Document ID: EPA-HQ-OPP-2003-0248-0048
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2008-04-16T04:00Z

UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

		     WASHINGTON, D.C. 20460

							                                             		

OFFICE OF PREVENTION, PESTICIDES AND TOXIC SUBSTANCES			

		

March 21, 2008

MEMORANDUM

SUBJECT:	Response to the Comments Received (2005) Relative to the Notice
of Availability of the Preliminary Risk Assessment for Creosote
Reregistration Eligibility Decision

FROM:	Talia Lindheimer, Chemist

		Nader Elkassabany, Team Leader

		Risk Assessment and Science Support Branch (RASSB)

Antimicrobials Division (7510P)

Timothy McMahon, Ph.D., Toxicologist

Najm Shamim, Ph.D., Chemist

Risk Assessment and Science Support Branch

Antimicrobials Division (7510P)

THRU:	Mark Hartman, Chief

		Regulatory Management Branch 2

Antimicrobials Division (7510P)

Norm Cook, Chief

Risk Assessment and Science Support Branch

Antimicrobials Division (7510P)

TO:		Public Docket EPA-HQ-OPP-2003-0248

	This document presents the Environmental Protection Agency’s (EPA or
“the Agency”) formal response to the comments received on the 2003
preliminary risk assessments for Creosote uses.  These comments were
received during the 60-day public comment period that ended in February
2005.   

	During the comment periods EPA received comments from approximately 12
stakeholders (see Table 1).  EPA’s responses to these comments are
presented by topic: Chemical Overview, Hazard, Human Exposure,
Occupational Assessment, Environmental Risk and Fate, Recommendations
and Insight, and Benefits and Alternatives.  Relative to the extensive
comments, the last four numbers identifying the docket have been
inserted after the comment summary because the entire detail of the
comments and appendices are too cumbersome to include in this response
document.

Table 1. Docket IDs by Respondent Name (last four digits are respondent
specific)

Docket ID	Respondent Name

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 21	Coalition for Health, Environmental and
Economic Rights

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 22	City/County of San Francisco, Department of
the Environment

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 23 	The Yale University

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 24	The California Regional Water Quality Control
Board

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 25 	The California Regional Water Quality
Control Board

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 26	Tri - TAC

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 27	Washington Toxics Coalition

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 28 	Beyond Pesticides

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 29 	Kenai Peninsula Borough

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 30 	Kerr-McGee Corporation

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 31 	Tri –TAC

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 32 	Utility Solid Waste Activities Group

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 33 	Toxicology Consultants, Inc.

  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 34 	U.S. Fish and Wildlife Service

Chemical Overview: Comments and Responses

Comment: Data on the different PAHs are needed (only 5 tested to date). 

EPA Response:

Comment: As indicated in the PRA, the American Wood-Preservers’
Association (“AWPA”) standard method for analysis of Pl/PI 3 and P2
creosotes are relied upon by industry to identify and specify creosote
suitable for use in wood preservation. As stated in the Product
Chemistry Assessment, analyses of the creosote samples used for data
development by the Council were performed using AWPA test methods that
were “similar to EPA’s Certified Limit Test.” The Council would
like EPA to explicitly acknowledge in the Revised Risk Assessment that
the AWPA test methods used to establish compliance with AWPA P 1/P13 and
P2 Creosote Standards, i.e.,identification of creosote, are the
appropriate Certified Limit Tests for creosote

EPA Response: The suggested changes are being made in the revised RA for
Creosote

Comment: The composition of creosote listed in Tables 1, 2 and 3 of the
Product Chemistry chapter appears to be incorrect, or at least
misleading. Constituent values listed in those tables are normalized for
each category of creosote component presented. For example, in Table 1
(“Polycyclic Aromatic Hydrocarbons (PAHs) in Coal Tar Creosote”) the
values of the PAHs listed appear to be inflated over actual
concentrations present in creosote because of the manner in which the
table is constructed. Anthracene may be 13% of the PAHs identified in
Table 1, but in fact it is only 2.2% of creosote. The same is true for
Tables 2 (“PhenolicConstituents in Coal Tar Creosote) and 3
(“Heterocyclic in Coal Tar Creosote”). Further, cresol (all three
isomers) and pentachlorophenol are erroneously shown in Table 2 as
constituents of creosote, and that should be corrected.

