure levels expected in the water
column. Guideline studies for acute and chronic toxicity testing with
freshwater and saltwater fish and invertebrates exposed to the PAH
complex would be needed to further characterize acute and chronic risks
to aquatic animals inhabiting the water column. Guideline data also are
not available to assess risks to aquatic plants. Uncertainties exist
with the available data on creosote leaching from treated wood into the
environment. Additional data would help to refine acute and chronic
EECs. Field monitoring of aquatic concentrations also could be
undertaken in areas of newly installed structures to further refine PAH
concentrations over time.

Based on findings from the Sooke Basin field study in Canada, PAH
accumulation in sediments is believed to be sufficiently high to pose a
risk to benthic organisms in the immediate vicinity of creosote-treated
pilings for at least a year. Risk could be better characterized if acute
and chronic sediment-toxicity guideline studies were available. These
guideline studies are outstanding for creosote. Moreover, movement into
and retention of PAHs in sediments around creosote-treated aquatic
pilings are likely to vary locally, depending on abiotic and biotic
factors such as current speed, amount of treated structure per unit
area, air and water temperature, salinity, and the infaunal species
occurring in the immediate area of the structures. Therefore, many
uncertainties exist in extrapolating findings from the Sooke Basin to
warmer locales in the southern U. S. Because of those uncertainties,
prior to installation of any new aquatic structures, a site evaluation
is essential to evaluate potential risks, particularly to listed (i. e.,
endangered or threatened) or other sensitive species or sensitive life
stages. Risk could be further characterized with additional field or
simulated field studies representing the environmental conditions and
species assemblages occurring in the southern U. S.

Existing aquatic structures are likely to continue leaching creosote to
the aquatic environment, but at lower rates than newly installed
structures. In some situations, such as noted at Sooke Basin after about
a year, leaching from submerged pilings might possibly be limited due to
the mass of organisms attached to the pilings. Even in those situations,
leaching may still occur in the pilings above the waterline, especially
in hot weather. In other areas, such as where herring or other organisms
attach their eggs directly to creosote-treated pilings, even pilings
that have been submerged for many years, eggs may not hatch or surviving
embryos may not develop normally. Developmental or other sublethal
impacts also might occur where aquatic organisms are exposed to low PAH
concentrations but for prolonged periods. Chronic guideline studies with
freshwater and saltwater fish and invertebrates would provide additional
information for assessing such risks.

Long-term findings from the Sooke Basin field study deserve mention. The
researchers reported that a substantial community of mussels, anemones,
and other invertebrates inhabited the creosote-treated pilings after the
first year. Sediment concentrations also decreased at that time, which
they speculate may have been due to the physical barrier of organisms
precluding additional movement of creosote into the water column and
sediments. However, despite the apparent lack of long-term adverse
affects on some organisms, sensitive species might be adversely affected
by short-term exposure. Additional acute-toxicity data generated in
guideline studies and refinement of initial EECs in the water column
would help address that risk, especially for listed species.

**Railroad ties**

Based on modeled EECs using PRZM/EXAMS scenarios, and the weighted
toxicity values for the PAH complex, acute risk is presumed for listed
freshwater and saltwater fish. Based on the scenario for wetter areas,
acute risk also is presumed for non-listed freshwater fish and aquatic
invertebrates exposed to PAHs in the water column. Chronic risk can not
be assessed due to the lack of chronic toxicity data, but some available
evidence indicates that chronic risk is possible to aquatic organisms
inhabiting the water column. As noted for aquatic structures, further
characterization of acute and chronic risks would require acute and
chronic toxicity testing with fish and aquatic invertebrates exposed to
the PAH complex in the water column. Acute and chronic EECs could be
refined from creosote leaching studies in the water column over time, or
from field monitoring in areas where railroad ties are in proximity to
surface waters. Data obtained from a mesocosm study indicate that
sediment PAH levels leached from railroad ties appear to be lower than
those around aquatic pilings, and the PAHs do not move any substantial
distance from the railway ballast.

**7.3 ENDANGERED SPECIES CONSIDERATIONS**

Section 7 of the Endangered Species Act (ESA), 16 U.S.C. Section
1536(a)(2), requires that federal agencies consult with the National
Marine Fisheries Service (NMFS) for marine and andronomus listed
species, or with the United States Fish and Wildlife Services (FWS) for
listed wildlife and freshwater organisms, if proposing an \"action\"
that may affect listed species or their designated habitat. Each federal
agency is required under the Act to insure that any action they
authorize, fund, or carry out is not likely to jeopardize the continued
existence of a listed species or result in the destruction or adverse
modification of designated critical habitat. To jeopardize the continued
existence of a listed species is to \"to engage in an action that
reasonably would be expected, directly or indirectly, to reduce
appreciably the likelihood of both the survival and recovery of a listed
species in the wild by reducing the reproduction, numbers, or
distribution of the species.\" 50 C.F.R. §402.02.

To comply with subsection (a)(2) of the ESA, EPA's Office of Pesticide
Programs has established procedures to evaluate whether a proposed
registration action may directly or indirectly appreciably reduce the
likelihood of both the survival and recovery of a listed species in the
wild by reducing the reproduction, numbers, or distribution of any
listed species (U.S. EPA 2004). If any of the Listed Species LOC
Criteria are exceeded for either direct or indirect effects in the
Agency's screening-level risk assessment, the Agency identifies any
listed or candidate species that may occur spatially and temporally in
the footprint of the proposed use. Further biological assessment is
undertaken to refine the risk. The extent to which any species may be at
risk determines the need to develop a more comprehensive consultation
package as required by the ESA.

The ecological risk assessment for creosote indicates a potential for
exposure of listed fish and aquatic invertebrate species that warrants a
more refined assessment to include direct, indirect, and habitat
effects. The refined assessment should involve clear delineation of the
action area associated with proposed use of creoste and best available
information on the temporal and spatial co-location of listed species
with respect to the action area. This analysis has not been conducted
for this assessment. An endangered species effect determination will not
be made at this time.

**8.0 INCIDENT REPORTS**

The following databases have been consulted for the poisoning incident
data on the active ingredient creosote (PC Code: 025002):

**[OPP Incident Data System (IDS)]{.underline}** - The Incident Data
System of The Office of Pesticide Programs (OPP) of the Environmental
Protection Agency (EPA) contains reports of incidents from various
sources, including registrants, other federal and state health and
environmental agencies and individual consumers, submitted to OPP since
1992. Reports submitted to the Incident Data System represent anecdotal
reports or allegations only, unless otherwise stated. Typically no
conclusions can be drawn implicating the pesticide as a cause of any of
the reported health effects. Nevertheless, sometimes with enough cases
and/or enough documentation risk mitigation measures may be suggested.

**[Poison Control Centers]{.underline}** - as the result of a data
purchase by EPA, OPP received Poison Control Center data covering the
years 1993 through 1996 for all pesticides. Most of the national Poison
Control Centers (PCCs) participate in a national data collection system,
the Toxic Exposure Surveillance System, which obtains data from about
65-70 centers at hospitals and universities. PCCs provide telephone
consultation for individuals and health care providers on suspected
poisonings, involving drugs, household products, pesticides, etc.

**[California Department of Pesticide Regulation]{.underline}** -
California has collected uniform data on suspected pesticide poisonings
since 1982. Physicians are required, by statute, to report to their
local health officer all occurrences of illness suspected of being
related to exposure to pesticides. The majority of the incidents involve
workers. Information on exposure (worker activity), type of illness
(systemic, eye, skin, eye/skin and respiratory), likelihood of a causal
relationship, and number of days off work and in the hospital are
provided.

**[National Pesticide Telecommunications Network (NPTN)]{.underline}** -
NPTN is a toll-free information service supported by OPP. A ranking of
the top 200 active ingredients for which telephone calls were received
during calendar years 1984-1991, inclusive, has been prepared. The total
number of calls was tabulated for the categories human incidents, animal
incidents, calls for information, and others.

**[Published Incident Reports]{.underline}** - Some incident reports
associated with creosote related human health hazard are published in
the scientific literature.

Incidents by database are summarized here:

**1) OPP's Incident Data System (IDS)**

The following cases from the IDS do not have documentation confirming
exposure or health effects. Registrants are not required to report
incidents involving exposure to previously treated wood, only direct
exposure to creosote itself. Therefore, it is possible that serious
adverse effects involving exposures to treated wood have been missed by
this review. Legal claims of severe damage to eyes and skin including
infections requiring amputation have been reported but only in a cursory
way and without enough documentation to be included in this review.

**[Incident#2796-100]{.underline}**

An incident was investigated in the United Kingdom in 1994 or 1995 (date
of incident unknown) involving creosote. After a landlord treated a
residence with creosote the male tenant complained of headache, stomach
ache, and respiratory irritation. No further information is available on
the disposition of this case.

**[Incident #2796-119]{.underline}**

An incident was investigated in the United Kingdom in 1994. After
creosoting work was done on the flat below theirs, a male and female
reported tearing, burning throat, nausea, and vomiting. No further
information is available on the disposition of this case.

**[Incident #8760-1]{.underline}**

In 1997 a 38 year old railroad worker alleged inhalation and dermal
exposure to creosote. The timing and duration of exposure are not
reported. A legal claim has been filed alleging nodular malignant
melanoma. No further information is available on the disposition of this
case.

**[Incident #8760-3]{.underline}**

A worker at a creosote plant was exposed in 1994 while testing boring
treated wood. He reportedly developed skin rash on wrists and forearms
and visited a dermatologist.

**2) Poison Control Center**

No data were reported in the Poison Control Center database covering the
years 1993 through 1996**.**

**3)** **California Data - 1982 through 1996**

Detailed descriptions of 124 cases submitted to the California Pesticide
Illness Surveillance Program (1982-1996) were reviewed. In 114 of these
cases, creosote was used alone and was judged to be responsible for the
health effects. Only cases with a definite, probable or possible
relationship were reviewed. Creosote ranked 88th as a cause of systemic
poisoning in California (1982-1994). Most of the cases that could
definitely be attributed to creosote (80% of the 50 cases categorized as
definite) involved workers who handled creosote directly but did not
have proper protection for eyes or skin. A significant number of cases
have resulted when workers have been exposed to treated wood, usually by
handling or sawing the wood. Most of these cases experienced chemical
burns to the skin or eyes.

**4) National Pesticide Telecommunications Network (NPTN)**

On the list of the top 200 chemicals for which NPTN received calls from
1984-1991 inclusively, creosote was ranked 118th with 26 incidents in
humans reported and no incidents in animals.

**5) Open Scientific Literature**

Dean et al. (1992) reported on a white ten week old female, who weighed
6 kilograms, and experienced cyanosis, irritability, metabolic acidosis,
and a lethal methehemoglobin level of 71.4%. She was taken to the
hospital and remained for three days. Three days earlier, the child\'s
father replaced an aluminum stove pipe leading from the wood-burning
stove to the chimney and installed a straight section of the stove pipe.
Green slab pine wood was continuously burning in the stove. Pine tar
fumes emitted from the stove were the suspected source of creosote oils.
The girl\'s cradle was approximately five feet from the stove.

Bowman et al. (1984) reported on a seventy year old man who was found
unconscious with a cup of creosote beside him. On admission to the
hospital, the man\'s respiratory effort was weak and on auscultation,
widespread crackles were heard. His face and clothes were stained with
vomit and creosote. He was immediately administered endotracheal
intubation and artificial ventilation. He experienced anuria and died.
After his death, a liter of mostly creosote fluid was found in his
stomach.

Thompson et al. (1994) reported that during 1989 to 1991, 250 children
(124 boys and 126 girls) under 10 years old out of 6, 478 cases were
taken to accident and emergency departments in the United Kingdom for
suspected pesticide poisoning. Seven percent of these cases were due to
creosote.

The following excerpts were taken directly for the Hazardous Substances
Data Bank (HSDB). HSDB is a toxicology data file on the National Library
of Medicine's Toxicology Data Network (TOXNET). Data are derived from "a
core set of books, government documents, technical reports and selected
primary journal literature. HSDB is peer-reviewed by the Scientific
Review Panel (SRP), a committee of experts in the major subject areas
within the bank's scope."

