EPA SCIENTIFIC ADVISORY COMMITTEE ON CHEMICALS
CHARGE TO THE PANEL - 1-BROMOPROPANE (1-BP)
CASRN: 106-94-5
As amended by the Frank R. Lautenberg Chemical Safety for the 21st Century Act on June 22,
2016, the Toxic Substances Control Act (TSCA), requires the U.S. Environmental Protection
Agency (EPA) to conduct risk evaluations on existing chemicals. In December of 2016, EPA
published a list of the initial ten chemical substances that are the subject of the Agency's
chemical risk evaluation process (	), as required by TSCA. 1-BP is one of the first
ten chemical substances to undergo a peer review by the Science Advisory Committee on
Chemicals (SACC). In response to this requirement, EPA has prepared and published a draft risk
evaluation for 1-BP. EPA has solicited comments from the public on the draft and will
incorporate them as appropriate, along with comments from peer ie\ iewers, into the final risk
evaluation.
The draft risk evaluation contains the following components:
Presentation of chemistry and physical-chemical properties
Characterization of uses/sources
Systematic review
Environmental fate and transport assessment
Occupational exposure assessment
Environmental, and consumer exposure assessment
Environmental hazard assessment
Human health hazard assessment
Risk characterization
Risk determination
The focus of this meeting is to conduct the peer review of the Agency's draft risk evaluation of
1-BP. At the conclusion of the peer re\ iew process, EPA will use the reviewers'
comments/recommendations, as well as public comment, to finalize the risk evaluation.
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CHARGE QUESTIONS:
EPA is seeking SACC advice on the clarity and scientific underpinnings of the overall
assessment. The peer review should consider whether the conclusions presented in the draft risk
evaluation are clearly presented, scientifically supported and based on the best available
scientific information. The SACC should also consider whether the methods employed to
generate the information are reasonable for and consistent with the intended use of the
information. As per TSCA, where unreasonable risks are identified, once finalized the risk
evaluation will be used to support rulemaking to mitigate identified risks.
Throughout the peer review, the SACC should be mindful thai TSCA now requires that EPA use
data and/or information in a manner consistent with the "best a\ ailable science" and that EPA
base decisions on the "weight of the scientific evidence" I - I'.Vs I'inal Rule, Procedures for
Chemical Risk Evaluation Under the Amended j ¦	ol Act (82 FR 33726).
defines "best available science" as science 1 hi.il is reliable and unbiased This involves the use of
supporting studies conducted in accordance with sound and objec1i\ e science practices,
including, when available, peer reviewed science and supporting studies and data collected by
accepted methods or best available methods (if the reliability of the method and the nature of the
decision justifies use of the data). The Final Rule also defines the "weight of the scientific
evidence" as a systematic review method, applied in a manner suited to the nature of the
evidence or decision, that uses a pre-eslablished protocol to comprehensively, objectively,
transparently, and consistently identify and e\ aluale each stream of evidence, including
strengths, limitations, and relevance of each study and to integrate e\ idence as necessary and
appropriate based upon strengths, limitations, and rele\ance
Below, are a set of charge questions lor each major element of the risk evaluation. The SACC is
expected to consider questions and issues raised during public comment as part of its
deliberations
1. Content ami Organization
EPA's I'inal Rule, .Pro,.,,..,.,,,	al Risk Evaluation Under the Amended Toxic
Substam	~ol Act (8	6) stipulates the process by which EPA is to
complete risk. e\ aluations under the Frank R. Lautenberg Chemical Safety for the 21st
Century Act. To that end. I-PA has completed a draft risk evaluation for 1-BP.
As part of this risk e\ aluation for 1-BP, EPA conducted an assessment of potential
environmental, occupational and consumer exposures. The evaluation considered
reasonably available information, including manufacturing, import, processing, distribution
in commerce, use, and disposal information. It is important that the information presented
in the risk evaluation and accompanying documents are clear and concise and describe the
process in a scientifically credible manner.
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/'/case comment on l/ic overall conienl. organization. andpresentation oj the
droit risk evaluation oj l-HI'.
I'lease provide surest ions for improving the clarity oj the injormalion
presented in the documents.
