Document ID: EPA-HQ-OPP-2003-0248-0066
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2008-11-19T05:00Z

SEQ CHAPTER \h \r 1 UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

WASHINGTON, D.C. 20460

OFFICE OF                  

PREVENTION, PESTICIDES AND 

TOXIC SUBSTANCES        

September 5, 2008			

					

MEMORANDUM			

SUBJECT:	Creosote:  Occupational and Residential Exposure and Risk
Assessment for the Reregistration Eligibility Decision (RED).  PC Codes
022003, 025003, and 025004. 

FROM:	Timothy Leighton, Environmental Scientist

Regulatory Management Branch II

		Antimicrobials Division

THRU:	Norm Cook, Branch Chief

Risk Assessment and Science Support Branch (RASSB)

		Antimicrobials Division

		

TO:		Jacqueline Campbell-McFarlane  SEQ CHAPTER \h \r 1 , Chemical
Review Manager

Antimicrobials Division

And

Timothy F. McMahon, Ph.D., Senior Toxicologist 

Antimicrobials Division

 TOC \f Table of Contents	2

Executive Summary	3

1.0 
Introduction……………………………………………………
……………………………5

2.0   Summary of Toxicity
Data………………………………………………………...
…………5    2.1 Acute Toxicology Categories	7

2.2 Summary of Endpoints of
Concern………………………………………………………..
..8

2.3 
FQPAConsideration………………………………………………
………………………10

3.0 Occupational Exposures and Risks at Pressure Treatment Facilities	10

3.1 Worker Exposure at Pressure Treatment Facilities	13

3.1.1 Pressure Treatment Process	13

3.1.2 Dermal Exposure Monitoring	14

3.1.3 Inhalation Exposure
Monitoring……………………………………………………..
.15

3.1.4 Exposure and Risk
Characterization………………………………………………
….16

3.2 Post-Application Exposures and Risks	21

4.0 Summary of Literature Exposure
Studies……………………………………………….22

5.0 Uncertainties and Limitations	26

6.0 References	27

 

EXECUTIVE SUMMARY

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. 

This chapter is a revision of the earlier draft Human Exposure RED
Chapter for Creosote completed in 2003.  Subsequent to the last release
of the creosote assessment, additional data were made available to
further refine the assessment.  The previous version of the human risk
assessment was based on relying on benzo(a)pyrene as an indicator of
creosote risk because creosote-specific data were not available.  Data
are now available to relate dermal absorption and cancer risks to
creosote.  The previous draft risk assessment also included scenarios
using data from the Pesticide Handlers Exposure Database (PHED) and the
Chemical Manufactures Association (CMA).  These scenarios have been
deleted in this current assessment based on the voluntary cancellation
of all non pressure treatment uses of creosote.

Toxicological endpoints have been selected for the dermal and inhalation
exposure routes to assess the exposure to creosote.  Both non cancer and
cancer endpoints are summarized in Table 2 below.  Because the
inhalation exposure samples from the Creosote Council’s worker
exposure study did not provide reliable air measurements for coal tar
pitch volatiles (CTPVs), the naphthalene air samples have been used to
indicate the need for inhalation exposure mitigation.  However, the use
of the naphthalene inhalation toxicology data is uncertain.  There are
notable species differences in the metabolism of naphthalene between
rodents and primates as discussed in the toxicology section below.  It
is understood that as further research is conducted with regard to the
species differences in naphthalene disposition and toxicity, that the
occupational inhalation assessment would be modified accordingly.

  

The results of the Creosote Council’s worker exposure study at
pressure treatment facilities indicate that the naphthalene inhalation
exposures trigger EPA’s non cancer risk level of concern for 16 of the
19 inhalation MOEs assessed.  The non cancer inhalation MOEs for worker
exposure to naphthalene range from 23 to 1,900 (i.e., target MOE of
300).  However, none of the average naphthalene air concentrations for
the various job functions exceeded the ACGIH TLV and OSHA PEL of 52
mg/m3.  Furthermore, the published literature for creosote exposure also
indicates naphthalene air concentrations in the range of that monitored
by the Creosote Council, with some upper ends of the range slightly
higher (but those concentrations are for “total vapor”).  The
results of the air concentrations reported in the literature support the
results of the Creosote Council’s worker exposure study indicating
that exposure to creosote should be reduced.

For dermal worker risks, 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).  

All of the cancer risks exceed the Agency’s level of concern of 1 x
10-6 but only 4 of the scenarios had risks exceeding 1 x 10-4 (i.e.,
risks range from 2.5 x 10-5 to 1.6 x 10-6).

 	The registrants submitted a probabilistic worker risk assessment for
creosote in February 2008.  This probabilistic assessment has been
included in the public docket.  A thorough EPA review of the
probabilistic assessment has not been conducted.  The methodology and
data inputs in this recent submission differ from that presented by EPA.
 EPA’s assessment herein presents a deterministic risk assessment.  In
summary, the Creosote Council’s probabilistic assessment includes
cancer risk results with and without the probabilistic analysis of the
cancer slope factor.  The mean and 95th percentile cancer risks reported
in Table 9 of the Creosote Council’s probabilistic assessment range
from  10-4 to 10-5.  These reported risks are within the range of the
risks presented by EPA in Table 6 of Section 3.1.4 below.  However,
EPA’s assessment reports one cancer risk lower than that reported in
the probabilistic assessment (i.e., 1.6 x 10-3 for the treatment
operators at a facility built in the 1940s).

1.0	Introduction

An occupational and/or residential exposure risk assessment is required
for an active ingredient if (1) certain toxicological criteria are
triggered and (2) there is potential exposure to handlers (mixers,
loaders, applicators, etc.) during use or to persons entering treated
sites after application is complete. For creosote, both criteria are
met.

On April 1, 1999, the EPA/OPP Health Effects Division's Hazard
Identification Assessment Review Committee (HIARC) evaluated the
toxicology data base of creosote and selected toxicological endpoints
for short-term, intermediate-term, and long-term occupational and
residential exposure risk assessments.  On September 3, 2003, the
Antimicrobials Division Toxicity Endpoint Selection Committee (ADTC) met
to verify the selected endpoints for dermal and inhalation risk
assessment.  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
(CARC) 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. 