> Death from large doses of creosote appears to be due largely to
> cardiovascular collapse. Fatalities have occurred 14 to 36 hr after
> the ingestion of about 7 g by adults or 1 to 2 g by children. The
> symptoms of systemic illness included salivation, vomiting,
> respiratory difficulties, thready pulse, vertigo, headache, loss of
> pupillary reflexes, hypothermia, cyanosis, and mild convulsions. The
> repeated absorption of therapeutic doses from the gastroenteric tract
> may induce signs of chronic intoxication, characterized by
> disturbances of vision and digestion (incr peristalsis & excretion of
> bloody feces). In isolated cases of \"self‑medication,\" hypertension
> & also general cardiovascular collapse have been described.
> \<NOINDEX\>\[Clayton, G. D. and F. E. Clayton (eds.). Patty\'s
> Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd
> ed. New York: John Wiley Sons, 1981‑1982. 2603\]
>
> \</NOINDEX\>
>
> Contact of creosote with the skin or condensation of vapors of
> creosote on the skin or mucous membranes may induce an intense burning
> and itching with local erythema, grayish yellow to bronze
> pigmentation, papular & vesicular eruptions, and gangrene and in
> isolated instances cancer. \... Heinz bodies have been noted in the
> blood of a patient one yr after his exposure to creosote. \... Similar
> observations following percutaneous absorption of this preparation.
> Eye injuries can include keratitis, conjunctivitis, and abrasion of
> the cornea. \... Permanent corneal scars result in about one third of
> such cases. Photosensitization has been reported \... and severe
> systemic illness. \<NOINDEX\>\[Clayton, G. D. and F. E. Clayton
> (eds.). Patty\'s Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C:
> Toxicology. 3rd ed. New York: John Wiley Sons, 1981‑1982. 2603\]
>
> \</NOINDEX\>
>
> Contact of liquid creosote with the eye has caused painful protracted
> keratoconjunctivitis. This has involved loss of corneal epithelium,
> clouding of the cornea, miosis, and long lasting irritability and
> photophobia. In one report concerned with creosote, two patients have
> been described, one examined 2 wk and the other 2 months after working
> with this material, both complaining of haziness of vision, which was
> found to be associated with numerous gray spots of varied size in the
> corneas, plus a superficial keratitis. \<NOINDEX\>\[Grant, W.M.
> Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas
> Publisher, 1986. 283\]\</NOINDEX\>
>
> Injuries to the skin or eyes have occurred mainly among men engaged in
> dipping or in \"pickling\" and handling \"sleepers,\" mine timbers,
> and woods for floors and other purposes. \... Calls attention to burns
> induced by fine particles of sawdust from creosote‑treated lumber.
> \... The burns were reduced to a minimum on rainy days, probably
> because of the decreased dispersion of both the wood particles and
> creosote. \<NOINDEX\>\[Clayton, G. D. and F. E. Clayton (eds.).
> Patty\'s Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C:
> Toxicology. 3rd ed. New York: John Wiley Sons, 1981‑1982.
> 2601\]\</NOINDEX\>
>
> Epitheliomas can result from prolonged exposure to creosote.
> \<NOINDEX\>\[Kirk‑Othmer Encyclopedia of Chemical Technology. 3rd ed.,
> Volumes 1‑26. New York, NY: John Wiley and Sons, 1978‑1984.,p. V22 592
> (1983)\]
>
> \</NOINDEX\>
>
> Vapor causes moderate irritation of nose and throat. Liquid may cause
> \... reddening and itching of skin. \<NOINDEX\>\[U.S. Coast Guard,
> Department of Transportation. CHRIS ‑ Hazardous Chemical Data. Volume
> II. Washington, D.C.: U.S. Government Printing Office, 1984‑5.\]
>
> \</NOINDEX\>
>
> Old creosote treated lumber \... retains a considerable portion of the
> oil for periods up to 25 or 30 years. \<NOINDEX\>\[Clayton, G. D. and
> F. E. Clayton (eds.). Patty\'s Industrial Hygiene and Toxicology:
> Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons,
> 1981‑1982. 2604\]\</NOINDEX\>

**6) Epidemiology Studies Associated with Creosote Exposure**

**Case Series Involving Chronic Effects Associated with Health Effects
of Creosote in Humans**

**[Garrett (1975)]{.underline}**

In a letter-to-the-editor, Garrett reported two patients diagnosed
within eighteen months with multi-focal transitional cell carcinoma of
the bladder with muscle invasion. Both men were determined to have had
chronic exposure to cresol and creosote, but no details of the exposures
were provided.

Reports of this kind may be useful when combined with other reports and
studies. Considered alone, no conclusion regarding association of
exposure to creosote with development of bladder cancer can be made.

**6.1 Cross-Sectional Studies Associated with Health Effects of Creosote
in Humans**

**Koppers (1979a)**

The Koppers Company sponsored a cross-sectional study of workers at four
wood preservative plants in Pennsylvania, South Carolina, West Virginia,
and Kentucky where creosote and creosote/coal tar were the predominant
treatments. The study was specifically aimed at identifying any health
problems known to be related to exposure to these major process
materials. An array of medical examinations were performed on 257
participants (73% of 351 total workers). The ratios of men to women
participants were similar among all four plants. However, the ratios of
black to white workers differed significantly among the plants,
therefore the ratios of black to white participants differed also. The
battery of examinations included a medical questionnaire, chemical
exposure questionnaire, chest x-ray, pulmonary function test, clinical
chemistry analysis, hematology analysis, urinalysis, sputum cytology
exam, and urine cytology exam.

No exposure parameter was evaluated in the health assessment other than
length of service. With the exception of a greater than expected number
of pustular eruptions of the skin, all other tests revealed only
infrequent and borderline abnormal findings. There was no evidence of
cancer at any site associated with work at these plants.

Due to the broad nature and limited depth of this study, only gross
negative health effects could be observed. Since no exposure assessment
for creosote was performed, no association between observed health
conditions and creosote exposure was possible. Within these limitations,
no evidence of detrimental health effects from working with creosote was
seen.

**Koppers (1979b,c and 1980a,b,c)**

Cross-sectional studies were conducted at five coal tar processing
plants to assess the health status of the work forces and thereby
identify possible adverse health problems associated with exposure to
coal tar and its derivatives. The studies were conducted by contracted
researchers as part of a continuing health and safety program sponsored
by the parent organization. The five plants studied were located in
California, West Virginia, Alabama, Ohio, and Illinois; all five
provided potential exposure to many industrial products, including
creosote, resulting from distillation of coal tar. From a toxicological
evaluation of coal tar products, an appropriate medical examination
protocol was designed to measure a number of health parameters that
should reveal toxic effects from the target coal tar products. Included
among the procedures were collection of medical and work history, chest
x-ray, pulmonary function test, clinical chemistry analysis, blood and
urological analysis, and sputum cytology examination.

The study populations included men and women, white and black, but
participation was voluntary resulting in an overall participation rate
of 42%. Length of employment ranged between less than one year to 50
years, but a majority of the workers who participated in the study
worked 10 years or less. No assessment of personal exposure to specific
substances was performed. The sole exposure parameter, which was
collected through the work history questionnaire, was the number of
years of potential exposure to coal tar and its derivatives.

Among the results from the broad medical examination, a number of
excesses and atypical findings were observed, although few could be
directly associated with working at the coal tar plants. Restrictive
respiratory deficits were found in the populations at all of the study
sites and considerable excesses were seen at three sites. A few
individuals at four of the five plants also were observed with
obstructive respiratory deficits. Increases in gamma glutamyl
transpeptidase (GGTP) and lactic dehydrogenase (LDH) levels were found
in a few individuals at two plants. Results from hematological
examinations showed atypical cells or abnormal cell counts in a few
workers at all five plants. Of particular interest were the increased
eosinophil counts observed in 13% of the workers at one plant. The only
notable result from the urine analyses was the observation of excess
RBCs (eight workers) and WBCs (11 workers) in 10% of the participants
from one plant. The prevalence of folliculitis was greater than expected
at three of the plants, with one of the plants having an incidence
significantly increased (11 out of 105 workers examined). At one plant,
no folliculitis was seen, but tar warts which are known to be associated
with exposure to coal tar, were in excess. In general, few atypical
cells were found during examinations of sputum. One exception was the
increased C-reactive protein observed in five workers at the same plant
at which the excess blood cells in urine and the greatest excess in
folliculitis occurred. No cancer at any site was discovered during the
broad medical examination program.

This group of studies showed evidence of increased prevalence of
folliculitis and tar warts consistent with prolonged exposure to coal
tar products. The only chronic health effect observed was an excess of
restrictive respiratory deficit. No excess cancer occurrence was
reported. The usefulness of results of this study are weakened by the
lack of specificity to creosote exposure, by only 42% participation of
eligible workers, and the lack of individual exposure assessment to coal
tar products.

**NIOSH (1981)**

Following a request from a carpenters' union, NIOSH conducted an
evaluation of exposure among six dock builders engaged in driving
creosote-preserved logs into a river bottom. Health surveys also were
administered for five of the six dock builders.

Breathing zone and area air concentration measurements collected for the
cyclohexane-extractable fraction of the coal tar pitch volatiles ranged
from below the detectable limit to 0.06 mg/m^3^. However, because of
atypical weather conditions on the day of sampling and because the pile
driver was in operation for less than one hour, the industrial hygiene
results were not representative of normal working conditions.

A medical questionnaire was administered to five of the six workers. The
questionnaire covered work conditions and work history, past exposures,
current health problems, medical history, the use of personal protection
and personal hygiene. Questions on health problems focused on skin,
respiratory, gastrointestinal, and central nervous system problems. The
five participating workers were also given skin examinations. The pile
drivers were between 24 and 61 years of age (average age 44.6 years),
and all had worked at the current site for at least five months. All of
the participants had been employed as pile drivers for an average of
16.6 years of which an average of 8.3 years had involved pile-driving
creosote-preserved piles. A number of health problems were reported by
the workers, including eye irritation, nausea, lightheadedness, and
swelling of the face, eyes, and hands. Skin problems reported by the
workers included irritation, rashes, erythema, burning, dryness,
desquamation, itching, and cracking. On hot days, symptoms were reported
to be worse, and in addition, the workers experienced tearing and
burning eyes, red eyes, swollen or puffy eyes, and photophobia. Four of
the five workers responding to the questionnaire reported that their
visual acuity had gradually worsened.

Skin examinations of the workers revealed erythema on the face, neck and
hands, dry skin with desquamation in sun exposed areas, black comedones,
plugged hair follicles on hands and forearms, and mild folliculitis on
the forearms.

The symptoms reported by the dock building workers and the observations
made during skin examinations were consistent with phototoxic skin
reactions. The folliculitis was consistent with prolonged and direct
contact with creosote. No chronic health effects, including cancers,
were reported or observed, and because of the small number of workers
examined, encountering these diseases would not be expected.

**EPA (1981a)**

A broad health evaluation was performed in 1981 on 59 workers (total of
79 workers eligible) at a wood preservative treatment plant in Ohio. The
workers (51 males, eight females) were aged between 20 and 69 years,
with only a slightly higher frequency of workers aged between 55 and 59
years. Creosote had been used at the plant since the 1920s, but had been
discontinued in 1979. A large battery of tests including chest x-rays,
pulmonary function tests, clinical chemistry analyses, hematology and
urology analyses, and sputum and urine cytology were used to assess
effects on organs and body systems known to be at risk from exposure to
chemicals used in the plant. No industrial hygiene monitoring data were
available, and no exposure assessments for individual participants were
made.

Fifteen workers were observed with restrictive or obstructive
respiratory deficits. One participant had elevated serum enzyme levels
indicative of liver disease. Two workers had proteinuria and one other
had evidence of urinary tract inflammation. Thirteen workers were found
to have elevated serum triglycerides, but only one with levels above
400mg/100ml.

This study identified no occupationally related disease and showed
little evidence of chronic effects from working for long periods in a
wood preservative treatment plant. The small size of the study cohort
and the lack of assessment of individual exposures, including the
absence of data on number of years employed, seriously limited the
possibility of observing negative health effects.

