1-BP RA Public Comments Collated 5/12/16

1.0. Background and Scope

Commenter Name: Eve Gartner

Commenter Affiliation: Earthjustice et al.

Document Control Number: EPA-HQ-OPPT-2015-0084-0016

Comment Excerpt Number: 2

Charge Question: 1-2 Scope and conceptual model

Comment Excerpt: 

1. The Draft Assessment must consider general and vulnerable population exposures to 1-BP

The Draft Assessment is incomplete because it does not address the risks posed to communities 

living near sources that use or manufacture 1-BP.[1] EPA states that it is excluding general 

population exposures “because no reliable exposure data for calculating general population risks 

are available.” There are three problems with this approach: First, ignoring known general 

population exposures is inconsistent with TSCA. Second, the Draft Assessment ignores evidence 

that communities are exposed to 1-BP as a result of emissions from facilities using this chemical. 

Third, general population exposures will likely have a disproportionate adverse impact on lowincome communities and communities of color.

 a. TSCA requires EPA to consider risks from all exposures

Under TSCA, in assessing a chemical substance, EPA must consider whether “the manufacture, 

processing, distribution in commerce, use, or disposal,” or “any combination of such activities,” 

“presents or will present an unreasonable risk.”[2] Moreover, in order to promulgate a rule under 

TSCA section 6(c), EPA must “consider and publish a statement with respect to ... the effects of 

such substance ... on health and the magnitude of the exposure of human beings to such 

substance....”[3] EPA cannot fulfill the requirements of TSCA to consider the “combination” of 

exposures and to document the “magnitude” of human exposures, unless its final 1-BP risk 

assessment takes into account the risks from all known exposures including the possibility, 

discussed immediately below, that communities in the vicinity of facilities using or 

manufacturing 1-BP will inhale the chemical as a result of its presence in ambient air.

 b. There is evidence of community exposure to 1-BP from ambient air

There is evidence that communities are exposed to 1-BP on an on-going basis. This is 

documented within the Draft Assessment’s “Schematic of Human and Environmental Exposure 

Pathways for 1-BP,” which shows that manufacturing and occupational uses of 1-BP result in 

emissions to outdoor air that can lead to oral, dermal and inhalation exposures by the general 

population.[4] Moreover, the Agency for Toxic Substances and Disease Registry’s (“ATSDR”) 

Draft Profile notes that “[e]xposure of 1-bromopropane to the general population may occur via 

inhalation of ambient air at locations in close proximity to the emissive use of 1-bromopropane, 

such as degreasing operations or dry cleaners (NTP 2011), where vapor may migrate.”[5] In 

addition, when the Occupational Safety and Health Administration (“OSHA”) nominated 1-BP 

for testing by the National Toxicology Program (“NTP”), it stated:
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 Various estimates have been made of the potential market for 1-BP in the key uses to 

which it is likely to be put: metal cleaning and degreasing, adhesives (especially for assembling 

polyurethane and other foam products), and aerosol spraying. Note that all of these uses are in 

practice highly emissive applications, resulting in substantial releases to the ambient 

environment and substantial exposure to workers....[6]

The potential for general population exposures via ambient air is confirmed by the following 

monitoring and modeling studies:

 In 2014, EPA’s Air Quality System database reported only positive detections of 1-

bromopropane at one monitoring location. 1-Bromopropane was detected in ambient air 

of Philadelphia, Pennsylvania at levels of 0.14–0.16 ppb (0.047–0.053 ppbv).[7]

 In 2009, average concentrations as high as 3.0 ppb (or 1.0 ppbv) were detected at a 

monitoring site directly east and upwind of the Superior Tube facility approximately 800 

feet from the southeast corner of the company building.[8] 77% of the samples taken 

from this location in 2009 found 1-BP at levels above the detection limit.[9]

 EPA itself has also used air dispersion modeling to estimate ambient 1-BP concentrations 

100 meters from facilities that use 1-BP as an adhesive. The estimated concentrations 

were 0.138 mg/m3[27.4 ppb] for facilities with average adhesive use and 1.38 mg/m3 

[274 ppb] for facilities with high adhesive use.[10] Inexplicably, this study is not 

included in the Draft Assessment.

 In comments submitted to the HAP docket, Professor Adam Finkel, former director of 

Health Standards Programs and Regional Administrator at OSHA, stated:

 In addition to documented concerns about indoor (in or adjacent to facilities using nPB) 

exposures, the air pollution modeling study done by Exponent in the docket reveals serious 

concern for outdoor exposure. Table 14 in that document estimates the maximum fenceline risk 

(lifetime excess cancer risk) from “Fabrication Company B” to be 2.1x10-5.[11]

Recent data from Massachusetts, where certain facilities must report 1-BP emissions,[12]

confirm that unregulated 1-BP is released from industrial sources at high levels. In 2010-2011, 

electronics facilities in Massachusetts reported that more than half of the amount of 1-BP that 

was used was released into the environment in each reporting year.[13] Although only three 

companies reported releases, 1-BP was the chemical with the 17th-largest releases reported in 

Massachusetts.[14] An electronic capacitor facility, Aerovox Corp., released 11,772 pounds of 1-

BP into the environment of the city of New Bedford, Massachusetts in 2012.[15]

No information is yet available in the Toxic Release Inventory (“TRI”) database regarding 

releases from facilities that manufacture or process 1-BP because this chemical was just added to 

the TRI list of reportable chemicals effective January 2016.[16] However, in adding 1-BP to the 

TRI list, EPA estimated that 131 facilities using or manufacturing 1-BP, not including dry 

cleaning facilities, will be required to report release and waste management data.[17] Moreover, 

in 2003, when EPA proposed listing 1-BP as an acceptable substitute for ozone-depleting 

substances under the SNAP program, it estimated that up to 7,330 small industrial end users used 

1-BP.[18] According to Appendix A to the Draft Assessment, the U.S. production volume of 1-

BP has increased significantly since 2003, so presumable there are either more small users, or 

some small users have increased their use.
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In addition to accounting for general population exposures from manufacturing and processing, 

the final risk assessment also must consider community exposures to 1-BP as a result of its use 

as a dry cleaning solvent replacing perc. Data about community exposures from the use of perc 

as a dry cleaning solvent can shed light on likely community exposures to 1-BP when it is used 

as a replacement for perc. Information gathered for the rule setting emission standards for perc 

shows that toxic air emissions from dry cleaners, over 34,000 nationwide, are often released into 

the environment.[19] The approximately 1,300 dry cleaners that are co-located in residential 

buildings are mostly found in urban areas.[20] In creating the perc rule, EPA found that 

individuals living in the same building as a dry cleaner are likely to receive significantly higher 

exposure to emissions of air pollutants from these types of sources.[21] In a study of emissions 

from New York City dry cleaners, those living in urban areas faced higher indoor levels of perc, 

and the mean perc levels inside households of people of color were four times higher than in 

white households.[22] It is unclear whether (and how many) dry cleaners co-located in 

residential buildings are using 1-BP. If they are, it is reasonable to assume that, as with perc, 

there will be chronic community exposures.

In sum, there is evidence of potential community exposures to 1-BP from the Draft Assessment, 

the ATSDR Draft Profile, OSHA’s statement nominating 1-BP for testing by NTP, modeling and 

monitoring studies, reporting data from Massachusetts, EPA’s economic analysis for the listing 

of 1-BP on the TRI, and by analogy to community exposures to perc. EPA must consider these 

potential exposures in the final risk assessment.

 c. EPA must consider disparate impact on communities of color and low-income 

communities

Exposure to 1-BP due to its presence in ambient air from dry cleaning, foam and furniture 

manufacturing[23] and chemical manufacturing likely disproportionately impacts low-income 

communities and communities of color. For example, EPA found that air emissions from foam 

fabricators covered by a separate air toxics rule created disproportionate exposure and other 

impacts for African Americans, since African Americans are over-represented in communities 

within a 3 mile radius of foam fabricators.[24] The African American population in areas 

surrounding foam manufacturing facilities exceeds the national average by 53% (19% versus 

13%).[25] In New Bedford, Massachusetts, where an electronic capacitator facility released 

11,772 pounds of 1-BP into the environment in one year, 16.7% of the population reporting to 

the Census as Hispanic and 23.5% of people live below the poverty line.[26] When it finalizes 

the 1-BP risk assessment, EPA should consider vulnerable and sensitive populations living in 

exposed communities and account for the potential health impacts of chronic exposures.

[1] Concerns about the scope of the Draft Assessment highlights why it is better practice for EPA 

to publish its problem formulations for public comment before moving on to the draft risk 

assessment. In the future, we urge EPA to allow the public to weigh in on the problem 

formulation and scope of the assessment.
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[2] 15 U.S.C. § 2605(a).

[3] 15 U.S.C. § 2605(c)(1)(A) (emphasis added).

[4] Draft Assessment at 35, Figure 1-2.

[5] ATSDR, Draft Toxicological Profile for 1-Bromopropane, Docket ID No. ATSDR-2016-

0003-0001 at 138 (Jan. 2016) (“ATSDR Draft Profile”). See also id. at 7 (“The general 

population may be exposed to 1-bromopropane in air when it is used during aerosol 

applications.”)

[6] Directorate of Health Standards Programs, OSHA, Nomination of 1_Bromopropane and 2-

Bromopropane for Testing by the National Toxicology Program 2 (Dec. 1999), 

https://ntp.niehs.nih.gov/ntp/htdocs/chem_background/exsumpdf/bromopropanes_508.pdf.

[7] ATSDR Draft Profile at 137 (internal citation omitted).

[8] Bureau of Air Quality, Pa. Dep’t of Envtl. Prot., Addendum to Collegeville Area Air 

Monitoring Project Third Report 2 (Apr. 22, 2010), 

https://www3.epa.gov/ttnamti1/files/20072008csatam/collegevilleaddendum.pdf.

[9] Id. at 5.

[10] Katy Wolf et al., Inst. for Research & Technical Assistance, UT Ctr. for Clean Products & 

Clean Techs., Alternative Adhesive Technologies: Foam Furniture and Bedding Industries, A 

Cleaner Technologies Substitutes Assessment D-1, Table D-1 (2003) (submitted herewith as 

Attachment 1).

[11] Adam Finkel, Comment on Petition to Add n-Propyl Bromide to the List of Hazardous Air 

Pollutants, Docket ID No. EPA-HQ-OAR-2014-0471-0047 at 3 (March 8, 2015) (noting 

increased cancer risk at fenceline for facility with indoor level of 1-BP at 30 ppm) (submitted 

herewith as Attachment 2).

[12] Facilities required to report 1-BP releases in Massachusetts are limited to miscellaneous 

metal products, semiconductors and related devices and electronic capacitors releasing 1,000 lbs. 

or more of 1-BP. TURI, Summary of Policy Analysis, Higher Hazard Substance Designation 

Recommendation: 1-Bromopropane (n-Propyl Bromide) CAS 106-94-5 at 4-5 (May 15, 2014), 

http://www.mass.gov/eea/docs/eea/ota/tur-prog/policy-analysis-npb-may2014.pdf.

[13] Id. at 4-6 (noting a lower reporting threshold would likely lead to more industries like dry 

cleaning to report 1-BP releases).

[14] Id. at 4.

[15] Mass. Toxics Use Reduction Inst., TURA Data (last visited May 9, 2016), 

http://turadata.turi.org/ [enter Company ID “331916”, click “Find ID”, then click “Chemical 

Quantity Detail for All Years”].
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[16] The Draft Assessment erroneously states that the TRI rulemaking has not been finalized. 

Draft Assessment at 29. The TRI rule was finalized in late 2015. See Addition of 1-

Bromopropane; Community Right-to-Know Toxic Chemical Release Reporting, 80 Fed. Reg. 

72,906 (Nov. 23, 2015).

[17] Abt Assocs., Economic Analysis of the Proposed Rule to add 1-Bromopropane to the 

EPCRA Section 313 List of Toxic Chemicals, Docket ID No. EPA-HQ-TRI-2015-0011-0011 at 

2-8 –2-9 (Feb. 17, 2015).

[18] Protection of Stratospheric Ozone: Listing of Substitutes for Ozone-Depleting Substances –

n-Propyl Bromide, 68 Fed. Reg. 33,284, 33,309 (June 3, 2003).

[19] National Perchloroethylene Air Emission Standards for Dry Cleaning Facilities, 71 Fed. 

Reg. 42,724, 42,725 (Jul. 27, 2006).

[20] Id. at 42,725, 42,738.

[21] Memorandum from Neal Fann, Risk and Exposure Assessment Group, EPA, OAQPS, to 

Dave Guinnup, Group Leader, Risk and Exposure Assessment Group, EPA, OAQPS, Docket ID 

No. EPA-HQ-OAR-2005-0155-0494, at 5 (July 2006).

[22] Michael J. McDermott et al., Tetrachloroethylene (PCE, Perc) Levels in Residential Dry 

Cleaner Buildings in Diverse Communities in New York City 5 (June 21, 2005), Docket ID No. 

EPA-HQ-OAR-2005-0155-0290.

[23] Foam, or fillable polyurethane, is a source where 1-BP is known to be used in some 

facilities. See Katy Wolf and Mike Morris, Inst. for Research & Technical Assistance, 

Assessment, Development, and Demonstration of Alternatives for Five Emerging Solvents 64 

(Oct. 2006), available at http://www.irta.us/reports/Five%20Emerging%20Chemicals.pdf; see 

also National Emission Standards for Hazardous Air Pollutants Residual Risk and Technology 

Review for Flexible Polyurethane Foam Production, 79 Fed. Reg. 48,073, 48,086 (Aug. 15, 

2014) (to be codified at 40 C.F.R. Part 63).

[24] Memorandum from Kaye Whitfield, EPA/OAQPS/SPPD, Docket ID No. EPA-HQ-OAR2012-0510-0070 at 2 (July 8, 2014).

[25] 79 Fed. Reg. at 48,086. In another furniture manufacturing rule, EPA also found 

disproportionate exposure and impacts for minorities, in particular Hispanic or Latino groups. 

See EC/R Inc., Risk and Technology Review - Analysis of Socio-Economic Factors for 

Populations Living Near Wood Furniture Manufacturing Operations Facilities, Docket ID No. 

EPA-HQ-OAR-2010-0786-0025 at 8 (Oct. 7, 2010).

[26] U.S. Census Bureau, QuickFacts, New Bedford city, Massachusetts (last visited Mar. 31, 

2015), http://quickfacts.census.gov/qfd/states/25/2545000.html.
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Commenter Name: Eve Gartner

Commenter Affiliation: Earthjustice et al.