Systematic Review (Draft Risk Evaluation and Supplemental Files)
To meet the TSCA scientific standards, EPA applied systematic review approaches and
methods to support the draft risk evaluation of 1-BP Information on the approaches and/or
methods is described in the draft risk evaluation as well as the following documents:
•	Application of Systematic Review in TSC.	( S. EPA. 2018a)
•	Strategy for Conducting Literature Searches for 1 -BP: Supplemental Document for the
TSCA Scope Document (U.S. EPA. 2C )
•	1-BP (CASRN: 106-94-5) Bibliography Supplemental Tile for the TSC A Scope Document
(' J." \ kIO-OPPT-2Ql''A>7 j | 004' )}
•	Scope of the Risk Evaluation for I -UP («i.	)
•	Problem Formulation for 1-Bromopropane (	b)
•	Draft Risk Evaluation for 1-Uromopropane (I -UP). Systematic Review Supplemental File:
Data Quality Evaluation of Environmental I ale and Transport Studies (EPA. )
•	Draft Risk Evaluation lor I-Uromopropane (I-UP). Systematic Review Supplemental File:
Data Extraction Tallies for I ji\ironmental I ale and Transport Studies (EPA. 2019b)
•	Draft Risk Evaluation for I -Uromopropane (I -UP), Systematic Review Supplemental File:
Data Quality I a aluation of I ji\ ironmental Release and Occupational Exposure Data (EPA.
)
•	Draft Risk I a aluation for I-Uromopropane (I-UP), Systematic Review Supplemental File:
Data Quality Evaluation of En\ ironmenlal Release and Occupational Exposure Data for
Common Sources (!¦";- \	)
•	Draft Risk Evaluation for 1-Bromopropane (1-BP), Systematic Review Supplemental File:
Data Quality F\ aluation for Consumer Exposure (EPA. 2019a)
•	Draft Risk I a aluation for 1 -Uromopropane (1-BP), Systematic Review Supplemental File:
Data Extraction for Consumer Exposure (EPA. 2019c)
•	Draft Risk Evaluation for 1 -Bromopropane (1-BP), Systematic Review Supplemental File:
Data Quality Evaluation of Ecological Hazard Studies (EPA. 2019d)
•	Draft Risk Evaluation for 1-Bromopropane (1-BP), Systematic Review Supplemental File:
Updates to the Data Quality Criteria for Epidemiological Studies (EPA. 2019j)
•	Draft Risk Evaluation for 1-Bromopropane (1-BP), Systematic Review Supplemental File:
Data Quality Evaluation of Human Health Hazard Studies - Epidemiologic Studies (EPA.
20190
•	Draft Risk Evaluation for 1-Bromopropane (1-BP), Systematic Review Supplemental File:
Data Quality Evaluation of Human Health Hazard Studies (EPA. 2019h)

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() 2.1
() 2.
I'lease comment oil l/ie approaches and or methods used lo support am/inform
the gathering. screentng. evaluation. am! integration of ilaia information used in
l/ie I h alt Risk I .valuation for l-Hromopropane (I-HI').
I'lease also comment on the clarity of the information as presented related to
systematic review and surest improvements as warranted.
3. Occupational Exposure Assessment (Section 2.3.1 of the Draft Risk Evaluation)
EPA evaluated acute and chronic exposures to workers lor conditions of use in industrial and
commercial settings. For exposure via the inhalation pathway: KPA quantified occupational
exposures for both workers and occupational non-users haseel on a combination of
monitoring data and modeled exposure concentrations I'or exposure via the dermal route,
EPA modeled exposure for workers, accounting lor the effect of \ olatilization and glove use.
EPA assumed dermal exposure would not occur lor occupational non-users.
EPA assumed that workers and occupational non-users would be adults of both sexes ( 16
and older, including women of reproductive age) based on occupational work permits
I'lease comment on the approaches am! estimation methods, models, ami data
used in the occupational exposure assessment.
I'lease provide any specific suggestions or recommendations for alternative
data, or estimation methods that could he considered hy the . Ityiicy for
conducting occupational exposure assessment.