EPA Response:  EPA has made the changes in the Tables 1, 2 and 3 as
suggested.

Comment: It also appears that information to construct Tables 1,2 and 3
was not derived from analysis of creosote, but instead derived from a
publication of analytical data on soil characterized as
“contaminated” (Mueller, et al, complete reference citation not
given). Selected analytical data actually developed on creosote is
presented in Table 4 (“Analytical Results of Creosote P2 and P 1/P13
Fractions”). These data (Table 4) were developed in accord with EPA
FIFRA Good Laboratory Practices (GLPs) in a laboratory that followed a
study protocol reviewed by EPA in advance of the initiation of the
analytical work. The performing laboratory and the study data were
subsequently audited by EPA FIFRA GLP inspectors and found to be in full
compliance with the protocol and with GLP regulations. The Council
believes that analytical data on the constituent composition of creosote
should originate from studies of creosote and not studies of soil with
unknown contaminants. This position is underscored by the fact the data
reliability of the analytical chemistry studies of creosote made
available to EPA is warranted by agency review of the study protocols
and the successful adherence to FIFRA GLP regulations. None of this can
be claimed for the contaminated soil data.

EPA Response: The Agency has made the suggested changes for Table
4.Hazard: Comments and Responses

Comment: Questioning if the risk assessment considers published and
peer-reviewed papers regarding the cancer causing properties of
benzo(a)pyrine and coal tars, and PAHs: 

L. Goldstein et al. 1998 'Tumors and DNA Adducts in Mice Exposed

to Benzo(a)pyrine and Coal Tars: implications for risk assessments' Env.
Health Perspectives:106 (Suppl. 6):1325-1333 

S. Nesnow et al. 1998 'Lung Tumorigenic Interactions in Strain A/J Mice
of Five Environmental Polycyclic Aromatic Hydrocarbons' Env. Health
Perspectives:106 (Suppl. 6):1337-1346.  

EPA Response:  The Agency has considered the published scientific
literature on the cancer-causing properties of benzo(a)pyrene, coal
tars, and PAHs. These data include those listed above as well as data
published by Gaylor et al (Risk Anal. 20(1): 81-85, 2000) and Schneider
et al. (J. Appl. Toxicol. 22: 73-83, 2002).  These studies showed that a
single chemical such as benzo(a)pyrene could not be used to estimate
absolute risk for coal tar mixtures, and that use of equivalency factors
to estimate risk from coal tar exposure tended to underestimate cancer
risk. However, it was also shown that the benzo(a)pyrene content of a
specific mixture could be suitable as an indicator of the relative
potency of the mixture for a specific exposure pathway. The Agency used
forestomach tumor response in a coal tar mixture as the cancer endpoint
for calculation of creosote cancer potency, which took into account the
point-of-contact nature of benzo(a)pyrene as a carcinogen. 

Comment: Taken as a whole the weight of evidence does not support a
conclusion that creosote is a known or potential human carcinogen.

EPA Response: The Agency has reviewed the data in both experimental
animals and in humans regarding the carcinogenicity of creosote. These
data are discussed within the Toxicology and Incident Report
disciplinary chapters of the creosote reregistration eligibility
decision.  A recently conducted study by Culp et al. (Carcinogenesis
19(1), pp. 117-124, 1998)  showed that 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. 

In humans, data are more tentative due to deficiencies in reporting of
the epidemiology studies available, but the data do show  increased
risks for development of a number of diseases including skin cancer and
nonmalignant skin disorders, bladder cancer, lung cancer and
nonmalignant respiratory diseases.

Comment:  Little or no supporting data exist from epidemiological
studies of creosote workers, and no demonstrable causal relationship
exists between creosote exposure and human cancer.

EPA Response: As previously mentioned, data in humans regarding
definitive conclusions about cancer and creosote exposure are tentative
based on study reporting deficiencies, but the available data do show 
increased risks for development of a number of diseases including skin
cancer and nonmalignant skin disorders, bladder cancer, lung cancer and
nonmalignant respiratory diseases.  These relationships need to be
examined further.  The data in experimental animals that do show a
clearly positive relationship between creosote exposure and cancer are
used in support of a weight-of-evidence determination that creosote has
carcinogenic potential in humans. The International Agency for Research
on Cancer (IARC) has classified creosote as a probable human carcinogen.