2.0 tc \l2 "4.1 	 Summary of Toxicity Data tc \l1 "Occupational  

Dermal tc \l3 "Dermal  Absorption:  Submitted studies on the dermal
absorption of creosote have been submitted and consist 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 results of these studies support the conclusion that
dermal absorption in human skin is approximately 8-fold lower than that
of rat skin. The results of the submitted studies also support a value
for dermal absorption of creosote in rat skin of approximately 34%.
Thus, estimated dermal absorption of creosote in human skin is
determined to be 5% (34% value divided by 8 and rounded to 5%).  A lower
dermal absorption value suggested by the registrant was not used because
of the lack of data on solubility limit of the creosote mixture itself
in the in vitro test system, and the continued absorption of creosote
observed after 8 hours in the in vivo study suggesting the availability
of creosote within the skin for absorption. 

Short-Term tc \l3 "Short-Term  Dermal (1 day - 1 month): An oral
maternal NOAEL of 50 mg/kg/day and a LOAEL of 175 mg/kg/day, based on
decreased body weight gain during the study, was chosen for this
endpoint (USEPA, 2008).  Although a 90-day dermal toxicity study was
available, the developmental toxicity study was chosen because dermal
toxicity studies (including the 2-week range-finding studies) did not
measure developmental endpoints, which are present in both developmental
toxicity studies.  An uncertainty factor (MOE) of 100 is applied to this
risk assessment (USEPA, 2008).  

Intermediate-Term tc \l3 "Intermediate-Term  Dermal (1 month to 6
months): A dermal NOAEL of 40 mg/kg/day, based on decreased body weight
gain in males at 400 mg/kg/day observed in the 90-day dermal toxicity 
study (MRID # 43616201).  An uncertainty factor (MOE) of 100 is applied
to this risk assessment (USEPA, 2008).

Long-Term tc \l3 "Long-Term  Dermal (greater than 6 months): A parental
oral LOAEL of 25 mg/kg/day, based on decreased pre-mating body weight,
was selected for this endpoint.  An extra uncertainty factor of 3x is
applied for use of a LOAEL in this study for occupational risk
assessments (USEPA, 2008).  Based on the results of this study, the
Parental Systemic NOAEL is < 25 mg/kg/day, and the Parental Systemic
LOAEL is 25 mg/kg/day, based on decreased pre-mating body weight.  The
developmental NOAEL in this study is < 25 mg/kg/day, and the
developmental LOAEL is 25 mg/kg/day, based on a dose-related decrease in
pup body weight for the F0 pups from days 14-21. The reproductive NOAEL
is < 25 mg/kg/day, and the reproductive LOAEL is 25 mg/kg/day, based on
reduced pregnancy and fertility indices in F1 female parental rats
(USEPA, 2008).			

Inhalation (any time-period):  An NOAEL of 0.0047 mg/L, based on
decreased body weight gain, altered hematology and clinical chemistry,
and increased absolute and relative weight of the liver and thyroid and
increased incidence of lesions of the nasal cavity observed at 0.048
mg/L in P2 creosote CMT in rats (USEPA, 2008).  In a 13-week inhalation
toxicity study (MRID # 43600901), 20 Sprague-Dawley rats/sex/group were
treated for 5 days/week, 6 hours/day with P2 Creosote CTM via whole body
exposure at doses of 0, 4.7, 48 or 102 mg/m3 (0, 0.005, 0.048 or 0.102
mg/L ) in air measured gravimetrically.  The aerosol size MMAD was
between 2.4 and 2.9 microns with a geometric standard deviation between
1.85 and 1.91.  

For worker risk, naphthalene was selected as an indicator because of
analytical difficulties encountered with the CTPV samples and because
all of the naphthalene inhalation samples monitored at the pressure
treatment facilities were detectable.  However, the Antimicrobials
Division is aware of recent developments regarding potential species
differences in toxicity of naphthalene.  “Critical research has been
published indicating that metabolic activation is a required step for
naphthalene’s respiratory toxicity (unmetabolized naphthalene is not
the cause of the cytotoxicity or tumors) and that there are notable
species differences in the metabolism of naphthalene between rodents and
primates (Buckpitt et al. 1992, 1995, 2002; Bogen et al. 2008).
 Available research to date indicates that the metabolism pathway in
rodents is more active than in humans (i.e., humans have a slower rate
of formation of the active metabolite) (Buckpitt et al. 1992, 1995,
2002; Bogen et al. 2008).” 

Recognizing that rodents may be more susceptible to the toxic effects of
naphthalene, but that the issue of human relevance is not fully
scientifically resolved, the Antimicrobials Division has at this time
based its creosote inhalation risk assessments for occupational workers
on the LOAEL of 52 mg/m3 selected from the naphthalene 2-year toxicity
study in mice (NTP, 1992), as discussed in the Agency’s IRIS
Toxicological Review for naphthalene
(http://www.epa.gov/ncea/iris/toxreviews/0436-tr.pdf).   Other reasons
for using naphthalene at this time are based on several significant
deficiencies in the inhalation monitoring study conducted on creosote
workers,  including (1) no attempt by the study sponsors to relate
inhalation levels found for polynuclear aromatics (PNAs) and coal tar
pitch volatiles (CTPVs) to "total creosote" -- a significant weakness
with the study; (2) analytical problems encountered with the CTPV
samples (all samples were non-detect); (3) the overall inhalation field
fortification percent recoveries for the coal tar pitch volatiles
(CTPVS) were poor (51-57%).    It is understood that as further research
is conducted with regard to the species differences in naphthalene
disposition and toxicity, that the occupational inhalation assessment
would be modified accordingly. 

Carcinogenicity tc \l3 "Carcinogenicity : In conjunction with Health
Canada’s Management Regulatory Agency (PMRA), 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 or 6.28 x 10-3 (mg/kg/day)-1 for the coal tar mixture 1
tested in this study was selected, on the basis of forestomach tumors
observed. 

2.1 tc \l2 "4.1.4 	Acute tc \l1 "Acute  Toxicology Categories

Table 1 provides the acute toxicity categories for creosote.  It also
provides the results of the toxicity tests (USEPA 2008).

 tc \l1 " Table tc \l3 "Table  1. Acute tc \l2 "Acute  Toxicity
Categories for Creosote

Test	

Results	

Toxicity Category

Acute Oral Toxicity	

LD50 = 2,451 mg/kg (M); 1,893 mg/kg (F)	

III

Acute Dermal Toxicity	

LD50 > 2,000 mg/kg	

III

Acute Inhalation Toxicity	

LC50 > 5 mg/L	

IV

Primary Eye Irritation	

Irritation clearing in 8-12 days	

II

Primary Dermal Irritation	

Erythema to day 14	

III

Dermal Sensitization	

Study unacceptable	

NA

NA - Not applicable, no toxicological endpoint.