4. Consumer Exposure. I ssessment (Section 2.3.2 of the Draft Risk Evaluation)
EPA e\ aluated acute inhalation exposure to consumers for the following product use
scenarios including adhesi\ e accelerants, general spray cleaners, spot cleaner/stain removers,
mold cleaning release, general cleaners-degreasers, degreasers-electronics, coin/scissors
cleaner, automobile AC Hush products, and insulation which contain 1-BP. EPA also
evaluated acute dermal exposure to consumers using general cleaners-degreasers,
coin/scissors cleaner, and automobile AC flush products containing 1-BP. Dermal exposure
was evaluated for these three uses based on the assumption that use could be a constant
supply of a product in contact with the skin such that evaporation from the skin does not
occur (submersion into a pool of product, or a product-soaked rag covering the skin).
Consumer uses of the above listed products are not expected to be chronic in nature and
therefore EPA did not evaluate chronic inhalation or dermal exposure.
EPA evaluated exposure to consumers in residential settings following acute exposure and
considered both users of a product and bystanders within the residence where the product
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was used. EPA considered users to be either adult (>21 years of age) or youth (16-20 years of
age). A second youth group (11-15 years of age) are included in the evaluation although this
age group is not expected to be a significant user of most product uses evaluated. Bystanders
within a residence where product is used include individuals of any age group (infants,
children, youth, adults, elderly).
Three models (CEM, MCCEM, and IECCU) were used to evaluate acute inhalation exposure
depending on the condition of use evaluated. These three models are defined and discussed in
detail within the 1-BP risk evaluation. Dermal exposure was evaluated using CEM.
Product specific consumer monitoring information was not identified during the systematic
review process, therefore, model inputs related to consumer use patterns (duration of use,
mass of product used, room of use, and similar inputs) are bused on survey data found in the
literature as described and referenced within the I -BIJ risk e\ alualion. Weight fraction of
chemical within products are based on product specific SDS sheets Default values utilized
within the models are based on literature i e\ ieued as part of model development as well as
EPA's Exposure Factors Handbook.
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I'lease comment on the approaches, models. exposure or use information (e.g..
information on duration, tmmher of user events, amount used) and estimates for
the nine consumer uses evaluated for this risk evaluation.
I'lease provide any specific suggestions or recommendations jor alternative
approaches, models, exposure or use information te. g.. information on duration,
number of user events, amount used) that could be considered by 1 hi
developing and or refining the exposure assumptions am! estimates for the nine
consumer uses evaluated for this risk evaluation.
/ K-rmal exposure was evaluated using a permeability method within ( L.\ / based
on the availability of a permeability coefficient found within the literature in a
study by \J( )SII. /he permeability method within ('IA / does not consider
evaporation when estimating exposure which is the primary basis for 1.1'. 1
evaluating dermal cxj'osiire only jor consumer uses where there is a constant
supply of product against the skin during use or a barrier prohibiting
evaporation. I'lease comment on the chosen approach and provide any
suggestions or recommendations jor alternative approaches, dermal methods,
models, or other information which may guide I1 in developing ami refining
the dermal exposure estimates.
5. Environmental Hazard and Risk Characterization (Sections 3.1 and 4.1 of the Draft Risk
Evaluation)
Available data indicates that 1-BP exhibits a moderate environmental hazard to aquatic
species. A screening-level analysis of potential risk to aquatic species indicates that expected
environmental concentrations are below hazard thresholds for aquatic species. In addition, a
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qualitative consideration of physical-chemical properties and the conditions of use in this
assessment indicate that risks to sediment-dwelling invertebrate species and terrestrial
species are not expected.
(hily a few environmental lest dam endpoinis {including IA II. IJ arc available in
the public domain for I-HI'. Mosi arc from llic IA HA wehsilc. I allempicd
lo ohlain llic full IA II. 1 si i lilies with no success. Since llic studies were in
Ircnch and Japanese land no I 'A. I. sponsor). I decided not to make further
allempis to find llic studies. (iiven that the IA II. 1 environmental test data results
arc in the public domain. Id'. 1 decided to use the experimental data, /'lease
comment oil the rcasonah/cncss oj this approach for llic environmental hazard
assessment <>1 I-HI'.
1 determined lhal there are no environmental risks hascil on a scrcening-
Icvcl assessment oj risk using environmental hazard data. IN/ exposure dam.
/ale in/ormalion. and physical chemical properties, /'lease comment on whether
llic in/ormalion presented supports the fim/ings oiiilincil in the dra/i risk
characterization seel ion.
