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1-BP RA Public Comments Collated 5/12/16
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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 low-income 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:
            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/m[3] [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.
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.
[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"].
[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-OAR-2012-0510-0070 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]
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-S-propylcysteine#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-HQ-TRI-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 metabolites of volatile organic compounds among children aged 6-11 years, 142 Envtl. Res. 461 (Oct. 2015).
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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:  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 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 physiologically-based 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.
[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-bromopropane-03242015.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)).
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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).
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.
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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:  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.
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.
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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:  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.
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
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.
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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:  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;..."
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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:  
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 knowledge-based 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 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 "co-residential 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).
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 co-residential buildings is prohibited (40 CFR §63.322 (o)(5)(i)).
 
During the RTR information gathering and comment process, OAQPS evaluated alternative non-Perc 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 co-residential 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).
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 non-residential 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 co-residential 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.
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.
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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 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(R), and scientific and business-to-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 n-Propyl Bromide in Adhesives, and Aerosol Solvents. Consumer Specialty Products Association.
[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"
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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 physical-chemical 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
 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.
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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 dose-dependent 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-of-evidence 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.
 

[1] The study sponsor, Albemarle, has included this study as part of their comments to this docket (comments dated May 9, 2016).
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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 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 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 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/R-12/001. 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).
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.
 

[1] EPA, 2012. Benchmark Dose Technical Guidance. Risk Assessment Forum. EPA/100/R-12/001. June
[2] EPA, 2012. Benchmark Dose Technical Guidance. Risk Assessment Forum. EPA/100/R-12/001. 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 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=CxEDxEFxWY / 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 well-acknowledged. 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]
 "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 age-dependent 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.
[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 x 260 days/yr x 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 Screening-Level 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 worst-case 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 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 dose-response, 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 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-system-iris-process. 
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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:  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 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-safety-health-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/osha-emphasizes-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. CDC-2016-0003-0011 (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.
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Commenter Name:  Lo Mariana
Commenter Affiliation:  Earthjustice
Document Control Number:  EPA-HQ-OPPT-2015-0084-0014
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. 
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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:  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 do not take into account consumer exposure or other important factors discussed in these comments.
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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:  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 re-substantiation 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.
 

[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.
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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-HQ-OPPT-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 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.
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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 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.
 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(R), 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 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.
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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-of- evidence 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.
 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 non-cancer POD and estimated exposure concentrations adjusted for durations." We suggest that the word "lowest" be substituted for "appropriate" in that sentence.
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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:  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 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.

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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
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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:  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. 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.