**[EPA (1986)]{.underline}**

A cross-sectional study was conducted on 113 of the total 140 workers at
a lumber preservative treatment plant. Thirty-nine of the participants
worked less than one year, 40 had worked between one and 10 years, and
34 had worked between 11 and 35 years. The plant had used creosote,
creosote/tar solution, Wolman salt (CCA), and pentachlorophenol (PCP)
for many years since 1946 as wood preservatives. A fire retardant, NCX,
also was used since 1978. The study focused on creosote and PCP since
these were considered the chemicals of concern.

Health effects from working at the wood treatment plant were evaluated
by a battery of tests including chest x-ray, pulmonary function test,
clinical chemistry analysis, hematology and urology analyses, and sputum
and urine cytology studies. Detailed medical and work history
questionnaires were administered, however, no individual exposure
assessment was conducted. Air concentrations for coal-tar pitch
volatiles were available from a single industrial hygiene survey
conducted in 1978.

No evidence of skin cancer, bladder cancer, or lung cancer were seen in
the study population. Pustular eruptions likely related to exposures at
the plant were observed in a greater than expected number of workers. A
number of workers had restrictive or obstructive pulmonary deficits, and
two workers showed evidence of liver disease. There was no evidence of
kidney disease or blood disease.

This study showed little evidence of chronic effects from working for
long periods in a wood preservative treatment plant. The small size of
the study cohort and the lack of assessment of individual exposures
limited the possibility of observing negative health effects.

**6.2 Cohort Studies Associated with Health Effects of Creosote in
Humans**

**EPA, (1981b and 1982)**

An in-depth study of mortality in 4048 males who worked at eight Koppers
coal tar plants was conducted by Tabershaw Occupational Medicine
Associates and reported by Koppers in 1981. The plants were located in
Illinois, West Virginia, California, New Jersey (two plants), Texas,
Alabama, and Ohio; and all plants except for one of the New Jersey
plants distilled crude coal tar. Creosote was among the distillation
by-products resulting from the plants' operations . The cohort was
initially defined as all males who worked at least 10 days between 1946
and 1977. Persons who worked in strictly clerical or secretarial
positions were excluded, as were women because of their small number.

The cohort consisted of 2,150 workers (53.1%) known to be white, 1,104
workers (27.3%) known to be black, and 794 workers (19.6%) whose race
was unknown. Demographic information including date of hire, date of
termination, and complete work history was collected from plant
personnel files. Vital status follow-up information was collected by
using plant records, SSA, motor vehicle bureaus, and finally local phone
directories. The total cohort provided 64,600 person-years of
observation with 9,917 person-years attributed to workers whose race was
unknown. Of the total cohort, 703 (17.4%) were identified as deceased,
and the vital status of 359 (8.9%) remained unknown.

During the analysis of the 1981 study, it was recognized that the lack
of race information for almost 20% of the cohort presented a serious
weakness in the study and imposed considerable difficulties with the
interpretation and validity of results. This was further complicated by
the fact that 163 of the workers classified as "race unknown" also had
unknown vital status. Because of this weakness, a re-analysis of data
for only those workers whose race was verified was performed in 1982,
therefore, the results from the 1981 study are not presented here. The
redefined cohort excluded the 794 workers with unknown race. The number
of person-years of follow-up was 36,635 for the white workers and 18,047
for the black workers. Within the cohort, 701 deaths had occurred by the
close of the study (12/31/77), and death certificates were retrieved for
632 workers (359 white, 273 black).

The second analysis looked at cause-specific deaths for six subgroups of
the total population of workers with known race. These groups were (1)
all white workers, (2) white workers employed for less than six months,
(2) white workers employed for six months or more, (4) all black
workers, (5) black workers employed for less than six months, (6) black
workers employed for six months or more.

For the entire population of white workers, the standard mortality r

atio (SMR) for all causes was 109. However, the SMR for deaths from all
cancers was considerably elevated (SMR=126) largely due to the
significant excess in cancers of the lung (SMR=160, p=0.05). Excesses
also were observed for cancers of the stomach, large intestine, rectum,
bladder, and kidney, however, none of the SMRs were statistically
significant. When only white workers employed for less than six months
were considered, a large excess in total mortality was observed
(SMR=137, p=0.01), and the SMR for deaths from all cancers was 125,
though not significant. The increases in overall mortality were due
largely to significant excesses in deaths from cirrhosis of the liver
(SMR=340, p=0.01), accidents (SMR=238, p=0.01), and cancer of the
stomach (four observed, 0.74 expected, SMR=540, p=0.05). When only white
workers employed for six months or more were considered, the only
significant excesses observed were for cancer of the respiratory system
(SMR=182, p=0.01), largely due to an excess of lung cancer (SMR=180,
p=0.01). Deaths from all other cause-specific cancers were within
expected numbers.

For the combined population of black workers, a number of statistically
significant excesses (p=0.05) were found, including deaths from all
causes (SMR=113), all cancers (SMR=138), cancer of the rectum (SMR=439),
and lung cancer (SMR=173). The number of deaths from accidents,
poisoning, and violence were also highly elevated (SMR=186, p=0.01).
When only black workers employed for less than six months were
considered, large excesses were seen for total mortality (SMR=154,
p=0.01), for deaths from all cancers (SMR=171, p=0.05), and for
accidents (SMR=241, p=0.01). The SMR for cancer of the respiratory
system was significantly increased (226, p=0.05), influenced greatly by
the SMR for lung cancer (SMR=243, p=0.01). The SMR for cancer of the
esophagus was also greatly increased (326), though it was based on only
three deaths with 0.92 expected. When only black workers employed for
more than six months or more were considered, the SMR for all causes of
death was 90, and the only significant excess observed was for bladder
cancer (SMR=531, p=0.05) based on three deaths. Nonsignificant excesses
also were observed for deaths from all cancers and several specific
diseases, including cancers of the digestive system and skin, diseases
of the hematopoietic system, and accidents. None of the excesses were
statistically significant and were based on small numbers of deaths.
Overall, mortality in the group of black workers employed six months
were higher than in the black workers employed less than six months.

This study provided a large amount of mortality data on a reasonably
large occupational cohort. Moderately convincing evidence is presented
that employment at the eight coal tar distillation plants may result in
increased risk of death from a range of malignancies. The study appeared
to be well planned and executed, though the validity of the findings is
limited by a number of shortcomings. These include the lack of race
information on a large fraction of the cohort, the small number of
deaths observed for many of the diseases reported in excess, and the
very crude measure of exposure based only on employment at one or more
of the plants.

**Steineck et al. (1989)**

Steineck, et al. employed a complex job-exposure matrix to estimate
exposure for calculating relative risk for development of renal pelvic
cancer (RPC) or bladder cancer (BC) in a Swedish population. The cohort
was defined as all males born in Sweden, aged 20-64 in 1960, who
reported themselves employed. Cases of renal RPC or BC occurring during
the 19-year study period were identified through the National Swedish
Cancer Registry.

The job-exposure matrix used to determine exposed and unexposed
subpopulations was based on self-reported job-related information
collected in 1960 for census purposes. Based on this information,
subjects were classified into 292 occupational titles and 308 industrial
categories, yielding 292 X 308 possible work tasks. Potential exposure
to 50 single agents or groups of substances were assigned for each
possible work task defined by the matrix. Among the potential exposures
selected for evaluation were most of those cited in the literature as
potential risk factors for the two cancers of interest, and creosote.

Relative risks were calculated after adjusting for age in 1960 (six
categories). For some calculations, adjustments also were made for
marital status, socioeconomic group, and urbanization of residence.
Among the total study population of 1,905,660 persons, 556, 429 were
judged to be exposed to at least one of the selected substances. During
the 19 years of observations within the study, there were 714 cases of
RPC with 542 cases occurring among the unexposed subjects. There were
10,123 cases of BC with 7,432 cases occurring within the unexposed
group. For individuals categorized as exposed to creosote, the relative
risk for BC was 1.4 (95% CI 0.7-2.6) compared to cohort members not
assigned any exposure. It is notable that all of the BC cases
categorized as exposed were leather tanners who were also assigned a
number of other exposures. When adjustments for applied for age, marital
status, socioeconomic group, and degree of urbanization, the relative
risk for BC remained between 1.25 and 1.30.

This study provides very limited evidence of association between
exposure to creosote and occurrence of bladder cancer. Weaknesses
include exposure assessment based solely on self-reported occupational
information from a single census observation, lack of control for
multiple exposures, and no consideration for nonoccupational exposures.

**Karlehagen et al. (1992)**

Karlehagen, et al. studied cancer incidence among 922 men exposed to
creosote at 13 wood impregnating plants in Sweden and Norway. Most
participants worked as impregnators while 36 men repaired or maintained
railroad cars used to transport creosote. Study participants were
employed at least one year between 1950 and 1975, and follow-up was
1958-1985 for the workers in Sweden and 1953-1987 for the workers in
Norway. Cancers were identified through national cancer registries in
both countries. Cancer registration is compulsory in both countries, and
quality and completeness of the registries was considered to be good.

No individual exposure measurements were available for participants,
however, levels of naphthalene and benzo(a)pyrene (major constituents of
creosote) at several of the plants had been determined to be 0.1-11
mg/m^3^ and 0.03μg/m^3^, respectively. Levels for both constituents were
well below accepted exposure limits. Consequently, exposure assessment
for study participants was based on minimum length of employment at
plants known to use creosote regularly. Information on the type of work
performed at each plant was collected through use of a questionnaire
completed by plant personnel, but not by participants. No differences in
exposure conditions among the 13 plants were observed.

The total incidence of cancer was lower than expected with 129 cases
observed and 137 cases expected. Some differences were seen between the
Swedish and Norway subgroups but the differences were small. Increased
risks were observed for lip cancer (SIR=2.50, P=0.05), nonmelanoma skin
cancer (SIR=2.37, P=0.02), and malignant lymphoma (SIR=1.9, P=0.06).
When a latency period of 20 years since first exposure was applied, the
SIRs for lip cancer, nonmelanoma skin cancer, and malignant melanoma
were 3.7, 2.0, and 2.2 respectively. Only the SIR for lip cancer (five
cases observed, 1.34 cases expected) was statistically significant. No
increase in the incidence of lung cancer was observed in this
population, with or without consideration for time since first exposure.

This study presents reasonable evidence that exposure to creosote, as
measured by employment at creosote plants, is likely associated with
development of nonmelanoma skin cancer. Increased risks of lip cancer
and malignant melanoma (Norway subgroup only), and malignant lymphoma
were also observed in the study population, but the risks were not
statistically significant. Because the workers in the study worked
outdoors part of the time, the validity of the associations observed,
particularly for lip cancer, nonmelanoma skin cancer, and malignant
melanoma, may be weakened.

**6.3 Case Control Studies Associated with Health Effects of Creosote in
Humans**

**Flodin et al. (1987)**

Risk factors for development of multiple myeloma (MM) were investigated
in a study of 131 cases and 431 controls in Sweden. The cases were
identified from records at six hospitals in southeast Sweden and were
required to be less than 81 years of age, of Swedish ethnicity, resident
in the catchment areas of the hospitals at the time of diagnosis, and
capable of responding to a questionnaire. The 131 cases represented
approximately one third of the total number of MM cases occurring in the
area as reported to the cancer registry. The discrepancy between total
number of cases and the number of cases identified from the six
hospitals was attributed to simple administrative record keeping and was
judged to not impose any bias on the study findings. Controls were
randomly selected from population registries for the same catchment
areas from which the cases were drawn. Differences in average age and
distributions of gender were found between cases and controls. The
average age for cases was 64 years and for controls, 58 years. Within
the 131 cases, 57 percent were males; within 431 controls, 46 percent
were males.

Assessment of exposure was through a nine-page questionnaire consisting
of 17 major questions of which 10 related to occupational exposures.
Some of the occupational questions also asked further questions
regarding details of exposures. Reported exposures lasting less than one
year and all reported exposures within five years prior to diagnosis
were ignored in the analyses.

Crude rate ratios were significantly increased for occupational exposure
to creosote (RR=6.0, 95% CI 2.00-18.2), fresh wood, engine exhaust,
farming, and bricklaying. When the cases and controls were stratified
into four age groups, the elevated risk ratios remained for creosote,
fresh wood, and engine exhaust. The increased risks associated with
creosote, engine exhaust, and fresh wood also remained significant when
analyses controlled for confounding effects of other determinants.