2.2 tc \l2 "4.1.5 	Summary tc \l1 "Summary  of Endpoints of Concern

Endpoints for assessing occupational and residential risks are presented
in Table 2 (USEPA 2008).  

Table tc \l3 "Table  2. Summary of Toxicological Endpoints tc \l2
"Endpoints  for Creosote.

EXPOSURE

SCENARIO	

DOSE

(mg/kg/day)	

ENDPOINT	

STUDY

Acute and Chronic Dietary	

Acute and Chronic Dietary risk assessment not required

Carcinogenicity

(dermal)	

Creosote has been shown to exert positive mutagenic effects in vitro,
and has been shown to be positive for carcinogenicity in an
initiation/promotion study.  Creosote has been classified as a B1
carcinogen in IRIS. An oral cancer slope factor of 6.28 x 10-3 (mg
CTM1/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  (Dermal)	

Oral NOAEL=50	

 decreased body weight gain at 175 mg/kg/day	

 Developmental Toxicity - Rat

	

Target MOE = 100 based on 10x interspecies variation and 10x
intraspecies extrapolation.  A 5 percent dermal absorption factor is
used to correct for use of oral endpoint.

Intermediate-term

(Dermal)	

Dermal NOAEL = 40	

Decreased body weight gain at 400 mg/kg/day	

90-Day Dermal Toxicity Study in the Rat

	

Target MOE = 100 based on  10x interspecies variation and 10x
intraspecies extrapolation 

Long-Term (Dermal)

	

Oral  LOAEL = 25 mg/kg/day 	

decreased pre-mating body weight	

2-generation reproduction study - Rat

	

Target MOE = 300 based on 10x interspecies, 10x intraspecies, and 3x 
for use of a LOAEL.

Inhalation

(any  time period)	Creosote

NOAEL = 0.0047mg/m3

	decreased body  weight, body weight gain, altered hematology

Target MOE = 100 based on  10x interspecies variation and 10x
intraspecies extrapolation	

90-day Inhalation Study in the Rat

	Naphthalene 

LOAEL = 52  mg/m3

[Note:  see Section 2.0 above for a discussion of the uncertainties in
the selection of this inhalation endpoint] 	nasal effects: hyperplasia
and metaplasia in respiratory and olfactory epithelium respectively

Target MOE = 300 based on 10x interspecies, 10x intraspecies, and 3x 
for use of a LOAEL.	Two year inhalation toxicity study - mouse (USEPA,
IRIS)

Dermal absorption 	

5%, determined from the results of in vivo / in vitro testing in rats
and in vitro testing using human skin. 

2.3 tc \l2 "4.1.3 	FQPA Considerations

	As there are no existing tolerances or other clearances for residues of
creosote in food, an FQPA assessment is not necessary.  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.  

	Although there are no current Agency guideline neurotoxicity studies
available for creosote, the existing studies on creosote indicate no
evidence of neurotoxicity for either the P1/P13 or P2 blends of creosote
(ATSDR, 2002). Based on the above, and realizing that creosote is
currently registered only for non -food use and is a restricted use
pesticide, no additional neurotoxicity testing will be required at this
time.

3.0 tc \l2 "4.2 	Occupational tc \l1 "Occupational  Exposures and Risks
at Pressure Treatment Facilities

	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. Table 3 provides a
summary of worker exposure scenarios at pressure treatment facilities. 
Although specific job functions have been defined within each exposure
scenario, EPA acknowledges the occasional need for workers to cross over
into other job functions.  Table 3 also provides the numbers of
monitoring events at each of four sites from MRID 453234-01.



Table 3:  Job Descriptions of Workers Exposed at Pressure Treatment
Facilities (Creosote Council Study – MRID 453234-01).

Job Function	

Description of worker activities	

Monitoring Events

Site	

Dermal	

Inhalation

Treatment Operator TO  (engineer)	

Operates and manages the treatment system; may open and close cylinder
doors; cleans accumulated creosote from doors and latches; operates
valves to transfer creosote solution between holding tanks and treatment
cylinders; handles leads and bands.	

A

B

C

D 	

total: 18 4, 1/day 

4, 1/day 

5, 1/day 

5, 1/day 	

total: 14

0

4, 1/day 

5, 1/day 

5, 1/day 

Treatment Assistant TA (helper)	

Performs and assists with tasks of the TO; charge preparation, cylinder
cleaning, maintenance, filter cleaning, mixing treatment solution;
loader operation and movement of charges.	

B	

total: 4

4, 1/day	

total: 4

4, 1/day

Oil unloader 

OU	

Operates creosote tank car unloading and transfer system; takes samples
from tank cars; inserts siphons into tanks.

(At site C, the tasks for this position were performed by the TO;
position was not monitored at Site B)	

A

D	

total: 9

4, 1/day

5, 1/day	

total: 5

0

5, 1/day

Loader Operator

CLO (cylinder area) 

LLO (load out area)	

Operates self-propelled vehicles for loading wood on and off trams,
moving charges in and out of cylinders, and to and from load out areas. 
Out-of-cab tasks include tram placement, and handling chains and leads.	

CLO

A

B

C

D 	

total: 18 

4, 1/day

4, 1/day

5, 1/day

5, 1/day	

total: 14

0

4, 1/day

5, 1/day 

5, 1/day

LLO

B

C

D 	

total: 19

4, 1/day

5, 1/day

10, 2/day	

total: 19

4, 1/day

5, 1/day

10, 2/day

Loader helper

CH; LH	

Assists the LO in some tasks; works mainly on the drip pad and load out
area, placing and removing charge leads, opening and closing cylinder
doors, retrieving leads, adjusting track switches, and banding and
unbanding charges.	

B

C

D	

total: 14

4 LH, 1/d

5 CH, 1/d 5 CH, 1/d	

total: 14

4 LH, 1/d

5 CH, 1/d 

5 CH, 1/d

Checker

CK	

Performed tasks of the loader helper as well as inspecting treated
lumber.  Worker part time in the treatment area.	