Document Control Number: EPA-HQ-OPPT-2015-0084-0016

Comment Excerpt Number: 3

Charge Question: 1-2 Scope and conceptual model

Comment Excerpt: 

2. EPA should acknowledge and assess the risk reflected by the widespread presence of urinary 

metabolites of 1-BP in biomonitoring and epidemiological studies

We are disappointed and concerned that the Draft Assessment does not mention, let alone 

attempt to explain, the fact that biomonitoring studies have found a urinary metabolite of 1-

Bromopropane -- N-Acetyl-S-(n-propyl)-L-cysteine – in a large proportion of the population. In 

finalizing the addition of 1-BP to the TRI list, EPA referred to N-Acetyl-S-(n-propyl)-L-cysteine 

as the “major metabolite” of 1-BP, and noted that it has been detected in the urine of exposed 

workers at levels that increased with increasing levels of 1-BP in ambient air. Multiple studies 

confirm that this metabolite is associated with 1-BP.[1]

A table from the most recent National Health and Nutrition Examination Survey (“NHANES”) is 

reproduced below. At the 50th percentile of concentration, all groups had measurable quantities 

of urinary N-Acetyl-S-(n-propyl)-L-cysteine, which CDC refers to as a metabolite of 1-BP.[2]

In addition, a very recent epidemiological study of 488 women in the third trimester of 

pregnancy in 7 locations around the country (who participated in the National Children’s Study) 

found that 99% of the participants had the 1-BP metabolite (N-Acetyl-S-(n-propyl)-L-cysteine) 

in their urine.[3]
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The high detection rate of N-Acetyl-S-(n-propyl)-L-cysteine in bio-monitoring studies raises 

serious questions about the possibility that the general population is experiencing continuous or 

frequent exposure to 1-BP. This is because the urinary metabolite is not expected to persist over 

long periods after a single exposure. While exposures to chemicals other than 1-BP could 

account for the presence of this metabolite, it is incumbent upon EPA to acknowledge the 

NHANES and National Children’s Study data and address whether these findings raise concerns 

about widespread exposures to 1-BP.[4]

If EPA cannot account for the NHANES and National Children’s Study findings, it should 

promptly move forward to obtain the information it needs to make sense of these data.[5]

Furthermore, EPA should investigate how these data might be useful in its risk estimate 

calculations, since these represent actual biomarker estimates of human exposures to 1-BP and 

would be indicative of the levels that the general population is being exposed to this chemical on 

a daily basis.

Although the widespread presence of N-Acetyl-S-(n-propyl)-L-cysteine in bio-monitoring 

studies suggests that the general population may be experiencing chronic exposures to 1-BP, the 

Draft Assessment considers only acute inhalation exposures for the general population based on 

consumer uses of a limited set of products. The potential that the the general population is 

experiencing chronic 1-BP exposures, which could be via dermal as well as inhalation routes, 

needs to be accounted for in the final risk assessment.

[1] See Nat’l Ctr. for Biotechnology Info., N-Acetyl-S-propyl-L-cysteine, PubChem Compound 

Database (last visited May 9, 2016), https://pubchem.ncbi.nlm.nih.gov/compound/N-acetyl-Spropylcysteine#section=Literature.

[2] Ctrs. for Disease Control, Fourth National Report on Human Exposure to Environmental 

Chemicals, Updated Tables 612 (Feb. 2015), 

http://www.cdc.gov/biomonitoring/pdf/FourthReport_UpdatedTables_Feb2015.pdf.

[3] Elizabeth Barksdale Boyle et al., Assessment of Exposure to VOCs among Pregnant Women 

in the National Children’s Study, 13 Int’l J. Res. & Pub. Health 376 (Mar. 29, 2016).

[4] Our concern is heightened by the fact that “1-BP can be used . . . as a chemical intermediate 

in . . . flavors, and fragrances.” Abt Assocs., Economic Analysis of the Proposed Rule to add 1-

Bromopropane to the EPCRA Section 313 List of Toxic Chemicals, Docket ID No. EPA-HQTRI-2015-0011-0011 at 1-5 (Feb. 17, 2015). These uses are not well-regulated and the identity 

of ingredients is often secret.

[5] This study makes clear that the exposure is not associated with direct or secondhand exposure 

to smoke, which is a major source for other VOCs. R. B. Jain, Levels of selected urinary 
1-BP Risk Assessment: Public Comments – Collated

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metabolites of volatile organic compounds among children aged 6-11 years, 142 Envtl. Res. 461 

(Oct. 2015).

Commenter Name: Eve Gartner

Commenter Affiliation: Earthjustice et al.

Document Control Number: EPA-HQ-OPPT-2015-0084-0016

Comment Excerpt Number: 4

Charge Question: 1-2 Scope and conceptual model

Comment Excerpt: 

3. EPA’s Draft Assessment fails to take into account the full range of exposures or the effects of 

exposure to multiple similar solvents

We are concerned that the Draft Assessment does not include potential harm to workers exposed 

through dermal contact, despite evidence that workers are harmed by exposure to 1-BP via this 

pathway. We also do not understand why the Draft Assessment does not include dermal 

pathways of exposure for consumer-users of 1-BP who are likely not using gloves or other 

personal protective equipment.

The Draft Assessment itself notes that “dermal and inhalation pathways are expected to be more 

relevant,” and exposure is possible in both occupational and consumer use scenarios through 

spilled solutions or by handling treated items without gloves.[1] The ATSDR Draft Profile 

reaches the same conclusion, noting: “Although the principal route of exposure was likely 

inhalation, dermal exposure could have been significant since often no gloves were used when 

handling 1-bromopropane, or the use of gloves, as noted in some reports, may have enhanced 

dermal uptake of 1-bromopropane by occlusion effect.”[2] The data show the potential for the 

same worker to be exposed simultaneously or additively to this chemical as a result of both 

inhalation and dermal pathways. EPA has no rational scientific basis for ignoring the dermal 

route in its own right, or in combination with inhalation exposure.

EPA excludes dermal exposure from the risk assessment because “dermal uptake is likely to 

be...lower than uptake by inhalation because 1-BP will evaporate quickly.”[3] This is 

problematic because internal doses are likely to be underestimated when dermal exposure is 

excluded. Only considering the dominant exposure pathway is not appropriate; if multiple 

exposure pathways would potentially occur, EPA must consider the cumulative exposures and 

resulting health effects from these exposures. EPA notes this deficiency but claims it is only an 

issue in the case of “no-risk” findings where reported margins of exposure (“MOEs”) are close

to, but still higher than the benchmark MOE. The benchmark MOE is calculated by dividing the 

point of departure (POD) by the estimated human exposure. The POD is often the exposure level 

at which no adverse effects are observed in observational studies. If later versions of this 

assessment revise the POD and incorporate a higher value, then excluding dermal exposure from 

the estimated exposure value may result in a reported MOE that is higher than the benchmark 

MOE. This inflated value would skew the final risk assessment toward allowing continued 

exposures at higher levels than what the benchmark MOE allows– an unacceptable result. EPA 
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Page 9

should consider all potential routes of exposure and incorporate all relevant routes into its final 

risk estimate to provide an accurate estimate of the potential risk, and not simply assume –

wrongly – that incorporating one exposure route would be sufficiently protective of all others.

Moreover, difficulty in quantifying dermal exposures is not a basis for ignoring this exposure 

pathway in the risk assessment. If dermal exposure was not quantifiable, then how can EPA say 

that it is likely to be “orders of magnitude lower than uptake by inhalation”?[4] Without 

providing data to justify this claim and the subsequent exclusion of the dermal route of exposure, 

some attempt must be made to estimate the extent of dermal exposure compared to inhalation 

exposure among people using products containing 1-BP. Although dermal uptake may be lower 

relative to inhalation uptake, it can still be significant and should not be ignored as a pathway of 

exposure. Additionally, the National Institute for Occupational Safety and Health (“NIOSH”) 

recently calculated that 1-BP has a skin dose to inhalation dose (SI) ratio higher than 0.1, which 

is the threshold that indicates that skin absorption may significantly contribute to the overall 

body burden of a substance.[5] Among the reasons stated for discounting the dermal route of 

exposure, one is that there is “no available toxicokinetic information to develop physiologicallybased pharmacokinetic models or route-to-route extrapolations.” Lack of data is not equivalent to 

the lack of potential hazard or risk.[6]

Finally, when EPA finalizes its risk assessment, we urge it to consider not only the health effects 

of exposure to 1-BP, but also the combined effects of exposures to 1-BP and other similar 

compounds. This is especially critical in the occupational setting where workers may be exposed 

to multiple VOC solvents, many of which are carcinogens. There is scientific consensus that 

carcinogenic risk is at least additive, and exposure to multiple carcinogens increases this risk.[7]

That is, the more carcinogens a person is exposed to, the greater their risk of cancer over their 

lifetime, and cancer risks should be summed together.[8]

EPA should acknowledge that there is particularly high risk for workers and community 

members exposed to 1-BP as well as other carcinogens through any combination of occupational, 

consumer, and community ambient air exposure.

[1] Draft Assessment at 83.

[2] ATSDR Draft Profile at 8. See also id. at 16 (“In occupational studies and case reports 

described below, exposure to 1-bromopropane occurred primarily via the inhalation route, but 

dermal exposure may have also occurred. Since in most cases, it is not known whether or not the 

workers were using protective clothing and/or respirators, the specific contribution of each route 

of exposure is not possible to determine. Therefore, the reader should keep in mind that both 

inhalation and dermal routes combined may have contributed to the effects described.”) 

(emphasis added).

[3] Draft Assessment at 36.
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[4] Id. at 36, 154.

[5] NIOSH, Skin Notation (SK) Profile, 1-Bromopropane [CAS No. 106-94-5] at 2-3 (2009), 

http://www.cdc.gov/niosh/docket/review/docket153c/pdfs/eid-tr-sk-1-bromopropane03242015.pdf.

[6] Indeed, in finalizing a Design for the Environment Alternatives Assessment, EPA correctly 

responded to a comment stating: “The absence of test data may be assumed by some readers to 

be an indication of no concern (i.e., they may incorrectly believe that no data is equivalent to the 

lack of potential hazard or risk).” EPA, Public Comments Submitted on the Draft Final Report, 

“Flame Retardants Used in Flexible Polyurethane Foam: An Alternatives Assessment Update” 

at 10 (Aug. 2015), https://www.epa.gov/sites/production/files/2015-

08/documents/ffr_response.pdf.

[7] See, e.g., Cal. EPA OEHHA, Risk Assessment Guidance Manual (finalized Mar. 6, 2015) at 

1-5, 2-4, 8-12, http://oehha.ca.gov/air/hot_spots/hotspots2015.html (“Cancer risks from all 

carcinogens addressed in the HRA [health risk assessment] are added.”; “Cancer risks from 

different substances are treated additively in risk assessment generally, and in the Hot Spots 

Program in part because many carcinogens act through the common mechanism of DNA 

damage.”).

[8] EPA has codified this scientific principle in its own guidelines. See, e.g., Residual Risk 

Assessment for Petroleum Refineries (Dec. 1, 2015) at 34, EPA-HQ-OAR-2010-0682-0800, 

https://www.regulations.gov/#!documentDetail;D=EPA-HQ-OAR-2010-0682-0800 (“To 

combine risks across multiple carcinogens, our assessments use the mixtures guidelines’ [37,38] 

default assumption of additivity of effects, and combine risks by summing them using the 

independence formula in the mixtures guidelines.”) (citing EPA, Guidelines for the Health Risk 

Assessment of Chemical Mixtures, EPA-630-R-98-002 (1986); EPA, Supplementary Guidance 

for Conducting Health Risk Assessment of Chemical Mixtures at 73, 125 & A-9, EPA-630/R-00-

002 (2000)).

Commenter Name: Lee Anderson

Commenter Affiliation: BlueGreen Alliance

Document Control Number: EPA-HQ-OPPT-2015-0084-0018

Comment Excerpt Number: 1

Charge Question: 1-2 Scope and conceptual model

Comment Excerpt: 

The BlueGreen Alliance supports the comments submitted by Earthjustice, NRDC and others on 

the Toxic Substances Control Act (TSCA) Work Plan Chemical Risk Assessment Peer Review 

Draft for 1-Bromopropane (n-Propyl Bromide) (“Draft Assessment”) prepared by the U.S. 

Environmental Protection Agency (EPA).
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Page 11

We share the concern expressed in those comments that the draft assessment needs to be 

substantially strengthened to protect workers and communities from the health impacts of 1-

Bromopropane. While we commend EPA for recognizing the need to review this highly toxic, 

high production volume chemical, the current draft’s exclusion of dermal, in utero, and long term 

fence-line community exposures will result in an assessment that does not adequately protect 

workers and their neighbors.

We urge you to revise the draft as recommended in the Earthjustice comments.

Commenter Name: Amy Kyle

Commenter Affiliation: School of Public Health, University of California, Berkeley

Document Control Number: EPA-HQ-OPPT-2015-0084-0019

Comment Excerpt Number: 2

Charge Question: 1-2 Scope and conceptual model

Comment Excerpt: 

Biomonitoring results indicate widespread exposure by the general population

EPA recognizes a method developed and implemented to measure a metabolite of 1‐

bromopropane (1‐BP) in urine referred to PBPM (N‐Acetyl‐s‐(n‐propyl)‐L‐cysteine.) (Mathias, 

Cheever et al. 2012) (Valentine, Amarnath et al. 2007). It is formed through conjugation during 

metabolism. Most of the literature cited by EPA in the risk assessment document pertained to 

measurements in occupational settings. The National Health and Nutrition Examination Survey 

(NHANE) run by the National Center for Health Statistics collected measurements of these 

metabolites for the first time in 2011‐12.

1. Two studies drawing on NHAHES show broad exposure in adults and in children 11 to 

16.

The NHANES data collected through the (NHANES) program was analyzed by Jain and shows 

widespread occurrence of 1‐BP urinary metabolites in the US adult civilian noninstitutionalized 

population (Jain 2015). The survey looked for 28 urinary metabolites of 18 VOCs, drawing on 

methods developed by Alwis (Alwis, Blount et al. 2012). The total number of participants was 

about 2600 and included males and females. Females had higher values for PBMA. Smokers did 

not.

Jain also evaluated the exposures of children age 6 to 11 using NHANES data (Jain 2015). 

Children’s exposures were higher than adults for many VOCs but not 1‐BP. The study reported 

that 60.8% of children had levels of the metabolite in their urine above the level of detection. It 

also reported that less than one percent of children had detectable levels of urinary metabolites 

that are linked to tetrachloroethylene.
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These studies also demonstrate that exposure to 1‐BP is not associated with direct or secondhand 

exposure to tobacco smoke. This is important because tobacco smoke is a major source for many 

other VOCs.

2. A study reporting biomonitoring results for the National Children’s Study shows 

widespread exposure among pregnant women.

Boyle et al reported that the urinary metabolite of 1‐BP known as BPMA was detected in the 

urine of 99% of women sampled in the National Children’s Study (Boyle, Viet et al. 2016). This 

was a group of 488 pregnant women from different geographic areas. This study reported that the 

values were not associated to direct or second hand cigarette smoke.

3. The widespread exposures would seem to suggest more continuous or frequent exposure 

to 1‐BP, rather than the pattern of infrequent, acute exposure that is provided in the 

assessment.

The cited studies show that exposure to 1‐BP is common in the general population. It may 

represent ongoing environmental exposures rather than infrequent product use, for example. This 

is because the urinary metabolite is not expected to be found over long periods after a single 

exposure but is thought to persist for days or maybe a couple of weeks. This does not seem to 

support the theory used in the risk assessment that exposure for the general population is 

infrequent and acute. The risk assessment considers only acute exposures for the general 

population. The evidence cited above suggests that there may be more continuous or frequent 

exposures.

4. Since children are exposed and are almost certainly not “consumers” of products 

identified in the analysis as sources of 1‐BP, the term “consumers” to describe the exposed 

population is rather misleading.

5. The broad exposure pattern does support the use of the benchmark response level of 

0.1% since a very large number of people could potentially be exposed. 

A more health protective level would appear to be warranted.

Commenter Name: Amy Kyle

Commenter Affiliation: School of Public Health, University of California, Berkeley

Document Control Number: EPA-HQ-OPPT-2015-0084-0019

Comment Excerpt Number: 3

Charge Question: 1-2 Scope and conceptual model

Comment Excerpt: 

Several key issues are not addressed including cumulative exposures to solvents, dermal 

exposures, and potential neurodevelopmental toxicity.
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1. Exposures to multiple solvents is well documented and may cause similar effects but are 

not considered

The assessment considers only 1‐BP and does not consider the combined effects of other similar 

chemicals. The sources cited, along with others, show widespread exposure to many VOCs. This 

would be expected to result in combined exposures to chemicals that may contribute to similar 

effects. Assessing and controlling each one separately will not be sufficient to protect the 

population from health effects.