Hazard and Dose-Response Assessments (Section 3.2 of I lie Draft Risk Evaluation)
EPA considered llic ad\crsc human health effects lor I-UP across organ systems and
screened to those that are relevant, sensili\ e. and found in multiple studies. The 1-BP human
health hazard systematic review process screened 813 studies and obtained 29 studies that
were relevant and applicable to the PF.CO statement. Five of these studies were unacceptable
based on data c\ aliiation criteria The remaining database of 24 studies included
epidemiological studies that examined associations between 1-BP exposure and endpoints
related to effects on the ncr\ ons system, as well as repeat-dose experimental animal studies.
For hazard identification and dose-response, EPA reviewed the evidence for 1-BP toxicity
and selected 1i\er toxicity, kidney toxicity, reproductive/developmental toxicity,
neurotoxicity, and cancer. Data on toxicity following acute exposures, and genotoxicity were
also considered. From these effects, EPA selected endpoints supported by the weight-of-the-
scientific evidence for non-cancer and cancer that demonstrated the most robust, sensitive
and consistent ad\ crsc human health effects for risk characterization, that were amenable to
quantitative analysis for dose-response assessment, and that were appropriate toxicological
studies to be used for acute and chronic exposure scenarios. EPA used benchmark dose
(BMD) modeling where practicable and, when BMD values were adequate, they were used
to generate the Point of Departure (POD) for characterizing chronic and acute exposure
scenarios. EPA determined that using developmental toxicity and neurotoxicity endpoints for
dose-response calculation would be protective of the most sensitive life stages, including the
developing fetus for non-cancer PODs and risk estimates.
For the non-cancer assessment, EPA identified liver toxicity, kidney toxicity,
reproductive/developmental toxicity, and neurotoxicity in the risk assessment as adverse

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human health effects for risk characterization. EPA used these endpoints to calculate PODs
to assess non-cancer risks associated with chronic inhalation exposures.
I.v pan of the review. please comment on the choice of these einlpomis as l'( )J >s
for assessing risks in humans associaieil inth acme am! chrome inhalation
exposures lo /-HI'. Specifically, are there other data thai /'./'. I could have
considered jor the hazard identification and dose-response associaieil with
acme inhalation exposures '' If so. please provide specific data am! references.
. Ire there other data thai I.!'. I could have considered jor l he hazard
identification ami dose response associated with chrome inhalation exposures '
If so. please provide specific data and references.
J'/ease comment on the II'()/. analysis for the choices of non-cancer endpoinis
for the acme am! chrome risk scenarios. J'lease provide additional data, dam
inierpreialion or information thai would have informed the II'(analysis and
select ion of critical studies for l he J'( )l >s.
The CSAC Peer Review of the Application of Systematic Review in IS(I Risk Evaluations
document (	£018 a) recommended that while llie majority of exposures are occurring
via inhalation, and inhalation exposure is llie most important, dermal exposures might be an
important contributor to overall exposure and an estimate lor dermal exposure should be included
in the evaluation, with gaps/limitations clearly staled to address another potential workplace
exposure pathway Limited toxicological data is a\ ailaMe hy the oral route, and no repeated-
dose toxicity studies In the dermal route were identified 011 I -BP. Physiologically based
pharmacokinetic pharmacodynamic (PBI'K I'D) models that would facilitate route-to-route
extrapolation ha\ e not been identified, and there are no relevant kinetic or metabolic
information for 1-BP that w ould facilitate de\ elopment of dosimetric comparisons.
Therefore, w hen N\\ deri\ ed HEDs for dermal exposures, the limited oral studies were not
used and III -l)s for dermal exposures were deri\ ed by extrapolating from the inhalation
PODs
/'/ease comment on the assumptions, strengths. am/ weaknesses of this approach
for determining derma!!'()/ >s in the non-cancer assessment.
In the 2016	ierrt (	SO 16). decreased live litter size (i.e. reduced
number of li\ e pups per litter) was the endpoint selected as most relevant for calculating risks
associated with developmental toxicity following chronic, exposures ( esearch. 2001).