C	

total: 5

5 CH, 1/d	

total: 5

5 CH, 1/d

Test Borer/QC Person

TB	

Takes core samples to test for creosote penetration; may test creosote
solution concentration (site C); other QC laboratory duties.  (These
tasks performed by CLO at site B) 	

A

C	

total: 9

4, 1/day

5, 1/day	

total: 5 

0

5, 1/day

Water Treatment System Operator 

WO	

Operates chemical/biological water recovery equipment (At Site C, the
tasks associated with this position were performed by the TB; position
not monitored at Site D)	

A

B	

total: 8

4, 1/day

4, 1/day	

total: 4

0 

4, 1/day

Drip pad cleaner

DP	

Steam-cleans drip pad area; disposes of sludge and treated wood waste;
other cleanup duties in treatment and drip pad area. 	

C

	

total: 4 

4, 1/day	

total: 4 

4, 1/day

Total	

	

	

108	

88

Site A is Florence, SC.  Site B is Delson, Quebec.  Site C is Denver,
CO.  Site D is Somerville, Tx.

	The worker exposure study on pressure treatment applications submitted
by the Creosote Council II to provide chemical-specific handler dermal
and inhalation exposure data in support of the re-registration of
pressure treatments of creosote (Creosote Council II, 2001, MRID
453234-01) is presented in Section 3.1.  Other published studies for
creosote are presented in Section 4.0. 

	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.  Nonetheless, other
studies available in the literature are also presented below in Section
4.0.

3.1	Worker Exposure at Pressure Treatment Facilities

	The 2001 Creosote Council II study was conducted to determine the
dermal and inhalation exposure of workers exposed to creosote while
performing routine tasks related to pressure treatment of lumber,
utility poles, and railroad ties.  The study was conducted at four
typical commercial treatment facilities in the U.S. and Canada, per the
requirements of the U.S. Environmental Protection Agency, Canada’s
Pesticide Management Regulatory Agency (PMRA), and the California
Department of Pesticide Regulation.  The four sites include older
facilities from the 1940s as well as more modern facilities with
additional engineering controls.  Therefore, the exposure and risk
estimates have been presented separately for each site.  The job
functions monitored in the study are presented in Table 3 above.  

	Previous drafts of the EPA’s creosote assessment have defined the job
functions at pressure treatment facilities as either handlers or
postapplication.  Since the job functions previously categorized as
handlers (treatment operators and assistants) perform many functions,
this creosote assessment does not highlight the job functions as being
either handler or postapplication.  Workers in the study performed
typical tasks related to their job functions and were monitored during a
full work cycle beginning at 7 AM and ending at 3 PM. 

Pressure tc \l3 "Pressure  Treatment Process 

	Pressure treatment is often required because of the resistance of wood
to deep penetration by preservatives. The pressure treatment process
begins when untreated wood is loaded onto rail/tram cars that are pushed
into the treating cylinder using locomotives, forklifts, or similar
equipment. The cylinder door is sealed via a pressure-tight door and the
operation remains a closed system during the entire treatment process.
Treating solutions are then pumped into the cylinder and the inside
pressure is raised. At the end of the treatment process, the excess
treating solution is pumped out of the treating cylinder and back to
storage for reuse. The cylinder is opened, and the rail/tram cars
holding the treated wood are pulled out of the cylinder using a
locomotive, forklift, or similar equipment. 

The amount of creosote handled in a given day among pressure treatment
facilities depends on such factors as the size of the facility and the
number of treatment cylinders on site. In a given facility, the amount
of creosote handled per day varies depending on the wood conditioning
techniques used for a given charge, on the type of wood being treated,
and the type of product being produced (e.g., marine piling vs utility
poles). 

According to information provided by industry sources (Krygsman, 1994),
wood pressure treatment of railroad ties in a retort may last anywhere
from 4 to 24 hours. A typical retort cylinder has a diameter of about 8
feet and a length of about 120 feet. About 16 rail/tram cars can be
placed in a retort at one time. The rail/tram cars usually are connected
together and are pushed in and out of the retort on railroad tracks
using a locomotive. Wood preservative is loaded into the wood pressure
treatment retort facilities from rail tank cars using hoses and metered
pumps. The wood preservative is stored in two or three holding tanks
that may be as large as 60,000 gallons. During the wood treatment
process the wood is sprayed under pressure in the enclosed retort. In
the retort, a “charge” of liquid preservative is pumped into the
trams and then later pumped out. After the wood preservative is pumped
out, the wood is dried through a vacuum treatment and the tram cars
containing wood (e.g. railroad ties) are then pulled out. Since the wood
in the tram cars is pulled by mechanical means there is very little
direct human contact with the exposed wood. Likely contact is through
dermal contact with equipment that was previously in the retort,
removing cables that separated layers of ties, dermal and inhalation
contact to vapors inside the retort before and after pressure treatment,
cleaning the retort, and inspecting wood pieces by coring the wood.

Dermal tc \l3 "Dermal  Exposure Monitoring 

	Since creosote is a complex mixture of over 100 chemicals including
phenols, creosol, and aromatic hydrocarbons, it is analytically
difficult and cost prohibitive to identify all of the chemicals in the
mix. In addition, creosote cannot be measured directly because of its
complex mixture.  Dermal exposure to “total creosote” was estimated
by measuring the levels of 10 individual polynuclear aromatic
hydrocarbon (PNA) compounds.  Each analyte was determined in each
whole-body dosimeter (WBD) and glove sample as if it represented total
creosote. The goal was to use these marker compounds to represent
“total creosote”.

The creosote dermal exposure to each worker was determined using a WBD,
consisting of a 100% cotton thermal shirt and long pants.  Each worker
at Sites A, C, or D wore his WBD under a fresh work uniform consisting
of a cotton long-sleeved work shirt and cotton work trousers (or
one-piece cotton coverall) provided by the test site.  The workers at
Site B were not provided uniforms therefore; each worker wore a WBD
under a fresh lightweight cotton/polyester sweat shirt and pants
purchased locally by study personnel.  The workers at all four sites
wore a lightweight 100% cotton glove dosimeter on each hand under his
chemical-resistant or work gloves, as appropriate. Each of these 10
analytes was determined for each WBD and glove sample as if it
represented total creosote.  The average of the analyte concentrations
were used to estimate the level of total creosote present in/on the
individual sample.