2. The dermal route of exposure (through the skin) may be important but is ignored.

EPA focuses entirely on inhalation exposure to 1‐BP and completely ignores a potential dermal 

route of exposures for the general population. The only justification given for ignoring this route 

is that they don't have any information about it.[1]

Federal Occupational health agencies note that 1‐BP passes through skin and even through many 

kinds of gloves, so they have found that dermal exposures occur and need to be protected against 

in occupational settings.

VOC solvents are often absorbed through skin, so there is no reason to conclude that dermal 

exposure would not be important.

The California occupational standard for 1‐BP includes a skin notation saying that workers 

should not be allowed to come into contact with the material.

The assessment says that the 1‐BP is used in "wipes" which suggests that there is a likelihood of 

dermal exposure unless wipes are always used with appropriate gloves, which is possible perhaps 

in a well‐controlled occupational setting but not in a general population setting. (This is at page 

28 of 403.)

It would be more scientifically appropriate for EPA to acknowledge the potential importance of 

dermal exposure, provide a best estimate, identify how the data gap can be filled, and take steps 

needed to obtain the data needed.

3. There may be neurodevelopmental impacts

Some animal evidence suggests potential for neurodevelopmental impacts, and this does not 

appear to have been assessed.

[1] At page 22 of 403, EPA says: Based on the physical‐chemical properties and use scenarios 

described in this
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assessment, EPA/OPPT expects inhalation to be the primary exposure route of concern for 1‐BP. 

Because of

limited toxicological data and the lack of toxicokinetic information needed to develop 

physiologically based

pharmacokinetic models for route‐to‐route extrapolations, EPA/OPPT did not evaluate dermal 

exposures.

Commenter Name: Amy Kyle

Commenter Affiliation: School of Public Health, University of California, Berkeley

Document Control Number: EPA-HQ-OPPT-2015-0084-0019

Comment Excerpt Number: 4

Charge Question: 1-2 Scope and conceptual model

Comment Excerpt: 

The document reflects limited understanding of the uses of 1-BP despite increasing use 

over two decades. EPA should identify and rectify critical data gaps.

The document suggests that EPA has essentially no idea when or how 1‐BP is being used in dry 

cleaning or products accessible to the general population or in facilities where children are 

found. This is a critical data gap that needs to be rectified.

There is some suggestion that 1‐BP is used for LEDs and this is something that should be 

investigated.

EPA should be mindful of the transition in use of solvents in dry cleaning as PERC is being 

phased out. It was known two decades ago that 1‐BP would be suggested or used as an 

alternative to PERC, a widely used dry cleaning solvent. It would be helpful to consider in the 

risk assessment the extent to which this transition is occurring and the implications of the 

transition.
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2.0. Human Exposure Assessment

Commenter Name: Christina Franz

Commenter Affiliation: American Chemistry Council (ACC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0012

Comment Excerpt Number: 3

Charge Question: 2-1 Worker exposure assessment approach

Comment Excerpt: 

EPA’s Risk Assessment Fails to Use “Best Science” Approaches, Which Are Critical to a 

Scientifically Defensible Assessment

EPA’s 1-bromopropane assessment applies inconsistent standards to existing scientific 

information, using methodology that does not comport with current “best science” approaches 

for the evaluation and integration of scientific information. For example, a systematic evaluation 

of the quality (including relevance and reliability) of each study is essential, but EPA has not 

included this review and evaluation in critical areas of the risk assessment (e.g., genotoxicity, 

developmental toxicity). When evaluating both hazard and exposure for 1-bromopropane, it is 

critical that EPA rely on studies of the highest quality, not simply those studies that produce the 

lowest points of departure (POD) or the highest exposure estimates. However, EPA consistently 

chose the lowest dose for each endpoint of toxicity and then drew conclusions based on results 

from the use of the lowest overall endpoint throughout the 1-bromopropane assessment, without 

any discussion at all regarding the quality of the available studies – with the exception of several 

cursory statements contained in tables.[1]

[1] For example, at page 120 of the draft assessment, EPA clearly states: “EPA/OPPT used 

margin of exposures (MOEs) to estimate acute or chronic risks for non‐cancer based on the 

following:1. the lowest HECs within each health effects domain reported in the literature;...”

Commenter Name: Christina Franz

Commenter Affiliation: American Chemistry Council (ACC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0012

Comment Excerpt Number: 5

Charge Question: 2-1 Worker exposure assessment approach

Comment Excerpt: 
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A.The 1-Bromopropane Exposure Assessment Is Outdated and Does Not Reflect Current 

Exposures in Occupational and Consumer Populations

EPA’s 1-bromopropane draft risk assessment identified occupational uses of concern, including 

its use in spray adhesives, dry cleaning (including spot cleaning), and degreasing (vapor, cold 

cleaning, and aerosol). The consumer uses of concern identified for 1-bromopropane included 

aerosol spray adhesives, aerosol spot removers, and aerosol cleaning and degreasing products. 

The Agency described (at page 24) a number of uncertainties associated with the available data 

and modeling approaches used, including “the sites used to collect exposure monitoring data 

were not selected randomly, and the data reported therein may not be representative of all 

exposure scenarios. Further, of necessity, exposure modeling approaches employed knowledgebased assumptions that may not apply to all use scenarios. Because site-specific differences in 

use practices and engineering controls exist, but are largely unknown, this represents another 

source of variability that EPA/OPPT could not quantify in the assessment. Consumer exposures 

were estimated based on modeling approaches due to the lack of monitoring information that 

could be used to assess consumer products. In addition, the inability to include dermal exposures 

results in potential underestimation of overall exposure and risk.”

ACC believes that the exposure assessment data used by EPA are not representative of current 

workplace/occupational exposures in 2016. ACC believes that workplace exposures for 1-

bromopropane have been rapidly declining based on changes in downstream applications. In a 

study previously conducted by Gradient Corporation, sponsored by Albemarle Corporation (see 

Albemarle comments submitted to EPA on the 1-BP Draft TSCA Work Plan Chemical Risk 

Assessment, May 9, 2016), workplace exposures were shown to have been declining in several 

occupational sectors, namely the dry cleaning industry, the spray adhesives industry, and the 

industrial metal cleaning industry. The 1-bromopropane risk assessment should account for this 

change in 1-bromopropane use patterns in the workplace.

Regarding EPA’s modeling of consumer exposures, EPA used the E-FAST-2/CEM model, 

stating: “CEM uses high‐end input parameters/assumptions to generate conservative, upper‐

bound inhalation exposure estimates for aerosol spray products.” (See page 74). In particular, 

for the consumer behavior patterns EPA states (at page 274): “By default, E‐FAST2/CEM uses 

pre‐set, high‐end values for a variety of consumer use scenarios when use information is not 

available for specific products. Under these conditions, the model results tend to over predict the 

exposure.” Therefore, by EPA’s own admission, it is very likely that EPA has overestimated 

consumer exposures.

A similar overestimation is likely to have occurred regarding workplace exposures. For instance, 

while EPA comments (at page 147) that “the use of 8-hr TWA is not expected to present a 

“worst case” or conservative exposure estimate,” EPA fails to mention that EPA is assuming 

that an individual is exposed at this level for an entire working life (40 years), as is reflected in 

Appendix H. By using only extreme values in a range, EPA fails to provide a sense of the 

average values of workplace exposure. Using central tendency estimates would be more useful 

and informative, particularly for the lifetime average daily concentrations (LADCs), which 

should be based on the average exposure concentration over time, rather than a single maximum 
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eight-hour time-weight-average (TWA). A refined exposure assessment that uses central 

tendency values should be conducted for all possible exposure scenarios in order to provide for 

realistic estimates of risk – as opposed to only worst-case scenario.

While EPA provides inputs in Appendix L for the 50th and 90th percentiles of exposure, the 

Agency fails to identify clearly the exposure values actually used for the MOE derivations. Since 

only 95th percentile values are presented in the risk characterization section of the assessment, 

we must assume that EPA used only the 90th percentile exposure estimates. Further clarity is 

needed from EPA on this point before ACC can comment further on the outputs used to inform 

the MOE calculations.

EPA’s reliance on outdated use and exposure data, in combination with estimated exposures and 

modeled data, very likely presents worst-case scenarios in the draft risk assessment. EPA should 

be very clear that the current draft risk assessment cannot identify actual risk, but rather can only 

identify exposure scenarios that require further refinement. EPA should refine the assessment 

using current/more recent exposure data and provide estimates of the range of modeled 

exposures.
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2.1. Occupational Exposures

Commenter Name: Ali Mirzakhalili

Commenter Affiliation: State of Delaware Department of Natural Resources & Environmental 

Control

Document Control Number: EPA-HQ-OPPT-2015-0084-0011

Comment Excerpt Number: 1

Charge Question: 2-2 Additional occupational exposure scenarios

Comment Excerpt: 

OPPT draft TSCA risk assessment overlooked one NPB receptor.

Delaware believes that a fourth NPB receptor needs to be included in the OPPT TSCA risk 

assessment for dry cleaning operations before the TSCA risk assessment is finalized. The fourth 

receptor is the person that resides in a building in which a NPB dry cleaning operation is also 

located. This belief is based on 1) information obtained and reported and 2) regulatory actions 

taken by the OAQPS as a result of the RTR process, as noted below.

On July 27,2006, the EPA/OAQPS completed its multi-year regulatory development process by 

1) undertaking the residual risk and technology reviews (RTR) of perchloroethylene (Perc) dry 

cleaning operations and 2) promulgating more health protective requirements in 40 CFR Part 63 

Subpart M (Sub M) (71 FR 42724,7/27/06).

During the RTR information gathering and comment process, OAQPS estimated that nearly 5% 

(-1,300) of the Perc dry cleaning operations were in co-residential buildings (71 FR 

42738,7/27/06). These co-residential dry cleaning operations are primarily found in urban areas 

(71 FR 42725,7/27/06).

During the risk assessment phase, OAQPS noted that estimates of ". . . cancer incidence are 

helpful in characterizing cancer risks, because such estimates account for the full range of 

exposures that have been captured by the monitoring and provide a metric of the aggregate 

health impact taking into account the number of people exposed to varying levels of risk. Our 

estimate of annual cancer incidence for the approximately 1300 co-residential sources currently 

in operation is in the range of 0.2 to 2 cases per year, which is on par with the estimated annual 

incidence of 0.4 to 4 cases per year for the approximately 27,000 other area source cleaners" (71 

FR 42738, 7/27/06). The fact that the estimated annual cancer incidences are roughly 10 times 

higher for co-residential dry cleaners than for other area source dry cleaners, indicated that "coresidential sources pose a disproportionate cancer incidence to their residents" (71 FR 42738, 

7/27/06).

During the rulemaking phase, OAQPS stated that "[after] reviewing technical developments in 

the industry, available public health risk information, and the comments received, we have 

concluded that the option that best satisfies the requirements of CAA section 112(d)(6) for 

existing co-residential area sources is to phase out the use of [Perc]" (71 FR 42738,7/27/06).
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Based on the above conclusion, OAQPS incorporated requirements into Sub M to eliminate the 

disproportionate cancer risk for residents in co-residential area sources by promulgating the 

following 2-step prohibition on the use of Perc in in co-residential buildings:

1. After December 21, 2005, no new Perc dry cleaning operations can be installed in 

co-residential buildings (40 CFR §63.322 (o)(4)) and

2. After December 21, 2020, the use of Perc in dry cleaning operations in coresidential buildings is prohibited (40 CFR §63.322 (o)(5)(i)).

During the RTR information gathering and comment process, OAQPS evaluated alternative nonPerc solvent cleaning technologies (EPA-HQ-OAR-2005-0155-0484). This evaluation found that 

except for the seldom used Stoddard solvent, which contains a small percentage of toluene and 

xylenes, none of the current non-Perc solvents cleaning technologies contain hazardous air 

pollutants or HAPs (EPA-HQ-OAR-2005-0155-0484). The emergence of and increased use of 

these alternative non-Perc solvent cleaning technologies was one of the factors in OAQPS's 

decision to adopt the above second step that would eliminated the use of Perc solvents in coresidential dry cleaning operations. (71 CFR 42734, 7/27/06)

To summarize the above, approximately 10 years ago, the EPA identified that a small, but 

measureable, percentage of Perc dry cleaning operations were housed in residential buildings. 

The EPA determined that the collocated residents, Perc receptors, in these buildings were 

exposed to a disproportionately high cancer risk and that high resultant cancer risk was 

unacceptable. Thus, the EPA promulgated measures in 2006 that 1) prevented any future 

installations of Perc dry cleaning operations in co-residential buildings and 2) prohibited the use 

of Perc solvent in dry cleaning operations in co-residential buildings after December 21, 2020. 

This same health protective measure allows, even encourages, the installation of new dry 

cleaning operation using non-Perc solvents and the conversion of existing Perc dry cleaning 

operations to ones using non-Perc solvents. Knowing the above, the EPA did not include this 

class of receptors in the draft TSCA risk assessment.

Is NPB an appropriate alternative non-Perc solvent cleaning technology?

As mentioned earlier, OAQPS evaluated alternative non-Perc solvent cleaning technologies 

during the RTR information gathering process and identified available alternatives to replace the 

use of Perc solvents. During the RTR information gathering and review process, NPB was not 

classified as 'reasonably anticipated to be a human carcinogen' by the National Toxicology 

Program (NTP); nor were any of the other alternative non-Perc solvent cleaning technologies 

that the EPA evaluated (EPA-HQ-OAR-2005-0155-0484).
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Since Perc was 'reasonably anticipated to be a human carcinogen' and safer alternative non-Perc 

solvent cleaning technologies existed, the EPA decision to reduce the disproportionate cancer 

risk associated with co-residential Perc dry cleaning operations was appropriate.

However, in the 2007-9 timeframe, the carcinogenic nature of NPB, a non-Perc alternative, 

began to gain notice. In June 2010, Adam M. Finkel summarized the current scientific 

information about the relative toxicity of Perc and NPB (EPA-HQ-OAR-2014-0471-0027). Mr. 

Finkel concluded...

 “To a reasonable degree of scientific certainty, equal exposures to nPB will harm more 

residents and workers than would exposures to Perc: both are harmful substances, but 

nPB is the more harmful of the two."

 “Even worse than comparable levels of exposure to the two solvents (in theory) would be 

the potential for much greater exposures to nPB than to Perc in actual practice", due to it 

higher volatility.

By 2014, NPB was, for the first time, classified as 'reasonably anticipated to be a human 

carcinogen' in the 13th Edition of the National Toxicology Program (NTP) “Report on 

Carcinogens" (2014). http://ntp.niehs.nih.gov/ntp/roc/content/listed_substances_508.pdf

To summarize the above, rather than being forced to shut down in December 2020, an owner of a 

co-residential Perc dry cleaning operation can opt to 1) relocate existing operation to nonresidential building, 2) remain in place and retrofit the Perc dry cleaning equipment to use NPB, 

or 3) remain in place and install a new non-Perc solvent cleaning technology, which could use 

NPB. There are indications that with NPB, a non-Perc alternative solvent, replacing Perc in a coresidential building, the current disproportionate cancer risk may actually worsen, rather than 

improve. Yet another reason, OPPT should include the residents that are collocated with a dry 

cleaning operation as an NPB receptor in the final TSCA risk assessment.

Recommendation

Delaware found the estimated cancer risk for the 3 classes of receptors at NPB dry cleaning 

operations staggering.