A BMR of 5% was used to address the severity of this endpoint (	) This
endpoint choice is a combination of reproductive effects where a BMR 10% relative deviation
would be used and developmental effects of post implantation loss which is considered a
severe effect like mortality where a BMR of 1% relative deviation would be used and so an
intermediate value of 5% was used. The POD for the decreased live litter size was a BMDL
of 43 ppm. The CSAC Peer Review of the	tft Risk Assessment (U.S. EPA. 2016)
recommended using nested modeling on this developmental endpoint to account for intra-
litter correlations and litter specific covariates. In response to this recommendation, EPA
used the BMDS nested dichotomous model, evaluated multiple covariates of dam weight and
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number of implantation sites and selected the NCTR model. However, this model can only be
applied to increases in effects and therefore, increased post-implantation loss was the
endpoint selected as most relevant for calculating risks associated with developmental
toxicity following chronic exposures (WIL Research. 2001) using nested modeling. A BMR
of 1% was used to address the severity of this endpoint which is considered a severe effect
like mortality (	1112.). The POD for the increased post-implantation loss was a
BMDL of 23 ppm.
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/'/case comment on the nested modeling approach and the selection of em/point
and whether lhe risk evaluation has adequately described the use of this model.
For the cancer risk assessment, EPA derived the inhalation unit risk (IUR) based on lung
tumors in female mice. The precise mechanism(s) models) of action of 1-BP carcinogenesis
are not clearly understood. There are, howe\ cr. an abundance of data, including in vitro tests,
metabolism across species, SAR and other potential mechanisms of action, that provide a
basis for a weight-of-evidence (WOE) e\ aliiation The WOE evaluation presented in the draft
1-BP Risk Evaluation proposes a mutagenic, and possibly additional, modes of action for
carcinogenesis. Other possible mechanisms of action oxidative stress, immunosuppression,
and cell proliferation—could act s\ nergistically to complete the multi-stage process of
carcinogenesis. Per EPA Guic s for Carcinogen	sessment, overall, the totality of
the available data/information and the WOE analysis lor the cancer endpoint was sufficient
to support a mutagenic mode of action for 1-IJP carcinogenesis
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LI'. I concluded in the risk assessment that I-lil' carcinogenesis occurs through
a mutagenic mode oj action (\ l.\ l().\) based on the totality oj the available
data information am! the IIY )L. I'lease comment w hether the cancer hazard
assessment has adequately described the li( )L regarding the \ l.\ l( 1I.
typically. LI'. I uses the benchmark dose modeling softw are (HMPSt with a
H\ IR oj /<>"» and the models are restricted to multistage models or the broader
suite oj dicholomons models in H.\ 11 >\ and a single best model is chosen for the
J'( )l K LI'. 1 used an alternative approach to calculate the cancer l'( )l > versus the
standard approach oj choosing best jn model and to assess the impact oj model
uncertainly. Hriej/y. 1.1'. I used two model averaging approaches fjrequeiitisi
and Hayesian) considering multiple benchmark dose models to calculate the
l'( )J > at benchmark response (H\ IR) levels oj I). !"<> and 10"" and jor added and
extra risk. I'lease comment on the assumptions, strengths and weaknesses oj the
model averaging approach jor determining the !'()! > in the cancer assessment.
In agreement with 1.1'. 1 's long-standing approach, all three tumor types from
the XII' sillily I	w ere dose-response modeled ivilli multistage models
using the typical constrained model coefficients ><> (LI'A. 20/2). I inler the I .S.
Id'. 1 's 200? cancer guidelines (	). qiiaimialive risk estimates
from cancer bioassay data w ere calculated by modeling the data in the observed
range to estimate a H.\ H I for a H\ IR of /0"„ extra risk, w hich is generally near
the low end of the observable ranifc for standard cancer bioassav data. Ihe
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Ii\ H 's ciin/1>.\ l( I s are show n /or each oj l/ic three cancer dalasels. /he results
for a IS.\ 1R oj 0. !"<> added risk arc presented for comparison, /'/case comment
on the assumptions, strengths am/ weaknesses oj the inn It is/age modeling
approach for determining the /'()/ > in the cancer assessment.
