# P ATTON B O

GGSLlP ATTORNEYS AT LAW



### Honorable LisaP. Jackson Administrator Environmental ProtectionAgency 1200 Pennsylvania Avenue, NW Washington, DC 20460 October 28, 2010 2550 M S tr

eet, NW Washing ton, DC 20037

-1350 202-457

-6000
Facsimile202-457

-6315 www.pattonboggs.com W. Caff ey Nonnan 202-457

-5270 cnonnan@pattonboggs.com



### Re: Petition to Add n-Propyl Bromide to List ofHazardous AirPollutants Regulated under § 

### 112 ofthe Clean Air Act Dear Ms. Jackson: Onbehalfofthe Halogenated Solvents Industry Alliance, Inc. ("HSIA"), an association ofproducers and users ofchlorinated solvents, I submit the enclosed petition pursuantto Clean Air Act ("CAA'' orthe "Act")§ 112(b)(3), 42 U.S.C. § 7412(b)(3). The petition seeks the addition ofn-propyl bromideto the list ofhazardous air pollutants codified at § 112(b)(1) 

### ofthe Act,42 U.S.C. § 

### 7412(b)(1), onthe basis that "emissions, ambient concentrations, bioaccumulation or deposition ofthe substance are known to cause ormay reasonably be anticipated to cause adverse effects to humanhealth or adverse environmental effects," CAA § 112(b)(3)(B), 42 U.S.C. § 

### 7412(b)(3)(B). The petition addresses uses ofand exposure ton-propylbromide. It

### then describes the scientific studies and otherinformation that demonstrate that emissions ofnPB areknownto cause or may reasonablybe anticipated to cause adverse effects to humanhealth. We believe that the case for listing is strong and we urge you to grant the petition well in advance ofthe 18- month statutory deadline for action. Please do nothesitate to have your staffcontact me ifwe canprovide further information that will assist in your review.

Enclosure
cc: Honorable Regina A. 

### McCarthy C. ScottFulton, Esq.

### Very**~** tlyyours, 

# tc_ ·

# ~Vj~ W. Caffey orman

Was hin gton DC I North ern Vi rg ini a 1 New Jerse y 1 New York 1 Dal la s 1 De nver 1 Anchorag e 1 Doha 1 Abu Dha bi

## BEFORETHE ENVIRONMENTALPROTECTIONAGENCY

Petition to Add n-Propyl Bromide to List ofHazardous AirPollutants Regulated under 

## § 112 ofthe Clean AirAct

HALOGENATED SOLVENTS INDUSTRYALLIANCE, INC. 1530 Wilson Boulevard

OF COUNSEL: W. Caffey Norman Patton Boggs LLP 2550 M Street,NW Washington, DC 20037

October28, 2010 Arlington, VA 22209

### Petition to Add n-Propyl Bromide to List ofHazardous Air Pollutants Regulated under § 112 ofthe Clean AirAct Introduction The CleanAirAct Amendments of 1990 establishedan initial list ofhazardous air pollutants, now codified at§ 112(b)(1) ofthe Clean AirAct ("CAA'' orthe "Act"), 42 U.S.C. § 7412(b)(l), sources ofwhichare subjectto regulationunder CAA §§ 112 (d), 

### (f), (k) and other subsections. CAA § 112(b)(3), 42 U.S.C. § 7412(b)(3), provides that any personmaypetition the Administrator to add or delete a substance to the list, and requires the Administratorto grant or deny the petition and to publish a written explanation ofthe reasons for her decision within 18 months after receipt ofthe petition. The Halogenated Solvents Industry Alliance, Inc. ("HSIA") submits this petitionpursuantto CAA § 112(b)(3), 42 U.S.C. § 7412(b)(3). HSIA is an association ofproducers and users ofchlorinated solvents. By its terms, CAA § 112(b)(3)(A), 42 U.S.C. § 7412(b)(3)(A), requires a petitionto add a substance to the list ofhazardous air pollutants to include a showingthatthere is adequate data
on the health orenvironmental effects ofthe pollutant in question to supportthe petition. Specifically, CAA § 112(b)(3)(B), 42 U.S.C. § 7412(b)(3)(B), provides that an air pollutant shall be added to the list if"emissions, ambient concentrations, bioaccumulation or deposition ofthe substance are known to cause or may reasonably be anticipated to cause adverse effects to humanhealth or adverse environmental effects." This petition addresses the uses ofand exposure ton-propyl bromide (also known as 1-bromopropane, and hereinafter as "nPB") (CAS No. 1 06-94-5). It then describes the scientific studies and other informationthat demonstrate that emissions ofnPB are known to cause or mayreasonably be anticipated to cause adverse effects to humanhealth. Use 

### and Production ofnPB NPB is a brominated hydrocarbon with a strong odor. Its chemical formula is C3H7 

### Br. NPB is used as a carrier solvent in aerosols and adhesives. Some brand names of products using nPB are: Abzol,® EnSolv,® and Solvon® cleaners; Pow-R-Wash® NRContact Cleaner, Superkleen Flux Remover 2311, and LPS NoFlashNU Electro Contact Cleaner aerosols; and Whisper Spray and Fire Retardant Soft Seam 6460 adhesives. It also is usedto

### remove wax, oil, and grease from electronics, metal, and othermaterials. 1 

### Specific applications include: 2 

### Aerosol Solvents. NPB is used as an aerosol solvent in lubricants, coatings, or cleaning fluids for electrical or electronic equipment; lubricants, coatings, or cleaning fluids for aircraft maintenance; and spinnerrette lubricants and cleaning sprays used in the production ofsynthetic fibers. Adhesives. NPB is used in adhesives for laminates, flexible foam, hardwood floors, tire patches, and metal to rubber adhesives. Ofthese applications, nPB-based adhesives have been used most widely in spray adhesives used in manufacture offoam cushions, and to a lesser degree in laminate adhesives. Electronics, Metal, and Precision Cleaning. NPB is used in open vapor degreasing applications to remove processing lubricants such as oils, greases, and waxes which have been applied to aid manufacture but need to be removed before further processing ofthe manufactured substance. Originally, nPB was used as a chemical intermediate in closed processes. It

### was nominated to the National Toxicology Program (NTP) for testing as a result ofits introduction into the emissive applications described above: "In the early to mid 1990s, 1-bromopropane was used primarily as an intermediate in the production ofpesticides, quaternary ammonium compounds, flavors and fragrances, pharmaceuticals, and other chemicals in well-controlled, closedprocesses. Inthe mid to late 1990s, it was introduced as a less toxic replacement for methylene chloride in emissive applications such as vapor and immersion degreasing operations and critical cleaning ofelectronics and metals. 1-Bromopropane was also introduced as a nonflammable, nontoxic, fast-drying, and inexpensive solvent for adhesive resins, and has beenmarketed as a replacement for ozone depleting refrigerants. 1-Bromopropane was nominated for study by the Occupational Safety and Health Administrationbased onthe potential for widespread occupational and environmental exposure and a lack of toxicity and carcinogenicity data. Male and female F344/N rats and B6C3F1 mice were exposed to 1-bromopropane (99% or greaterpure) by inhalation for 2 weeks, 3 months, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium and Escherichiacoli and mouse peripheral blood."3

172 Fed. Reg. 30168,30171 (May 30, 2007).

3 NTP Technical Report 564 (Board Draft), copy enclosed.


### 2

### As a result ofthe growing emissive use, global production ofnPB was estimatedto be 20,000-30,000 metric tonnes in 2007. 4 

### It

### is assumed to be produced in China, France, India, Israel, Japan, Jordan, and the United States. China is estimatedto have produced around 20,000 metric tonnes in 2008, ofwhich approximately 40% were exported. Use as a solvent was reported to be growing at a rate of 15-20% per year inthe United States (5,000 metric tonnes) and Asian countries otherthan China. Solvent use inJapan was 1,100- 1,200 metric tonnes in 2009. No information was available to the United Nations Environment Programme (UNEP) for otherregions.5


### Exposure to nPB 

### Attached is a summary ofworkplace exposure data for nPB collected bythe EPA SignificantNewAlternatives Policy (SNAP) program from a variety ofsources. 6 