Delaware recommends that the EPA, if they haven't already, bring its OPPT and OAQPS 

resources together to provide a holistic human health risk characterization that identifies the 

health impacts on those people working in the NPB dry cleaning facility, the public living around 

the NPB dry cleaning facility, and the residents that are collocated in a building with the NPB 

dry cleaning facility.

If unacceptable risk is identified, the EPA should take appropriate measures to reduce the 

estimated risk to an acceptable level, either under Section 5 or 6 of the TSCA (OPPT) or under 

Section 112 of the CAA (OAQPS) or both, if necessary.
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Delaware looks forward to EPA's continued efforts to reduce the impact of toxic substances and 

HAPs on the public health, safety, and welfare. Thank you for considering these comments, and 

if you have any questions do not hesitate to contact Jim Snead at 302-323-4542 or contact me at 

302-739-9402.

Commenter Name: Jared Snyder

Commenter Affiliation: New York State Department of Environmental Conservation (DEC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0013

Comment Excerpt Number: 1

Charge Question: 2-2 Additional occupational exposure scenarios

Comment Excerpt: 

The New York State Department of Environmental Conservation (DEC) offers these comments 

on the Toxics Substance Control Act (TSCA) Work Plan Chemical Risk Assessment of 1-

Bromopropane (n-Propyl Bromide): Spray Adhesives, Dry Cleaning and Degreasing Uses (the 

“TSCA Assessment”), prepared by the United States Environmental Protection Agency (EPA) 

Office of Chemical Safety and Pollution Prevention. DEC supports EPA’s efforts to reevaluate 

the end uses of n-Propyl Bromide (n-PB) and believe the determinations contained in the TSCA 

Assessment could provide EPA with the supporting information necessary to restrict or ban the 

end use of n-PB by drycleaners, especially in collocated buildings.

Overall the TSCA Assessment is a thorough and comprehensive review with some exceptions. 

The document adequately describes the need for EPA to pursue risk reduction and other possible 

actions under TSCA to reduce n-PB exposure based on the unacceptable health risks 

demonstrated to exist for all the end uses that were evaluated. We do, however, have additional 

concerns about the end use of n-PB by dry cleaners in collocated and stand-alone settings. The 

TSCA Assessment is also silent on the potential exposure of residents and bystanders in 

locations that are collocated with drycleaners that may use n-PB. In addition, the TSCA 

Assessment does not mention that some of the adverse neurological health effects from n-PB 

occupational exposures appear to be irreversible and may result in permanent nerve damage.

In summary, NYSDEC believes the determinations contained within the document provide the 

necessary support for EPA to act on these end uses of n-PB under TSCA and provides additional 

support to our petition to list n-PB as a hazardous air pollutant under the Clean Air Act.

Thank you for the opportunity to comment on the TSCA Assessment.
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2.2. Consumer Exposures

Commenter Name: Steven Bennett

Commenter Affiliation: Consumer Specialty Products Association (CSPA)

Document Control Number: EPA-HQ-OPPT-2015-0084-0015

Comment Excerpt Number: 1

Charge Question: 3-1 Consumer exposure assessment approach

Comment Excerpt: 

The Consumer Specialty Products Association (CSPA)[1] appreciates the opportunity to provide 

the following information in response to the agency’s TSCA draft Work Plan Risk Assessment 

of 1-bromopropane (1-BP) released by the agency on March 8, 2016. As a trade association 

representing the manufacturers of specialty formulated products, we have expertise regarding the 

formulation and appropriate use of these products.

We are particularly concerned that the draft risk assessment and Draft Peer Review Charge 

Questions focus extensively on consumer exposures to 1-bromopropane present in these 

products, which to the best of our knowledge, should not occur with our members’ products as 

they are manufactured and intended for industrial and commercial users: While there is limited 

existing usage of formulated products containing 1-bromopropane in industrial and commercial 

(workplace) settings, 1-BP products are not manufactured, distributed, marketed nor intended to 

be sold for consumer uses. We are concerned that there are numerous references throughout the 

document to “consumer uses” that are unsubstantiated and urge that the EPA update the 

information in the final risk assessment to accurately reflect existing 1-BP uses to minimize the 

expenditure of agency resources and to clarify existing uses to better inform the risk assessment 

and any future rulemakings based on the risk assessment.

As 1-BP products are designed and intended for workplace use, the labeling and GHS-compliant 

Safety Data Sheets (SDS) reflect requirements as dictated by the Federal Hazard 

Communications Standard2[2] providing hazard information to employers and workers including 

appropriate handling, storage and use information. In addition, 1-BP products are distributed via 

industrial supply chains or directly to industrial customers.

CSPA would also call attention to activity related to the EPA SNAP program, specifically to a 

CSPA-initiated survey of 1-BP product manufacturers and customers conducted in response to a 

proposed ban in 2007 cited in the draft risk assessment[3]. A review of the survey and comments 

clearly shows that the 1-BP products described were used exclusively in industrial environments 

and were not manufactured, distributed, marketed, nor intended to be sold to consumers. There 

are no indications from CSPA members that this has changed.

On page 185, the draft Risk Assessment notes “(t)he NIH Household Products Database and 

Kirk-Othmer Encyclopedia of Chemical Technology contained no relevant information on 

consumer products containing 1-BP. Through other search means, EPA/OPPT identified a 

number of products available to consumers which contain 1-BP.” It is puzzling that italicized 
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Page 23

statements are put forward without any support or indications that the described events are 

happening in the marketplace. For example, is there information that 1-BP products are currently 

listed for sale on legitimate websites? Or is there information that an industrial supplier, i.e., 

Grainger, is marketing these products to consumers?

In addition, also on page 185, the draft Risk Assessment indicates “(t)here may be other 

consumer products containing 1-BP which are available to consumers since not all SDSs display 

a complete list of chemical ingredients, therefore, some products may contain 1-BP but this 

cannot be confirmed by EPA.” A product containing 1-BP would be required to list its chemical 

name and concentration since 1-BP is characterized as a health hazard per paragraph (d) of 

§1910.1200 of the Federal Hazard Communication Standard.[4] Consequently, the statement is 

either inaccurate or describes a product that is non-compliant with the Federal Hazard 

Communication Standard requirements.

EPA cites the 1987 Westat “Household solvent products: A national usage survey”[5] of 

chlorinated solvents indicating that the “survey aligned with the description of the products 

chosen for modeling in this exposure assessment.”[6] We question the appropriateness of 

utilizing information contained in a thirty-year old consumer survey that “presents the results of 

a nationwide study of consumer usage of products thought to contain methylene chloride or five 

other chlorinated solvents used in combination with or as substitutes for methylene chloride.”[7]

and applying the result to a non-chlorinated solvent for industrial applications. This survey is 

simply not reflective of the properties or uses of 1-BP products.

[1] The Consumer Specialty Products Association (CSPA) is the premier trade association 

representing the interests of companies that manufacture, formulate, distribute and sell more than 

$100 billion annually in the U.S. of familiar consumer products that help household and 

institutional customers create cleaner and healthier environments. CSPA member companies 

employ hundreds of thousands of people globally. Products CSPA represents include 

disinfectants that kill germs in homes, hospitals and restaurants; candles, and fragrances and air 

fresheners that eliminate odors; pest management products for home, garden and pets; cleaning 

products and polishes for use throughout the home and institutions; products used to protect and 

improve the performance and appearance of automobiles; aerosol products and a host of other 

products. Through its product stewardship program, Product Care®, and scientific and businessto-business endeavors, CSPA provides members a platform to effectively address issues 

regarding the health, safety and sustainability of their products. For more information, please 

visit www.cspa.org.

[2] http://www.osha.gov/dsg/hazcom/HCSFinalRegTxt.html

[3] CSPA. (2007). Supplemental Comments to CSPA Opposition to Unacceptable Listing of nPropyl Bromide in Adhesives, and Aerosol Solvents. Consumer Specialty Products Association.
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[4] Section 3 of Appendix D to §1910.1200 - Safety Data Sheets (Mandatory), 

https://www.osha.gov/dsg/hazcom/hazcom-appendix-d.html

[5] https://hero.epa.gov/hero/index.cfm/reference/details/reference_id/1005969

[6] Appendix L Consumer Exposure Assessment portion of draft Risk Assessment

[7] Pg lvii of Westat study “Household solvent products: A national usage survey”

Commenter Name: Steven Bennett

Commenter Affiliation: Consumer Specialty Products Association (CSPA)

Document Control Number: EPA-HQ-OPPT-2015-0084-0015

Comment Excerpt Number: 4

Charge Question: 3-1 Consumer exposure assessment approach

Comment Excerpt: 

CSPA is concerned with the numerous additional references to “consumer” and “consumer use” 

throughout the draft risk assessment and recommends the references should either be removed, 

substantiated or updated appropriately. CSPA would like to point out the following specific 

passages for particular scrutiny:

 Page 22, “Consumer uses of concern identified for 1-BP include those that involve 

aerosol spray adhesives, aerosol spot removers, and aerosol cleaning and degreasing 

products – many of which were identified to contain 60-100% 1-BP.”

 Page 23, “For the consumer exposure assessment, EPA/OPPT relied on models 

incorporating information on generalized consumer use patterns, and the physicalchemical properties of 1-BP to estimate potential inhalation exposures.”

 Page 24-25, “EPA/OPPT also examined risks for acute exposure scenarios for consumer 

uses. EPA/OPPT assumed that consumers would be individuals (> 16 and older; both 

sexes including women of childbearing age) that intermittently use 1-BP in aerosol spray 

adhesives, aerosol spot cleaners, and aerosol degreasers/cleaners, although exposures to 

younger non-users may be possible in residential settings. Non-users may be individuals 

of any age group (e.g., children, adults, and elderly) who are nearby during product 

application.

 Page 31, “7. Consumer use in aerosol spray adhesives (consumer users and non-users), 8. 

Consumer use in aerosol spot removers (consumer users and non-users), and 9. Consumer 

use in aerosol cleaners and degreasers (including engine degreasing, brake cleaning and 

electronics cleaning scenarios for consumer users and non-users)”

 Page 72-82, Section 2-2 Consumer Exposures

 Page 118, Table 4-2 Use Scenarios, Populations of Interest and Toxicological Endpoints 

for Assessing Consumer Risks Following Acute Exposures to 1-BP Use In Aerosol Spray 

Adhesives, Aerosol Spot Removers, and Aerosol Cleaners and Degreasers
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 Page 125, Table 4-15 Non-Cancer Risk Estimates for Acute Inhalation Exposure

Following Consumer Uses of 1-BP

 Page 148, 4.4.2 Uncertainties of the Consumer Exposure Assessment

 Page 148, 4.4.2.1 Consumer Use Information

 Page 185, Section A-8 Consumer Uses

 There were numerous additional references to consumer and consumer use
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2.2.1. Approach and Methodology

Commenter Name: Steven Bennett

Commenter Affiliation: Consumer Specialty Products Association (CSPA)

Document Control Number: EPA-HQ-OPPT-2015-0084-0015

Comment Excerpt Number: 2

Charge Question: 3-1 Consumer exposure assessment approach

Comment Excerpt: 

CSPA is concerned that the “Aerosol Paint” E-FAST2 Consumer Exposure Model noted in 

2.2.1.4 Consumer Model Results overestimates potential exposures. 1-BP products are dispensed 

as a liquid directly to the surface (often utilizing straws or nozzles) rather than aerosolized as in 

an aerosol paint product. CSPA recommends that the E-FAST2 CEM model be updated to better 

reflect the exposure patterns of 1-BP products. Further CSPA recommends that the exposure 

scenarios be updated for the corresponding modeling runs throughout the draft risk assessment.

Commenter Name: Steven Bennett

Commenter Affiliation: Consumer Specialty Products Association (CSPA)

Document Control Number: EPA-HQ-OPPT-2015-0084-0015

Comment Excerpt Number: 3

Charge Question: 3-1 Consumer exposure assessment approach

Comment Excerpt: 

In addition, we are concerned that Section F-4 Estimates for Number of Workers Potentially 

Using Aerosol Degreasing overestimates the number of workers are potentially exposed to 

degreasing solvents. CSPA members manufacture and market products for engine degreasing 

and brake cleaning but do not manufacture or know of any 1-BP products designed for engine 

degreasing and brake cleaning. Products formulated with other ingredients are much more 

suitable for brake cleaning and engine degreasing. CSPA recommend that the NAICS categories 

811111, 811112, 811113, 811118, 811121, 811122, 811191, 811192, 811198 be removed from 

Table F-14 and that the 222,940 establishments among the industry sectors be lowered to better 

reflect the number of workers and occupational non-users that would be potentially exposed.
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3.2.2. Cancer Hazard Identification

Commenter Name: Christina Franz

Commenter Affiliation: American Chemistry Council (ACC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0012

Comment Excerpt Number: 11

Charge Question: 4-1 Cancer hazard assessment and WOE

Comment Excerpt: 

The Discussion of the Potential Genotoxicity of 1-Bromopropane in the EPA Risk 

Assessment Is Incomplete

EPA’s 1-bromopropane draft risk assessment indicates that genotoxicity studies have 

demonstrated mixed results in tests using bacteria. 1-Bromopropane was stated to be a dosedependent mutagen in in vitro studies with Salmonella typhimurium (S. typhimurium) strains 

TA100 and TA1535 when the assay was conducted using closed chambers/desiccators 

specifically designed for testing volatile substances (Barber et al., 1981). While other Ames tests 

cited in EPA’s assessment were identified as negative for mutagenicity, the Agency noted that a 

major deficiency in these negative studies was the fact that the system was an “open” rather than 

“closed” system. However, there is additional Ames test data now available that have not been 

considered by EPA in its draft risk assessment (BioReliance, 2014)[1]. This new study replicated 

the closed system used by Barber et al. (1981), but demonstrated that 1-bromopropane was not 

mutagenic in vitro, either with or without metabolic activation. These data impact the weight-ofevidence for genotoxicity of 1-bromopropane and should be considered by EPA in its 

assessment.

With respect to the available genotoxicity data in assays other than the Ames assay, an in vitro

L5178Y mouse lymphoma cell assay was also positive; however, the increased mutation 

frequency was noted only at levels that produced cytotoxicity. Therefore, these data do not 

provide strong evidence for genotoxicity potential of 1-bromopropane. The only other in vitro

assay suggesting 1-bromopropane may be genotoxic was a Comet assay for DNA damage that 

employed human leukocytes from venous blood of unexposed workers. This assay had several 

experimental limitations that affect the interpretation of study results and the weight accorded to 

the study in any genotoxicity assessment. First, the assay did not include a S9 fraction; without 

the S9 fraction data, the effect of metabolic capacity as observed in vivo was not examined, 

limiting the utility of the data in the weight-of-evidence assessment. In addition, leukocytes of 

one donor only were used and no positive control was included in the assay. Overall, the quality 

of this Comet assay is questionable. All of the in vivo mutagenicity studies, including three 

micronucleus assays, two dominant lethal mutation assays, and one in vivo Comet assay were 

negative. ACC believes that the weight-of- evidence for a mutagenic mode of action for 1-

bromopropane does not exist. The EPA draft risk assessment should be revised to reflect the new 

data and to re-evaluate the issue of mutagenic mode of action.
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[1] The study sponsor, Albemarle, has included this study as part of their comments to this 

docket (comments dated May 9, 2016).