This study provides moderate evidence that exposure to creosote, as
measured by self-reporting via mailed questionnaire, may be linked to
development of MM. The association is less convincing because the
numbers of cases and controls reporting exposure to creosote were quite
small. Also, the study suffers the same limits as other studies using
similar assessment methods.

**Persson et al. (1989)**

A case-control study was conducted in Sweden by Persson, et al. to
investigate associations between exposure to creosote and subsequent
development of Hodgkin disease (HD) or non-Hodgkin's lymphoma (NHL).
Cases were 160 patients (101 men, 59 women) with HD or NHL identified
through the registry at Orebro Medical Centre Hospital and diagnosed
between 1964 and 1986. The cases remained alive at least through the
data collection period in 1986 and were required to be at least 20 years
of age at diagnosis, born in Sweden, living in the area of the hospital
at time of diagnosis, less than 80 years of age at time of data
collection, and mentally capable of responding to the study
questionnaire. The 275 controls (157 men, 118 women) were a subset of a
larger set of controls, previously used in earlier studies, randomly
drawn from general population registries in catchment areas of several
hospitals. For the current study, only individuals in the catchment area
from which the patients were drawn were used as controls. The controls
were required to meet the applicable inclusion criteria used for
patients.

Information for assessment of exposures was collected through a nine
page questionnaire mailed to each case and control. Of 17 main
questions, 10 questions addressed occupational exposures with some of
the occupational questions having additional subquestions asking for
details. Questions also were asked about exposures during leisure
activities. Exposures reported for periods of less than one year were
not considered. A latency period between exposure and development of
disease was imposed by considering only exposures within five to 45
years prior to diagnosis for the cases. For the controls, exposures were
only considered if they occurred five to 45 years before the point in
time of selection.

Age ranges for cases and controls were similar; 20-73 for HD, 22-79 for
NHL, and 20-77 for controls. Crude odds ratios (ORs) for both HD and NHL
were increased for exposure to wood preservatives and for exposure to
creosote specifically (OR 10.5 for HD, OR 13.6 for NHL). Although the
numbers of cases and controls exposed to creosote were small, logistic
analyses were performed to control for age at time of case diagnosis,
gender, and two exposure determinants, i.e., farming and exposure to
fresh wood. For HD, the logistic OR for occupational exposure to
creosote was still elevated (OR 10.7, CI 90% 1.1-103). For NHL, the
logistic OR was 9.4 (CI 90% 1.2-69).

Assuming the instrument for exposure assessment and the methodology for
administration was not biased, this study provides good evidence that
exposure to creosote is a risk factor for development of both HD and
HNL. The study is somewhat weakened by the small of number of persons
reporting creosote exposure.

**Feingold et al. (1992)**

Feingold, et al. studied associations between parental exposures and
cancers in children born subsequent to the exposures. The 252 incident
cases, identified from a Colorado cancer registry, were in children 0-14
years of age, diagnosed between 1976 and1983. The cases were compared
with 222 controls selected by random digit dialing in the same
geographical area as the cases and matched on age (+/- three years),
gender, and telephone exchange area.

Assessment of parental exposure was based on job history information
(including job title, industry, and employment dates) collected by
personal interview. A job-exposure matrix, derived from past industrial
hygiene surveys and knowledge of industrial processes, was used to
assign exposures to individuals on the basis of job title and industry
of employment. All jobs held for six months or longer by mothers and
fathers during the year prior to birth of the child were linked to all
chemicals assigned to the job. Analyses were then performed to determine
associations between cancer incidence and parental exposure to a large
number of substances.

Creosote was not identified as an exposure for any of the mothers of
cases or controls. An adjusted odds ratio of 2.5 (CI = 0.8-8.1) was
found for association of fathers' exposure to creosote during the year
prior to birth of children with any type of cancer in the offspring.
When associations between fathers' exposure to creosote and the
incidence of specific cancers in children born subsequently were
investigated, an odds ratio of 3.7 (CI = 0.8-16.6) was observed for
childhood brain cancer. Fathers assigned exposure to creosote were
chiefly in the construction industry or were farmers.

The major limitation of this study is the imprecision of the exposure
assessment. Exposures to individuals with the same job titles and
working in the same industries vary widely. Therefore, assignments of
exposures to specific chemicals, such as creosote, based entirely on job
titles and industries may be invalid for some individuals. Also, the
credibility of occupation information collected from mothers for fathers
is likely to be only 60-80%. However, exposure misclassification
resulting from the lack of individual exposure data, or due to the
necessary use of information from surrogates, is likely to be equal
among parents of cases and controls and therefore, should be
nondifferential.

**Persson et al. (1993)**

A case-control study was conducted in Sweden by Persson, et al. among
124 patients with HD or NHL to reexamine earlier findings of
associations between exposure to creosote and HD and NHL. Cases
diagnosed between 1975 and 1984 were identified through a regional
cancer registry located at a university hospital serving a three county
area. Only men were included in the study, and were required to be at
least 20 year of age, born in Sweden, living in the area of the hospital
at time of diagnosis, less than 80 years of age at time of data
collection and mentally capable of responding to the study
questionnaire. The 204 controls were randomly drawn from general
population registries for the catchment area of the university hospital
from which the patients were drawn. The controls were required to meet
the applicable inclusion criteria used for patients.

Information for assessment of exposures was collected through a nine
page questionnaire mailed to each case and control. Of 17 main
questions, 10 addressed occupational exposures with some of the
occupational questions having additional subquestions. Exposures of less
than one year were not considered, and only exposures five to 45 years
prior to diagnosis were considered pertinent for the cases. For the
controls, the window of time during which exposures were considered had
been determined based on the time of diagnosis of the patients in
earlier studies.

None of the cases, and only four controls reported exposure to creosote.
Assuming a null hypothesis for association of creosote with HD or NHL,
the number of cases expected to report creosote exposure would be 2.4
based on the number of controls reporting creosote exposure and the
ratio of cases to controls. This study shows no evidence of an
association of creosote exposure with these diseases.

**Tynes et al. (1994)**

A nested case-control study was conducted to assess the presence of an
association between exposure to electromagnetic fields existing at
Norwegian railways and occurrence of brain tumors or leukemia in railway
workers. Limited information on exposure to creosote was collected for
analysis as a confounder.

The cohort from which the cases were selected included 13,030 male
railroad workers employed in 1957 on either electric or non-electric
railways and included line workers, outdoor station workers, and
electrical workers. The cases identified from the Norway Cancer Registry
to which all new cancer cases are reported included men diagnosed with
brain tumors or leukemia during the follow-up period between 1958 and
1990. Four or five controls were selected for each case matched on year
of birth. Controls were required to survive to the age at which the
matching case was diagnosed. Information on whether the participants
ever smoked was collected through telephone interviews.

Assessment of exposures to electromagnetic fields for the cases and
controls was based on job titles, work histories, and job descriptions.
Exposures to other potential hazards, including creosote, were estimated
and analyzed as confounders. An exposure matrix was constructed using
categories of exposure frequency (0=never, 1=monthly, 2=weekly, 3=daily)
and years of employment as factors.

No association of brain tumors or leukemia with estimated exposure to
creosote was observed in this study. As is true in many similar studies,
assessment of exposures was based on qualitative information relevant to
jobs and departments, and therefore is not precise, or accurate for any
particular individual.

**Schildt et al. (1999)**

Associations between a number of occupational exposures including
creosote with oral cancer was investigated in a case-control study in
Sweden. The population-based study included 410 verified cases of
squamous cell oral cancer reported to a four-county cancer registry
during 1980-1989 and 410 controls drawn from a national population
registry. Among the cases (175 alive, 235 deceased) were 134 women and
276 men. A control was matched to each case on age, gender, and county
of residence. For deceased cases, deceased controls were selected from
the the National Registry for Causes of Death. In addition to the other
matching criteria, deceased controls also were matched on year of death.

Assessment of exposures was based on information collected through
mailed questionnaires. For deceased participants, the questionnaire was
sent to the next-of-kin in the order of spouse, child, parent, sibling,
or other. The questionnaire included a lifetime work history and other
questions concerning exposure factors of interest for oral cancer.
Exposures associated with occupations held for less than one year were
ignored.

Analysis of association between exposure to creosote and oral cancer
showed no increased risk (OR = 0.5, CI = 0.1-2.0). The reliability of
this result is weakened by the method of exposure assessment and by the
small numbers of individuals exposed (three cases and six controls).

**9.0 REFERENCES**

**[Product Chemistry References]{.underline}**

None American Wood Preservers' Association Standards, 1998, pp 3-4.

None MacKay D. et al., 1992. Illustrated Handbook of Physical-Chemical
Properties and Environmental Fate for Organic Chemicals, Lewis
Publishers.

None Mueller J.G. et al., 1989. Environ. Sci. Technol., Volume 23(10):
1197-1201.

None USEPA Document 540-RS-88-066. Guidance for the Registration of
Pesticide Products containing Coal Tar/Creosote.

None Cited in reference 4 above.

None Cited in reference 4 above.

44141101 Wade, Terry L. 1992. Product Chemistry Methods Development and
Validation for Creosote. Analysis and Certification of Product
Ingredients: Aristech Creosote P1/P13. Pesticide Assessment Guidelines
Reference Series 62. U.S.E.P.A. Pesticide Assessment Guidelines
Subdivision D: Product Chemistry. Unpublished study prepared by
Geochemical and Environmental Research Group, Texas A&M University, for
Aristech Chemical Corporation and John H. Butala, Technical Advisor,
Creosote Council II. July 23, 1992.

44141102 Wade, Terry L. 1992. Product Chemistry Methods Development and
Validation for Creosote. American Wood Preservers Association (AWPA)
Standard Physical Characteristics: Aristech Creosote P1/P13. AWPA
Standard Methods for Analyses of Creosote and Oil-Type Preservatives
(A1-89). U.S.E.P.A. Pesticide Assessment Guidelines Subdivision D:
Product Chemistry. Unpublished study prepared by Geochemical and
Environmental Research Group, Texas A&M University, for Aristech
Chemical Corporation and John H. Butala, Technical Advisor, Creosote
Council II. August 29, 1992.

44141103 Wade, Terry L. 1992. Product Chemistry Methods Development and
Validation for Creosote. Analyses of Physical and Chemical
Characteristics: Aristech Creosote P1/P13. Pesticide Assessment
Guidelines Reference Series 63. U.S.E.P.A. Pesticide Assessment
Guidelines Subdivision D: Product Chemistry. Unpublished study prepared
by Geochemical and Environmental Research Group, Texas A&M University,
for Aristech Chemical Corporation and John H. Butala, Technical Advisor,
Creosote Council II. September 15, 1992.

44141104 Wade, Terry L. 1992. Product Chemistry Methods Development and
Validation for Creosote. Analysis and Certification of Product
Ingredients: Aristech Creosote P2. Pesticide Assessment Guidelines
Reference Series 62. U.S.E.P.A. Pesticide Assessment Guidelines
Subdivision D: Product Chemistry. Unpublished study prepared by
Geochemical and Environmental Research Group, Texas A&M University, for
Aristech Chemical Corporation and John H. Butala, Technical Advisor,
Creosote Council II. July 23, 1992.

44141105 Wade, Terry L. 1992. Product Chemistry Methods Development and
Validation for Creosote. American Wood Preservers Association (AWPA)
Standard Physical Characteristics: Aristech Creosote P2. AWPA Standard
Methods for Analyses of Creosote and Oil-Type Preservatives (A1-89).
U.S.E.P.A. Pesticide Assessment Guidelines Subdivision D: Product
Chemistry. Unpublished study prepared by Geochemical and Environmental
Research Group, Texas A&M University, for Aristech Chemical Corporation
and John H. Butala, Technical Advisor, Creosote Council II. August 29,
1992.

44141106 Wade, Terry L. 1992. Product Chemistry Methods Development and
Validation for Creosote. Analyses of Physical and Chemical
Characteristics: Aristech Creosote P2. Pesticide Assessment Guidelines
Reference Series 63. U.S.E.P.A. Pesticide Assessment Guidelines
Subdivision D: Product Chemistry. Unpublished study prepared by
Geochemical and Environmental Research Group, Texas A&M University, for
Aristech Chemical Corporation and John H. Butala, Technical Advisor,
Creosote Council II. September 15, 1992.