 

3.1.3	Inhalation tc \l3 "Inhalation  Exposure Monitoring 

	Inhalation exposure for each worker was monitored by a personal air
sampling train.  Inhalation exposure was estimated for 11 individual PNA
compounds as well as for benzene-soluble PNAs and related compounds
collectively known as coal tar pitch volatiles (CTPVs).  The
Polytetrafluroethylene (PTFE) filter retained the CTPVs, while the PNAs
were retained in the XAD-2 resin tubes. Each worker wore a sampling
train consisting of a PTFE filter upstream from two in-line XAD-2
resin-filled air sampling tubes.  However, there was no attempt by the
study sponsors to relate inhalation levels found for PNAs and CTPVs to
"total creosote" -- a significant weakness with the study.  Moreover,
there were analytical problems encountered with the CTPV samples and all
samples were non detect.  Therefore, EPA did not rely on the CTPV
inhalation exposure monitoring results.  Instead, naphthalene was used
to indicate inhalation exposure concerns (see Section 2.0 above for a
discussion of the uncertainties in the selection of the inhalation
toxicological endpoint for naphthalene).

Inhalation exposure monitoring at Site A was unsuccessful because a
single XAD-2 tube was used along with a non-solvent-resistant filter
cassette.  Therefore, the sampling methodology was changed to include
the use of a second XAD-2 resin tube in the sampling train prior to
sampling at Sites B, C, and D.  Inhalation exposure monitoring was
performed successfully at these sites.  Each worker at Sites B, C, and D
was equipped with an air sampling train consisting of a PTFE filter in
an opaque, solvent-resistant plastic cassette connected upstream from
two in-line XAD-2 resin-filled air sampling tubes.  The intake orifice
of the filter was placed in the worker’s breathing zone, directed
downward.  Air was pulled through the sampling train by a portable air
sampling pump attached to the worker’s belt.  The pump drew air
through the sampling tube at approximately 1 L/minute while the worker
performed his tasks.  Pumps were calibrated immediately prior to and
after each monitoring period using a mass flow meter or bubble
calibrator.  The pumps were turned on at the beginning of each work
cycle and were left running during restroom, coffee, or other short
breaks, but were turned off or set on “hold” during lunch breaks.  

The pumps and samplers were removed from the worker during the lunch
break.  At the conclusion of the lunch break, the pump and sampling
train were reinstalled and the pump restarted.  All start and stop times
for breaks were recorded.  

During each work cycle, start times and end times of each task performed
by the worker were recorded.  Pump parameters during use were also
recorded.  At the end of each work cycle, the pumps and sample trains
were collected.  Each filter cassette and sampling tube were capped,
labeled, bagged, and placed on dry ice for shipment to USX Engineers and
Consultants, Inc. (UEC) for extraction and analysis.  After the
collection of the air samples, the air sampling pump was re-calibrated. 

3.1.4 tc \l2 "4.2.2 	 tc \l1 "Handler Exposure and Risk Characterization

Estimated Dose:  The short-term dermal endpoint is based on a maternal
toxicological endpoint; therefore, a female body weight of 60 kg was
used for the dose calculation.  The median adult male/female body weight
of 70 kg was used for the intermediate-term, long-term, and cancer
endpoints.  Short-term, long-term, and cancer endpoints are all based on
oral administrations.  Therefore, the 5 percent dermal absorption factor
was used to estimate an absorbed dermal dose for comparison to an orally
administered dose in the toxicity studies.  The intermediate-term
endpoint is based on a dermal toxicity study, and therefore, no
absorption factor was necessary.  A route specific inhalation assessment
has been developed comparing the air concentrations monitored for
workers directly to the human equivalent concentration (HEC) without the
need for an extrapolated dose estimate. 

	The following equation was used to estimate the dermal dose.  Because
EPA traditionally uses an adult body weight of 70 kg and female body
weight of 60 kg in its exposure assessments which is slightly different
then the 71.8 kg body weight used in the Creosote Council II exposure
assessment, the doses used in this assessment had to be normalized back
to daily dermal exposures. The normalization was performed by
multiplying the exposure dose times the 71.8 kg body weight. 
Subsequently, the dermal exposure was converted into an absorbed and/or
potential dose using the 60 and 70 kg body weights.

Absorbed Daily Dermal Dose (mg/kg/day) = Dermal Exposure (mg/day) x
Dermal Absorption (%) x (1/Body Weight)

	The estimated absorbed dermal lifetime average daily dose (LADD) is
based on the following equation:

LADD[absorbed] (mg/kg/day) = Absorbed dermal dose (mg/kg/day) x (250
days worked/365 days) x (35 years worked/70 year lifetime)

Estimated Non Cancer and Cancer Risks:  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 = LADD[absorbed] (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 (Table 4):  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).  



Table 4.  Creosote Dermal MOEs.

 

Job

 	 

Site

 	 

n=

 	 

Site Description

 	Potential

dermal dose

(mg/kg/day)	Absorbed

Dermal Dose

(mg/kg/day)	Dermal MOEs

 

ST	IT	 

LT

TO	A	4	1940s; manual	0.414	0.021	2415	97	1208

 	B	4	1983; Eng. Controls	0.015	0.001	67568	2703	33784

 	C	5	1940s	14.800	0.740	68	3	34

 	D	5	1970s; Automated	0.132	0.007	7576	303	3788

TA	B	4	1983; Eng. Controls	0.025	0.001	40323	1613	20161

OU	A	4	1940s; manual	0.887	0.044	1127	45	564

 	D	5	1970s; Automated	0.938	0.047	1066	43	533

CLO	A	4	1940s; manual	0.212	0.011	4717	189	2358

 	B	4	1983; Eng. Controls	0.089	0.004	11299	452	5650

 	C	5	1940s	2.120	0.106	472	19	236

 	D	5	1970s; Automated	0.117	0.006	8547	342	4274

LLO	B	4	1983; Eng. Controls	0.018	0.001	55249	2210	27624

 	C	5	1940s	0.203	0.010	4926	197	2463

 	D	10	1970s; Automated	0.077	0.004	12953	518	6477

LLO(F)	D	 	1970s; Automated	0.244	0.012	4098	164	2049

LH	B	4	1983; Eng. Controls	0.023	0.001	43860	1754	21930

 	C	5	1940s	1.810	0.091	552	22	276

 	D	5	1970s; Automated	0.383	0.019	2611	104	1305

CK	C	5	1940s	0.822	0.041	1217	49	608

TB	A	4	1940s; manual	0.112	0.006	8929	357	4464

 	C	5	1940s	1.060	0.053	943	38	472

WO	A	4	1940s; manual	0.204	0.010	4902	196	2451

 	B	4	1983; Eng. Controls	0.047	0.002	21322	853	10661

DP	C	4	1940s	0.150	0.008	6667	267	3333

Site A,B,C,D indicate differences in site setup (e.g., eng controls).