Commenter Name: Christina Franz

Commenter Affiliation: American Chemistry Council (ACC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0012

Comment Excerpt Number: 12

Charge Question: 4-1 Cancer hazard assessment and WOE

Comment Excerpt: 

The Female Mouse Lung Tumor is of Limited Relevance for Human Cancer Risk 

Assessment

A cancer risk assessment was performed in EPA’s risk assessment based on an increased 

incidence of alveolar/bronchiolar adenomas or carcinomas (combined) in female B6C3F1 mice 

that had been exposed to 1-bromopropane via inhalation for two years (NTP, 2011)[1]. This 

result was limited to one species (only mice) and only one sex (female). Mouse lung tumors have 

been the subject of scientific discussion in recent years, with significant investigation and 

discussion around the relevance of these tumors to human cancer risk assessment. EPA held a 

“State-of-the-Science Workshop on Chemically-induced Mouse Lung Tumors” (Workshop) in 

2014.[2] At that Workshop, data was presented addressing the issue of human relevance 

(presentation by Dr. Daniel Krewski). After performing an analysis of known human carcinogens 

as identified by the International Agency for Research on Cancer (IARC) and comparing human 

and animal data, Dr. Krewski reported that the concordance of human and mouse lung tumors 

was only “slight,” while the concordance of human and rat lung tumors was only somewhat 

better and ranked as “moderate.” Therefore, positive lung cancer results for 1-bromopropane, 

which were limited to female mice only, occurred in the rodent species that was found to only 

slightly correlate with human cancer occurrence. This lack of human concordance should be 

considered as part of the 1-bromopropane risk assessment process.

In order to determine why there is a lack of concordance between mouse and human lung tumor 

occurrence, researchers at the EPA Workshop suggested several factors may be involved. In a 

presentation by Dr. Gary Boorman (Covance), the pathology of human versus mouse lungs was 

discussed. Dr. Boorman described a series of potentially important differences between the lungs 

of humans and mice that included: 1) differences in the gross anatomy of the mouse lung and 

human lung; 2) dominance of the Clara cell in epithelial cells lining mouse lung; and 3) 

metabolic differences between mouse, rat and human lung. Each of these factors indicates that 

mouse lung tumors are not relevant for quantitative cancer risk assessment and for predicting 

human risk. These issues are discussed in detail in comments provided by Albemarle (dated May 
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Page 29

9, 2016) and ACC believes they provide important support for the lack of relevance of mouse 

lung tumors to human cancer risk.

[1] NTP, 2011. NTP Technical Report on the Toxicology and Carcinogenesis Studies of 1-

Bromopropane (CAS No. 106-94-5) in F344/N Rats and B6C3F1 Mice (Inhalation Studies). 

(NTP TR 564; NIH Publication No. 11-5906). Research Triangle Park, NC.

[2] http://www2.epa.gov/iris/mouse-lung-tumor-workshop
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3.3. Weight of Evidence/Multiple Lines of Evidence Supporting Critical Effects

Commenter Name: Christina Franz

Commenter Affiliation: American Chemistry Council (ACC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0012

Comment Excerpt Number: 10

Charge Question: 4-3 WOE analysis and non-cancer endpoints

Comment Excerpt: 

There Are Insufficient Data to Establish a Mode of Action for 1-Bromopropane 

Carcinogenicity

The EPA draft risk assessment states: “1-BP is expected to be a good alkylating agent because 

bromine is a good leaving group.” “Four possible mechanisms---genotoxicity, oxidative stress, 

immunosuppression, and cell proliferation—have been suggested.” “The exact mechanism/mode 

of action for 1-BP carcinogenesis is not clearly understood. More research (e.g., organ-specific 

in vivo DNA adduct studies, oxidative stress) is needed to identify key molecular events” (page 

322).

The limited toxicokinetic data indicate that glutathione (GSH) conjugation and oxidation via 

cytochrome P450 (CYP450) significantly contribute to the metabolism of 1-bromopropane. As 

discussed by EPA in the draft 1-bromopropane risk assessment (see page 84), 1-bromopropane is 

rapidly absorbed and eliminated from the body following inhalation in humans. The metabolism 

of the chemical in mammals involves: (1) conjugation, principally with glutathione, leading to 

release of the bromide ion and formation of mercapturic acid derivatives; and (2) oxidation 

(catalyzed by cytochrome P-450) of parent material and metabolites leading to metabolites with 

hydroxyl, carbonyl, and sulfoxide groups, and to CO2.

According to EPA, over 20 metabolites have been identified or hypothesized in rodent studies, 

including four metabolites that have been identified in human urine. While glycidol and 

propylene oxide have been identified as reactive intermediate, and have been reported to be 

genotoxic, as discussed above, a weight-of-evidence assessment of the genotoxicity potential of 

1-bromopropane indicates that the compound is most likely non-genotoxic. As a result, there is 

no sound basis for any specific mode of action for 1-bromopropane, and any statements based on 

the available data are pure speculation. As EPA states in the draft risk assessment: “The exact 

mechanism/mode of action for 1-BP carcinogenesis is not clearly understood. More research 

(e.g., organ-specific in vivo DNA adduct studies, oxidative stress) is needed to identify key 

molecular events.” ACC encourages EPA to make these conclusions clear as the draft risk 

assessment is revised.

Regarding mechanism/mode of action, EPA repeatedly states in the draft assessment (at pages 

95, 99, 152, and 322 of 403, and in the charge questions to the Peer Review Panel[1]) that 

“oxidative stress, immunosuppression and cell proliferation can act synergistically to complete 

the multi-stage process of carcinogenesis.” EPA provides no scientific support for this sweeping 
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statement and has not connected this finding to any of the 1-bromopropane experimental data. 

These statements do not support a mutagenic mode of action for 1-bromopropane. ACC 

recommends that EPA either delete these statements or conduct a more robust scientific review 

to provide justification for them.

[1] The EPA/OPPT Work Plan Risk Assessment for 1-Bromopropane (1-BP) Draft Peer Review 

Charge Questions dated February 29, 2016
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3.4. Dose-Response Assessment

Commenter Name: Christina Franz

Commenter Affiliation: American Chemistry Council (ACC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0012

Comment Excerpt Number: 6

Charge Question: 5-1 MOE approach for acute exposure

Comment Excerpt: 

EPA Has Used Very Conservative Benchmark Dose Modeling Response Levels without 

Describing the Rationale for Its Choices

EPA has used benchmark dose modeling (BMD) rather than NOAEL/LOAEL and RfD/RfC 

methods for dose-response assessment applied to 1-bromopropane datasets. EPA states at pages 

100-101 of the assessment that it followed its 1991 EPA guidance (EPA, 1991)[1] and its 2012 

BMD Technical Document (EPA, 2012)[2] regarding the selection of BMRs when 

developmental endpoints indicate increased severity. A review of both guidance documents, 

however, reveals important differences between what the guidance recommends and what EPA 

actually did in the 1-bromopropane risk assessment.

For instance, the 1991 guidance document refers to the use of BMD modeling, but states that its 

use in developmental toxicity datasets has not yet been validated. The 2012 Technical Document 

states that although use of BMD modeling for quantal datasets has been refined and the Agency 

provides specific guidance on its use for quantal datasets, EPA also cautions that use of the 

approach for continuous datasets is not straightforward (see page 20 of the guidance).

In addition, on page 19 of the 2012 Technical Document, Section 2.2., Selection of the 

Benchmark Response Level (BMR), EPA states: “Selecting a BMR(s) involves making 

judgments about the statistical and biological characteristics of the dataset and about the 

applications for which the resulting BMDs/BMDLs will be used. The EPA does not currently 

have guidance to assist in making such judgments for the selection of the response levels, or 

BMRs, to use with BMD modeling for most applications (e.g., for calculating reference doses or 

relative potency factors), and such guidance is beyond the scope of this document.” EPA’s lack 

of transparency regarding its justification for the choices of BMRs in the 1-bromopropane 

assessment makes it virtually impossible to understand the bases for EPA’s decisions. Noting 

that EPA followed Agency guidance is not sufficient.

The choice of a BMR is critical to the MOE calculations presented. Therefore, additional details 

on why certain very conservative choices for BMR were made is very important to understand 

how to interpret EPA’s results, as well as to understand whether the risks presented are actually

worst case, which appears to be the case, given the inadequate level of detail provided. For 

example, the EPA BMD modeling appears in some cases to represent a 1% response in rodents 

(see Table Apx P-2). This level is inconsistent with the Agency’s guidelines, which state that the 

model should only be used within the range of observable effects (typically 10%) to determine a 
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POD. As stated at page 20 of the EPA 2012 BMD Technical Document: “It is important to 

recognize that the BMR need not correspond to a response that the study could detect as 

statistically significantly different from the control response, provided that the response is 

considered biologically significant.” Given the very low response level chosen, (below 5% in 

some cases), EPA should provide a discussion of why these response levels would be 

biologically significant and are superior to NOAEL/LOAEL methods with application of 

uncertainty factors.

[1] EPA, 1991. Guidelines for Developmental Toxicity Risk Assessment. Published on 

December 5, 1991, Federal Register 56(234):63798-63826.

[2] EPA, 2012. Benchmark Dose Technical Guidance. Risk Assessment Forum. EPA/100/R12/001. June
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3.4.1. Non-Cancer Dose-Response Assessment

Commenter Name: Christina Franz

Commenter Affiliation: American Chemistry Council (ACC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0012

Comment Excerpt Number: 9

Charge Question: 4-2 Endpoints and PODs: acute and chronic exposure

Comment Excerpt: 

EPA’s Benchmark Dose Modeling of Reproductive and Developmental Toxicity Datasets Is 

Inconsistent with EPA Guidance and Decisions that Depart from Guidance Are Not 

Explained Adequately

ACC has commented above regarding the reproductive toxicity endpoints and assessing risks of 

non-cancer effects in adult males. ACC reviewed EPA’s use of the WIL study data in BMD 

modeling as applied to non-cancer risk assessment for adult males and pregnant women, for 

acute and chronic exposure scenarios, and has identified additional inconsistencies. ACC is 

concerned that EPA has failed to explain adequately the modeling and data choices/decisions it 

made in the 1-bromopropane risk assessment as it applies to both endpoints of toxicity (i.e., 

reproductive and developmental endpoints). Consistent with comments above, the key issues 

ACC has identified concern EPA’s choice of BMR levels for BMD modeling and the lack of 

consistency of those choices with current EPA Technical Guidance (EPA, 2012)[1].

As discussed on pages 102 and 103 in EPA’s draft risk assessment for 1-bromopropane, the 

Agency indicates it will use “a BMR of 5%” to address the severity of the developmental 

endpoint for both acute and chronic exposures in humans. The endpoint selected is from the WIL 

2001 study in rats and was described as “decreased live litter size” at post-natal day 0 (birth) in 

the F1 generation (see Table 3-1, page 107). Given that this endpoint is a continuous endpoint, 

EPA’s 2012 Technical Document indicates that a BMR of 1 standard deviation (1SD) from the 

control mean is recommended (EPA, 2012[2]). EPA also states that a justification should always 

be provided for the selected BMR. The 2012 Technical Document also indicates that a 0.5SD 

can be used for more severe effects (where a 0.5SD is assumed to correspond to a 5% BMR as 

may be applied to quantal datasets), yet the basis for such decisions should be discussed in the 

risk assessment. Interestingly, the support provided by EPA for the use of a 0.5 SD level, 

assumed to equate here to the 5% BMR, is a paper from 1995 (Kavlock, 1995)[3] (see page 323 

of the 1-bromopropane risk assessment). However, Kavlock’s paper addresses the issue of BMR 

choice by pointing out that in the analysis of the validity of BMR choices for developmental 

toxicity endpoints, the BMD calculations produced values that were similar to NOAELs 

observed in the same studies (see page 212, right hand column of Kavlock et al. 1995). This is 

not true of EPA’s BMR choices and the resulting modeling where use of any standard other than 

the 1SD standard resulted in BMD and BMDL values that were very different from the NOAEL 

for live litter size from the WIL study (see values in Table Apx P-2 of the 1-bromopropane risk 

assessment).
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ACC also notes that in Table Apx P-2, EPA indicates that they have used “relative deviation” 

instead of SD. The use of “relative deviation” is not mentioned or supported by the 2012 EPA 

Technical Guidance. Therefore, ACC questions the validity of any use of “relative deviation” in 

the 1-bromopropane assessment, particularly given the lack of discussion of modeling choices in 

the current draft assessment. The choice to use “relative deviation” in place of SD has a 

significant impact on the risk assessment and further justification is needed if EPA is going to 

rely on this endpoint.

Importantly, the Kavlock paper cited by EPA as support for its 1-bromopropane assessment 

states that the first step in the BMR assessment is to determine what change will be considered 

biologically significant, emphasizing the importance of this step to the validity of the BMD 

modeling (see page 216 under “Discussion” of Kavlock et al. 1995). Nowhere in the 1-

bromopropane risk assessment does EPA provide a rationale or discussion of what change in live 

litter size would be considered biologically significant.

A search of the published literature by ACC failed to identify any specific guidance on this issue. 

What was found, as mentioned above, is a discussion of the fact that BMD modeling of 

developmental toxicity endpoints that are continuous data points, such as live litter size, are 

generally similar to NOAEL values for those same endpoints when robust developmental 

toxicity studies were evaluated in a meta-analysis (Kavlock, 1995; Kimmel, 1995[4]; Allen. 

1994[5]).

Evaluating the actual data for live litter size as presented in Table Apx P-1 (see page 323), and 

the results of modeling in Table Apx P-2 (page 324), it is clear that EPA has not provided 

adequate explanation for the choices made in terms of modeling the WIL study data. For 

example, the live litter size data demonstrates that the control mean litter size was 14.4 with a SD 

of 2.21. This means that there was a 15% difference in the mean value and the value representing 

1SD from that mean in the control group. Yet, a 5% BMR value as used by EPA represents only 

0.72, or less than one fewer rat pups per litter, a value that is unlikely to be biologically relevant 

given that the control group varied by much more than one rat pup from litter to litter. EPA 

should provide a scientifically-based discussion, not a statistical discussion, of the biological 

relevance of 0.72 as the 5% BMR for the dataset. If EPA were to use the approach from its 2012 

Technical Guidance, the BMR representing 1SD would be applied, which would result in 

estimates of a BMD that is essentially identical to the NOAEL of 250 ppm identified in the study 

(see EPA calculations in Table Apx P-2). Moreover, the BMDL1SD of 158 ppm (see Apx P-2) 

would make logical sense as well, given that 100 ppm was also a NOAEL exposure level in the 

study. EPA must provide a rationale for use of a BMD and BMDL other than 256 ppm and 158 

ppm in the 1-bromopropane risk assessment.

ACC notes that use of the BMD of 256 ppm and a BMDL of 158 ppm would result in increases 

in the HEC values for the 1-bromopropane risk assessment that are at least 3-fold higher. Given 

the 2012 Technical Guidance and publications concerning the use of BMD modeling for 

developmental toxicity study data, ACC finds no support for the use of an alternative approach, 

including the inappropriate use of the “relative deviation”, particularly given the lack of 

discussion of biological relevance of the very small changes in live litter size of 0.7.
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[1] EPA, 2012. Benchmark Dose Technical Guidance. Risk Assessment Forum. EPA/100/R12/001. June

[2] EPA, 2012. Benchmark Dose Technical Guidance. Risk Assessment Forum. EPA/100/R12/001. June (page 21).

[3] Kavlock et al. 1995. Dose-response assessment for developmental toxicity. IV. Benchmark 

doses for fetal weight changes. Fund. Appl. Toxicol. 26:211-222.

[4] Kimmel et al. 1995. The application of benchmark dose methodology to data from prenatal 

developmental toxicity studies. Toxicol. Lett. 82/83:549-554.