7. Human Health Risk Characterization (Section 4.2 of the Draft Risk Evaluation)
EPA quantified non-cancer risks based on the Margin of Exposure (MOE), which is the
product of dividing the scenario specific exposure into the hazard point of departure which is
no adverse effect level, based on animal and/or human studies. EPA calculated MOEs for
acute or chronic exposures separately based on the appropriate noncancer POD and estimated
exposure concentrations adjusted for durations. To determine if unacceptable risks were
present for relevant exposure scenarios, 1he end point-specific MOF.s were compared to the
endpoint-specific benchmark MOEs. The benchmark MOEs were the product of all of the
relevant UFs identified for each non-cancer POD If the MOE estimate was less than the
benchmark MOE, the exposure scenario lor non-cancer endpoints was interpreted as a human
health risk. Cancer risk estimation consisted of multiplyinu the occupational scenario-
specific exposure estimates by the cancer IUR to estimate the extra cancer risk. Extra lifetime
cancer risk estimates from 1 -EiP exposure were compared to benchmark cancer risk levels of
10"6, 10"5 and 10"4 (i.e., 1 in 10,000, 1 in 100,000 and 1 in 1.000,000).
The Frank R. Laulenbei u Chemical Safety for the 21 st Century Act (2016; amended TSCA
(TSCA §§ 6b[4a|) states that "potentially exposed or susceptible subpopulations" (PESS)be
considered in the risk e\ aluation process. "Ihe . \dministrator shall conduct risk evaluations
pursuant to this paragraph to determine whether a chemical substance presents an
unreasonable risk of in/ury to health or the environment, without consideration of costs or
other non-risk factors, including an unreasonable risk to a potentially exposed or susceptible
subpopnlation identified as relevant to the risk evaluation by the Administrator, under the
conditions of use. " Further, amended TSCA specifically includes infants, children, and
pregnant women in its definition of PESS (TSCA §§ 3[ 12] )- "The term 'potentially exposed
or susceptible subpopulaiion' means a group of individuals within the general population
identified by the . idmimsiraior who, due to either greater susceptibility or greater exposure,
may be at greater risk than the general population of adverse health effects from exposure to
a chemical substance or mixture, such as infants, children, pregnant women, workers, or the
elderly. "
EPA interpreted the endpoint of decreases in live litter size following exposure to 1-BP
before and during gestation, as a surrogate for frank developmental effects, as relevant to
humans per EPA's Guidelines for Developmental Toxicity Risk Assessment. EPA used this
endpoint to calculate a point of departure (POD) to assess non-cancer risks associated with
acute inhalation exposures to 1-BP.
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I'lease comment on the assumptions, strengths ami w eaknesses of the ,\ l( d.
approaches nseil to estimate the non-cancer risks to workers and occupational
non-users fe.g. adults oj reproductive age) follow ing acme inhalation exposures
to I-HI', including lhe .\ l( )/\s presented in the document. Specifically,
please suggest alternative data thai could he used. I'lease comment on the
selection of uncertainly factor values in deriving the benchmark /()l. for acme
inhalation exposures.
I'lease comment on the assumptions, strengths ami w eaknesses oj the \ H d.
approaches used to estimate the non-cancer risks to consumers follow ing acme
inhalation exposures to l-HJ'. including the \l( d .s presented m the document.
Specifically, please suggest alternative data thai could he used. I'lease comment
on the selection oj uncertainly factor values in deriving the benchmark \ Hdfor
acute inhalation exposures.
I'lease comment on the assumptions, strengths and w eaknesses oj the \ H d.
approaches used to estimate the non-cancer risks to workers am! occupational
non-users follow ing chrome inhalation exposures io /-/>/'. including the \ l( )Ls
presented in the document. I'lease comment on the selection of uncertainly
factor values in deriving the benchmark \ H d. for chronic inhalation exposures.
I'lease comment on the assumptions, strengths ami w eaknesses of the approach
used to estimate extra lifetime cancer risks lo workers w hich Id', \-denved from
an inhalation mm risk based on lung minors hi female mice for estimating
incremental or extra individual lifetime cancer risk.
I'lease comment on whether the risk characterization has adequately described
the assumptions, uncertainties and data /imitations in the methodology used lo
assess risks from l-HI'. /'lease comment on whether this information am!risk
conclusions are presented in a logical, transparent manner ami provide
suggestions thai could increase clarity in the risk characterization.
/'/ease comment on whether the risk characterization has adequately ii/cnlificil
and characterized the "potentially exposed or susceptible siibpopulalions "
(J'LSS) based on a thorough review of the available I-III' exposure and health
effects data on both potentially exposed and biological susceptible
siibpopulalions.