45355601 Sparacino, Charles M. 2000. Product Chemistry for North
American CTM Creosote P1/P13 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45355602 Sparacino, Charles M. 2000. Product Chemistry for North
American CTM Creosote P2 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45355701 Sparacino, Charles M. 2000. Product Chemistry for Western Tar
Products Corp. Creosote P1 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45355702 Sparacino, Charles M. 2000. Product Chemistry for Western Tar
Products Corp. Creosote P2 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45355801 Sparacino, Charles M. 2000. Product Chemistry for KMG-Bernuth,
Inc. Creosote P2 Storage Stability and Corrosion Characteristics.
Unpublished study prepared by Research Triangle Institute. March 31,
2000.

45355802 Sparacino, Charles M. 2000. Product Chemistry for KMG-Bernuth,
Inc. Creosote P1/P13 Storage Stability and Corrosion Characteristics.
Unpublished study prepared by Research Triangle Institute. March 31,
2000.

45355901 Sparacino, Charles M. 1998. Product Chemistry for Trenton
Sales, Inc. Creosote P1/P13 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. October 15, 1998.

45356001 Sparacino, Charles M. 2000. Product Chemistry for Coopers Creek
Chemical Corp. Creosote P2 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45356002 Sparacino, Charles M. 2000. Product Chemistry for Coopers Creek
Chemical Corp. Creosote P1/P13 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45356101 Sparacino, Charles M. 2000. Product Chemistry for Koppers
Industries, Inc. Creosote P1/P13 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45356102 Sparacino, Charles M. 1999. Product Chemistry for Koppers
Industries, Inc. Creosote P2 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. October 26, 1999.

45356201 Sparacino, Charles M. 2000. Product Chemistry for Reilly
Industries, Inc. Creosote P1/P13 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45356202 Sparacino, Charles M. 2000. Product Chemistry for Reilly
Industries, Inc. Creosote P2 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45363901 Sparacino, Charles M. 2000. Product Chemistry for Allied Signal
Incorporated Creosote P1/P13 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45363902 Sparacino, Charles M. 2000. Product Chemistry for Allied Signal
Incorporated Creosote P2 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

**[Toxicology References]{.underline}**

**[BIBLIOGRAPHY]{.underline}**

MRID 43032101: North American P1/P13 Creosote: Acute Oral Toxicity Study
in Rats. Study conducted by IRDC, Mattawan, MI for the Creosote Council
II. Unpublished. HED document no. 011033.

MRID 43032102: North American P1/P13 Creosote: Acute Dermal Toxicity
Study in Rats. Study conducted by IRDC, Mattawan, MI for the Creosote
Council II. Unpublished. HED document no. 011033.

MRID 43032103: North American P1/P13 Creosote: Acute Inhalation Toxicity
Study in Rats. Study conducted by IRDC, Mattawan, MI for the Creosote
Council II. Unpublished. HED document no. 011033.

MRID 43032104: North American P1/P13 Creosote: Eye Irritation Study in
Rabbits. Study conducted by IRDC, Mattawan, MI for the Creosote Council
II. Unpublished. HED document no. 011033.

MRID 43032105: North American P1/P13 Creosote: Primary Dermal Irritation
Test in Rabbits. Study conducted by IRDC, Mattawan, MI for the Creosote
Council II. Unpublished. HED document no. 011033.

MRID 43032106: North American P1/P13 Creosote: Dermal Sensitization
Study (Buehler) in the Albino Guinea Pig. Study conducted by IRDC,
Mattawan, MI for the Creosote Council II. Unpublished. HED document no.
011033.

MRID 43032301: North American P2 Creosote: Acute Oral Toxicity Study in
Rats. Study conducted by IRDC, Mattawan, MI for the Creosote Council II.
Unpublished. HED document no. 011033.

MRID 43032302: North American P2 Creosote: Acute Dermal Toxicity Study
in Rats. Study conducted by IRDC, Mattawan, MI for the Creosote Council
II. Unpublished.

MRID 43032303: North American P2 Creosote: Acute Inhalation Toxicity
Evaluation in Rats.Study conducted by IRDC, Mattawan, MI for the
Creosote Council II. Unpublished. HED document no. 011033.

MRID 43032304: North American P2 Creosote:Eye Irritation Study in Rats.
Study conducted by IRDC, Mattawan, MI for the Creosote Council II.
Unpublished. HED document no. 011033.

MRID 43032305: North American P2 Creosote: Primary Dermal Irritation
Test in Rabbits.Study conducted by IRDC, Mattawan, MI for the Creosote
Council II. Unpublished. HED document no. 011033.

MRID 43032306: North American P2 Creosote: Dermal Sensitization Study
(Buehler) in the Albino Guinea Pig. Study conducted by IRDC, Mattawan,
MI for the Creosote Council II. Unpublished. HED document no. 011033.

MRID 43601001: North American P1/P13 Creosote: Thirteen Week Subchronic
Inhalation Toxicity Study on North American P1/P13 Creosote CTM in Rats:
Study conducted by IRDC, Mattawan, MI for the Creosote Council II.
Report No. 671-016 (1995). Unpublished.

MRID 43600901: North American P2 Creosote: Thirteen Week Subchronic
Inhalation Toxicity Study on North American P2 Creosote CTM in Rats:
Study conducted by IRDC, Mattawan, MI for the Creosote Council II.
Report No. 671-018 (1995). Unpublished.

MRID 43616101: North American P1/P13 Creosote: 90-Day Subchronic Dermal
Toxicity Study in Rats. Study conducted by IRDC, Mattawan, MI for the
Creosote Council II. Report No. 671-013 (1995). Unpublished.

MRID 43616201: North American P2 Creosote: 90 Day Subchronic Dermal
Toxicity Study in Rats. Study conducted by IRDC, Mattawan, MI for the
Creosote Council II. Report No. 671-014 (1993). Unpublished.

MRID 43584201: North American P1/P13 Creosote: Developmental Toxicity
Study in Rats. Study conducted by IRDC, Mattawan, MI for the Creosote
Council II. Report No. 671-020 (1995). Unpublished.

MRID 43584202: North American P2 Creosote: Developmental Toxicity Study
in Rats. Study conducted by IRDC, Mattawan, MI for the Creosote Council
II. Report No. 671-022 (1995). Unpublished.

York, Raymond G. (1994): Developmental Toxicity Study in New Zealand
White Rabbits. Study conducted by IRDC, Mattawan, MI for Koppers
Inductries, Pittsburgh, PA. Report no. 672-002. Unpublished.

York, Raymond G. (1995): Two Generation Reproduction/Fertility Study in
Rats. Study conducted by IRDC, Mattawan, MI for Koppers Inductries,
Pittsburgh,

PA.Report no. 672-006. Unpublished.

MRID 44844401: A 6-Month Dermal Oncogenicity Study of Creosote in Mice.
Study conducted by WIL Research Laboratories, Ashland, OH for Koppers
Industries,

Pittsburgh, PA. Report no. WIL-100005. Unpublished.

McMahon, Timothy F.: Creosote: Report of the Hazard Identification
Assessment Review Committee. May, 1999. HED document no. 013375.
Unpublished.

USEPA, 1984: Wood Preservative Pesticides: Creosote, Pentachlorophenol,
Inorganic Arsenicals. Position Document 4

Agency for Toxic Substances and Disease Registry (1990): Toxicological
Profile for Creosote. U.S. Department of Health and Human Services:
Public Health Service.

Culp, S.J., Gaylor, D.W., Sheldon, W.G., Goldstein, L.S., and Beland,
F.A. (1996): DNA adduct measurements in relation to small intestine and
forestomach tumor incidence during the chronic feeding of coal tar or
benzo\[a\]pyrene to mice. *Polycyclic Aromatic Compounds* 11, 161-168.

Culp, S.J., Gaylor, D.W., Sheldon, W.G., Goldstein, L.S., and Beland,
F.A. (1998): A comparison of the tumors induced by coal tar and
benzo\[a\]pyrene in a 2-year bioassay. *Carcinogenesis* 19(1): 117-124.

Gaylor, D.W., Culp, S.J., Goldstein, L.S., and Beland, F.A. (2000):
Cancer Risk Estimation for Mixtures of Coal Tars and Benzo\[a\]pyrene.
*Risk Analysis* 20(1): 81-85.

Schneider, K., Roller, M., Kalberlah, F., and Schumacher-Wolz, U.
(2002): Cancer Risk Assessment for Oral Exposure to PAH Mixtures. *J.
Appl. Toxicol.* 22: 73-83.

**[Exposure References]{.underline}**

Agency for Toxic Substances and Disease Registry (ATSDR, 1990).
Toxicological Profile for Creosote. U.S. Public Health Service. February
16, 1990.

Agency for Toxic Substances and Disease Registry (ATSDR, 1995).
Toxicological Profile for Creosote. U.S. Public Health Service.

Butala J. H. February, 1999. Creosote Council II memorandum with
attachment to Nader Elkassabany, U.S. Environmental Protection Agency,
Antimicrobial Division.

Creosote Council II, 1998. "Assessment of Potential Creosote Inhalation
and Dermal Exposure Associated with Pressure- Treatment of Wood with
Creosote." Submitted by John H. Buttala, Creosote Council II. Field work
by George M. Singer, Ph.D, American Agricultural Services Inc.
Analytical work by David A. Winkler, EN-CAS Laboratories.

Creosote Council II, 2001. "Assessment of Potential Creosote Inhalation
and Dermal Exposure Associated with Pressure Treatment of Wood with
Creosote." Submitted by John H. Butala, Creosote Council II. Field work
by Mark G. Bookbinder, Ph.D, c/o American Agricultural Services Inc.
Analytical work by Bert Clayton, EN-CAS Laboratories and Stephanie
Guilyard, USX Engineers and Consultants. MRID 453234-01.

Flickinger and Lawrence, 1982. Occupational Health Experience in the
Wood Preserving Industry. Koppers Company, Inc. MRID 447595-02.

Heikkila PR, Hameila M, Pyy L, et al. 1987. Exposure to Creosote in the
Impregnation and Handling of Impregnated Wood. Scand J Work Environ
Health 13:431‑437.

Krygsman, Adrian 1994. "Wood Preservation. An Overview of Biocide Use
and Application." NIOSH (1980a). Industrial Hygiene Report,
Comprehensive Survey of Wood Preservative Treatment Facility at Santa Fe
Centralized Tie Plant, Somerville, Texas. National Institute for
Occupational Safety and Health, Division of Surveillance, Hazard
Evaluations and Field Studies, Cincinnati, OH. (by Todd AS & Timbie CY).
NTIS PB83‑133892.

Markel, H.L.; Ligo, R.N.; Lucas, J.B. 1977. Health Hazard
Evaluation/Toxicity Determination Report 75-117-372. Koppers Company,
Inc. North Little Rock, Arkansas.

NIOSH (1980). Industrial Hygiene Report, Comprehensive Survey of Wood
Preservative Treatment Facility at Santa Fe Centralized Tie Plant,
Sommerville, Texas. National Institute of Occupational Safety and
Health, Division of Surveillance Hazard Evaluations and Field Studies,
Cincinnati, OH. (by Todd AS and Timbie CY). NTIS PB83-133892.

NIOSH (1981a). Industrial Hygiene Report, Comprehensive Survey of Wood
Preservative Treatment Facility at Cascade Pole Company, McFarland
Cascade, Tacoma, Washington. National Institute for Occupational Safety
and Health, Division of Surveillance, Hazard Evaluations and Field
Studies, Cincinnati, OH. (by Todd AS and Timbie CY). NTIS PB82‑174160.

NIOSH (1981b). Health Hazard Evaluation: New York Port Authority,
Brooklyn, New York. U.S. Department of Health and Human Services,
National Institute for Occupational Safety and Health, Cincinnati, OH.
(by Baker D & Fannick N). HHE 80‑238‑931.

Personal Communication, 1998. Personal Communication with industry
experts and members of the Creosote Council II and Pentachlorophenol
Task Force on April, 1998.

*Pentachlorophenol Task Force*

> a\) Mr. John Wilkinson, Vulcan Chemicals, Phone (202) 293-0635.

b\) Mr. Gene Meyer, Vulcan Chemicals, Phone (205) 877-3543.