[5] Allen et al. 1994. Dose-response assessment for developmental toxicity. III. Statistical 

models. Fund. Appl. Toxicol. 23:496-509.
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3.5. Summary of Health Hazard

Commenter Name: Christina Franz

Commenter Affiliation: American Chemistry Council (ACC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0012

Comment Excerpt Number: 8

Charge Question: 4-2 Endpoints and PODs: acute and chronic exposure

Comment Excerpt: 

The Use of Non-GLP Study Data Instead of GLP Quality Data for the Reproductive 

Toxicity Hazard Assessment is Not Adequately Explained and Errors in the Risk 

Assessment Need Correction

EPA identifies reproductive toxicity in its draft risk assessment as one of the hazards of 1-

bromopropane. As shown in Table 3-1, EPA identifies the available data used in its hazard 

assessment and non-cancer dose-response assessment. The key studies identified and used by 

EPA in its risk assessment for non-cancer effects include a guideline GLP study by WIL 

Research (2001) and a research study by a Japanese group referred to as Ichihara et al. (2000b). 

A careful review of the use of these two studies in EPA’s risk assessment identified some 

important discrepancies that call into question the use of the Ichihara study over the WIL study 

for dose-response assessment of reproductive toxicity.

The Ichihara et al. (2000b) study is a non-GLP research study conducted in male Wistar rats only 

where animals were exposed by whole body inhalation exposure. The only details of the study 

available to EPA were those from the publication itself. In Appendix O of EPA’s assessment, it 

states that this study is said to be a “GLP” study, but this conclusion is erroneous based on the 

published paper itself. Therefore, EPA has misstated a key quality concern for this study. 

Consequently, the Ichihara et al. study is not as robust as another GLP-guideline reproductive 

toxicity study, i.e., WIL (2001).

Another error exists in Table 3-4, where EPA identifies the lowest human equivalent 

concentrations (HECs) for non-cancer effects for 1-bromopropane. The entry in the table 

mistakenly identifies the WIL (2001) study as evidence supporting reproductive system toxicity, 

i.e., the data presented in Table 3-4 actually relates to the Ichihara et al. (2002b) study; not the 

WIL study. These two errors lead us to question the quality of the study evaluation made by EPA 

and, given the significance of these studies to the risk assessment for 1-bromopropane, the 

assessment needs to be corrected.

The use of the Ichihara et al. (2000b) study for the 1-bromopropane assessment, rather than the 

more robust reproductive study known as WIL (2001), is never fully discussed, except to state 

that the Ichihara study apparently had a lower NOAEL. The Ichihara study tested exposures from 

200 to as high as 800 ppm 1-bromopropane, and the authors reported that there was no NOAEL 

level identified for reproductive effects. Instead, the authors report a LOAEL of 200 ppm based 

on decreases in absolute and relative seminal vesicle weights. However, the WIL 2001 study 
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identified a NOAEL of 250 ppm 1-bromopropane in a whole body inhalation exposure study 

conducted in Sprague-Dawley rats exposed to levels from 100 ppm to as high as 750 ppm. The 

LOAEL of 500 ppm was associated with decreased percentage of motile sperm and an increase 

in estrous cycle length. The WIL study saw no significant effects on seminal vesicle endpoints at 

exposures up-to-and-including 250 ppm 1-bromopropane. It is also important to note that effects 

on sperm parameters are considered a more sensitive measure of toxicity and are typically 

associated with biologically relevant changes in reproductive organ effects (EPA, 1996)[1], such 

as were observed in the 2001 WIL study. Given the fact that Wistar rats are not the standard 

strain used in chemical toxicology testing in the United States, the possibility of strain-specific 

differences cannot be ruled out. EPA’s risk assessment should explain why the more robust GLP 

study was set aside in favor of the non-GLP study.

It is also critical to emphasize that the use of the WIL (2001) reproductive toxicity study instead 

of the non-GLP study by Ichihara et al. (2000b) to choose a POD for use in the 1-bromopropane 

risk assessment would result in a 4-fold increase in the MOEs for adult workers based on 

reproductive endpoints (HEC of 200 ppm as compared to an HEC of 53 ppm), without 

refinements to the exposure assessment component of the 1-bromopropane risk assessment, 

which are also necessary (as discussed above).

[1] EPA, 1996. Guidelines for Reproductive Toxicity Risk Assessment. Published on October 

31, 1996, Federal Register 61(212):56274-56322.
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4.0. Human Health Risk Characterization

Commenter Name: Christina Franz

Commenter Affiliation: American Chemistry Council (ACC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0012

Comment Excerpt Number: 7

Charge Question: 5-1 MOE approach for acute exposure

Comment Excerpt: 

EPA Fails to Consider Its Own Guidance Regarding Developmental Toxicity Risk 

Assessment

EPA has developed guidance regarding developmental toxicity studies and risk assessment 

(EPA, 1991).[1] In that guidance, EPA discusses interpretation of fetal and pup study data in 

light of maternal toxicity (see pages 18-19 of EPA, 1991). In the 1-bromopropane risk 

assessment, EPA relies on study data from a rat reproduction study known as WIL (2001) in 

order to derive an acute toxicity BMDL (see page 117) for pregnant women. In the WIL (2001) 

study (see page 107), Sprague-Dawley rats were exposed to 1-bromopropane via inhalation

exposure at levels from 100 to 500 ppm, 6 hours/day during mating, throughout mating, and up 

to gestation day (GD) 20 for first generation litters. In another study – Huntingdon (2001) (cited 

by EPA on page 315), Sprague-Dawley rats also were exposed to 1-bromopropane via inhalation 

at exposure levels of 103, 503 or 1005 ppm, 6 hours/day on GDs 6-19 (see page 315). In the 

Huntingdon study there was no effect on litter size, and just as was observed in WIL (2001), 

there was no significant effect on pre- or post-implantation loss. In fact, the only reported toxic 

effects in offspring in this study were non-specific effects seen in the presence of maternal 

toxicity. In comparison, WIL (2001) reported a statistically significant effect on live litter size 

only at an exposure level (500 ppm) that was also associated with signs of maternal toxicity. 

Therefore, using EPA guidance on developmental toxicity risk assessment, the data from both 

GLP quality rat studies, one a reproductive toxicity study (WIL, 2000) and the other a 

developmental toxicity study (Huntingdon, 2001), should be interpreted in light of the maternal 

toxicity data as discussed in EPA’s own guidance. Yet, EPA fails to provide such study data 

discussion in its 1-bromopropane draft risk assessment.

[1] EPA, 1991. Guidelines for Developmental Toxicity Risk Assessment. Published on 

December 5, 1991, Federal Register 56(234):63798-63826.
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4.1. Risk Estimation Approach

Commenter Name: Eve Gartner

Commenter Affiliation: Earthjustice et al.

Document Control Number: EPA-HQ-OPPT-2015-0084-0016

Comment Excerpt Number: 5

Charge Question: 4-2 Endpoints and PODs: acute and chronic exposure

Comment Excerpt: 

4. EPA’s risk calculation fails to fully account for risks to pregnant women and from in utero 

exposure

EPA states that it is addressing pregnant women’s exposure as a highly vulnerable endpoint. But, 

EPA’s risk assessment does not make clear how, if at all, EPA’s risk values actually account for 

the increased vulnerability caused by in utero exposure. Failing to quantitatively account for such 

vulnerability within the risk assessment values would mean that EPA’s risk values are 

underestimates of real-world risk for the most vulnerable population.

EPA appropriately recognizes that pregnant workers are likely to be exposed to 1-BP.[1] Further, 

exposures during pregnancy are likely to occur among consumers, for whom EPA also calculates 

risk, and for the community populations in the vicinity of 1-BP sources, as discussed above. 

However, the equations EPA uses to calculate the cancer and chronic non-cancer risk for 

workers do not appear to use any age-dependent adjustment factors based on the window of 

exposure.[2]

EPA states that it is using the following equation to calculate “acute and chronic exposures for 

non-cancer and cancer risk”[3]:

ADC or LADC=C×ED×EF×WY / AT.

In this equation, there appears to be no input reflecting uncertainties relevant to early-life 

exposure and exposure of other vulnerable populations.[4] However, these uncertainties are wellacknowledged. For example:

 “While it is anticipated that there may be differential 1-BP metabolism based on 

lifestage; currently there are no data available, therefore the impact of this cannot be 

quantified.”[5]

 “The available data clearly indicate that the nervous system is a target for 1-

bromopropane toxicity in humans and animals. Data in humans show that 1-

bromopropane can induce morphological alterations in neurons, which may lead to motor 

and sensory deficits. Studies in animals show that 1-bromopropane can induce 

biochemical, morphological, electrophysiological, and neurobehavioral alterations by

mechanisms yet to be elucidated.”[6]
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 “Overall, the available human data are inadequate to assess the reproductive toxicity of 1-

bromopropane. The available animal data suggest that the reproductive system may be a 

potential target of concern for 1-bromopropane toxicity in humans.” [7]

In summary, there are many uncertainties and data gaps in relevant health and developmental 

endpoints, mechanism, and extrapolations from animal data to human risk. While we support 

EPA’s choice of a POD based on developmental toxicity as a starting point,[8] without 

additional uncertainty factors, EPA is likely underestimating risk and failing to protect all 

vulnerable populations, and relevant health endpoints.

We are also concerned that the Draft Assessment understates risks to children resulting from 

consumer uses. EPA acknowledges likely bystander exposure from consumer use as a result of 

the fact that the majority of consumers reported using the chemical inside their home, with no 

open window, door, or exhaust fan, and with the door of the room of use open to the rest of the 

house.[9] EPA recognizes that children may be exposed in this way. Such early-life exposure is 

likely to be greater due to children’s lower body weights. However, EPA does not use any 

increased vulnerability factor to acknowledge higher risks due to such exposure. The use of an 

age-dependent adjustment factor would be appropriate to avoid underestimation of health risks. 

The result of not using any such factor means EPA’s risk assessment assumes that adults and 

children are equally vulnerable to health impacts at the same rate of exposure. This is not correct. 

Children are not little adults.[10] Children exposed are both likely to take in more of the 

chemical and to be more vulnerable to adverse health effects. EPA’s assessment of consumer 

risk is an underestimate because it does not include children’s increased vulnerability.

As a further concern, there appears to be no specific risk assessment value used to account for 

risk from in utero exposure for pregnant women, or the increased vulnerability resulting from 

such exposure. This is true even though EPA recognizes that “[t]here is some evidence for 

mutagenicity and DNA damage associated with exposure to 1-BP in vitro.”[11] The failure to 

account for this within the risk assessment value calculation also causes an underestimation of 

health risks.

Finally, EPA acknowledges in the risk assessment that 1-BP has a mutagenic mode of action.[12]

Consequently, to follow the agency’s own guidelines on cancer risk, EPA must use agedependent adjustment factors within the calculation of risk to account for the increased 

vulnerability due to early-life exposure.[13]

[1] Draft Assessment at 24.

[2] See Draft Assessment, App. H at 210.

[3] Id.
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[4] In Appendix H, id., EPA states that the inputs to the equation are as follows:

ADC = average daily concentration (8-hr TWA) used for chronic non-cancer risk calculations

LADC = lifetime average daily concentration (8-hr TWA) used for chronic cancer risk 

calculations

C = contaminant concentration in air (8-hr TWA)

ED = exposure duration (8 hr/day)

EF = exposure frequency (260 days/yr)

WY = working years per lifetime (40 yr)

AT = averaging time (LT × 260 days/yr × 8 hrs/day.

[5] Draft Assessment at 150.

[6] ATSDR Draft Profile at 67.

[7] ATSDR Draft Profile at 72.

[8] Draft Assessment at 150.

[9] Draft Assessment, App. L at 249-51.

[10] Nat’l Research Council, Pesticides in the Diets of Infants and Children 3 (1993).

[11] Draft Assessment at 94.

[12] Id. at 24 (“The weight-of-evidence analysis for the cancer endpoint is sufficient to support a 

probable mutagenic mode of action for 1-BP carcinogenesis.”).

[13] Even if EPA did not find a mutagenic mode of action, EPA should use age-dependent 

adjustment factors to assess cancer risk for all carcinogens, as California’s state Office of 

Environmental Health Hazards has recognized is a scientifically appropriate method to attempt to 

more fully account for such risks.
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4.5. Risk Assessment Conclusions

Commenter Name: Christina Franz

Commenter Affiliation: American Chemistry Council (ACC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0012

Comment Excerpt Number: 2

Charge Question: 5-4 Risk characterization assumption, uncertainty

Comment Excerpt: 

A.The 1-Bromopropane Risk Assessment Employs Methods Consistent with ScreeningLevel Risk Assessment -- Not a Refined Risk Assessment -- Which Should be Reflected in 

the Risk Assessment Conclusions

The methodology described in the 1-bromopropane risk assessment consistently employs worstcase and high-end assumptions regarding both hazard and exposure throughout the assessment. 

This very conservative methodology is consistent with a screening-level assessment, where 

health protective assumptions are used for parameters employed to calculate hazards and 

exposures to assure that potential risks are not underestimated. Screening-level assessments are 

not designed to provide accurate estimates of risk. When a screening-level assessment indicates 

an acceptable level of risk, the Agency has a high degree of confidence that the potential risks 

are much lower than the calculation, and therefore, the actual risks are often much lower and/or 

perhaps non-existent. However, when a screening-level risk assessment indicates a potential 

concern for a health or environmental effect, this does not mean that the actual risks are 

significant and warrant action. Rather, it means that the risk evaluation should be refined using 

more realistic and accurate parameters in the methodologies to calculate risks.[1] The outcome is 

then a refined risk assessment that more accurately quantifies actual risks. The screening-level 

assessment is, therefore, a “first look” at the available data to determine if more work is needed 

(the MOE was not adequate), or more work is not necessary with use of worst-case assumptions 

(MOE is adequate). Significantly, EPA fails to state throughout the assessment that this risk 

assessment is a screening-level assessment and must be refined before reliable and/or realistic 

conclusions about potential risks can be made.

For example, the Agency states in the Executive Summary: “The Agency is performing risk 

assessments for chemicals in the work plan. If an assessment identifies unacceptable risks to 

humans or the environment, EPA will pursue risk management.” However, pursuing risk 

management after conducting a worst-case scenario risk assessment is not appropriate. Instead, 

refinement of the assessment should first be pursued for those exposures where 1-bromopropane 

MOEs have been found to be unreasonable.

The significance of the distinction between a screening-level and refined risk assessment is 

apparent in EPA’s, “Main Conclusions of this Risk Assessment.” (see page 25). The Agency 

discusses cancer risk and describes risks in the range of 1 in 100 for use of spray adhesives 

containing 1-bromopropane. However, given the use of outdated exposure data, as well as 

questionable cancer rodent data to define the hazard, the conclusions EPA should have described 
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here would be the need to refine the cancer risk assessment in order to understand the magnitude 

of the risk.

In addition, EPA’s discussion in Part 4 of the human health risk characterization for 1-

bromopropane is inconsistent with EPA’s own Risk Characterization Handbook (EPA, 2000)[2]. 

In Part 4 of the 1-bromopropane risk assessment, EPA presents only the findings for the 95th 

percentile. In contrast, EPA’s Handbook states at page 40: “Assessments should address the 

resulting variability in doses received by members of the target population. Individual exposure, 

dose, and risk can vary widely in a large population. Central tendency and high end individual 

risk descriptors capture the variability in exposure, lifestyles, and other factors that lead to a 

distribution of risk across a population.”

Furthermore, the National Academies reiterated the importance of providing central estimates for 

hazard values in 2014.[3] The EPA section on risk characterization in the draft assessment has 

not provided any central tendency estimates of risk. By failing to provide the full range of 

available risk estimates, risk managers will not have a complete and full understanding of the 

data and the findings. This critical information must be provided not only when conducting doseresponse, but also in the final risk characterization section. This failure to discuss central 

tendencies, and presenting only the 95th percentile responses, is consistent with a screening-level 

approach.