Comment: The weight of evidence suggests that aside from skin problems
likely associated with chronic irritation and phototoxicity, creosote
does not pose significant cancer or other health risks to workers.

EPA Response:  Several epidemiology studies in workers do show health
risks associated with exposure to creosote in addition to the known
irritancy of creosote. As noted in the Agency for Toxic Substances and
Disease Registry’s Toxicological Profile for Creosote (ATSDR, 2002;
available at:    HYPERLINK "http://www.atsdr.cdc.gov" 
http://www.atsdr.cdc.gov ), “workers exposed to coal tar creosote,
cola tar, coal tar pitch, and coal tar pitch volatiles in various
industrial environments [showed] increased cancer risk involving a
number of tissues including the respiratory tract, skin, lung, pancreas,
kidney, scrotum, prostate, rectum, bladder, and central nervous system.
Leukemia and lymphoma have also been diagnosed.”  

Comment:  The use of a single component (i.e., B(a)P) from a complex
mixture like creosote to estimate cancer risk is likely to result in
erroneous results and is inappropriate, particularly when the mixture
has been studied and sufficient, high- quality data are available to
assess the mixture directly.

EPA Response: The Agency acknowledges the possibility of obtaining
results with BaP that are not entirely accurate when studying a mixture
such as creosote.  Thus, as indicated earlier, the Agency has used data
conducted specifically with creosote or coal tar creosote to assess both
non-cancer and cancer risks. 

Comment: In this chapter of the PRA, OPP identifies eye irritation with
Pl/P13 creosote, mutagenicity, carcinogenicity, and possible
cardiomyopathy from inhalation of creosote aerosol, as toxicological
effects of concern. OPP also expresses concern about qualitative
developmental toxic effects. According to the PRA, the teratogenic
potential of creosote cannot be ruled out because high-dose fetal
malformations were observed in rats (but not in rabbits) at
maternally-toxic dose levels of PUP13 creosote, even though such changes
were not seen with P2 creosote in rats or rabbits. In addition, OPP
expresses concern about the potential for reproductive toxicity as a
result of its review of the reproductive toxicity testing conducted by
the Council. Moreover, EPA indicates that the dermal sensitization
studies submitted by the Council are not acceptable. 

Each of these concerns is addressed below as well as in extensive
details within the comment submission and the appendices to these
comments (Docket -  HYPERLINK
"http://www.regulations.gov/fdmspublic/custom/jsp/search/searchresult/do
cketDetail.jsp" \l "#" \o "EPA-HQ-OPP-2004-0402-0016" 
EPA-HQ-OPP-2003-0248-00 33).

There is a discussion of rabbit eye testing and the results within the
comments.  In summary, EPA should consider this evidence as possibly
qualifying creosote for Pesticide Category I11 Acute Toxicity Category
for Eye Irritation; but, in no case is it evidence of “significant
irritation” as stated by EPA in the PRA.

The relevance of reports of creosote mutagenicity and animal
carcinogenicity to human health are fully discussed by Dr. Tardiff in
Appendix I to these comments.

Cardiotoxicity (and pulmonary changes) are cited as toxicological
effects of concern by EPA. These concerns issue from the 90-day, or
subchronic, toxicity studies conducted on creosotes by the Council The
No-Observed Adverse Effect (NOAEL) for these studies was the low
exposure concentration, about 5 mg/ m3, meaning that exposure to a
creosote aerosol at this level was without exposure-related effects. 

The agency has misread the developmental toxicity studies submitted by
the Council. In reviewing the P 1/P 13 rat developmental toxicity study,
the agency failed to consider that treatment-related developmental
effects did not occur in the absence of maternal toxicity.  EPA does not
disagree with this reading of the study data, but maintains that the
“teratogenic potential of Pl/P13 Creosote cannot be ruled out”. This
unsupportable view of the rat developmental toxicity data on Pl/P13
creosote should be revisited by EPA. The absence of developmental or
phototoxic effects at maternally nontoxic dose levels in the rabbit
developmental toxicity study with Pl/P13 creosote also supports the
position that P 1/P13 creosote should not be regarded as a [potential
teratogenic or developmental toxicant. 