> c\) Mr. Martin Rollins, H.M. Rollins Co. Inc., Phone (601) 832-1738.

d\) Mr. Herbert Estreicher, Consultant on Task Force, Phone (202)
662-6000.

*Creosote Council II.*

> a\) Dr. John Butala, Consultant for the Creosote Council II, Phone
> (724) 443-0097.
>
> b\) Dr. Mark Bookbinder, Consultant for the Creosote Council II, Phone
> (301) 540-5622.

Personal Communication, 1999. Personal Communication with Dr. Timothy
McMahon, Senior Toxicologist EPA/OPP/AD/RASSB. April 19, 1999.

Pesticide Handler Exposure Database (PHED) Surrogate Exposure Guide,
1997. Estimates of Worker Exposure from the Pesticide Handler Exposure
Database (PHED) Version 1.1. May, 1997.

Rotard W, Mailahn W (1987). Gas Chromatographic-Mass Spectrometric
Analysis of Creosotes Extracted from Wooden Sleepers Installed in
Playgrounds. Anal. Chem. 59:65-69.

SRI. 1993. Directory of chemical producers: United States of America.
SRI International, Menlo Park, CA.

The Environmental Degradation of Creosote, 1998.

http://inweh1.uwaterloo.ca/biol447new/assignments/creo2.html.

United States Environmental Protection Agency (USEPA), 1984. "Wood
Preservative Pesticides: Creosote, Pentachlorophenol, Inorganic
Arsenicals. Position Document 4." Registration Division. Office of
Pesticides and Toxic Substances. Washington, DC. July, 1994.

United States Environmental Protection Agency (USEPA), 1997a. Standard
Operating Procedures for Residential Exposure Assessments. December,
1997. Residential Exposure Assessment Work Group, U.S. Environmental
Protection Agency.

United States Environmental Protection Agency (USEPA), 1997b. Exposure
Factors Handbook. Volume 1. Office of Research and Development.
Washington, DC. EPA/600/P-95/002Fa.

United States Environmental Protection Agency (USEPA), 1998a. Route to
Route Extrapolations. Memorandum from John E. Whalan EPA/OPP/HED to
Margaret Stasikowski, Director EPA/OPP/HED.

United States Environmental Protection Agency (USEPA), 1998b. Creosote
LUIS Database. USEPA Report Run Date 3/09/98.

United States Environmental Protection Agency (USEPA), 1998c.
International Harmonization Position Paper. Antimicrobial Exposure
Databases. An Overview of the NAFTA Member Agencies Regulatory Authority
Over Antimicrobial Pesticides And An Evaluation of Existing Databases
Used in Antimicrobial Exposure Assessments. Prepared by Antimicrobial
Division. Office of Pesticide Programs.

United States Environmental Protection Agency (USEPA), 1998d. Inhalation
Risk Characterizations and the Aggregate Risk Index (ARI). Memorandum
from John E. Whalan, EPA/OPP/HED, to Margaret Stasikowski, Director,
EPA/OPP/HED.

United States Environmental Protection Agency (USEPA), 1998e. Integrated
Risk Information System (IRIS) database.

United States Environmental Protection Agency (USEPA), 1999. Creosote -
Report of the Hazard Identification Review Committee, April 1, 1999.

United States Environmental Protection Agency (USEPA), 2001. Assessment
of Potential

Creosote Inhalation and Dermal Exposure Associated with
Pressure-Treatment of Wood with

Creosote. Office of Pesticides and Toxic Substances, January 30, 2001.

Product Chemistry References

[MRID]{.underline}

None American Wood Preservers' Association Standards, 1998, pp 3-4.

None MacKay D. et al., 1992. Illustrated Handbook of Physical-Chemical
Properties and Environmental Fate for Organic Chemicals, Lewis
Publishers.

None Mueller J.G. et al., 1989. Environ. Sci. Technol., Volume 23(10):
1197-1201.

None USEPA Document 540-RS-88-066. Guidance for the Registration of
Pesticide Products containing Coal Tar/Creosote.

None Cited in reference 4 above.

None Cited in reference 4 above.

44141101 Wade, Terry L. 1992. Product Chemistry Methods Development and
Validation for Creosote. Analysis and Certification of Product
Ingredients: Aristech Creosote P1/P13. Pesticide Assessment Guidelines
Reference Series 62. U.S.E.P.A. Pesticide Assessment Guidelines
Subdivision D: Product Chemistry. Unpublished study prepared by
Geochemical and Environmental Research Group, Texas A&M University, for
Aristech Chemical Corporation and John H. Butala, Technical Advisor,
Creosote Council II. July 23, 1992.

44141102 Wade, Terry L. 1992. Product Chemistry Methods Development and
Validation for Creosote. American Wood Preservers Association (AWPA)
Standard Physical Characteristics: Aristech Creosote P1/P13. AWPA
Standard Methods for Analyses of Creosote and Oil-Type Preservatives
(A1-89). U.S.E.P.A. Pesticide Assessment Guidelines Subdivision D:
Product Chemistry. Unpublished study prepared by Geochemical and
Environmental Research Group, Texas A&M University, for Aristech
Chemical Corporation and John H. Butala, Technical Advisor, Creosote
Council II. August 29, 1992.

44141103 Wade, Terry L. 1992. Product Chemistry Methods Development and
Validation for Creosote. Analyses of Physical and Chemical
Characteristics: Aristech Creosote P1/P13. Pesticide Assessment
Guidelines Reference Series 63. U.S.E.P.A. Pesticide Assessment
Guidelines Subdivision D: Product Chemistry. Unpublished study prepared
by Geochemical and Environmental Research Group, Texas A&M University,
for Aristech Chemical Corporation and John H. Butala, Technical Advisor,
Creosote Council II. September 15, 1992.

44141104 Wade, Terry L. 1992. Product Chemistry Methods Development and
Validation for Creosote. Analysis and Certification of Product
Ingredients: Aristech Creosote P2. Pesticide Assessment Guidelines
Reference Series 62. U.S.E.P.A. Pesticide Assessment Guidelines
Subdivision D: Product Chemistry. Unpublished study prepared by
Geochemical and Environmental Research Group, Texas A&M University, for
Aristech Chemical Corporation and John H. Butala, Technical Advisor,
Creosote Council II. July 23, 1992.

44141105 Wade, Terry L. 1992. Product Chemistry Methods Development and
Validation for Creosote. American Wood Preservers Association (AWPA)
Standard Physical Characteristics: Aristech Creosote P2. AWPA Standard
Methods for Analyses of Creosote and Oil-Type Preservatives (A1-89).
U.S.E.P.A. Pesticide Assessment Guidelines Subdivision D: Product
Chemistry. Unpublished study prepared by Geochemical and Environmental
Research Group, Texas A&M University, for Aristech Chemical Corporation
and John H. Butala, Technical Advisor, Creosote Council II. August 29,
1992.

44141106 Wade, Terry L. 1992. Product Chemistry Methods Development and
Validation for Creosote. Analyses of Physical and Chemical
Characteristics: Aristech Creosote P2. Pesticide Assessment Guidelines
Reference Series 63. U.S.E.P.A. Pesticide Assessment Guidelines
Subdivision D: Product Chemistry. Unpublished study prepared by
Geochemical and Environmental Research Group, Texas A&M University, for
Aristech Chemical Corporation and John H. Butala, Technical Advisor,
Creosote Council II. September 15, 1992.

45355601 Sparacino, Charles M. 2000. Product Chemistry for North
American CTM Creosote P1/P13 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45355602 Sparacino, Charles M. 2000. Product Chemistry for North
American CTM Creosote P2 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45355701 Sparacino, Charles M. 2000. Product Chemistry for Western Tar
Products Corp. Creosote P1 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45355702 Sparacino, Charles M. 2000. Product Chemistry for Western Tar
Products Corp. Creosote P2 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45355801 Sparacino, Charles M. 2000. Product Chemistry for KMG-Bernuth,
Inc. Creosote P2 Storage Stability and Corrosion Characteristics.
Unpublished study prepared by Research Triangle Institute. March 31,
2000.

45355802 Sparacino, Charles M. 2000. Product Chemistry for KMG-Bernuth,
Inc. Creosote P1/P13 Storage Stability and Corrosion Characteristics.
Unpublished study prepared by Research Triangle Institute. March 31,
2000.

45355901 Sparacino, Charles M. 1998. Product Chemistry for Trenton
Sales, Inc. Creosote P1/P13 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. October 15, 1998.

45356001 Sparacino, Charles M. 2000. Product Chemistry for Coopers Creek
Chemical Corp. Creosote P2 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45356002 Sparacino, Charles M. 2000. Product Chemistry for Coopers Creek
Chemical Corp. Creosote P1/P13 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45356101 Sparacino, Charles M. 2000. Product Chemistry for Koppers
Industries, Inc. Creosote P1/P13 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45356102 Sparacino, Charles M. 1999. Product Chemistry for Koppers
Industries, Inc. Creosote P2 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. October 26, 1999.

45356201 Sparacino, Charles M. 2000. Product Chemistry for Reilly
Industries, Inc. Creosote P1/P13 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45356202 Sparacino, Charles M. 2000. Product Chemistry for Reilly
Industries, Inc. Creosote P2 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45363901 Sparacino, Charles M. 2000. Product Chemistry for Allied Signal
Incorporated Creosote P1/P13 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

45363902 Sparacino, Charles M. 2000. Product Chemistry for Allied Signal
Incorporated Creosote P2 Storage Stability and Corrosion
Characteristics. Unpublished study prepared by Research Triangle
Institute. March 31, 2000.

**Environmental Fate References**

Al-Bashir, B. et al. 1990. Appl. Microbiol. Biotech. 34:414-419.

Bauer, J.E. et al. 1985. Appl. Environ. Microbiol. 81-90.

Bauer, J.E. et al. 1988. Appl. Environ. Microbiol. 1649-1655.

Behymer, T.D. and R.A. Hites. 1985. Environ. Sci. Technol.
19(10):1004-1006.

Bestari, K.T. Jim et al. 1998a. Distribution and composition of
polycyclic aromatic hydrocarbons within experimental microcosms treated
with liquid creosote. Environ. Toxicol. Chem. 17(12):2359-2368.

Bestari, K.T. Jim et al. 1998b. Distribution and composition of
polycyclic aromatic hydrocarbons within experimental microcosms treated
with creosote-impregnated douglas fir pilings. Environ. Toxicol. Chem.
17(12):2369-2377.

Bieri, R.H. et al. 1986. Polycyclic aromatic hydrocarbons in surface
sediments from the Elizabeth River subestuary. Int. J. Environ. Anal.
Chem. 26:97-113.

Bouwer, E.J. and P.L. McCarty. 1983. Appl. Environ. Microbiol.
45:1295-1299.

Bouwer, E.J. et al. 1996. Annals of New York Academy of Sciences. pp.
103-115.

Bruner, K.A. et al. 1994. J. Great Lakes Research. 20:725-734.

Callahan, M.A. et al. 1979. Water Related Environmental Fate of 129
Priority Pollutants, EPA-440-4-79-029a,b.

Chapman, P.J. et al. 1995. Fossil Fuel Biodegradation: Laboratory
Studies. Environ. Health Perspec. 103, Supplemental 5:80-83.

Elder, J.F. and P. Dresler. 1988. Accumulation and bioconcentration of
polycyclic aromatic hydrocarbons in a nearshore estuarine environment
near a Pensacola (Florida) creosote contamination site. Environmental
Pollution. 49:117-132.

Electric Power Research Institute (EPRI). 1992. Document EPRI
TR-01000870.

Ehrlich, G.G. et al. 1982. Groundwater. 20(4):703-710.

Flyvberg, J.E. et al. 1993. J. Contamin. Hydrology. 12:133-150.

Fowler, M.G. et al. 1993. Preliminary results from a field experiment
investigating the fate of some creosote components in a natural aquifer.
Org. Geochem. 22:641-649.

Fukuda, K. et al. 1988. Chemosphere. 17(4):651-659.

Gevao, B. and K.C. Jones. 1998. Kinetics and potential significance of
polycyclic aromatic hydrocarbon desorption from creosote-treated wood.
Environ. Sci. Tech. 32:640-646.

Gile, J.D. et al. 1982. J. Agric. Food Chem. 30:295-301.