Another example illustrating the significance of the important difference between screening-level 

and refined assessments is found in the Executive Summary of the assessment (see page 24), 

where EPA states: “A concern for adverse developmental effects was identified for all acute 

consumer exposure scenarios (i.e., MOEs were below the benchmark MOE of 100), with 1-BP 

use in aerosol spray cleaners and degreasers showing the greatest risk.” However, if an adequate 

MOE is not achieved based on the use of worst-case assumptions in a screening-level 

assessment, this does not mean there is a risk. Instead, the conclusion properly drawn is that an 

adequate MOE was not achieved based on the use of worst-case, non-refined assumptions, and 

the assessment should be refined to understand whether a real concern exists or not.

Given that the 1-bromopropane risk assessment employs a methodology consistent with a 

screening-level assessment, EPA must very carefully describe any conclusions drawn in the draft 

risk assessment in order to avoid confusion and misinterpretation by overstating any potential 

risks identified. In addition, ACC strongly encourages EPA to refine the current risk assessment 

with participation from industry before finalizing the assessment and contemplating any risk 

management measures.

[1] This well accepted approach is consistent with EPA’s general approach to risk evaluation. 

This is perhaps best articulated in EPA’s 2001 bulletin on ecological risk assessment, which 

states: “Screening-Level Ecological Risk Assessments are conservative assessments in that they 
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provide a high level of confidence in determining a low probability of adverse risk, and they 

incorporate uncertainty in a precautionary manner. It must be stressed that SLERAs are not 

designed nor intended to provide definitive estimates of actual risk, generate cleanup goals and, 

in general, are not based upon site-specific assumptions. Rather, the purpose of SLE RAs is to 

assess the need, and if required, the level of effort necessary, to conduct a detailed or “baseline” 

ecological risk assessment for a particular site or facility. Therefore, refinement of contaminants 

of concern occurs in the baseline risk assessment rather than in the SLERA.” Further details can 

be found here: https://www.epa.gov/sites/production/files/2015-09/documents/slera0601.pdf.

[2] EPA, 2000. Science Policy Council Handbook: Risk Characterization. Office of Science 

Policy. Office of Research and Development. EPA 100-B-00-002. December.

[3] See: http://www.nap.edu/catalog/18764/review-of-epas-integrated-risk-information-systemiris-process.

Commenter Name: Eve Gartner

Commenter Affiliation: Earthjustice et al.

Document Control Number: EPA-HQ-OPPT-2015-0084-0016

Comment Excerpt Number: 7

Charge Question:

Comment Excerpt: 

6. We support EPA’s conclusions that 1-BP poses serious risks in a range of applications and 

urge it to prohibit these uses.

It is scientifically appropriate that EPA recognizes the serious risks that use of 1-BP poses when 

used in spray adhesives, dry cleaning machines, spot cleaning, vapor degreasing, and aerosol 

degreasing in both acute and chronic exposure scenarios. There is extensive evidence of harm to 

workers attributable to worker exposures. For example, in the dry cleaning and laundry industry, 

which employs approximately 110,000 people, the use of 1-BP is linked to emergency room 

visits for a number of neurological effects.[1] Acute and chronic health effects of those working 

in the cushion or foam fabricator industry were highlighted in a 2013 New York Times article.[2]

There are over 300 foam fabricators in the United States,[3] and workers in this industry have 

experienced devastating injuries from exposure, including prolonged numbness, stinging in their 

feet, spinal pain, and long-term mobility problems.[4] The science also supports EPA’s 

recognition of the serious acute inhalation risks to consumers using products containing 1-BP. 

This chemical is too toxic for consumer use.

We urge EPA to conclude that use of 1-BP– both in occupational and consumer applications --

poses “unreasonable risks” within the meaning of TSCA, and to move forward promptly with a 

Section 6 rulemaking to prohibit its use. We believe that the exposure and risk estimates to 1-BP 

presented in this Draft Assessment support this conclusion, and that this would represent a 
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Page 46

significant step towards adequately protecting the health of the general population as well as 

those exposed through their occupation.

We strongly urge EPA not to conclude wrongly that engineering controls offer adequate 

protection for workers. Indeed, in April 29, 2016 comments to the CDC in connection with the 

Draft Criteria for a Recommended Standard: Occupational Exposure to 1-Bromopropane, an 

EPA scientist stated that use of engineering controls when using 1-BP in occupational settings 

“may not be sufficient to achieve the proposed [recommended exposure limit].”[5] Moreover, 

use of engineering controls such as ventilation has significant potential to lead to more 1-BP in 

the ambient air and is likely to increase exposure for community members living, working, and 

attending school near these sources.

Furthermore, due to the high risks EPA has quantified, and the risks known to be present but not 

quantified, particularly for consumers and community members, EPA should make clear in this 

risk assessment that there is no known use for which 1-BP could be considered safe. Finally, in 

view of the high risks EPA has found and the additional information showing that EPA’s risk 

assessment likely underestimates such risks, EPA should remove 1-BP as an acceptable 

substitute in the SNAP program. EPA also should use all other available authority to prevent and 

reduce exposure to community members, particularly children, including listing 1-BP as a known 

hazardous air pollutant.

[1] Ctrs. for Disease Control, Neurologic Illness Associated with Occupational Exposure to the 

Solvent 1-Bromopropane—New Jersey and Pennsylvania, 2007–2008, 57 Morbidity & Mortality 

Wkly Rep. 1300 (Dec. 5, 2008), http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5748a2.htm.

[2] Ian Urbina, As OSHA Emphasizes Safety, Long-Term Health Risks Fester, N.Y. Times, Mar. 

31, 2013, at A1, available at http://www.nytimes.com/2013/03/31/us/osha-emphasizes-safetyhealth-risks-fester.html.

[3] See Katy Wolf and Mike Morris, Inst. for Research & Technical Assistance, Assessment, 

Development, and Demonstration of Alternatives for Five Emerging Solvents 63 (Oct. 2006), 

available at http://www.irta.us/reports/Five%20Emerging%20Chemicals.pdf.

[4] Id. at 47; Ian Urbina, As OSHA Emphasizes Safety, Long-Term Health Risks Fester, N.Y. 

Times, Mar. 31, 2013, at A1, available at http://www.nytimes.com/2013/03/31/us/oshaemphasizes-safety-health-risks-fester.html.

[5] Margaret Sheppard, EPA, Comments on External Review Draft of “Criteria for a 

Recommended Standard: Occupational Exposure to 1-Bromopropane,” Docket ID No. CDC2016-0003-0011 (Apr. 29, 2016).
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Commenter Name: Amy Kyle

Commenter Affiliation: School of Public Health, University of California, Berkeley

Document Control Number: EPA-HQ-OPPT-2015-0084-0019

Comment Excerpt Number: 6

Charge Question:

Comment Excerpt: 

The conclusions of the analysis are difficult to see and should be brought forward.

The document seems to conclude overall that there are current exposures of concern for both the 

occupational and general populations that would warrant action. These findings are buried in 

many tables and repetitive discussion and hard to find and are obscured in the text of the 

executive summary.

These are important findings should be explained clearly in a way that will be accessible to a 

motivated lay audience and does not require the reader to deconstruct jargon.
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5.0. References

Commenter Name: Christina Franz

Commenter Affiliation: American Chemistry Council (ACC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0012

Comment Excerpt Number: 4

Charge Question: 5-4 Risk characterization assumption, uncertainty

Comment Excerpt: 

EPA Failed to Include a Systematic Review of Study Quality, Reliability, and Relevance

A systematic evaluation of the quality (including relevance and reliability) of each study is a 

necessary part of a scientifically defensible risk assessment process. When evaluating both 

hazard and exposure, it is critical that EPA rely on the studies of the highest quality, not simply 

those studies that produce the lowest points of departure, or the highest exposure estimates. EPA 

should develop, through an open and transparent process, clear procedures and protocols that 

will promote consistent and scientifically sound assessments that can be compared and 

evaluated.

Unfortunately, while EPA identifies inhalation endpoints that are considered suitable in Table 3-

1, EPA fails to provide information regarding the quality of the individual studies. Appendix M 

does identify some quality considerations; however, EPA does not provide any information 

regarding its own findings from its quality review of the individual studies. No information is 

provided to describe how considerations were applied and what constitutes a study of “high 

quality” (as cited on page 100) or “good quality” (as cited on page 113). An evaluation of 

scientific evidence should begin with a transparent application of clear criteria to evaluate the 

quality of individual studies. Simply referencing some considerations without describing how 

each relevant study compares to applicable criteria is neither transparent nor sufficient. Without a 

robust evaluation, studies of lower quality can be accorded too much weight in the overall 

assessment, leading to a flawed evaluation. It is very important that EPA rely on studies that are 

of the highest quality, not simply those studies that produce the lowest points of departure (as 

EPA states it has done on page 120). While it is possible that EPA has conducted such an 

evaluation, EPA should be transparent about how that evaluation was conducted and the criteria 

used. ACC strongly recommends that EPA include this information in its final risk assessment 

and provide evidence-based determinations of the chosen endpoints based on the quality of the 

data. Simply selecting the lowest value in not appropriate unless EPA acknowledges that this 

assessment of 1-bromopropane is strictly a screening-level assessment.

Commenter Name: Lo Mariana

Commenter Affiliation: Earthjustice

Document Control Number: EPA-HQ-OPPT-2015-0084-0014
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Comment Excerpt Number: 1

Charge Question:

Comment Excerpt: 

EPA should consider all of the relevant scientific information contained in Docket CDC-2016-

0003/NIOSH 057-A. To assist in this review, we have uploaded the docket index and some of 

the relevant scientific documents contained in this docket. 

Commenter Name: Eve Gartner

Commenter Affiliation: Earthjustice et al.

Document Control Number: EPA-HQ-OPPT-2015-0084-0016

Comment Excerpt Number: 8

Charge Question:

Comment Excerpt: 

7. EPA’s assessment should incorporate evidence from other recent regulatory dockets

As EPA is undoubtedly aware, other agencies and other EPA Offices are also considering the 

toxicity of 1-BP and the risks it poses. ATSDR has recently published for public comment a 

Draft Toxicological Profile of 1-BP.[1] The State of New York has petitioned to add 1-BP to the 

list of hazardous air pollutants (HAPs) under section 112(b) of the Clean Air Act, 42 U.S.C. § 

7412(b) and numerous commenters, including the National Association of Clean Air Agencies, 

and individual state regulators, filed comments in support of that listing. In addition, the Center 

for Disease Control and Prevention has sought comment on its Draft Criteria for a 

Recommended Standard for Occupational Exposure to 1-BP. The ATSDR Draft Profile materials 

are available at docket number ATSDR 2016-0003; HAP petition materials are available at 

docket number EPA-HQ-OAR-2014-0471; the CDC draft criteria materials are available at 

docket number CDC-2016-0003-0001. We urge EPA to review the material in these dockets, 

including comments, and to incorporate any new information about the toxicity of 1-BP into its 

final 1-BP risk assessment.[2]

[1] ATSDR, Draft Toxicological Profile for 1-Bromopropane, Docket ID No. ATSDR-2016-

0003-0001 (Jan. 2016) (“ATSDR Draft Profile”).

[2] We recommend that EPA take stronger action under TSCA than the CDC draft criteria 

reflect, however, as those criteria would allow an unacceptably high cancer risk for workers, and 
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do not take into account consumer exposure or other important factors discussed in these 

comments.

Commenter Name: Amy Kyle

Commenter Affiliation: School of Public Health, University of California, Berkeley

Document Control Number: EPA-HQ-OPPT-2015-0084-0019

Comment Excerpt Number: 5

Charge Question:

Comment Excerpt: 

All sources of information should be drawn upon for the assessment including confidential 

business information

The document states at several points that EPA is reporting publically available data. It is 

certainly appropriate to use and report publically available data. However, EPA may also possess 

data that is protected as confidential business information. It is not appropriate to exclude from 

an analysis such as this data that are submitted as confidential business information. This creates 

the wrong incentives for development and disclosure of data in the chemical industry.

The existence of pertinent confidential business information should be disclosed. EPA should 

carefully assess whether restrictions on the disclosure of any such information is genuinely

supported. For too long, CBI claims have offered convenient ways to shield inconvenient data, 

and this is not in the public interest.

EPA should consult with the European Union and the European Chemicals Agency to determine 

whether there are data held by those entities that could be drawn upon to fill key data gaps in this 

assessment.
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6.0. Appendices

Commenter Name: Eve Gartner

Commenter Affiliation: Earthjustice et al.

Document Control Number: EPA-HQ-OPPT-2015-0084-0016

Comment Excerpt Number: 6

Charge Question:

Comment Excerpt: 

5. Incomplete information about the manufacturing of 1-BP compromises the Draft Assessment

Appendix A to the Draft Assessment indicates that only two companies currently manufacture 1-

BP in the United States, though a third company is listed as a “possible manufacturer.” All 

information about one of the two known manufacturers is shown as “CBI,” including the name 

of the company and its location.[1] The location of the “possible manufacturer” is not revealed, 

though its name – Diaz Chemical Corporation -- is provided.

We are concerned in two respects. First, the invocation of “CBI” in the Draft Assessment 

conceals important information about where in the United States 1-BP is manufactured, and thus 

which communities may be exposed to ambient 1-BP. We also question why the identity of a 1-

BP manufacturer is CBI. Given the very high domestic production volume (over 15 million 

pounds in 2012), it is important to look at where 1-BP manufacturing plants are located in 

relation to communities and to assess the potential for exposure. We ask EPA to seek resubstantiation of the CBI claims at issue here, and if the CBI designation is no longer warranted, 

information about the second manufacturer, including the manufacturing location, should be 

included in the final risk assessment.

We also note that documents recently received from EPA through a Freedom of Information Act 

Request by the Environmental Health Strategy Center, reveals that Chemtura Corporation, 

manufactures 1-BP at a facility called Great Lakes Chemical-Central in Eldorado, Arkansas.[2] It 

is unclear whether Chemtura is the claimed-to-be-CBI manufacturer, or if it is yet another 

manufacturer that was simply not identified in Appendix A. Either way, the fact that Chemtura 

manufactures 1-BP in Arkansas should be reflected in the final risk assessment.

Second, we are troubled that Diaz Chemical Corporation may be manufacturing 1-BP without 

reporting its production, or the location of its production, to EPA under the CDR.[3] The location 

that Diaz Chemical Corporation might be manufacturing 1-bromopropane is especially important 

information because in 2002 this company was responsible for a major release of VOCs at a 

facility in New York State. Many neighboring residents were forced to vacate their houses and 

the site remains on EPA’s Superfund list.[4] We strongly urge EPA to investigate. If it turns out 

that Diaz Chemical Corporation is in violation of TSCA section 8(a), we ask EPA to seek 

appropriate penalties.
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[1] Some of the organizations that submit these comments have filed a Freedom of Information 

Act request seeking the substantiation that this information is validly CBI, but we have not 

received a response as of the date these comments were due.

[2] See Chemtura, Great Lakes, Eldorado Arkansas, 2012 Non-CBI CDR Submissions, 

submitted herewith as Attachment 3.

[3] Draft Assessment, App. A-2 at 182.