Pl/P13 and P2 creosotes were evaluated for the ability to produce
allergic skin sensitization in Guinea pigs. Reports of the initial
evaluations were submitted to EPA in November, 1993 and were
subsequently determined to be unacceptable because of a failure in the
laboratory positive control test for these assays. These studies were
assigned MRID numbers 43032 106 and 43032306 for Pl/P 13 and P2
creosotes, respectively. Each dermal sensitization assay was repeated
and proper results obtained. These studies were resubmitted to EPA in
June, 1995 but are not referenced or considered in the PRA. The MRID
numbers for those studies are 43675301 and 43675201 and the results of
the studies showed that P 1/P13 and P2 creosotes are not dermal
sensitization properties in the Guinea Pig.

EPA Response: The Agency will examine the results from the two
submissions cited above to determine if the results will change the
conclusions regarding creosote as a dermal sensitizer.  The Agency will
re-visit the teratogenic potential statements made for creosote and make
appropriate changes if needed.  It is noted that no special uncertainty
factors were applied in the creosote risk assessment regarding
susceptibility of infants or children. 

Comment: In the Human Risk Characterization chapter, OPP once again
inappropriately relies on the approach of using a single component of
creosote, B(a)P, as an indicator of toxicity. Specifically, OPP uses the
B(a)P cancer slope factor for creosote assessment. This approach to
assessment of a mixture is fully addressed in Dr. Tardiff’s appended
cancer risk assessment (Docket ID -0033). As explained, the use of a
single component (ie.,B(a)P) from a complex mixture like creosote to
estimate cancer risk is likely to result in erroneous results and is
inappropriate, particularly when the mixture itself has been studied
extensively and sufficient, high-quality data are available to assess
the mixture directly. In the case of creosote and coal tar products,
such studies are available and a better source of information on the
possible toxicity of creosote and cancer risk to exposed workers than
that of individual PAHs. This position comports with the conclusions of
the National Research Council. Accordingly B(a)P content alone cannot be
considered a reliable indicator of the potential carcinogenicity of a
complex hydrocarbon mixtures and should not be used as a surrogate in
classifying creosote or conducting a quantitative risk assessment of
occupational exposure to creosote.

EPA Response:  The Agency has since modified the cancer risk assessment
and has used the data of Culp et al. (1998) for characterization of
creosote cancer potential. The Agency is no longer using surrogate data
on benzo(a)pyrene for cancer risk assessment. 

Comment: The final paragraph of section 4.3 (“Summary and Conclusions
of the Health Effects of Creosote in Humans”) of this chapter appears
to be inconsistent with the statements appearing earlier in that section
about the important limitations of the extant epidemiology studies. A
detailed presentation of the literature and its applicability to
creosote is presented in the cancer risk assessment appended to these
comments (Docket ID -0033). The findings of that literature review
indicate that limited data exist from epidemiological studies of
creosote workers, and no demonstrable causal relationship exists between
creosote exposure and human cancer. Specifically, in the case of
creosote, epidemiological studies carried out on U.S. creosote workers
have not provided evidence of increased cancer morbidity or mortality
due to cancer (or any other chronic disease for that matter). Given
creosote’s long history of widespread use, it would be surprising that
no strong supporting evidence of an association exists if creosote were
a potent human carcinogen. The weight of evidence presented in these
studies suggests that aside from skin problems likely associated with
chronic irritation and phototoxicity, creosote does not pose significant
cancer or other health risks to workers.

EPA Response: The Agency notes the association of creosote exposure with
increased risk for several types of non-cancerous and cancerous
responses in humans as noted above.  However, the lack of a strong
causal association in human studies is based in part on significant
limitations in the reported data with respect to objective measurement
of exposure. 

Human Exposure (residential and dietary): Comments and Responses

Comment:  Two major shortcomings of the human health risk assessment
are: 1.)  The assessment is based on 2 surrogate chemicals rather than
the full mixture, 2.)  The assessment does not consider likely human
exposures to creosote-treated railroad ties that are widely used in home
gardens, retaining walls, and public landscapes.  The EPA has probably
underestimated the risk to human health by only considering 2 components
of creosote [benzo(a)pyrene and naphthalene].  The human health risk
assessment is too uncertain and surrogate data should not be use.  How
is EPA planning on handling the disposal issues?