### Given its use across a variety ofapplications, some ofwhich are uncontrolled, 

### itis not surprisingthatthere is a wide range ofexposures inthe workplace, from a few parts per million ("ppm") up to 150 ppm or more. A recently published study ofexposure to nPB inNewJersey dry cleaning shops, attached, found exposures as high as 54 ppm. 7 

### The report states: "This study suggested that some green or organic alternative solvents in the dry cleaning industry intended to replace PERC may result in significant exposures above acceptable guidelines among some workers. One dry cleaning worker reported serious adverse health effects resulting in an emergency room visit. Careful consideration and study ofpotential exposures and health effects

4 Montreal Protocol On Substances that Deplete the Ozone Layer, Report ofthe UNEP Technology and Economic Assessment Panel (Progress Report, Volume 2, May 2010), 59. http://www.unep.org/ozone/teap/Reports/TEAP Reports/. Because ofits ozone depleting potential, the Parties to the Protocol have sought to limit nPB use to those situations where more economically feasible and environmentally friendly alternatives are not available (Decision XIII/7).
5/d. UNEP reports that "Obtaining more complete and accurate data on production and uses ofn-PB, as well as its emissions, continues to be difficult. No governmental records are available on emission or uses since nPB is not classified orregistered as a controlled chemical substance like CFCs, and HCFCs (ODS class I and II) nor designated as a hazardous air pollutant in the Clean Air Act in the USA orreportable compound for pollution release (emission) and transfer (PRTR) in Europe and Japan."
6 EPA-HQ-OAR-2002-0064-0015.
7 Blando, et al., Preliminary Study ofPropyl Exposure among New Jersey Dry Cleaners as a Result ofa Pending Ban on Perchloroethylene, J. Air & Waste Manage. Assoc. 60(9): 1049-56 (2010).
3

### among workers using new chemicals or newprocesses mustprecede any regulatory attemptto facilitate substitution for environmental purposes." Health Effects ofnPB
1. Reproductive Toxicity In a proposed rule to list nPB as acceptable for certain applications and unacceptable for others under its SNAP program, EPA discussed the available reproductive toxicity data in some detail.8 

### EPA based its analysis ofoccupational exposures on effects on sperm motility observed in a two-generation reproductive toxicity study employing a benchmark dose (BMD) calculation.9 

### Since that time, additional BMD calculations have been developed based on effects on estrus cycle inthe same multigeneration study. Petitionerhas reviewed the documents provided by EPA detailing the selection ofendpoints, the choice ofstudy, and the preferred calculations ofBMD and the lower 95% confidence limit onthe BMD (BMDL). We agree that the BMDL values selected (169 ppm based on sperm motility, 162 ppmbased on effects on estrus cycle) are appropriate and follow accepted methods and principles. These values were then adjusted to take into account the temporal differences betweenthe exposure regime in the rat study (6 hours per day, 7 days per week) and occupational exposures of8hours per day, 5 days per week. The resultant human equivalent concentrations (HECs) are 177 ppm and 170 ppm for male and female reproductive toxicity, respectively. The HEC value canprovide apoint ofdeparture (POD) for calculation ofa recommended exposure limit (REL) for noncancer effects. EPA's approach to setting a limit for occupational exposure is similarto that for calculation ofthe reference concentration (RfC) which defines the inhalation concentration at which even sensitive members ofthe general population are unlikely to experience adverse effects. We have modified EPA's calculations to derive an RfC for the general population. Although potential reproductive effects remain ofconcern, more recent evidence ofneurotoxicity in workers and carcinogenicity in rodents may nowindicate effects ofgreater concern.

8 72 Fed. Reg. 30168 (May 30, 2007).
9 WIL, An Inhalation Two-Generation Reproductive Toxicity Study of 1-Bromopropane in Rats, sponsored by the Brominated Solvents Consortium (May 24, 2001).

### 4

### EPA modified its normal procedure to calculate an RfC as abasis for determining a recommended exposure limit for workers. This calculation involves applying a sequence of uncertainty factors to the POD based onthe extrapolation ofanimal data to human exposures, variability among the population, and the completeness ofthe database. The maximum uncertainty factor applied for the animal to human extrapolation is 10-fold (i.e., man is 10-foldmore sensitive than the laboratory animal). This factor of 10 is considered to include a 3-fold safety factor for pharmacodynamic species differences (sensitivity atthe site ofaction) and a 3-fold factor for pharmacokinetic differences (delivery ofthe active moiety to the site ofaction). For nPB, EPA adopted a 3-folduncertainty factor for pharmacodynamic differences betweenrat and man, but elected to include no uncertainty factor (i.e., 

### a factor of 1) for pharmacokinetic differences. EPA'sjudgmentthat no uncertainty factor is necessary for dose-response extrapolation from rat to man was based on a higherblood/airpartition coefficient for nPB in rats than in man (11.7 versus 7.1). EPA concludedthat, for a given external concentration, "the delivered dose of nPB into the bloodstream ofrats is slightly higherthan inhumans." This relatively small difference in blood/airpartition coefficients is insufficient, however, to overcome the many remaining uncertainties. The partition coefficient itselfis only an indication ofrelative solubility and the targettissues in rat and man may be similar in ability to dissolve nPB suchthat, ifnPB is poorly metabolized/cleared, the level achieved inthe target tissue may be the same in the two species at equilibrium. There are only certain situations in whichthe blood/airpartition coefficient is the controlling factor in determining the level ofthe active moiety atthe site ofaction. Without information onnPB metabolism in humans, this level cannotbe predicted withphysiologicallybased pharmacokinetic ("PBPK") modeling for humans. The factors that supportthe application ofa full 3-folduncertainty factor for pharmacokinetics are the following: • the active moiety or moieties for reproductive effects are not known,

• the relationship between blood level and active moiety is unknown,

• the nature and extent ofnPB metabolism and general pharmacokinetics inman are not known,

• the difference in blood/airpartitioncoefficients is small, and

5

### • the blood/airpartition coefficient is only controllingunder certain conditions that can only be defined through PBPKmodeling for man. Taken together, these uncertainties are highly significant and support the application ofa safety factor of3 for pharmacokinetics for extrapolation from rat to man. Combined withthe 3-fold safety factor for pharmacodynamics, Petitioner believes that the full10-fold uncertainty factor should be applied for the interspecies (rat to man) extrapolation. This is particularly important when one considers the greater human sensitivityto reproductive toxins relative to responses inthe rat. The ratpossesses huge overcapacity in reproductive capabilities whereas man is considered to be much closerto infertility as a species. This fact suggests that humans are fundamentally more susceptible to reprotoxins thanthe rat. Although this sensitivity is captured, to a limited extent, in the 3-folduncertainty factor for pharmacodynamics, it may not be sufficientto account for the greater sensitivity ofhumans. Regarding human variability, the RfC methodology allows up to a 10-folduncertainty factor to account for the variability in sensitivity withinthe general population. In some circumstances, Petitioner acknowledges thatthis factor canbe reduced for a workingpopulation because ofthe general good health required for employment. We agree with EPA's conclusion that there may be sensitive individuals for reproduction inthe workforce because poor reproductive health may exist in individuals generally fit enough to work. EPA considers that variability in the worker population may be less than inthe general population and that an uncertainty factor of 1 0-fold is greaterthan necessary. This is also areasonable assumption and Petitioner supports the use ofan intraspecies uncertainty factor of3-fold for variations in sensitivity in a worker

### population exposed to nPB. As indicated by EPA, the general population is usually considered to include sub-populations that are more sensitive than the relatively "healthy" workers. This would indicate that an uncertainty factor of 10 should be applied for human variability inthe general population. At the time that EPA was deriving the occupational exposure limit, there was no informationregarding effects oflong-term exposures to nPB. This normally leads to inclusion of a "database uncertainty factor" ofupto 10-fold. The subsequentresults ofNTP 2-year cancer bioassays in rats and mice (discussed below) showthat such an uncertainty factor should have been included for workers and a full factor of 10 would have been appropriate for the general population. The composite uncertainty factor for the general population is therefore 1 000 and
6