Godsy, E.M. et al. 1992. Ground Water. 30(2):232-242.

Goerlitz, D.F. et al. 1985. Environ. Sci. Tech. 19(10):955-961.

Grbic-Galic, D. et al. 1991. Anaerobic degradation of aromatic
hydrocarbons and aerobic degradation of trichloroethylene by subsurface
microorganisms. In: Organic Substances and Sediments in Water, R.A.
Baker, Ed., Lewis Publishers, Michigan:239-266.

Harris, J.C. 1982. Handbook of Chemical Property Estimation Methods.
W.J. Lyman, W.F. Reehl, D.H. Rosenblatt, Eds. McGraw-Hill Book Company,
New York: Chapters 7-8.

Hellou, J.G. et al. 1990. Polycyclic aromatic hydrocarbons in muscle
tissue of marine mammals from the Norhtwest Atlantic. Marine Pollution
Bulletin. 21(10):469-473.

Howard, P.H., R.S. Boethling, W.F. Jarvis, W.M. Meylan, E.M. Michalenco,
Eds. 1991. Handbook of Environmental Degradation Rates, Lewis
Publishers, Inc. Chelsea, Michigan, USA.

Hurst, C.J. et al. 1996. Polycyclic aromatic hydrocarbon biodegradation
as a function of oxygen tension in contaminated soil. J. Haz. Materials.
51:193-208.

Karthikeyan, R. and A. Bhandari. 2001. Anaerobic biotransformation of
aromatic and polycyclic aromatic hydrocarbons in soil microcosms: a
review. Journal of Hazardous Substance Research. 3:3-19.

Kirso, U. et al. 1991. Photochemical oxidation of PAH and heteroaromatic
analogues in different model conditions. Polycyclic Aromatic
Hydrocarbons: Proceedings of the Thirteenth International Symposium on
Polynuclear Aromatic Hydrocarbons.

Kuhn, E.P. et al. 1988. Appl. Environ. Microbiol. 54:490:496.

Lindhardt, B. and T.H. Christensen. 1996. Volatilisation of aromatic
hydrocarbons from soil: part II, fluxes from coal tar contaminated soils
residing below the soil surface. Water Air Soil Pollution. 92:375-389.

Long, E.R. et al. 1995. Incidence of adverse biological effects within
ranges of chemical concentrations in marine and estuarine sediments.
Environ. Management. 19:81-97.

Mabey, W. et al. 1982. Aquatic Fate Process for Organic Priority
Pollutants. EPA Report No. 440/4-81-14.

Mattraw, H.C. and B.J. Frank. 1986. Movement and fate of creosote waste
in ground water, Pensacola, Florida; U.S. Geological Survey toxic waste
\-- ground-water contamination program. U.S. Geological Survey Water
Supply Paper No.: 2285.

McGroddy, S.E. and J.W. Farrington. Sediment porewater partitioning of
polycyclic aromatic hydrocarbons in three cores from Boston Harbor,
Massachusetts. Environ. Sci. Technol. 29(6):1542-1550.

Merril, E.G. and T.L. Wade. 1985. Carbonized coal products as a source
of aromatic hydrocarbons to sediments from a highly industrialized
estuary. Environ. Sci. Technol. 19:597-603.

Middaugh, D.P. et al. 1991. Archives of Environ. Contamin. pp. 244-254.

Mihelcic, J.R. et al. 1988. Appl. Environ. Microbiol. 54:1182-1187.

Mill, T. et al. 1981. Chemosphere. 10:1283-1293.

Miller, M.M. et al. 1985. Environ. Sci. Technol. 19:522-529.

Mississippi State University. 1981. Cooperative Agreement Number 12-156.

Mueller, J.G. et al. 1991. Biodegradation of creosote in contaminated
groundwater: chemical and biological assessment. Applied and
Environmental Microbiology. 57(5):1277-1285.

Mueller, J.G. et al. 1993. Strategy using bioreactors and specially
selected microorganisms for bioremediation of groundwater contaminated
with creosote and pentachlorophenol. Environ. Sci. Technol.
27(4):691-698.

National Oceanic and Atmospheric Administration (NOAA). 1988. A Selected
Summary of Data of Chemical Contaminants in Sediments Collected During
1984-1987, NTIS.

Neff, J.M. et al. 1976. Marine Biology. Volume 38:279-289.

Padma, T.V. et al. 1999. Toxicity of creosote water-soluble fractions
generated from contaminated sediments t the bay mysid. Ecotoxicology and
Environmental Safety. 42:171-176.

Politzer, I.R. et al. 1985. Impact on Human Health of Petroleum in the
Marine Environment, American Petroleum Institute (API), Washington, DC.

Priddle, M.W. and K.T.B. MacQuarrie. 1994. Dissolution of creosote in
groundwater: an experimental and modeling investigation. Journal of
Contaminant Hydrology. 15:27-56.

Rutherford, P.M., M.R. Gray, and M.J. Dudas. 1997. Desorption of
\[^14^C\]naphthalene from bioremediated soils contaminated with creosote
compounds. 31:2515-2519.

Sharak Genther, B.R. et al. 1977. Arch. Environ. Contamin. Toxicol.
32:99-105.

Shocken, M.J. et al. 1984. Bacterial oxidation of the polycyclic
aromatic hydrocarbons acenaphthene and acenaphthylene. Appl. Environ.
Microbiol. 48(1):10-16.

Smith, J.H. et al. 1978. Environmental Pathways of Selected Chemicals in
Fresh Water Systems: Part II. Laboratory Studies: 304. EPA-600/7-78-074,
USEPA, Athens, Georgia.

Southworth, R.G. 1977. Aquatic Toxicology, ASTM ATP 667. L.L. Marking,
R.A. Kimerle, Eds., American Society for Testing and Materials: 359-380,
Philadelphia.

Southworth, G.R., J.J. Beauchamp, and P.K. Schmieder, 1978. Water
Research. 12:973-977.

Spacie, A. et al. 1983. Uptake, depuration, and biotransformation of
anthracene and benzo\[a\]pyrene in bluegill sunfish. Ecotoxicology and
Environmental Safety. 7:330-341.

Stegman, J.J. and J.M. Teal. 1973. Marine Biology. 22:37-44.

Tay K.L. et al. 1992. Sediment bioassessment in Halifax Harbour.
Environmental Toxicology and Chemistry. 11:1567-1581.

Verasani, U. et al. 1978. Toxicol. Appl. Pharmacol. 44:277-289.

Villholth, K.G. 1999. Colloid characterization and colloidal phase
partitioning of polycyclic aromatic hydrocarbons in two
creosote-contaminated aquifers in Denmark. Environ. Sci. Technol.
33:691-699.

Wan, M.T. 1994. Utility right-of-way contaminants: polycyclic aromatic
hydrocarbons. J. Environ. Quality. 23:1297-1304.

Webb, D.A. No date available. Creosote, its use as a wood preservative
in the railroad transportation industry with environmental
considerations. American Wood Preserver's Association.

Wendt, P.H. et al. 1996. Wood preservatives leachates from docks in an
estuarine environment. Arch. Environ. Contamin. Toxicol. 31:24-37.

Zepp, R.G. et al. 1980. Assessing the photochemistry of organic
pollutants in aquatic environments. In, Dynamics, Exposure and Hazard
Assessment of Toxic Chemicals. R. Haque, Ed. Ann Arbor Sci. Publ. Inc.,
Ann Arbor, Michigan: 69-110.

**Ecological Toxicity References**

Brooks, K.M. 2004. Polycyclic aromatic hydrocarbon migration from
creosote-treated railway ties into ballast and adjacent wetlands. USDA.
Forrest Service. Research paper FPL-RP-617

EPA, 2006. "PE5 User's Manual for PRZM EXAMS Modeling Shell, Version
5.0." Environmental Fate and Effects Division. Office of Pesticide
Programs, U.S. Environmental Protection Agency. November 15 2006.

Parker, Ronald. 2007. Office of Pesticide Programs. U.S. Environmental
Protection Agency. Personal communication with ICF. November.

Anderson, J.W., J.M. Neff, B.A.Cox, H.E.Tatem, and G.M. Hightower. 1974.
The effects of oil on estuarine animals: Toxicity, uptake and
depuration, respiration. In: F.J. Vernberg and W.B.Vernberg (Eds.),
Polution and Pysiology of Mar. Organisms, Academic Press, NY :285-310.

Bestari, K.T. Jim, R.D. Robinson, K.R. Solomon, T.S. Steele, K.E. Day
and P.K. Sibley. 1998. Distribution and composition of polycyclic
aromatic hydrocarbons within experimental microcosms treated with
creosote-impregnated Douglas fir pilings. Environ. Toxicol. Chem.
17(12):2369-2377.

Brooke, L.T. 1991. Results of freshwater exposures with the chemicals
atrazine, biphenyl, butachlor, carbaryl, carbazole, dibenzofuran,
3,3'-dichlorobenzidine, dichlorvos, 1,2-epoxyethylbenzene (Styene
Oxide), isophorone, isopropalin (truncated). Ctr. For Lake Superior
Environ. Stud., U. Of WI-Superior, Superior, WI: 110 p.

Brooke, L.T. 1993. Conducting toxicity tests with freshwater organisms
exposed to dieldrin, fluroanthene, and phenanthrene. US EPA contract no
68-C1-0034, work assignment No 5 to R.L. Spehar, Duluth, MN.

Brooks, K.M. 2000. Assessment of the environmental effects associated
with wooden bridges preserved with creosote, pentachlorophenol, or
chromated copper arsenate. Res. Paper FPL-RP-587. Madison, WI: U.S.
Department of Agriculture, Forest Service, Forest products Laboratory.
100 p.

Brooks, K.M. 2004. Polycyclic aromatic hydrocarbon migration from
creosote-treated railway ties into ballast and adjacent wetlands. Res.
Paper FPL-RP-617. Madison, WI: U.S. Department of Agriculture, Forest
Service, Forest products Laboratory. 53 p.

Cairns, M.A., and A.V. Nebeker. 1982. Toxicity of acenaphthene and
isophorone to early stages of fathead minnows. Arch. Environ. Contam.
Toxicol. 11(6):703-707.

Call, D.J., L.T. Brooke, S.L. Harting, S.H. Poirier, and D.J. McCauley.
1986. Toxicity of phenanthrene to several freshwater species. Final
report to Battelle Research Institute, Columbus, OH. Center for Lake
Superior Environmental Studies, University of Wisconsin-Superior. 18 pp.

Canadian Institute of Treated Wood - Western Wood Preservers Institute.
1997. Best Management Practices for the Use of Treated Wood in Aquatic
Environments. Developed For Use In Specifying Materials For Use In
Aquatic Projects in Canada and the Western United States.

Carls, M.G., S.D. Rice and J.E. Hose. 1999. Sensitivity of fish embryos
to weathered crude oil: Part I. Low-level exposure during incubation
causes malformations, genetic damage, and mortality in larval Pacific
herring (*Clupea pallasi*). Environ. Toxicol. Chem. 18:481-493.

Champlin, D.M. and S.L. Poucher. 1991. Chronic toxicity of fluoranthene
to the mysid, *Mysidopsis bahia*. Memorandum to D.J. Hansen, USEPA.

DeWitt, T.H., M.S. Redmnod, J.E. Sewall, and R.C. Swarz. 1992.
Development of a chronic sediment toxicity test for marine benthic
amphipods. US EPA-Erlin, Newport, OR

De Witt, T.H., R.C. Swartz, and J.O. Lamberson. 1989. Measuring the
acute toxicity of estuarine sediments. Environ. Toxicol. Chem.
8:1035-1048.

Diamond, S.A., J.T. Oris, and S.I. Guttman. 1995. Adaptation to
fluoranthene exposure in a laboratory population of fathead minnows.
Environ. Toxicol. Chem. 14(8):1393-1400.

EPA. 1993a. Sediment Quality Criteria for the Protection of Benthic
Organisms: Fluoranthene. USEPA Office of Water and Office of Research
and Development, Washington, DC, EPA-822-R-93-012, September, 1993. 102
pp.

EPA. 1993b. Sediment Quality Criteria for the Protection of Benthic
Organisms: Phenanthrene. USEPA Office of Water and Office of Research
and Development, Washington, DC, EPA-822-R-93-014, September, 1993. 86
pp.