Dermal exposures are not normalized to the various amount of wood
treated.

Arithmetic mean of the dermal dose from Table 9 of the PMRA worker study
review.

Abs Dermal Dose (mg/kg/day) = dermal dose (mg/kg/day) x 5% dermal
absorption

 Where ST NOAEL is 50 mg/kg/day (Target MOE = 100) and LT LOAEL is 25
mg/kg/day (Target MOE = 300).

Where IT NOAEL is 40 mg/kg/day (Target MOE = 100) from a dermal study.

Inhalation MOEs (Table 5):  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 ACGIH TLV and
OSHA PEL of 52 mg/m3.  Additional research is being conducted on the
inhalation toxicological endpoint for naphthalene.  Therefore, the risks
presented in Table 5 maybe an overestimate of the actual risk as
discussed in Section 2.0 above.  Nonetheless, these risks are presented
as a conservative estimate to indicate the need for inhalation exposure
mitigation.

Table 5.  Inhalation MOEs for Naphthalene.

 

Job	 

Site	 

n=	 

Site Description	Average

Naphth (ug/m3)	Average

Naphth (mg/m3)	 

% of TLV	MOE

(Target 300)

TO	A	4	1940s; manual	NA	NA	NA	NA

 	B	4	1983; Eng. Controls	221	0.221	0.4	235

 	C	5	1940s	1320	1.32	2.5	39

 	D	5	1970s; Automated	802	0.802	1.5	65

TA	B	4	1983; Eng. Controls	406	0.406	0.8	128

OU	A	4	1940s; manual	NA	NA	NA	NA

 	D	5	1970s; Automated	925	0.925	1.8	56

CLO	A	4	1940s; manual	NA	NA	NA	NA

 	B	4	1983; Eng. Controls	227	0.227	0.4	229

 	C	5	1940s	2033	2.033	3.9	26

 	D	5	1970s; Automated	574	0.574	1.1	91

LLO	B	4	1983; Eng. Controls	27	0.027	0.1	1926

 	C	5	1940s	694	0.694	1.3	75

 	D	10	1970s; Automated	195	0.195	0.4	267

LLO(F)	D	 	1970s; Automated	679	0.679	1.3	77

LH	B	4	1983; Eng. Controls	43	0.043	0.1	1209

 	C	5	1940s	1870	1.87	3.6	28

 	D	5	1970s; Automated	2251	2.251	4.3	23

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. Controls	917	0.917	1.8	57

DP	C	4	1940s	347	0.347	0.7	150

Site A,B,C,D indicate differences in site setup (e.g., eng controls)

TLV = 10 ppm (52 mg/m3) STEL 15 ppm (79 mg/m3)

mg/m3 = ug/m3 / 1000

% of TLV = (mg/m3 / 52) x 100

MOE = HEC / air conc; Where HEC = 52 mg/m3.

Cancer Risks (Table 6):  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).

Table 6.  Creosote Dermal Cancer Risks.

 

Job

 	 

Site

 	 

n=

 	 

Site Description

 	Potential

dermal dose

(mg/kg/day)	 

Abs Dermal Dose

(mg/kg/day)	 

Abs LADD

(mg/kg/day)	 

Creosote

Risk

TO	A	4	1940s; manual	0.414	0.0207	0.0071	4.5E-05

 	B	4	1983; Eng. Controls	0.0148	0.0007	0.0003	1.6E-06

 	C	5	1940s	14.8	0.7400	0.2534	1.6E-03

 	D	5	1970s; Automated	0.132	0.0066	0.0023	1.4E-05

TA	B	4	1983; Eng. Controls	0.0248	0.0012	0.0004	2.7E-06

OU	A	4	1940s; manual	0.887	0.0444	0.0152	9.5E-05

 	D	5	1970s; Automated	0.938	0.0469	0.0161	1.0E-04

CLO	A	4	1940s; manual	0.212	0.0106	0.0036	2.3E-05

 	B	4	1983; Eng. Controls	0.0885	0.0044	0.0015	9.5E-06

 	C	5	1940s	2.12	0.1060	0.0363	2.3E-04

 	D	5	1970s; Automated	0.117	0.0059	0.0020	1.3E-05

LLO	B	4	1983; Eng. Controls	0.0181	0.0009	0.0003	1.9E-06

 	C	5	1940s	0.203	0.0102	0.0035	2.2E-05

 	D	10	1970s; Automated	0.0772	0.0039	0.0013	8.3E-06

LLO(F)	D	 	1970s; Automated	0.244	0.0122	0.0042	2.6E-05

LH	B	4	1983; Eng. Controls	0.0228	0.0011	0.0004	2.5E-06

 	C	5	1940s	1.81	0.0905	0.0310	1.9E-04

 	D	5	1970s; Automated	0.383	0.0192	0.0066	4.1E-05

CK	C	5	1940s	0.822	0.0411	0.0141	8.8E-05

TB	A	4	1940s; manual	0.112	0.0056	0.0019	1.2E-05

 	C	5	1940s	1.06	0.0530	0.0182	1.1E-04

WO	A	4	1940s; manual	0.204	0.0102	0.0035	2.2E-05

 	B	4	1983; Eng. Controls	0.0469	0.0023	0.0008	5.0E-06

DP	C	4	1940s	0.15	0.0075	0.0026	1.6E-05

Site A,B,C,D indicate differences in site setup (e.g., eng controls)

Dermal exposure not normalized to various amounts of wood treated per
site

Arithmetic mean from Table 9 of the PMRA review.

Abs Dermal Dose (mg/kg/day) = dermal dose (mg/kg/day) x 5% dermal abs

Creosote Risk = LADD (mg/kg/day) x creosote oral CSF of 6.28E-3
(mg/kg/day)-1

3.2	 tc \l1 "Occupational 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.  For creosote-treated wood that is
recycled into the residential landscaping market, 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
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.  However, as a post-RED
activity, EPA plans to work with the creosote registrants as well as the
rail road industry on the diversion issue of recycled rail ties that are
being used in the residential market.

  

4.0	Summary tc \l3 "Summary  of Literature Exposure Studies 

	Additional creosote exposure studies in the literature are summarized
below and presented in Table 7.  Some of the air concentrations in Table
7 from these published studies exceed the inhalation level of concern
for creosote outlined in this risk assessment as well as the ACGIH TLV
and PEL of 0.2 mg/m3 for CTPV.  The results of the air concentrations
reported in the literature support the naphthalene air concentration
results from the Creosote Council’s worker exposure study indicating
that inhalation exposure mitigation measures are needed.  