### this, applied to the HEC based on the BMDL, leads to an RfC of0.17 ppm for male and female reproductive effects. 2. Neurotoxicity Earlierreviews ofthe neurotoxicity ofnPB focused on animal studies in which hind-limb weakness and neurophysiological measurements indicated effects onthe peripheral nervous system. More recently, there have been a number ofreports ofsevere neurotoxicity in workers exposed to nPB. In particular, the human effects noted relate to lower limbperipheral nerve effects with adverse sensory responses. These effects are qualitatively similarto those seen in rat experiments-- limb weakness progressing in some cases to paralysis. Central nervous system effects also were reported in aproportion ofhuman cases. The consistency ofsevere effects across multiple independent investigations is remarkable and, although the measurements ofatmospheric levels have limitations, the similarity ofexposure levels associated with effects is striking. Many ofthe case subjects needed hospitalization and the reversibility ofthe effects is still in question. A publicationby Majersik 

### etal. provides a complete clinical analysis ofthe effects and indications ofthe slowrecovery, if any, observed in patient follow- up. 10 

### More recently, two cases were reported involving workers exposed to nPB (in vapor degreasing and dry cleaning, respectively) who were diagnosed with clinical manifestations ofnPB. 11 

### Petitioner believes that neurotoxicity inhumans exposedto nPB is ofsubstantial concern. A recently published study showing neurophysiological effects in workers exposedto a range of levels allows for derivation ofa dose response relationship for female workers. 12 

### This wellconducted study allowed the authors to calculate the lowest dose level at which female workers would be likely to experience measurable adverse effects (neurological and red blood cell reduction in number). This exposure is 1.28 ppm (presumably an 8hourtime-weighted average). Li 

### etal. also report various effects associated with exposure to nPB and provide a

10 Majersik et al., Severe Neurotoxicity Associated with Exposure to the Solvent 1-Bromopropane (nPropyl Bromide), Clinical Toxicology45: 270-276 (2007).
11 Perrone et al., Neurologic Illness Associated with Occupational Exposure to the Solvent 1- Bromopropane- New Jersey and Pennsylvania, 2007-2008, Morbidity andMortality Weekly Report 57(48): 1300-1302 (2008).
12 Li et al., Dose-Dependent Neurologic Abnormalities in Workers Exposed to 1-Bromopropane, J. Occup. Environ. Med52: 769-777 (2010). 

### 7

### clear definition ofa dose-response relationship indicated in an earlier study. 13 

### Takingthe results ofLi 

### eta!. and translating them to an RfC value for the general population involves adjusting the 1.28 ppm from an 8 hour, 5 days per week occupational exposure to a continuous exposure, which a lowest-observed-adverse-effect level (LOAEL) of0.3 ppm. Althoughthis is based on effects observed in humans, EPA will still apply uncertainty factors in deriving an RfC. Thus, an uncertainty factor as high as 10-fold would be applied for a LOAEL in the absence ofa noobserved-adverse-effect level (NOAEL). In this case, a factor of3 is probably sufficient since the calculated number is presumedto reflect the lowest level ofdetection. As the LOAEL is based onresponses ofworkers, a factor for sensitive sub-populations in the general population would be applied. A factor of3 may be sufficientto coverthis uncertainty. The composite uncertainty factor to apply is thus 1 0-fold and the resultant RfC wouldbe 0.03 ppm. 3. Carcinogenicity Perhaps the most significant recent information relevant to the healthhazard on nPB are the results of2-year carcinogenesis studies conducted and reviewed byNTP. The enclosed draft report, which was unanimously approved by the NTP Technical Reports Review Subcommittee, shows:

• Clearevidence ofcarcinogenicity in female F344 rats (adenomas in large intestine and equivocal evidence for skintumors)

• Some evidence ofcarcinogenicity in male F344 rats (adenomas in large intestine, skintumors, and equivocal findings for mesotheliomas and pancreatic adenomas)

• Clear evidence ofcarcinogenicity in female B6C3Fl mice (lung tumors)

• No evidence ofcarcinogenicity in male B6C3Fl mice Atthis time, there are no reasons to assume that the mode, or modes, ofactionby which tumors are induced by nPB are notrelevant to man and thus a linear, no-threshold dose-response relationship should be assumed. Using standard methodology for the calculation ofcancer potency and risk estimation (the linearized multistage model) applied to the incidence ofmouse lung tumors yields a q1

### *term. This value is the 95% confidence limit ofthe linear term resulting from the model. The cancerpotency term for mouse lung tumors from the NTP bioassay is a
13 Ichihara eta!., Neurological Abnormalities in Workers ofa 1-Bromopropane Factory, Environmental Health Perspectives 112(13): 1319-1325 (2004).


### 8

### risk of 1.95 x 1 

# o-3

### perppm (lifetime exposure). This potency value indicates that a lifetime risk of 1in 1million is potentially associated with an exposure of0.5 ppb or 2.5 11g/m3• 

### Recommendations/Regulatory Measures ofOtherAuthorities 1. American Conference ofGovernmental Industrial Hygienists (ACGIH) Threshold LimitValues (TLVs®) TLVs® refer to airborne concentrations ofchemical substances and represent conditions under which it is believed that nearly all workers may be repeatedly exposed, day after day, over a working lifetime, without adverse health effects. The TLy®for nPB is 10 ppm as an 8-hour time-weighted average (TWA). This limit was set without regard to the recently reported cancer bioassay results, and is likely to be lowered in the future. 2. CaliforniaWorkplace Limit The California Occupational Safety and Health Standards Board establishes workplace standards for toxic materials that assure, to the extent feasible, that no employee will suffer material impairment ofhealth orfunctional capacity ifexposed for a working lifetime. The Board recently adopted a Permissible Exposure Limit (PEL) for nPB of5 ppm as an 8-hour TWA. Its rationale was as follows: "Anew Permissible Exposure Limit for 1-bromopropane is proposed as an 8-hourtime-weighted average of5ppm TWA (25 mg/M3). The PELproposed differs from the TLV of 10 ppm adopted bythe ACGIH in 2005. 1- bromopropane is apotential substitute for solvents used to clean metals and electronics such as in specialized aircraftpart degreasing operations and has been used as a solvent in adhesives. The documentation ofthe TLV for 1- bromopropane indicates that it was adopted to provide protection against the potential for neurotoxicity, hepatotoxicity, and reproductive and developmental toxicity. The PELproposed also differs from the recommendation ofthe Committee for a PEL of 1ppm. The Committee at its meeting January 9, 2004 considered two possible 8-hour TWAPELrecommendations presented by Julia Quint ofHazard Evaluation Systems and Information Service (HESIS): 1ppm based on 2003 HESIS and Office ofEnvironmental Health Hazard Assessment (OEHHA) documents and 3.3 ppmbased on an assessmentby the National Toxicology Program's (NTP) Center for the Evaluation ofRisks to Human Reproduction (CERHR). The OEHHA assessment, dated December 2, 2003, was conducted for the CaliforniaAir Resources Board and was based on reproductive system effects in male rats reported by Ichiharaet al. in 2000. The CERHR assessment, dated October 2003, was based onreproductive system effects in bothmale and female rats reported in a studyby WIL Research Laboratories in 2001 sponsored by the Brominated Solvents Consortium. The 9

### value of3.3 ppm is calculated from theNo Observed Adverse Effect Concentration (NOAEC) of 100 ppmin test animals in the WIL Research study, application ofan interspecies uncertainty factor of3.16 (the square root of 10) and an intraspecies uncertainty factor of 10, and adjustment for an 8-hour workday and 5-day workweek. At the May 18, 2005 advisory meeting, representatives of manufacturers and vendors of 1-bromopropaneproducts commented onthe Committee's recommendation ofa PEL of 1ppm. Their comments included concerns that a PEL of 1ppm would amount to a ban onthe use of 1- bromopropane in California and thatthere were flaws inthe Ichihara study underlying the OEHHA Interim Reference Exposure Level. They also noted the importance ofskin absorption and suggested that a PEL for 1-bromopropane should include a "skin" notation. In light ofconcerns with the Ichihara study expressed by these stakeholders and by the authors ofthe CERHRreport, this rulemaking proposes aPEL of5 ppm (8-hourTWA) for 1-bromopropane, along with a "skin"notation. The PEL of5ppmis arounding up from the level of3.3 ppm to a more standardized PEL value." 14 