EPA Response:  The creosote assessment has been revised based on new
data for creosote.  The revised assessment is based on the
carcinogenicity of creosote.  The previous assessment using BaP as an
indicator of potential worker cancer risk has been removed.  The use of
inhalation exposure to naphthalene is still regarded as relevant to
worker risk.  The landscaping use of creosote-treated lumber is
considered to be a misuse of the product.  The Agency does not typically
estimate risks based on misuse of pesticides.  The disposal of creosote
treated lumber will be considered during the risk mitigation and RED
development phase.

Comment This EPA creosote risk assessment does not adequately provide
the basis for protecting people and the environment from the risks of
creosote.  Because creosote is a persistent, bioaccumulative, and toxic
chemical (PBT), it should be phased out of production.  Re-cycled
railroad ties often end up in home and public landscapes, or are
disposed of in landfills.  The EPA should base its human health risk
assessment on all components of creosote, not just two.  EPA must also
assess important non-occupational exposures to landscape timbers
(dietary exposure, direct skin contact, children exposure).  

EPA Response:  See response above.

Comment: Real world residential post-application exposure scenarios must
be considered for recycled crossties, soil contamination from leaching. 

EPA Response: The landscaping use of creosote-treated lumber is
considered to be a misuse of the product.  The Agency does not typically
estimate risks based on misuse of pesticides.

Occupational Assessment: Comments and Responses

 

Comment: In the docket (-0023) the following published/peer reviewed
journal article was provided to be used in the creosote human exposure
risk assessment: “Borak, J, G. Siranni, H. Cohen, S. Chemerynski, and
F. Jongeneelen.  2002.  Biological vs. ambient exposure monitoring of
creosote facility workers.  Journal of Occupational and Environmental
Medicine, 44:310-319.”  (A PDF copy was attached to the e-mail).	

EPA Response:  Additional literature results have been incorporated into
the occupational assessment as well as the incident chapter.

Comment:  The EPA should suspend all creosote registrations and deny any
further registrations based on it’s own human health risk assessment
(pressure treatment handler scenarios and cancer risk estimates for all
occupational handler scenarios exceed the level of concern 1/1,000
exposed will get cancer).  

EPA Response:  The risk mitigation phase of the creosote RED will
determine the appropriate outcome based on risks and benefits of
creosote.

Comment:  Since…only 390 to 600 individuals are actually involved in
pressure-treated with creosote, the upper-bound estimate suggests no
additional cancer cases would result in out of a normal background
incidence of between 98 and 125 cases of cancer in a population of this
size.  The best estimate would suggest that no additional cases of
cancer would occur in this population given the exposure potential and
carcinogenic potency of creosote.

EPA Response:  The risk mitigation phase of the creosote RED will
determine the appropriate outcome based on risks and benefits of
creosote.

Comment: In view of the small population exposed, the proper
interpretation of these cancer risk estimates is that wood treatment
workers exposed to creosote over the course of a working lifetime will
experience no additional cancers.  Accordingly, any added cancer risk
posed by exposure to creosote falls within normally accepted regulatory
risk and poses no elevated cancer risk.

EPA Response: The risk mitigation phase of the creosote RED will
determine the appropriate outcome based on risks and benefits of
creosote.

Comment: Based on the differences in product content and use patterns,
it is clear that use of coal tar-derived products other than creosote to
assess the risk of creosote is likely to result in an over-estimate of
risk due to a higher content of carcinogenic PAHs and other compounds
and to products use patterns that result in higher exposure potential to
workers using these products.

EPA Response: The creosote assessment has been revised based on new data
for creosote.  The revised assessment is based on the carcinogenicity of
creosote.  The previous assessment using BaP as an indicator of
potential worker cancer risk has been removed.  The use of inhalation
exposure to naphthalene is still regarded as relevant to worker risk.