Todd and Timbie (NIOSH 1980) estimated occupational exposures of workers
to creosote in a railroad tie treatment plant in Somerville, Texas. 
Petroleum oil/creosote solutions of 70/30 and 50/50 were used
respectively to treat the cross ties and bridge timbers in the plant.
The concentrations of creosote (i.e., coal-tar pitch volatiles; CTPV) in
personal air samples over a two-day monitoring period ranged from 0.002
to 1.211 mg/m3.  

Another NIOSH study (NIOSH 1981a) of occupational exposure to creosote
at a wood-treatment facility in Tacoma, Washington reported CTPV
concentrations in personal air samples ranging from less than 0.0004 to
0.112 mg/m3 with the highest concentration found at the end of the
treatment process when the cylinder was opened. NIOSH also reported
creosote exposures of dock builders ranging from zero to 0.059 mg/m3
based on cyclohexane extractable fraction of CTPV (NIOSH; 1981b).  

Studies conducted by Markel et al. (1977) and SRI (1993) indicated that
particulate polycyclic organic materials (PPOM) was within 0.1 mg/m3,
the NIOSH permissible level for CTPV, when estimating occupational
exposure to creosote in wood treatment plants. The concentrations of
naphthalene, methylnaphthalene, and acenaphthene (the only components in
the vapor-phase fractions that could be reliably measured) ranged from
0.54 to 2.0 mg/m3. Benzene-soluble particulates (PPOM) ranged from 0.02
to 0.10 mg/m3. 

Hiekkila et al. (1987) conducted an occupational study in Finland
estimating workers’ exposure to creosote in the creosote impregnation
plants and when they were handling the impregnated wood. The average
vapor concentrations (naphthalene being the major component) ranged from
0.5 to 71 mg/m3 in the impregnation plants; while the vapor
concentrations ranged from 0.1 to 11 mg/m3 in the handling of
impregnated wood. Most of the airborne contaminants in workers’
breathing zones were in the vapor phase; the proportion of particulate
polycyclic aromatic hydrocarbons (PAHs) to total concentration of vapors
was less than 0.5 to 3.7 percent. 

Rotard and Mailahn (1987) reported high levels of carcinogenic PAHs,
such as benzo[a]pyrene, benzo[b]-fluoranthene, and benzo[j]fluoranthene,
and cocarcinogenic PAHs in samples of wooden sleepers (railroad cross
ties) installed in playgrounds.

Borack et. al. 2002 conducted air sampling and biological monitoring of
36 workers at a wood treatment plant where railroad ties were treated
with creosote.  There were 18 low exposure workers who worked as
secretaries or clerical staff, 13 moderate exposure workers who
transported cured ties to the shipment yard and 3 high exposure workers
who worked in the retort building and handled ties immediately after
creosote application.   Air sampling was conducted with a filters and
adsorbent tubes both of which were analyzed for benzene soluble PAHs. 
Six filter samples had detectable levels of particulate PAHs and the
highest level was 0.33 ug/m3 for pyrene.  Thirty two of the tube samples
had detectable levels of vapor phase PAHs but levels were generally low.
  The highest levels were for pyrene and naphthalene measured in the
high exposure group and ranged from 1.5 to 2.5 ug/m3 for pyrene and 210
ug/m3 to 330 ug/m3 for naphthalene.   Biomonitoring was performed using
urinary 1-hydroxypropene and the results suggested that more than 90% of
the measured 1-hydroxypropene could be attributed to dermal exposure. 

Elovarra et.al. 1995 conducted air sampling and biological monitoring of
six workers (1 impregnator, 2 assistant operators, 1 lorry driver and 2
tie platers) at an impregnation plant in Russia where railroad ties were
treated with creosote.  The air sampling was conducted for five
consecutive days using filters and adsorbent tubes.  The filters were
analyzed for nine PAHS other than naphthalene and the tubes were
analyzed for naphthalene.  The results for the filter samples ranged
from 1.23 to 13.74 ug/m3 with a GM of 4.77 ug/m3 and an AM of 5.7 ug/m3.
  The naphthalene results of the tube samples ranged from 370 to 4200
ug/m3 with a GM of 1536 ug/m3 and an AM of 1254 ug/m3.   Biomonitoring
was performed using urinary 1-hydroxypropene and indicated that dermal
uptake was much greater than inhalation uptake. 

Flickinger and Lawrence, 1982 data was cited in Wong and Harris, 2005
which is an epidemiological study of creosote workers at 11 plants in
the United States.  This data indicates that 95 percent of the workers
at the woodtreating plants were exposed to no more than 0.14 mg/m3
CTPV-BSF.  In terms of specific jobs, the typical time-weighted average
of treating operators at the participating plants ranged from 0.04 to
0.11 mg/m3 CTPV-BSF with most measurements centered on 0.05 or 0.06
mg/m3 CTPV.  Because of the limited nature of the data, however, the
epidemiology study was based on job/exposure categories rather than the
data.

Heikkila et. al. 1997 conducted air sampling and biological monitoring
of six workers at an impregnation plant where railroad ties were treated
with creosote.  The air sampling was conducted for one workweek and
samples were analyzed for ten PAHs and naphthalene.  The mean exposures
were 1.5 mg/m3 for naphthalene vapor, 5.9 ug/m3 for particulate PAHs and
1.4 ug/m3 for PAHs with 4-6 aromatic rings.   Biomonitoring was
conducted in conjunction with the air sampling and indicated that
airborne naphthalene correlated fairly well with urinary 1-napthol (r =
0.745).  It was also determined, however, that urinary 1-naphthol alone
is not a suitable marker for inhalatory or cutaneous exposure to PAH
originating from creosote. 

Baker and Fannick, 1980 surveyed worker exposures to coal tar pitch
volatiles during a NIOSH health hazard evaluation on October 14, 1980 at
the New York Port Authority. The evaluation was requested by a union
representative on behalf of six workers engaged in pile driving creosote
preserved wood logs for a dock underpinning. Personal and area air
samples were collected.  Breathing zone CPTV concentrations ranged up to
0.06 mg/m3 and area CPTV concentrations ranged up to 0.02 mg/m3. These
concentrations were below the NIOSH recommended limit of 0.1 mg/m3,
however weather conditions on the sampling day probably caused
substantial reductions in exposure. The authors concluded that on
typical days workers may be exposed to significant amounts of CPTV. 