### As in the case ofthe TLV®recommendation discussed above, this limit was set without regard to the recently reported cancerbioassay results, and is likely to be lowered inthe future. 3. CaliforniaProposition 65 Effective December 7, 2004, nPB was listed as a chemical known to the state of Californiato cause reproductive toxicity for purposes ofthe Safe Drinking Water and Toxic Enforcement Act of 1986 ("Proposition 65"). The listing was based on a formal identification by an authoritative bodythat nPB 15 

### causes developmental and female and male reproductive toxicity. A "safe harbor" exposure level has not yet been adoptedbut is normally 1000-fold belowthe no observed effect level for reproductive toxicity, and thus is likely to be in the region of 1 -2 ppb. 4. European Union Classification and Labelling The following "riskphrases" have been assigned to nPB: R 11 (highly flammable), R36/37/38 (irritantto eyes/skin/respiratory system), R 48/20 (danger ofserious damage to health by prolonged exposure/harmful by inhalation), R 60 (may impair fertility), R 63 (possible risk of harm to the unborn child), R 67 (vapors may cause drowsiness and dizziness). The results ofthe

14 California Occupational Safety and Health Standards Board, Initial Statement ofReasons, Airborne Contaminants (March 19, 2009); https://www.dir.ca.gov/oshsb/airborne_contaminants09_ISOR.doc.
15 National Toxicology Program Center for the Evaluation ofRisks to Human Reproduction Expert Panel Report on the Reproductive and Developmental Toxicity of 1-Bromopropane (nPB) (March 2002).


### 10

### NTP carcinogenicity bioassay are notreflected inthis listbutwould be expectedto add an additional risk phrase to be displayed on labels and safety data sheets.


### Conclusion Chlorinated solvents are listed as hazardous airpollutants and industrial sources of chlorinated solvent emissions are stringently regulatedunder CAA §§ 112(d) and (f). NPB is being aggressively marketed as an unregulated alternative to chlorinated solvents. 16 

### Indeed, sales literature for nPB emphasizes that it is essentially unregulated. Sales ofnPB in adhesive and solvent cleaning uses are already substantial and appearpoised for further growth. The results ofthe recently reported carcinogenicity bioassays show "clearevidence of carcinogenic activity" in female rats and female mice. An estimate ofcarcinogenic potency using standard methodology shows that the cancerpotency is similar to or higher than that ofthe regulated materials nPB is being marketedto replace. Moreover, observations oftoxic effects of nPB in animal experiments and workers exposed at various levels demonstrate that exposed populations may face other serious healthrisks, including reproductive effects (male and female), liver and kidney toxicity, immunotoxicity, and effects onred blood cells and hemoglobin. High levels ofworker exposure have led to a number ofdocumented cases oflower limb paralysis that has been slowto improve; the onset ofadverse effects onperipheral nerves has been detectable in workers exposed at very low levels (estimated lowest-observed-effect level was 1.28 ppm). This translates to concern for the general population exposed to very low levels.

16 E.g., http://www.envirotechint.com/products/dry-cleaning/: "Being "Green" has never been easier with DrySolv. The first environmentally responsible replacement solvent for your dry cleaning machine!

• DrySolv is non-flammable, showing no flashpoint in multiple tests and test methods.(ASTM D-56 TCC, ASTM D-92 COC, ASTM D-93 TCC). • DrySolv is also non-chlorinated. • DrySolv is non-hazardous.(DOT, OSHA, NESHAP, RCRA, Clean WaterAct) • DrySolv is not a hazardous air pollutant, is SNAP approved, and does not contribute to global warming. (NESHAP, SignificantNew Alternative Program-SNAP approved (Federal EPA), NotTitle V) • The USEPA states that DrySolv's main ingredient is less persistent in the environmentthan many other solvents, is oflow to moderate concern for movement in soil, does not warrant listing under the Toxics Release Inventory and is not prone to bioaccumulation. (USEPA

- Federal Register May 30, 2007). • DrySolv does not have a hazardous decomposition orhazardous polymerization."



### 11

### Clearly, nPB meets the statutory criteria for listing as ahazardous air pollutant under CAA § 112(b)(3)(B), 42 U.S.C. §7412(b)(3)(B). We urge EPA forthwith to grantthis petition.
Attachments

127



# ABSTRACT

1-BROMOPROPANE CAS No. I06-94-5 MolecularWeight: 122.99 Synonyms: 1-BP; propyl bromide; n-BP; N-propyl bromide

In the early to mid 1990s, 1-bromopropane was used primarily as an intermediate in the production ofpesticides, quaternary ammonium compounds, flavors and fragrances, pharmaceuticals, and other chemicals in well-controlled, closed processes. In the mid to late 1990s, it was introduced as a less toxic replacement for methylene chloride in emissive applications such as vapor and immersion degreasing operations and critical cleaning ofelectronics and metals. 1-Bromopropane was also introduced as a nonflammable, nontoxic, fast-drying, and inexpensive solvent for adhesive resins, and has been marketed as a replacement for ozone depleting refrigerants. 1-Bromopropane was nominated for study by the Occupational Safety andHealth Administration based on the potential for widespread occupational and environmental exposure and a lack oftoxicity and carcinogenicity data. Male and female F344/N rats and B6C3Fl mice were exposed to 1-bromopropane (99% or greaterpure) by inhalation for 2 weeks, 3 months,

or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium and Escherichia coli and mouse peripheral blood.

Board Draft NOT FORDISTRIBUTION ORATTRIBUTION8 1-Bromopropane, NTP TR564
2-WEEK STUDY IN RATS Groups offive male and five female rats were exposed to I-bromopropane vapor at concentrations ofO, I25, 250, 500, I,OOO, or 2,000 ppm, 6 hours plus T90 (I2 minutes) per day, 5 days per week for I6 days. All rats survived to the end ofthe study except one 500 ppm male. Mean body weights of2,000ppm rats were significantly less than those ofthe chamber controls. The absolute kidney weight ofI,000 ppmmales, relative kidney weights ofall exposed groups ofmales, and absolute and relative kidney weights ofall exposed groups offemales were significantly increased. The absolute and relative liver weights ofI,000 ppm males, relative liver weights of500 and 2,000 ppm males, and absolute and relative liver weights of500 ppm orgreater females were significantly increased. Nasal lesions included suppurative inflammation in males exposed to 500 ppm or greater, respiratory epithelial necrosis in I,OOO and 2,000 ppm males, and respiratory epithelial regeneration in I,OOO and 2,000 ppm females.

2-WEEK STUDY IN MICE Groups offive male and five female mice were exposed to I-bromopropane vapor at concentrations ofO, I25, 250, 500, 1,000, or 2,000 ppm, 6 hours plus T90 (12 minutes) per day, 5 days per week for 17 days. All 2,000 ppm males, two 2,000 ppm females, four 500 ppm males, one I,000 ppmmale, and one I,000 ppm female died early. The mean body weight gain of 1,000 ppm males was significantly less than that ofthe chamber controls. Abnormal breathing, lethargy, and eye discharge were observed primarily during week 1in groups exposed to 500 ppm or greater. Liver weights of 1,000 ppm males and offemales exposed to 500 ppm orgreater were significantly increased. Kidney weights of 1,000 and 2,000 ppm females were significantly increased. Microscopic lesions related to 1-bromopropane exposure occurredin the lung, liver, and nose ofmales and females and were primarily seen in mice exposed to 500 ppm or greater.