Comment: “[T]he potential for development of non-cancer hazards
associated with creosote exposures in the workplace is very low and,
given the type of effects most likely to occur, would not be considered
irreversible or serious detriments to the long-term health or well-being
of the creosote wood treating workers if they occurred.”

EPA Response: The risk mitigation phase of the creosote RED will
determine the appropriate outcome based on risks and benefits of
creosote.

Comment: EPA revised worker exposure scenarios to reflect the
registrants’ voluntary cancellation of all non-pressure treatment
uses, particularly those scenarios in the draft PRA that relied on the
Pesticide Handlers and Exposure (“PHEDS”) and Chemical Manufacturers
Association (“CMA”) data bases. In light of this revision, it is not
clear why in Table 1 of the Human Exposure chapter of the PRA that EPA
indicates that the source of data for Exposure Scenario (1a)
(“Mixing/Loading/Applying Liquids at a Pressure Treatment Facility
(treatment operator)”) is exposure study data from Creosote Council II
and PHED. 

EPA Response:  EPA agrees and the assessment has been updated to reflect
the cancellation of non pressure treatments.

Comment: The Human Exposure chapter of the PRA expresses the tentative
and preliminary view that workers engaged in pressure-treatment of wood
with creosote may receive inhalation and or dermal exposure that results
in a risk exceeding the target margin of exposures (MOEs) for both
cancer and non-cancer risks. The Council commissioned Dr. Robert Tardiff
of The Sapphire Group, Inc. to conduct probabilistic assessments for the
cancer and non-cancer risks to workers engaged in pressure-treatment of
wood with creosote. Those assessments are included as Appendices 1 and 2
to these comments and warrant OPP’s careful review and consideration.
In summation, the results of the Dr. Tardiff s probabilistic risk
assessments indicate that the weight of evidence suggests that aside
from skin problems likely associated with chronic irritation and
phototoxicity, creosote does not pose significant cancer or other health
risks to workers. 

The assessment concludes: 

that the upper-bound estimate for cancer incidence in creosote wood
treating workers suggests that no additional cancer cases would result
out of a normal background incidence of between 98 and 125 cases of
cancer in a population of this size. The best estimate would suggest
that no additional cases of cancer would occur in this population given
the exposure potential and carcinogenic potency of creosote.

Estimated workplace risks for creosote workers also fall well below the
OSHA level of acceptable cancer risk in the workplace (1 x 10E-3).

Added cancer risk posed by exposure to creosote during wood pressure
treatment operations falls within normally accepted regulatory risk (E-6
to E-4), and thus poses no elevated cancer risk. In other words, in view
of the small population exposed, the proper interpretation of the
probabilistic cancer risk estimates is that wood treatment workers
exposed to creosote over the course of a working lifetime will
experience no additional cancers.

The probabilistic assessment of non-cancer risks to workers engaged in
pressure treatment of wood with creosote generally fall below the Hazard
Index of 1.0. This demonstrates that non-cancer hazards associated with
creosote exposure are low, and given the type of non-cancer effects that
are most likely to occur, effects of overexposure would be most likely
reversible and not result in long-term health detriments if they
occurred.

EPA Response:  The creosote human risk assessment has been substantially
revised.

Comment: The PRA’s review of the Council’s Creosote Worker Exposure
Study is essentially unchanged from the draft PRA. The Council again
requests OPP to consider its February 2003 comments on the draft PRA,
specifically those provided by Dr. Mark Bookbinder.

EPA Response: The creosote human risk assessment has been substantially
revised.

 

Environmental Risk and Fate: Comments and Responses

Comment:  Other essential types of data are also missing, such as
environmental fate data to estimate whole creosote and individual PAH
leaching from treated wood in aquatic environments.

EPA Response:  The Agency has tried as best as possible to incorporate
as much available data as possible; however, it is the concentrations of
PAHs and other components in the waterways are present from so many
sources that it is not possible to conduct an unambiguous environmental
fate assessment

Comment: As to the environmental/ecological risk assessment for
creosote, the Council again urges OPP to abandon its current approach,
and instead, utilize the definitive work of Dr. Kenneth Brooks, who has
conducted a holistic assessment of the environmental fate of creosote in
marine, estuarine, and terrestrial environments.  

EPA Response:  The amended fate chapter has included Brooks’ studies,
and comments have been added.

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