General Risk Characterization (Sections 4.1, 4.2, and 4.3 of the Draft Risk Evaluation)
After consideration of all information identified by EPA that pertains to 1-BP, EPA
concluded that 1-BP presents an unreasonable risk of injury to health or the environment
under the conditions of use. EPA made these determinations considering risk to potentially
exposed or susceptible subpopulations identified as relevant, under the conditions of use
without considering costs or other non-risk factors.

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/'/case comment on the ob/ectivity of the iinderlying data used to support the
risk characterizations and the sensitivity of I \ conclusions lo analytic
assumptions.
I'lease comment on the characterization oj uncertainties and assumptions
including w hether 1 has presented a clear exphnalion of underlying
assumptions, accurate coniexiiiahzalion of uncertainties ami. as appropriate,
the probabilities associated i villi both optimistic ami pessimistic pro/ecltons.
including best-case and worst-case scenarios.
J'lease provide information on additional uncertainties ami assumptions that
I1 has not adequately presented.
I'lease comment on w hether the information presented supports the fiinlings
outlined m the draft risk characterization section. If not. please suggest
alternative approaches or information that could be used to develop a risk
finding in the context of the requirements of I \ I tnal Rule, 1'rocedures jor
('hemical Risk /. valuation I nder the . Intended loxic Substances ('ontrol. let
f\2 I R it-y».
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References
(2019a). Draft Risk Evaluation for 1-Bromopropane (1-BP), Systematic Review
Supplemental File: Data Extraction for Consumer Exposure.
(2019b). Draft Risk Evaluation for 1-Bromopropane (1-BP), Systematic Review
Supplemental File: Data Extraction Tables for Environmental Fate and Transport Studies.
(2019c). Draft Risk Evaluation for 1-Bromopropane (1-BP), Systematic Review
Supplemental File: Data Quality Evaluation for Consumer Exposure.
(2019d). Draft Risk Evaluation for 1-Bromopropane (1-BP), Systematic Review
Supplemental File: Data Quality Evaluation of Ecological Hazard Studies.
(2019e). Draft Risk Evaluation for 1-Bromopropane (1 -BP), Systematic Review
Supplemental File: Data Quality Evaluation of Environmental Fate and Transport
Studies.
(2019f). Draft Risk Evaluation for 1-Bromopropane (I-liP). Systematic Review
Supplemental File: Data Quality Evaluation (if Environmental Release and Occupational
Exposure Data.
(2019g). Draft Risk Evaluation for I -Ikomopropane (1-BP), Systematic Review
Supplemental File: Data Quality Evaluation of I -n\ iron mental Release and Occupational
Exposure Data for Common Sources.
(2019h). Draft Risk Evaluation for 1-Bromopropane (1-BP), Systematic Review
Supplemental File: Data Quality Evaluation of Human I lealth Hazard Studies.
(2019i). Draft Risk Evaluation for 1-Bromopropane (1-BP), Systematic Review
Supplemental File: Data Quality Evaluation of I luman Health Hazard Studies -
Epidemiologic Studies.
(2019j). Draft Risk Evaluation for I-Bromopropane (1-BP), Systematic Review
Supplemental File: Updates to the Data Quality Criteria for Epidemiological Studies.
U.S. EPA. (2005). Guidelines for carcinogen risk assessment [EPA Report] (pp. 1-166).
(I-IW P-<).i 001F). Washington, DC: U.S. Environmental Protection Agency, Risk
Assessment I orum. http://wiyiv2.epa.gov/osa/guidelines-carcinoeen-risk-assessment
U.S. (2) TSCA work plan chemical risk assessment: Peer review draft 1-
bromopropane' (n-Propvl bromide) spray adhesives, dry cleaning, and degreasing uses
CASRN 11IO-D4-5 [I P \ Report], (EPA 740-R1-5001). Washington, DC.
https://wwv	Toduction/files/2016-03/documents/l -
bp report z	:es final.pdf
(2017a). Scope of the risk evaluation for 1-Bromopropane [EPA Report], (EPA- 740-
R1-7009). https://www.epa.gOv/sites/production/files/2 /documents/bp scope 06-
22-17.pdf
U.S. EPA. (2017b). Strategy for conducting literature searches for 1-Bromopropane (1 -bp):
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