3-MONTH STUDY IN RATS Groups of 10 male and 10 female rats were exposed to 1-bromopropane vapor at concentrations ofO, 62.5, I25, 250, 500, or 1,000 ppm, 6 hours plus T90 (10 minutes) per day, 5 days per week for 14 weeks. Additional clinical pathology groups of 10 male and 10 female rats were exposed to the same concentrations for 23 days. All rats

NOT FOR DISTRIBUTION OR ATTRIBUTION Board Draft1-Bromopropane, NTP TR564 9
survived to the end ofthe study. Mean body weights of 1,000 ppm males were significantly less than those ofthe chamber controls. The increases in sorbitol dehydrogenase activities in 500 ppm males and 1,000 ppmmales and females were consistent with the histopathologic evidence ofmild hepatotoxicity causedby 1-bromopropane. Liver weights ofmales exposed to 250 ppm or greater and offemales exposed to 125 ppm or greater were significantly increased. Spleen andkidney weights of 1,000ppm females were significantly increased. Results ofsperm count and vaginal cytology evaluations showed exposure concentration-related decreases in sperm motility and counts in male rats, reaching 28% and 37%, respectively, in the 1,000 ppm group. Female rats in all three exposure groups evaluated exhibited altered estrous cycles, spending significantly more time in extended estrus and less time in extended diestrus. The incidences ofcytoplasmic vacuolization ofthe liver were significantly increased in males exposed to 250ppm or greater and in females exposed to 500 ppm orgreater. Hepatocyte degeneration was also observed in 1,000 ppm females.

3-MONTH STUDY IN MICE Groups of 10 male and 10 female mice were exposed to 1-bromopropanevapor at concentrations ofO, 62.5, 125, 250, or 500 ppm, 6 hours plus T90 (10 minutes) per day, 5 days per week for 14 weeks. One 250 ppm male and four males and five females in the 500 ppm groups died early. Mean body weights ofexposed groups were similar to those ofthe chamber controls. Lethargy was observed in males and females exposed to 500 ppm, and abnormal breathing was observed in moribund mice. The kidney, liver, and lung weights of500 ppm females were significantly greater than those ofthe chamber controls. The kidney weights of500 ppm males were significantly decreased. Male mice in the 500 ppm group had decreased sperm counts that were 28% less than that in the chamber controls. Female mice exhibited altered estrous cycles, with females in the 500 ppm group spending significantly more time in extended diestrus and those in the 250 ppm group spending significantly more time in extended estrus compared to the chamber controls. Nonneoplastic lesions were observed in the nose, larynx, trachea, lung, and liver of500 ppm males and females and in the adrenal cortex of500 ppm females.

Board Draft NOT FORDISTRIBUTION ORATTRIBUTION10 1-Bromopropane, NTP TR 564
2-YEAR STUDY IN RATS Groups of50 male and 50 female rats were exposed to 1-bromopropane vapor at concentrations of0, 125, 250, or 500 ppm, 6 hours plus T90 (10 minutes) per day, 5 days perweekfor 105 weeks. Survival of500 ppmmales was significantly less than that ofthe chamber control group. Mean body weights ofexposed groups were similar to those ofthe chamber controls.

Increased incidences ofmacroscopic, soft, pale-yellow to green, variably sized nodules were seen predominantly in the nose and skin ofexposed rats. The number ofanimals with multiple masses was increased in the 500 ppm groups. In most cases, these lesions were microscopically shown to be suppurative inflammation, many with Splendore-Hoeppli material.

The incidence ofadenoma ofthe large intestine (colon orrectum) in 500 ppm females was significantly greater than that in the chamber control group. The incidence ofadenoma ofthe large intestine in 250 ppmmales exceeded the historical control ranges for inhalation studies and all routes.

The incidences ofkeratoacanthoma, basal cell adenoma, basal cell carcinoma, or squamous cell carcinoma (combined) in all exposed groups ofmales were significantly greater than that in the chamber control group and exceeded the historical control range for inhalation studies. The incidences ofkeratoacanthoma and of keratoacanthoma or squamous cell carcinoma (combined) in 250 and 500 ppm males were also significantly increased and exceeded the historical control ranges for inhalation studies. In 500 ppmfemales, the incidence of squamous cell papilloma, keratoacanthoma, basal cell adenoma, orbasal cell carcinoma (combined) exceeded the historical control range for inhalation studies.

The incidence ofmalignant mesothelioma in 500 ppm males was significantly greater than that in the chamber control group.

The incidences ofpancreatic islet adenoma in all exposed groups ofmales and ofpancreatic islet adenoma or carcinoma (combined) in 125 and 250 ppm males were significantly increased.

NOT FORDISTRIBUTION OR ATTRIBUTION Board Draft1-Bromopropane, NTP TR 564 11

Treatment-related nonneoplastic lesions were observed in the respiratory system ofexposed male and female rats. In the nose, the incidences ofsuppurative chronic inflammation, chronic active inflammation, glandular hyperplasia, respiratory epithelial hyperplasia (females), and respiratory metaplasia ofthe olfactory epithelium (females) were increased in all exposed groups. In the larynx, the incidences ofchronic active inflammation and squamous metaplasia (except 125 ppm females) were increased in all exposed groups, and the incidences ofsuppurative chronic inflammation were increased in the 500 ppm groups. In the trachea, there were increased incidences of chronic active inflammation in all exposed groups offemales and 500 ppm males, and the incidence ofepithelial hyperplasia was increased in 500 ppm females.


### 2-YEAR STUDY IN MICE Groups of50 male and 50 female mice were exposed to 1-bromopropanevapor at concentrations ofO, 62.5, 125, or 250 ppm, 6 hours plus T90 (10 minutes) per day, 5 days perweekfor 105 weeks. Survival ofexposed groups was similar to that ofthe chamber controls. Mean body weights ofall exposedgroups were similar to those ofthe chamber controls throughout the study.

In the females, there were increased incidences ofalveolar/bronchiolar adenoma, alveolar/bronchiolar carcinoma, and alveolar/bronchiolar adenoma or carcinoma (combined); the incidences ofalveolar/bronchiolar adenoma or carcinoma (combined) were significantly increased in all exposed groups offemales. There were significantly increased incidences ofcytoplasmic vacuolization ofthe bronchiolar epithelium in all exposed male groups and regeneration ofthe bronchiolar epithelium in all exposed groups ofmales and females.

In the nose, there were significantly increased incidences ofcytoplasmic vacuolization ofthe respiratory epithelium in all exposed groups ofmales and in 125 and 250 ppmfemales. There were significantly increased incidences of respiratory epithelial hyperplasia in all exposed female groups and in 62.5 and 250 ppm males. There were significantly increased incidences ofrespiratory metaplasia ofolfactory epithelium in 62.5 and 125 ppm males and 125 and 250 ppmfemales.

Board Draft NOT FORDISTRIBUTION ORATTRIBUTION12 1-Bromopropane, NTP TR 564
There were significantly increased incidences ofcytoplasmic vacuolization ofrespiratory epithelium in the larynx and trachea ofall exposed male groups and in the trachea of62.5 and 125 ppmfemales.

GENETIC TOXICOLOGY 1-Bromopropane was not mutagenic in either oftwo independentbacterial mutagenicity assays, each conducted with and without induced rat liver activation enzymes. Bacterial strains tested included S. typhimurium strains TA97, TA98, TA100, and TA1535, as well as E. coli strain WP2 uvrA/pKM101. In addition, no increases in the frequencies ofmicronucleated normochromatic erythrocytes were seen in male or female B6C3F1 mice exposed for 3 months to 62.5 to 500 ppm 1-bromopropane via inhalation.

CONCLUSIONS
Under the conditions ofthese 2-year inhalation studies, there was some evidence of carcinogenic activity* of 1-bromopropane in male F344/N rats based on the occurrence ofrare adenomas ofthe large intestine and increased incidences ofneoplasms ofthe skin. Increased incidences ofmalignant mesothelioma and pancreatic islet adenoma may also have been related to 1-bromopropane exposure. There was clearevidence of carcinogenic activity of 1-bromopropane in female F344/N rats based on increased incidences ofadenoma ofthe large intestine. Increased incidences ofneoplasms ofthe skin may also have been related to 1-bromopropane exposure. There was no evidence of carcinogenic activity of 1-bromopropane in male B6C3F1 mice exposed to concentrations of62.5, 125,

or 250 ppm 1-bromopropane. There was clear evidence of carcinogenic activity of 1-bromopropane in female B6C3F1 mice based on increased incidences ofalveolar/bronchiolar neoplasms.
Exposure to 1-bromopropane resulted in increased incidences ofnonneoplastic lesions in the nose ofrats and mice, the larynx ofrats and male mice, the trachea offemale rats and male and female mice, and the lung ofmice. Suppurative inflammatory lesions with Splendore-Hoeppli material were present primarily in the nose and skin of male and female rats exposed to 1-bromopropane.