Unwin et. al. 2006 conducted air sampling and biological monitoring of
eleven workers at a timber impregnation plant as part of a larger study
of PAH occupational exposure in the U.K that was funded by the British
Health Executive.  The workers included 2 pole fabricators, 2 pole
loaders, 1 timber loader, 2 creosote plant operators, 1 unchainer, 2
labourers and 1 QC inspector.  The air sampling was conducted for one
day using an IOM fitted with glass fiber filters and followed by an
XAD-2 adsorbent tube.  The air samples were analyzed for 17 PAHs
including napthalene.  The results expressed as total PAH ranged from
29.9 to 1913 ug/m3 with a mean of 835 ug/m3.   The PAH profile was
dominated by naphthalene and the results for total 3-6 ring PAH and BaP
were much lower with mean values of 0.05 ug/m3 for 3-6 ring PAH and 0.01
ug/m3 for BaP.   Biomonitoring was performed using urinary
1-hydroxypropene and indicated that the creosote workers had the highest
exposure among the 25 workplaces surveyed. 

Table tc \l3 "Table  7.  Summary tc \l2 "Summary  of Occupational
Inhalation Exposure Studies of Creosote

Study	

Setting/Subjects	

Components Reported (Analyzed)	

Concentration

(mg/m3)

NIOSH; 1980 (Todd & Timbie)	

railroad tie treatment plant	

coal-tar pitch volatiles (CTPV)	

0.002-1.211 

NIOSH; 1981a (Todd & Timbie)	

wood treatment facility	

CTPV	

0.0004-0.112 

NIOSH; 1981b (Baker & Fannick)	

dock builder	

CTPV (cyclohexane extractables)	

ND-0.059 

Markel et al. (1977) and SRI (1993)	

wood treatment facility	

polycyclic organic materials (PPOM)	

<0.1 

Hiekkila et al. (1987)	

creosote impregnation plant;	

average total vapor (naphthalene being the major component)	

0.5-71 

Hiekkila et al. (1987)	

handling impregnated wood	

average total vapor (naphthalene being the major component)	

 0.1-11

Elovaara et. al., 1995	Railroad Tie impregnation plant in Russia/six
workers, 5 days	10 PAHs include Naphthalene	0.40 to 4.2 Naphthalene

Borak,  et.al., 2002	Railroad Tie impregnation plant /34 workers, all
jobs including office/1 days	Benzene Soluble Fraction/16 PAHS	0.21 –
0.33 Naphthalene

0.015 to 0.0025 pyrene

Flicker and Lawrence, 1982 

Cited in Wong and Harris, 2005	Wood Preserving Industry/Treating
Operators	CTPV-BSF	0.04 – 0.11

Heikkila et. al. 1997	Railroad tie impregnation plant/six workers/one
week	Naphthalene and 10 PAHs	1.5 Naphthalene (mean)

0.0059 PAH (mean)

Baker and Fannick, 1980	Pile Driving Creosote Dock/New York Port
Authority/six workers/one day	CPTV	Up to 0.06 (n=6)

Unwin et. al. 2006	Timber impregnation/UK	Total PAH (Primarily
naphthalene)	0.030 – 1.9 (n=11)

5.0	Uncertainties tc \l1 "Uncertainties  and Limitations

	This section summarizes the uncertainties and data limitations in the
creosote assessment.  

The amount of product applied and the amount of active ingredient
handled by each worker was not calculated because the creosote was
applied in a closed system which recovered and retained excess treatment
solution from the wood and treatment vessel while sealed.  The amount of
wood treated at the 4 sites is believed to be representative of the
industry.

The number of field fortification samples collected at the sites was
less than the required number to satisfy Series 875 guidelines. 
According to the guidelines, there should be at least one fortification
sample per worker per monitoring period (8 hour shift) per fortification
level (three levels) for each matrix and at least one field blank per
worker per monitoring period for each matrix.  There were more workers
monitored than there were field fortifications and field blank samples
collected.

The overall inhalation field fortification percent recoveries for the
coal tar pitch volatiles (CTPVS) were poor.  The overall recovery for
Site B was 57%.  The overall recoveries for Sites C and D were 51% and
57%, respectively.  The analytical method for quantifying CTPVs in the
creosote study was inadequate and only one filter had a detectable
level.  Therefore, inhalation exposure to CTPVs was not determined. 
Instead, risk concerns are indicated using the results of the
naphthalene inhalation samples.  See Section 2.0 above for a discussion
of the uncertainties and ongoing research on the inhalation
toxicological endpoint for naphthalene. 

table low recoveries for gloves.  As an example, for a 60 μg/sample
“total creosote” fortification for Site B, the recoveries for the
WBD’s were as high as 150% and recoveries for the gloves as low as
52.3%.   There were measurable amounts of total creosote found in each
of the control samples prepared at each facility.

The study sponsors made no attempt to relate inhalation levels found for
PNAs and CTPVs to "total creosote" -- a significant weakness with the
study.

6.0 tc \l2 "4.6 		References tc \l1 "References 

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.

Baker and Fannick, 1980. HHE-80-238-931 New York Port Authority,
Brooklyn New York, NIOSH 1980.

Borak et. al. 2002.  Biological Versus Ambient Exposure Monitoring of
Creosote Facility Workers, JOEM, Vol. 44, No. 4, April 2002.

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

Elovaara et. al. 1995.  Significance of Dermal and Respiratory Uptake in
Creosote Workers: Exposure to Polycyclic Aromatic Hydrocarbons and
Urinary Excretion of 1-hydroxypyrene, Finnish Institute of Occupational
Safety and Health, Occup. Environ Med 1995: 52:196-203.

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

Flickinger and Lawrence, 1982.  Occupational Health Experience in the
Wood-Preserving Industry, American Wood-Preservers Association, 1982
(Cited in Wong and Harris).

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.

Heikkila et.al. 1997. Urinary 1-naphthol Excretion in the Assessment of
Exposure to Creosote in an Impregnation Facility, Scand J. Work Environ
Health, 1997.

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
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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.

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.

 

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Wong and Harris, 2005.  Retrospective Cohort Mortality Study and Nested
Case Control Study of Workers Exposed to Creosote at 11 Wood-Treating
Plants in the United States, JOEM, Vol. 47, no. 7, July 2005.

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