[4] ATSDR, Public Health Assessment, January 5, 2002 Air Release, Diaz Chemical 

Corporation (last updated Oct. 22, 2009), 

http://www.atsdr.cdc.gov/HAC/pha/pha.asp?docid=185&pg=1#sum; 

https://cumulis.epa.gov/supercpad/cursites/csitinfo.cfm?id=0203341.
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7.0. Other

Commenter Name: Lee Anderson

Commenter Affiliation: BlueGreen Alliance

Document Control Number: EPA-HQ-OPPT-2015-0084-0007

Comment Excerpt Number: 1

Charge Question:

Comment Excerpt: 

The BlueGreen Alliance, as a partnership of 15 of the country’s largest labor unions and 

environmental organizations, appreciates the work being done by EPA under the draft TSCA 

Work Plan Chemical risk assessment for 1-Bromopropane (1-BP). Our organization and our 

partners have worked for many years seeking to protect workers, the environment, and the public 

from hazards associated with chemical exposures.

Given the critical importance to the public of properly assessing 1-BP and for ensuring that all 

stakeholders are given the fullest opportunity for comment, the BlueGreen Alliance requests that 

the current March 9, 2016 deadline for the submission of public comments be extended by thirty 

(30) days until Wednesday, June 1st, 2016.

The BlueGreen Alliance and our partner organizations applaud the administration for 

undertaking this important work, thank you for your consideration of our request for an 

extension of this comment period’s deadline, and look forward to continuing to work 

productively with the EPA.

Commenter Name: Tracey Woodruff

Commenter Affiliation: Program on Reproductive Health and the Environment, University of 

California

Document Control Number: EPA-HQ-OPPT-2015-0084-0010

Comment Excerpt Number: 1

Charge Question: 1-1 General comment on Section 1 

Comment Excerpt: 

We are submitting this letter to request that the U.S. Environmental Protection Agency (EPA) 

extend the public comment period for the TSCA Work Plan Chemical risk assessment document 

for 1-Bromopropane (1-BP) by 45 days. This request applies to Docket ID Number EPA-HQOPPT-2015-0084.

We welcome EPA’s important efforts to characterize the risks posed by 1-BP. With large 

quantities of production and import to the US (estimated at over 15 million pounds in 2011) and 

its high potential for occupational and consumer exposure from to its extensive use in spray 
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Page 54

adhesives, dry cleaning, degreasing, and other cleaning products, an accurate and comprehensive 

assessment of the potential risks is extremely important and of great interest to various 

stakeholders and the public. We welcome the opportunity to review this draft risk assessment 

and to provide public comments.

However, the 1-BP and appendices document is over 400 pages long and the 60-day comment 

period does not provide us with adequate time to review these important documents and provide 

meaningful comments. As academics, our review of these documents and preparation of public 

comments is often external to research time funded through grants. As such, a 60-day period is 

an extremely short amount of time to undertake an extensive review of the multiple exposure 

scenarios and potential endpoints for hazard. Accordingly, we ask that you extend the comment 

period by 45 days to June 23, 2016.

Thank you very much for your consideration. We would be happy to discuss this request at your 

convenience.

Commenter Name: Christina Franz

Commenter Affiliation: American Chemistry Council (ACC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0012

Comment Excerpt Number: 1

Charge Question:

Comment Excerpt: 

I. Introduction:

The American Chemistry Council (ACC)[1] appreciates the opportunity to comment on the draft 

chemical risk assessment for 1-bromopropane announced in the Federal Register on March 8, 

2016. ACC has a longstanding and strong interest in risk assessments conducted by the 

Environmental Protection Agency (EPA), including those conducted under its Work Plan 

Chemical program under the Toxic Substances Control Act (TSCA).

ACC agrees with the general direction that EPA has taken in the Work Plan Chemicals program 

to prioritize chemicals for further review and conduct targeted assessments that may be used to 

consider whether regulatory action is warranted. In general, ACC agrees that this type of 

approach, with some important and essential refinements, will enable the Agency to evaluate 

existing chemicals in commerce effectively.

ACC commends the Agency for conducting targeted quantitative assessments that focus on the 

potential risks associated with certain uses and applications of the Work Plan chemicals, and for 

employing a margin of exposure (MOE) approach for human health evaluations. The MOE 

approach used for non-cancer assessments, consistent with the approach used by EPA’s Office of 

Pesticide Programs (OPP), the European Union, and Canada, is a robust methodology that 
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Page 55

improves transparency and is preferable to those that use reference values (RfCs or RfDs).[2]

Targeted quantitative assessments and use of the MOE are important steps for the Agency to take 

in its risk assessments. When properly implemented, these methodologies should allow EPA 

focus its resources confidently and consistently on uses that present the greatest potential for 

concern.

II. Executive Summary:

ACC has a number of comments and suggestions to improve the overall risk assessment of 1-

bromopropane and ensure a scientifically rigorous approach to evaluate risks associated with this 

chemical. In addition, in Section IV, we identify specific suggestions to improve the peer review 

charge questions. The key issues identified by ACC are:

 The 1-bromopane risk assessment uses methods consistent with a screening-level risk 

assessment, not a refined risk assessment, which must be reflected in the conclusions in 

the draft assessment. EPA should work with industry to refine the draft 1-bromopropane 

draft risk assessment.

 EPA’s risk assessment fails to use “best science” approaches, which are critical to a 

scientifically defensible assessment. Failure to use best science approaches is a critical 

flaw in EPA’s 1-bromopropane risk assessment. Specific comments relating to the 

benchmark dose modeling, the non-cancer and cancer risk assessments, and the exposure 

assessment components of the risk assessment are provided in these comments below.

 A systematic review of study quality, relevance, and reliability is missing from the 

assessment and must be included in order to adequately review and evaluate EPA’s 

decisions. A systematic evaluation of each study used is a necessary part of a 

scientifically defensible risk assessment.

 The 1-bromopropane exposure assessment is outdated and does not reflect current 

exposures in occupational and consumer populations. ACC believes that EPA should 

work with industry to refine and update the 1-bromopropane exposure assessment.

 EPA has failed to describe adequately the scientific basis for decisions made when 

applying benchmark dose modeling to reproductive and developmental toxicity datasets. 

The risk assessment should incorporate significant additional discussion and explanation 

of the benchmark dose modeling process used. Without a discussion of the details of the 

modeling, risk assessors cannot judge the validity of certain modeling outputs and 

decisions.

 EPA has failed to consider its own guidance regarding developmental toxicity and relies 

on a study endpoint and dose where maternal toxicity was present. EPA has failed to 

discuss why this endpoint is appropriate in light of maternal toxicity. In addition, EPA 

has not articulated its consideration of study quality when selecting studies upon which to 

rely.

 EPA has used very conservative benchmark dose modeling response levels without 

describing the rationale for the choices made. EPA indicates that it followed its own 

guidance, yet a review of the two documents cited reveals important differences between 

the recommendations contained in EPA’s guidance and what EPA actually did in the 1-

bromopropane risk assessment.
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 The genotoxicity discussion in the 1-bromopropane risk assessment is incomplete. A 

weight-of-evidence assessment, which includes all available data, indicates that 

genotoxicity is not the mode of action for tumor induction in rodents exposed for a 

lifetime to 1-bromopropane by whole body inhalation. ACC agrees with EPA statements 

in the draft 1-bromopropane assessment that a mode of action for cancer is not known, 

based on available data.

The female mouse lung tumor is not relevant for the 1-bromopropane human cancer risk 

assessment. EPA should refine the risk assessment to consider data related to this type of tumor 

as discussed at the 2014 EPA State-of-the-Science Workshop on Chemically-induced Mouse 

Lung Tumors.

ACC elaborates on each of the points raised in the Executive Summary as follows:

IV.Conclusion:

In conclusion, ACC strongly urges EPA to:

 Acknowledge that its assessment of 1-bromopropane is a screening-level assessment that 

should be refined to determine if unreasonable risks exist in the occupational and/or 

consumer applications that are the focus of the assessment;

 Refine the 1-bromopropane assessment using “best science” approaches in all aspects of 

the assessment, i.e., benchmark dose modeling, non-cancer and cancer risk assessments, 

and the exposure component;

 Conduct a systematic review of study quality, relevance, and reliability of each study 

used in the revised and refined assessment;

 Refine the exposure assessment with current data and information in both occupational 

and consumer settings with the assistance of industry stakeholders;

 In a refined assessment of 1-bromopropane, describe in adequate detail the scientific 

basis for decisions made when applying modeling to reproductive and developmental 

toxicity datasets;

 Consider its own guidance regarding developmental toxicity and explain the endpoints 

relied upon for its conclusions; and

 Consider all available data regarding genotoxicity and apply a weight-of-evidence 

approach in drawing conclusions from the data;

[1] The American Chemistry Council (ACC) represents the leading companies engaged in the 

business of chemistry. ACC members apply the science of chemistry to make innovative 

products and services that make people's lives better, healthier and safer. ACC is committed to 

improved environmental, health and safety performance through Responsible Care®, common 

sense advocacy designed to address major public policy issues, and health and environmental 

research and product testing. The business of chemistry is an $801 billion enterprise and a key 

element of the nation's economy. It is the nation’s largest exporter, accounting for fourteen 
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percent of all U.S. exports. Chemistry companies are among the largest investors in research and 

development. Safety and security have always been primary concerns of ACC members, and 

they have intensified their efforts, working closely with government agencies to improve security 

and to defend against any threat to the nation’s critical infrastructure.

[2] ACC prefers the use of the MOE for these assessments. When reference values are used they 

incorporate science policy judgments, in the form of uncertainty factors that are not immediately 

transparent to risk managers. Using an MOE approach, the risk manager can more clearly 

determine if the differential between the exposure level and the effect level is appropriate 

considering the populations exposed, endpoints of concern, strength of the evidence and other 

key factors that are often built into uncertainty factors but are not immediately transparent to the 

risk manager.

Commenter Name: Christina Franz

Commenter Affiliation: American Chemistry Council (ACC)

Document Control Number: EPA-HQ-OPPT-2015-0084-0012

Comment Excerpt Number: 13

Charge Question:

Comment Excerpt: 

Comments on 1-Bromopropane Draft Peer Review Charge Questions

Consistent with EPA’s Scientific Advisory Board practices, we recommend that the peer review 

discussions begin with a robust discussion of each of the charge questions and allow stakeholder 

comment as part of this discussion. ACC has a number of comments and concerns regarding the 

1-bromopropane draft peer review charge questions. In general, the draft charge questions 

frequently fail to solicit direct opinions concerning the specific scientific issues that are critical to 

the risk assessment. For example:

 In the “Hazard and Dose-Response Assessment” and “Rick Characterization” sections, 

EPA should include the following key question: “Did we choose the appropriate critical 

GLP studies that were available and present a sound scientifically balanced weight-ofevidence discussion of the key critical endpoints for the non-cancer and cancer 

assessments as well as the acute and chronic risk scenarios?”

 Questions 2-1, 2-3, 2-4 and 3-1: EPA should specifically request comment regarding the 

inputs used in the exposure modeling and subsequent calculations.

 The introduction to the hazard and dose-response charge questions discusses EPA’s 

review of the evidence. EPA should explicitly state that its calculations were based on the 

lowest human equivalent concentrations (HECs) rather than on the quality of the 

individual studies, and request comment on this approach.
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 Question 4-1: EPA should revise this question to ensure that it accurately reflects the 

assessment and ensure that comment is requested on whether EPA’s finding is 

appropriate. We suggest the following replacement language:

“EPA/OPPT concluded that 1-BP carcinogenesis occurs through a possible mutagenic mode of 

action based on the totality of the available data/information and the WOE. Please comment on 

whether the cancer hazard assessment has described adequately the relevance of the animal 

tumors to human risk assessment? Has the Agency adequately described the WOE, using all 

appropriate critical GLP studies, to address the proposed mutagenic mode of action?”

 Question 4-2: In framing this question, EPA should state that the endpoints chosen were 

those with the lowest HECs. EPA should specifically take comment on the scientific 

robustness of this approach.

 Question 4-3: We suggest that EPA add the following question: “Did the Agency choose 

the appropriate critical GLP studies for this analysis”

 Question 4-4: This question should explicitly request comment on EPA’s use of the 

“relative deviation” in place of the standardized “standard deviation.” The question 

should also request comment on all aspects of the BMR modeling, not only the model 

averaging approach.

 Risk Characterization: In the introductory section to the charge questions concerning risk 

characterization, EPA states in the first paragraph, second sentence that “EPA/OPPT 

calculated MOEs for acute or chronic exposure separately based on the appropriate noncancer POD and estimated exposure concentrations adjusted for durations.” We suggest 

that the word “lowest” be substituted for “appropriate” in that sentence.

Commenter Name: Eve Gartner

Commenter Affiliation: Earthjustice et al.

Document Control Number: EPA-HQ-OPPT-2015-0084-0016

Comment Excerpt Number: 1

Charge Question:

Comment Excerpt: 

As we explain below, we are concerned that the Draft Assessment does not take into account the 

full range of exposures to 1-BP. In particular, it fails to consider exposures for communities in 

the vicinity of facilities where 1-BP is used, processed, or manufactured – nor for the fact that 

the people affected are likely to be disproportionately low-income and from communities of 

color. In addition, the Draft Assessment does not address the fact that a urinary metabolite 

indicative of 1-BP exposure is widely found in the general population, indicating widespread 

exposure to the general population. The assessment also does not account for dermal exposures 

despite acknowledging that such exposures occur, nor for cumulative exposures to multiple 

carcinogenic solvents. Failure to include the full scope of exposures to 1-BP in the risk 

assessment will result in an underestimation of risk. This underestimation is of great concern, as 
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it could mean that 1-BP will continue to be used in settings that lead to harmful exposures and 

serious health impacts. As we discuss in more detail below, we urge EPA to include the risks 

from human exposures to 1-BP via all pathways in the final risk assessment, as TSCA requires. 

In addition, in accounting for the risk to pregnant women and from in utero exposures, EPA’s 

risk calculation must reflect the uncertainties and data gaps relevant to early life exposure.

Finally, we are troubled that some information about where 1-BP is manufactured is concealed 

due to a claim of Confidential Business Information (“CBI”). We are also concerned that EPA 

itself is not certain that all domestic manufacturers of 1-BP are reporting their production. In 

order to ensure appropriate transparency in the Agency’s work, we urge EPA to re-substantiate 

all claimed CBI that is cited in its Work Plan Chemical assessments and to pursue enforcement 

actions against chemical manufacturers that have failed to comply with reporting requirements.

Commenter Name: Eve Gartner

Commenter Affiliation: Earthjustice et al.

Document Control Number: EPA-HQ-OPPT-2015-0084-0017

Comment Excerpt Number: 1

Charge Question:

Comment Excerpt: 

Please find the attachments referenced in the comments submitted by Blue Green Alliance, 

Earthjustice, Environmental Health Strategy Center, Natural Resources Defense Council, Safer 

Chemicals, Healthy Families and Sierra Club Toxics Committee. Thank you

Commenter Name: Amy Kyle

Commenter Affiliation: School of Public Health, University of California, Berkeley

Document Control Number: EPA-HQ-OPPT-2015-0084-0019

Comment Excerpt Number: 1

Charge Question:

Comment Excerpt: 

Assessments should support public understanding of the implications of chemical uses

The purpose of the TSCA Work Plan assessments is to support better understanding of the 

hazards and risks of a chemical that is already in use, by EPA, the public, chemical 

manufacturers and importers, and businesses that create, sell or use chemical products. The 

assessment is not geared toward a single regulatory or management context or authority. 
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Consequently, assessments should be useful and understandable for a variety of potential 

contexts and audiences and hazards and risks defined broadly rather than narrowly.

A full discussion of options for conceptualizing and assessing potential hazards and risks under 

this TSCA Work Plan process are beyond this scope of these comments but quite important to 

the Chemical Safety Advisory Committee and US EPA. EPA indicates that these will be 

examined, and that would be an important step as the process moves forward.