• Explanation ofLevels ofEvidence ofCarcinogenic Activity is on page 14.

NOT FORDISTRIBUTION OR ATTRIBUTION Board Draft1-Bromopropane, NTP TR 564 13**Summar~** ofthe 2-Year Carcinogenesis and Genetic**Toxicolog~** Studies of1-BromoJ.!rOJ.!ane

Concentrations in air Body weights
Survival rates Nonneoplastic effects

Neoplastic effects

Equivocal findings

Level ofevidence of carcinogenic activity Genetic toxicology Bacterial gene mutations: Male F344/N Rats
0, 125,250, or 500 ppm Exposed groups similarto the chamber control group 23/50, 26/50, 18/50, 13/50 Nose: inflammation, suppurative, chronic (0/50, I/48, 2/48, 7/50); inflammation, chronic active (29/50, 33/48, 34/48, 35/50); glands, hyperplasia (5/50, 14/48, 14/48, 15/50) Larynx: inflammation, chronic active (21150, 28/50, 31150, 26/50)

Large intestine: adenoma (0/50, 0/50, 2/50, 1/50) Skin: keratoacanthoma (0/50, 3/50, 6/50, 6/50); keratoacanthoma or squamous cell carcinoma (1/50, 4/50, 6/50, 8/50); keratoacanthoma, basal cell adenoma, basal cell carcinoma, or squamous cell carcinoma (1/50, 7/50, 9/50, 10/50) Malignant mesothelioma: (0/50, 2/50, 2/50, 4/50) Pancreatic islets: adenoma (0/50, 5/50, 4/50, 5/50)
Some evidence

Micronucleated erythrocytes

Mouseperipheral blood in vivo:

Board Draft Female Male Female F344/N Rats B6C3Fl Mice B6C3Fl Mice
0, 125,250, or 500 ppm 0, 62.5, 125, or 250 ppm 0, 62.5, 125, or250 ppm Exposed groups similar to Exposed groups similar to Exposed groups similar to the chambercontrol group the chambercontrol group the chambercontrol group 34/50, 33/50, 30/50, 24/50 37/50, 33/50, 32/50, 36/50 36/50, 40/50, 37/50, 42/50 Nose: inflammation, Lung: bronchiole, Lung: bronchiole, suppurative, chronic vacuolization cytoplasmic regeneration (0/50, 45/50, (0/50, 1/50, 3/49, 7/50); (0/50, 18/50, 19/49, 43/50, 49/50) inflammation, chronic 17/49); bronchiole, active (24/50, 37/50, regeneration (1/50, 44/50, Nose: respiratory 37/49, 36/50); glands, 38/49, 47/49) epithelium, vacuolization hyperplasia (6/50, 23/50, cytoplasmic (0/50, 3/50, 28/49, 30/50); respiratory Nose: respiratory 5/50, 8/50); respiratory epithelium, hyperplasia epithelium, vacuolization epithelium, hyperplasia (5/50, 13/50, 9/49, 18/50); cytoplasmic (0/50, 12/50, (11/50, 25/50, 28/50, olfactory epithelium, 19/50, 20/50); respiratory 27/50); olfactory metaplasia, respiratory epithelium, hyperplasia epithelium, metaplasia, (3/50, 4/50, 6/49, 9/50) (16/50, 29/50, 23/50, respiratory (0/50, 4/50, 26/50); olfactory 5/50, 14/50) Larynx: inflammation, epithelium, metaplasia, chronic active (18/50, respiratory (0/50, 7150, Trachea: vacuolization 25/50, 30/50, 32/50); 6/50, 3/50) cytoplasmic (0/50, 8/49, metaplasia, squamous 7/50, 4/50) (3/50, 2/50, 6/50, 21/50) Larynx: vacuolization cytoplasmic (0/48, 5/50, Trachea: inflammation, I0/48, 11150) chronic active (0/50, 4/50, 1/50, 6/50); epithelium, Trachea: vacuolization hyperplasia (0/50, 0/50, cytoplasmic (0/49, 15/50, 0/50, 4/50) 24/47, 24/50) Large intestine: adenoma None Lung: (0/50, 1150, 2/50, 5/50) alveolar/bronchiolar adenoma (1/50, 6/50, 4/50, I0/50); alveolar/bronchiolar carcinoma (0/50, 7/50, 5/50, 4/50); alveolar/bronchiolar adenoma or carcinoma (1150, 9/50, 8/50, 14/50)

Skin: squamous cell None None papilloma, keratoacanthoma, basal cell adenoma, orbasal cell carcinoma (1/50, 1/50, 1/50, 4/50)
Clear evidence No evidence Clearevidence Negative in Salmonella typhimurium strains TA97, TA98, TAIOO, and TA1535 with and without S9; and in Escherichia coli WP2 uvrA!pKMIOI with and without S9 Negative

NOT FORDISTRIBUTION ORATTRIBUTION14 1-Bromopropane, NTP TR564
EXPLANATION OF LEVELS OF EVIDENCE OF CARCINOGENIC ACTIVITY
TheNational Toxicology Program describes the results ofindividual experiments on a chemical agent and notes the strength ofthe evidence for conclusions regarding each study. Negative results, in which the study animals do not have a greater incidence ofneoplasia than control animals, do not necessarily mean that a chemical is not a carcinogen, inasmuch as the experiments are conducted under a limited set ofconditions. Positive results demonstrate that a chemical is carcinogenic for laboratory animals under the conditions ofthe study and indicate that exposure to the chemical has the potential for hazard to humans. Other organizations, such as the International Agency for Research on Cancer, assign a strength ofevidence for conclusions based on an examination ofall available evidence, including animal studies such as those conductedby the NTP, epidemiologic studies, and estimates ofexposure. Thus, the actual determination ofrisk to humans from chemicals found to be carcinogenic in laborat01y animals requires a wideranalysis that extends beyond the purview ofthese studies. Five categories ofevidence ofcarcinogenic activity are used in the Technical Report series to summarize the strength ofevidence observed in each experiment: two categories for positive results (clear evidence and some evidence); one category for uncertain findings (equivocal evidence); one category for no observable effects (no evidence); and one categoryfor experiments that cannot be evaluated because ofmajor flaws (inadequate study). These categories ofinterpretative conclusions were first adopted in June 1983 and then revised onMarch 1986 for use in the Technical Report series to incorporate more specifically the concept ofactual weight ofevidence ofcarcinogenic activity. For each separate experiment (male rats, female rats, male mice, female mice), one ofthe following five categories is selected to describe the findings. These categories refer to the strength ofthe experimental evidence and not to potency or mechanism.