EPA. 1993c. Sediment Quality Criteria for the Protection of Benthic
Organisms: Acenaptrene. USEPA Office of Water and Office of Research and
Development, Washington, DC, EPA-822-R-93-013, September, 1993. 94 pp.

Gendusa, A.C. 1990. Toxicity of chromium and fluroanthene from aqueous
and sediment sources to selected freshwater fish. Ph.D. Thesis, Univ. of
North Texas: 138 p.

Goyette, D. and K.M. Brooks. 2001. Addendum Report: Continuation of the
Sooke Basin Creosote Evaluation Study (Goyette and Brooks, 1998); Year
four -- Day 1360 & Day 1540. Prepared for: Creosote Evaluation Steering
Committee Regional Program, Report PR00-03, May 12, 2001.

Goyette, D. and K.M. Brooks. 1998. Creosote Evaluation: Phase II Sooke
Basin Study - Baseline to 535 Days Post Construction 1995-1996. Prepared
for: Creosote Evaluation Steering Committee Regional Program, Report
PR98-04, December, 1998.

Hatch, A.C. Jr. 1999. Photo-induced toxicity on PAHs to *Hyalella
azteca* and *Chironomus tentans*: Effects of mixture and behavior.
Environ.Pollut. 106(2):157-167.

Heintz, R. A., J. W. Short, and S. D. Rice. 1999. Sensitivity of fish
embryos to weathered crude oil: Part II. Increased mortality of pink
salmon (*Oncorhynchus gorbuscha*) embryos incubating downstream from
weathered Exxon Valdez crude oil. Environ. Toxicol. Chem. 18(3):
494-503.

Heitmuller, P.T., T.A. Hollister, and P.R. Parrish. 1981. Acute toxicity
of 54 industrial chemicals to sheepshead minnows. Bull. Environ. Contam.
Toxicol. 27(5):596-604

Holcombe, G.W., G. Phipps, and J.T. Fiandt. 1983. Toxicity of selected
priority pollutants to various aquatic organisms. Ecotoxicol. Environ.
Saf. 7(4):400-409.

Horne, J.D., M.A. Swirsky, T.A. Hollister, B.R. Oblad, and J.H. Kennedy.
1983. Aquatic toxicity studies of five priority pollutants. Report No.
4398, EPA Contract No. 68-01-6201, NUS Corp., Houston, TX. 93 pp.

Howard, P.H., R.S. Boethling, W.F. Jarvis, W.M. Meylan, E.M. Michalenco,
Eds. 1991. Handbook of Environmental Degradation Rates, Lewis
Publishers, Inc. Chelsea, Michigan, USA.

Hutton, K.E. and S.C. Samis. 2000. Guidelines to protect fish habitat
from treated wood used in aquatic environments in the Pacific region.
Canadian Tech. Rep. Fisheries and Aquatic Sci. 2314. Habitat and
Enforcement Branch, Fisheries and Ocenas Canada, Vancouver, BC.

Ingram Jr., L.L, G.D. McGinnis, L.R. Gjovik and G. Roberson. 1982.
Migration of creosote and its components from treated piling sections in
a marine environment. Proc. Annual Meeting Amer. Wood-Preserver's Asso.
78:120-128.

Kagan, J., E.D. Kagan, I.A. Kagan, and P.A. Kagan. 1987. Do Polycyclic
Aromatic Hydrocarbons, Acting as Photosensitizers, Participate in the
Toxic Effects of Acid Rain? In: W.J.Cooper and R.G.Zika (Eds.),
Photochemistry of Environmental Aquatic Systems, Chapter 14,
m.Chem.Soc.Symp.Ser.No.327, Washington, D.C.:191-204

Karrow, N.A., H.J. Boermans, D.G. Dixon, A. Hontella, K.R. Solomon, J.J.
Whyte, and N.C. Bols. 1999. Characterizing the immunotoxicity of
creosote to rainbow trout (*Oncorhynchus mykiss*): a microcosm study.
Aquatic Toxicol. 45:223-239.

Korn, S., D.A. Moles, and S.D. Rice. 1979. Effects of temperature on the
median tolerance limit of pink salmon and shrimp exposed to toluene,
naphthalene, and Cook Inlet crude oil. Bull.Environ.Contam.Toxicol.
21(4/5):521-525.

Kuhn, A. and S. Lussier. 1987. Phenanthrene results of acute and chronic
tests (flow-thru) with *Mysidopsis bahia*. Memorandum to D.J. Hansen,
August 3, 1987. 3 pp.

Mayer, F.L., Jr., and M.R. Ellersieck. 1986. Manual of Acute Toxicity:
Interpretation and Data Base for 410 Chemicals and 66 Species of
Freshwater Animals. Resour. Publ. No. 160, U.S. Dept. of the Interieo,
US FWS, Wash., DC:505 p.

McCloskey, J.T., and J.T. Oris. 1991. Effect of water temperature and
dissolved oxygen concentration on the photo-induced toxicity of
anthracene to juvenile bluegill sunfish (*Lepomis macrochirus*).
Aquat.Toxiol. 21:145-156.

Moore, M.N., D.R. Livingston, and J. Widdows. 1989. Hydrocarbons in
marine mollusks: biological effects and ecological consequences. In:
Metabolism of Polycyclic Aromatic Hydrocarbons in the Aquatic
Environment. U. Varanasi, ed., Boca Raton, FL, CRC Press, Inc. 321 pp.

NAS. 1982. Round robin testing of the midge (Tanytarsus): acute and
chronic toxicity tests of 2,4,6-trichlorophenol and acenaphthene.
Northwestern Aquatic Sciences, Inc., Newport, OR report to USEPA,
ERL-Duluth, MN. 66 pp.

Neff, J.M. 1979. Polycyclic aromatic hydrocarbons in the aquatic
environment; sources, fates and biological effects. London: Applied
Science Publishers LTD. ISPN 0-85334-832-4.

Oris, J. T. and J. P. Giesy. 1987. The photo-induced toxicity of
polycyclic aromatic hydrocarbons to larvae of the fathead minnow
(*Pimephales promelas*). Chemosphere 16:1395-1404.

Padma, T.V., R.C. Hale, and M.H. Roberts, Jr. 1998. Toxicity of
water-soluble fractions derived from whole creosote and
creosote-contaminated sediments. Environ. Toxicol. Chem. 17:1606-1610.

Pastorok, R.A., D.C. Peek, J.R. Sampson, and M.A. Jacobson. 1994.
Ecological risk assessment for river sediments contaminated by creosote.
Environ. Toxicol. Chem. 13:1929-1941.

Pelletier, M.C., R.M. Burgess, K.T. Ho, A. Kuhn, R.A. McKinney, and S.A.
Ryba. 1997. Phototoxicity of individual polycyclic aromatic hydrocarbons
and petroleum to marine invertebrate larvae and juveniles. Environ.
Toxicol. Chem. 16:2190-2199.

Poston, T. 2001. Treated Wood Issues Associated with Overwater
Structures in Marine and Freshwater Environments. White Paper submitted
by Battelle to the Washington Department of Fish and Wildlife,
Washington Department of Ecology, and Washington Department of
Transportation. 96 pp.

Rice, S.D. and R.E. Thomas. 1989. Effedct of pre-treatment exposures of
toluene or naphthalene on the tolerance of pink salmon (*Oncorhynchus
gorbuscha*) and kelp shrimp (*Eualis suckleyi*). Comp.Biochem.Physiol.C
94:289-293.

Rossi, S. and J.M. Neff. 1978. Toxicity of polynuclear aromatic
hydrocarbons to the polychaete *Neanthes arenaceodentata*. Mar. Pollut.
Bull. 9:220-223.

SCI. 2005. Creosote-treated wood in aquatic environments: technical
review and use recommendations. Prepared for NOAA Fisheries, Santa Rosa,
CA by Stratus Consulting Inc., Boulder, CO with Duke University, Durham,
NC.

Sibley, P.K., M.L. Harris, K.T. Bestari, T.A. Steele, R.D. Robinson,
R.W. Gensemer, K.E. Day, and K.R. Solomon. 2001a. Response of
zooplankton communities to liquid creosote in freshwater microcosms.
Environ. Toxicol. Chem. 20:394-405.

Sibley, P.K., M.L. Harris, K.T. Bestari, T.A. Steele, R.D. Robinson,
R.W. Gensemer, K.E. Day, and K.R. Solomon. 2001b. Response of
phytoplankton communities to liquid creosote in freshwater microcosms.
Environ. Toxicol. Chem. 20:2785-2793.

Spehar, R.L., S. Poucher, L.T. Brooke, D.J. Hansen, D. Champlin, and
D.A. Cox. 1999. Comparative toxicity of fluoranthene to freshwater and
saltwater species undr fluorescent and ultraviolet light. Arch. Environ.
Contam. Toxicol. 37(4):496-502.

Suedel, B.C., J.H. Rodgers, Jr., and P.A. Clifford. 1993.
Bioavailability of fluoranthene in freshwater sediment toxicity tests.
Environ. Toxicol. Chem. 12(1):155-165.

Swartz, R.C., D.W. Schuts, T.H. DeWitt, G.R. Ditsworth, and J.O.
Lamberson. 1990. Toxicity of fluoranthene in sediment to mrine
amphipods: A test of the equilibrium partitioning approach to sediment
quality criteria. Environ. Toxicol. Chem. 9(8):1071-1080.

Swartz, R.C. 1999. Consensus sediment quality guidelines for polycyclic
aromatic hydrocarbon mixtures. Environ. Toxicol. Chem. 18:780-787.

Swartz, R.C. 1991. Acenaphthene and phenanthrene files. Memorandum to D.
J. Hansen, June 26, 1991. 160 pp. \[in EPA 1993c\]

Tagatz, M.E., G.R. Plaia, C.H. Deans, and E.M. Lores. 1983. Toxicity of
creosote-contaminated sediment to field- and laboratory-colonized
estuarine benthic communities. Environ. Toxicol. Chem. 2:441-450.

Thursby, G.B., W.J. Berry, and D. Champlin. 1989. Flow-through acute and
chronic tests with acenaphthene using *Mysidopsis bahia*. Memorandum to
D.J. Hansen, September 19, 1989. 5 pp. \[in EPA 1993c\]

Trucco, R.G., F.R. Engelhardt, and B. Stacey. 1983. Toxicity,
accumulation, and clearance of aromatic hydrocarbonbs in *Daphnia
pulex*. Environ. Pollut. Ser. A 31(3):191-202.

Valle, S., M.A. Panero and L. Shor. 2007. Pollution Prevention and
Management Strategies for Polycyclic Aromatic Hydrocarbons in the New
York/New Jersey Harbor. New York Academy of Science, New York. 171 pp.

van Brummelen, T.C., B. van Hattum, T. Crommentuijn, and D. F. Kalf.
1998. Bioavailability and Ecotoxicty of PAH. In: Neilson, A. H. (ed.).
PAH and Related Compounds -- Biology. (Vol. 3-J, The Handbook of
Environmental Chemistry). Springer-Verlag, Berlin Heidenberg. pp.
203-263.

Vines, C.A., T. Robbins, F.J. Griffin, and G.N. Cherr. 2000. The effects
of diffusible creosote-derived compounds on development in Pacific
herring (*Clupea pallasi*). Aquatic Toxicol. 51:225--239.

Vlosky RP. 2006. Statistical Overview of the U.S. Wood Preserving
Industry: 2004. Louisiana State University Agricultural Center.

Ward, G.S., P.R. Parrish, and R.A. Rigby. 1981. Early life-stage
toxicity tests with a saltwater fish: Effects of eight chemicals on
survival, growth, and development of sheepshead minnows. J,. Toxicol.
Environ. Health 8(1-2):225-240.

WHO. 2004. Coal Tar Creosote. Concise International Chemical Assessment
Document (CICAD) 62, World Health Organization, Geneva, Switzerland.
<http://www.inchem.org/documents/cicads/cicads/cicad62.htm>

Xiao, Y., J. Simonsen, and J.J. Morrell. 2002. Effects of water flow
rate and temperature on leaching from creosote-treated wood. Res. Note
FPL-RN-0286. Madison, WI: U.S. Department of Agriculture, Forest
Service, Forest Products Laboratory. 6 p.