• Clear evidence ofcarcinogenic activity is demonstrated by studies that are interpreted as showing a dose-related (i) increase of malignant neoplasms, (ii) increase ofa combination ofmalignant and benign neoplasms, or (iii) marked increase ofbenign neoplasms ifthere is an indication from this or other studies ofthe ability ofsuch tumors to progress to malignancy. Some evidence ofcarcinogenic activity is demonstrated by studies that are interpreted as showing a chemical-related increased incidence ofneoplasms (malignant, benign, or combined) in which the strength ofthe response is less than that required for clear evidence. • Equivocal evidence ofcarcinogenic activity is demonstrated bystudies that are interpreted as showing a marginal increase of neoplasms that may be chemical related. No evidence ofcarcinogenic activity is demonstrated by studies that are interpreted as showing no chemical-related increases in malignant orbenign neoplasms Inadequate study ofcarcinogenic activity is demonstrated by studies that, because ofmajorqualitative or quantitative limitations, cannotbe interpreted as valid for showing either the presence or absence ofcarcinogenic activity. For studies showing multiple chemical-related neoplastic effects that ifconsidered individuallywould be assigned to different levels ofevidence categories, the following convention has been adopted to convey completely the studyresults. In a studywith clear evidence ofcarcinogenic activity at some tissue sites, other responses that alone might bedeemed some evidence are indicated as ''were also related" to chemical exposure. In studies with clear orsome evidence ofcarcinogenic activity, otherresponses that alone might be termed equivocal evidence are indicated as "mayhave been" related to chemical exposure. When a conclusion statement for a particular experiment is selected, consideration must be given to key factors that would extend the actual boundary ofan individual category ofevidence. Such consideration should allow for incorporation ofscientific experience and current understanding oflong-tenn carcinogenesis studies in laboratory animals, especially for those evaluations that maybe on theborderline between two adjacent levels. These considerations should include:

• adequacy ofthe experimental design and conduct; occunence ofcommon versus uncommon neoplasia; progression (or lack thereof) from benign to malignant neoplasia as well as from preneoplastic to neoplastic lesions; somebenign neoplasms have the capacity to regress butothers (ofthe same morphologic type) progress. At present, it is impossible to identifY the difference. Therefore, where progression is known to be a possibility, the most prudent course is to assume that benign neoplasms ofthose types have the potential to become malignant; combiningbenign and malignant tumor incidence known or thought to represent stages ofprogression in the same organ or tissue; latency in tumor induction; multiplicity in site-specific neoplasia; metastases; supporting information from proliferative lesions (hyperplasia) in the same site ofneoplasia or other experiments (same lesion in another sex or species); • presence or absence ofdose relationships; statistical significance ofthe observed tumor increase; concunentcontrol tumor incidence as well as the historical control rate andvariability for a specific neoplasm; • survival-adjusted analyses and false positive orfalse negative concerns; structure-activity correlations; and in some cases, genetic toxicology.

NOT FORDISTRIBUTION ORATTRIBUTION Board Draft

### Summary ofData on Workplace Exposure ton-Propyl Bromide

The U.S. Environmental Protection Agency's (EPA) Significant New Alternatives Policy (SNAP) Programhas received workplace exposure data for n-propylbromide (nPB) from several different sources. The sources include:



### •
• Data from organic vapor monitoring badges wornby workers using vapor degreasing equipment Data from charcoal tube samplers wornby workers using vapor degreasing equipment, cold batch cleaning equipment, aerosols, spray adhesives in foam fabrication, adhesives used for flooring, and manual cleaning Area samples takenusing both organic vapor monitoring badges and charcoaltube samplers Data from three manufacturers or suppliers ofproducts containing nPB Data from the National Institute for Occupational Safety and Health from four different facilities Data from spray adhesives, a highly emissive use, both before and after improvements to ventilation The Agency considered these data in determining whether it is feasible to meet the recommended workplace exposure limit for nPB using available, affordable control or ventilation equipment. Description ofexposure data by sector 

### Non-aerosol solvent cleaning Almost all samples for solvent cleaning were taken for vapor degreasing. • There are approximately 500 personal samples in all, roughly 90% taken using organic


### • badge monitors (3M or SKC). There are approximately 40 area samples, most taken with charcoal tube
. Data sources for personal samples include exposure data from customers oftwo suppliers ofnPB-based solvents for vapor degreasing, 2003. For area samples, EPA also considered data from R.L. Smith, 1998a and 1998b. Approximately 75% ofthe personal samples were below 10 ppmon an 8 hour timeweighted average (TWA) >87% ofpersonal samples were below 25 ppm (8 hr TWA) In several situations where samples indicated workplace exposure greater than 25 ppm, the supplier and user worked to reduce emissions, and brought thembelow 25 ppm Earlier samples taken in 1997 had higher average concentrations than later samples. This may reflect that some manufacturers reduced their recommended workplace exposure limit in 2000, and therefore, users made greater efforts to attain lower emissions. There also was a Health Hazard Evaluation (HHE) by the National Institute for Occupational Safety and Health (NIOSH) for an air-tight "cold" batch cleaner with ventilation.Before use ofthe air-tight cleaning equipment, workers complained ofadverse health effects such as headaches, nausea, vomiting, feeling faint, and irritation ofthe mucous membranes (NIOSH, 2000c). After installing the new equipment, NIOSH measured workplace exposure. NIOSH found that samples taken on 20 employees all read concentrations less than lppmofnPB. These data from NIOSH are not included in the more than 500 personal samples mentioned above, which are all for vapor degreasing. Figure 1. Distribution ofExposure Data for Vapor Degreasing 

## Distribution of nPB Exposure DataforVapor Degreasing -C') 

### co s:::: 

# g·c;; 35.0%

### ~ 

# m 30.0% C1) I.. 

### c.. C') 25.0% '+- C1) 0 

## c 20.0% C1) I.. 15.0%**C')~** 

### co In 10.0% 

# c C1) C1)
- 5.0% 

### (.)c. s.. 

## E 

## o.o% C1) 

### co C..tl)


### Concentration, 8 1-t

### TWA (ppm) • Percentage of Sarrples in Range

EPA also examined data for two other "cold cleaning" applications that are not currently regulated under SNAP: flushing and hand wiping. At one site, personal exposure levels for manual flushing ofcoils ranged from 5 to 42 ppm, with three samples taken with charcoal tubes. EPA has data for three different sites for hand wiping. The personal samples were all greater than 25 ppm. Table 1. Exposure Data from Hand Wiping Application

Site #ofSamples Avg Cone. Cone. Range (ppm)

Hand Wipe Site #3 4 Not available 28 to 47 (6 to 10 min. exposure) Sources: Smith, R.L. 1998; November 16, 2001 Email from Mick Kassem, Albemarle Corporation.
2AerosolSolvents Ofthe three major applications that EPA evaluated, there was the least amount of exposure data for aerosol solvents. There are: Eight personal samples onan eight-hour TWAbasis, most takenusing organic badge monitors Four area samples, all taken with charcoal tube samplers Eight 15-minute samples, suitable for comparison with a short-term exposure limit (STEL) Sources ofdata include Kassem, 2001 and Aerosol data, 1998. • The eight personal samples on an eight-hour TWAbasis ranged from 5 ppm to 30.2 ppm. Seven ofthe eight personal samples on an eight-hour TWAbasis were below 25 ppm. The eight 15-minute samples ranged from 45.1 ppmto 254 ppm. 

### Figure 2. Distribution ofnPB Exposure Data for Aerosol Solvent Use (8 hr TWA)

1/) 0.4 Q) Q. E 0. 3 5 n:l en 'iii 0.3 1:: 0 0.2 5 1/)

.... Q) a. 0.2 0 1/) 0 0.1 5 .... Q) 

### <



### .... 0. 1 0 1:: 0 0. 0 5 :;::; (.) n:l 0 .... u. Dis trib u tio n of n P 8 Exposure Data for Aero so I Solvent Use

< 1 1 to 6 to 11 1 6 21 2 6 31 41 5 10 to to to to to to 15 20 25 30 40 50 Concentration, 8 hr TWA (ppm)**m~Fraction** ofaerosol sam pies in range

The 15 minute samples are useful for a comparison with a short-termexposure limit (STEL). The samples taken on a eight-hour time-weighted average are usefi.il for comparison with a workplace exposure limit.

3

### Figure 3. Distribution ofShort-Term nPB Exposure Data for Aerosol Solvent Use (15 Minute Exposures) 

### Distribution of Short-Term nPB Exposure Data for Perosol Solvent Use
ctJ r::: 0 

### 0.3**~~~""'~**

### ~ !I> 

### 0.25 c..**~** 

### 0.2 

# o E" o.15 r::: ctJ 

### 0.1 111 Fraction ofsamples in range 0 

## en 0.05 ;; 

## (.) 0 ctJ


## .... u.. 

### 1to 

### 51 101 151 201 251 50 to to to to to 

### 1

00 150 200 250 300 15-min Concentration, ppm

Adhesives Almost all ofthe exposure data for adhesives were for spray adhesives using nPB as a carrier solvent in foam fabrication and construction ofseat cushions. In addition, there were a few sites where nPB-based adhesives were applied for flooring. There are: Approximately 90 personal samples, all taken with charcoaltube samplers Five area samples, all taken with charcoaltube samplers Data sources include Smith, R.L. 1998, Kassem2001, NIOSH 2000a, NIOSH 2000b, NIOSH 2001, NIOSH 2002a, and NIOSH 2002b. There is a marked difference in the exposure data at two sites where NIOSH worked together with the facilities to improve their ventilation. Less than halfofthe personal samples were below 50 ppmon an 8 hour TWAbefore improving ventilation; 97% ofthe personal samples were below 50 ppm after improving ventilation. The mean concentration before improving ventilation was 141.7 ppm; the mean concentration after improving ventilation was 18.3 ppm. After improving ventilation, 78% percent ofthe samples were at 25 ppm or below.

41/) Q) 

### c. E co (/) iii s:: 0 1/) 

### ... Q) c..



### .... 0 Q) Cl co 

# - s:: Q) (..)


### ... Q) c.. 

### Figure 4. Distribution ofnPB Exposure Data for Adhesives Distribution ofnPB Exposure Data forAdhesives
16.0% 14.0% 12.0% 10.0%

8.0% 6.0% 4.0% 2.0% 0.0%**~** 0 0 0 0 0 v**~** N (") 1.() 1'- .8 .8 .8 .8 .8 c.o c.o c.o**~** 10**~** N Concentration, 8 0 1.() 0) N .8**~** 00 .8 0 0**~** Hr TWA 1.() 0 1'- 1.()**~** N .8 .8 

### u; ;;**~** N (ppm)**m~Percentage** ofall sam pies. after ventilation 1i111111Percentage of all samples, before ventiIation

Figure 4 shows the distribution ofpersonal samples taken in adhesives application both before and after making improvements to ventilation. Percentages are a percentage ofall personal samples for adhesives for which we have data. Approximately 58% ofthe person samples are from after ventilation was improved and 42% are from before ventilation was improved. To see percentage ofsamples within each category, see Figure 5 below. Figure 4 does not include data from the Letter from Dept. ofHealth and Human Services (HHS) to Custom Products, Inc., December 1, 1999. The nPB exposure data at this plant were relatively high before NIOSH assisted CustomProducts in improving ventilation. However, the individual measurements are not available, and thus they are not included in the distribution above. Table 2 summarizes the data from NIOSH's 1999 letter to CustomProducts. Workplace exposure levels at CustomProducts ranged from 60 ppmto 381.2 ppmduring NIOSH's initial evaluation. The mean exposure level for the plant was 168.9 ppm. By comparison, after improving ventilation, the mean exposure level dropped almost tenfold to 18.9 ppm, with a range from 1.2 to 58 ppm.

5Table 2. Summary ofnPB Exposure Data from Adhesives at Custom Products, Prior to Ventilation**Im~rovements** Exposure, ppm ofnPB (8 HourTWA) Job Title Department #of Samples Mean Minimum Maximum Assembly 36 169.8 60.0 250.7 Sprayers Assembly 15 193.0 115.3 250.7 Assemblers Assembly 20 154.7 60.0 234.9 Sprayers Covers 21 197.0 117.3 381.2 Saw Operator Saw 12 117.1 85.1 159.2 All Exposure Data 69 168.9 60.0 381.2

Conclusions Exposure levels to nPB in the workplace are much lower for vapor degreasing and for airtight cleaning equipment than for other applications. Most vapor degreasers are capable of containing nPB exposure levels to less than 10 ppm. There are limited nPB exposure data available for aerosol and cold cleaning applications. These data indicate that aerosol users are likely to attain workplace exposure levels below 20 ppm. On the other hand, hand wiping appears to be a highly emissive application with exposure levels consistently above 25 ppm. Exposure levels are the highest for adhesives. Itis possible to make improvements to ventilation when using adhesives that can reduce exposure levels below 20 ppm on average. Without proper ventilation, nPB exposure from spray adhesives canbe extremely high, into the hundreds ofparts per million.

6Figure 5. Distribution ofnPB Exposure Data by Use Category

Distribution ofnPB Exposure Data by Use Category
40.0%**-.:~~-:--.-~.~. ~-**  ..**~-"":··**

35.0%**~** 

### g, 30.0% .! m (.) .:::**~** 25.0% 

### a. E m (/)**~** 20.0% 0 !!! Q) c..

### ~ 15.0% Cl m "E Q)**~** Q) 10.0% c..

5.0%

0.0%**~ ~** **~ ~** **~ ~** **~ ~** **~ ~** **~ ~** **~ ~** **~ ~** **~ ~** **~ ~** **~** ,o 0 0 0 0 0 0 0 0 0 0 0 " " " " '"); '"); "j**~** " lo'"" "'"" lo'"" ""' fO"' "'"" ""' ""' "'"" """' ""' ,o ,o ,o ,o ,o ,o ,o ..., " "**~** '"); "j**~ ~**  lo**~ ~** **~ ~** **~ ~** **~ ~** **~** >-.: ,__v " " '"); '"); Concentration, 8 Hr TWA (ppm)
7 IE! Vapor Degreasing IIIIIIAerosols DAdhesives (Before Ventilation) DAdhesives (After Ventilation)References Aerosol data, 1998. Airborne Exposure Assessment of 1-Bromopropane, 1998 (Docket A-2001-07, item II-D-89) Kassem, 2001. November 16, 2001 Email from Mick Kassem, Albemarle Corporation, concerning exposure levels using nPB in various applications. (Docket A-2001-07, item ll-A-19) NIOSH, 1999. Letter from Dept. ofHealth and Human Services to Custom Products, Inc., December 1, 1999. Re: results ofDec. 1998 survey ofworkplace exposure to nPB at Custom Products. (Docket A-2001-07, item ll-D-6) NIOSH, 2000a. Letter from Dept. ofHealth and Human Services to MarxIndustries, Inc., February 1, 2000. Re: results ofnPB exposure assessment survey conducted Nov. 16-17, 1999. (Docket A-2001-07, item ll-D-7) NIOSH, 2000b. Letter from Dept. ofHealth and Human Services to CustomProducts, Inc., December 21, 2000. Re: results ofnPB exposure assessment survey conducted Nov. 16, 2000. (Docket A-2001-07, item ll-D-8) NIOSH, 2000c. NIOSH Health Hazard Evaluation Report ofnPB exposure from cold vapor degreasers at Trilithic, Inc. (HHE Report 2000-0233-2845; Docket A-2001-07, item ll-D-11) NIOSH, 2001. Letter from Dept. ofHealth and Human Services to STN Cushion Company, March 7, 2001. Re: Results ofnPB exposure assessment survey conducted November 14, 2000. (Docket A-2001-07, item ll-D-9) NIOSH, 2002a. NIOSH Health Hazard Evaluation Report: HETA#2000-0410-2891, STN Cushion Company, Thomasville, NC, August 2002 (Docket A-2001-07, item Il-A31) NIOSH, 2002b. NIOSH Health Hazard Evaluation Report: HETA#98-0153-2883 CustomProducts, Inc. November 2002. (Docket A-2001-07, itemll-A-49) Smith, R.L. 1998a. Assessments ofoccupational exposure to nPB in adhesive spray and metal cleaning applications. Written communications from Robert Smith, Albemarle Corporation to EPA, March 19 through June 26, 1998. (a) 3/19/98; (b) 4/21198; (c) 4/22/98; (d) 4/23/98; (e) 4/24/98; (f) 5/1198; (g) 5/29/98; (h) 6/3/98; (i) 6/26/98 (Docket A-91-42, item X-A-57) Smith, R.L. 1998b. Additional information from Robert Smith (Docket A-91-42, item VID-114)
8Vapor degreasing data, 2003. Exposure data from customers oftwo suppliers ofnPBbased solvents for vapor degreasing, 2003 (see attached spread sheet and emails)

9