### Report on Carcinogens, Thirteenth Edition

National Toxicology Program, Department of Health and Human Services 

### For Table of Contents, see home page: http://ntp.niehs.nih.gov/go/roc13 

## 1-Bromopropane CAS No. 106-94-5 Reasonably anticipated to be a human carcinogen First listed in the Thirteenth Report on Carcinogens (2014) Also known as n -propyl bromide C H 2 H 2 C Br CH 3 

### Carcinogenicity 1-Bromopropane is reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity from studies in exper imental animals. 1-Bromopropane, either directly or via reactive me tabolites, causes molecular alterations that typically are associated with carcinogenesis, including genotoxicity, oxidative stress, and glu tathione depletion. These alterations, observed mainly in vitro and in toxicity studies in rodents, are relevant to possible mechanisms of human carcinogenicity and support the relevance of the cancer stud ies in experimental animals to human carcinogenicity. Cancer Studies in Experimental Animals Inhalation exposure to 1-bromopropane caused tumors in two ro dent species and at several different tissue sites, including one tissue site in rats at which tumors are rare (NTP 2011). In male rats, 1 - bromopropane caused significant dose-related in creases in the incidences of several types of benign and/or malignant skin tumors (keratoacanthoma; keratoacanthoma and squamous-cell carcinoma combined; and keratoacanthoma, squamous-cell carci noma, basal-cell adenoma, and basal-cell carcinoma combined). Both female and male rats showed an increased incidence of large-intestine tumors (adenoma of the colon and rectum), which are rare tumors in rats. In females, the incidence was dose-related and statistically significantly higher than in concurrent controls, and it exceeded the historical control range for all routes of exposure used in studies, in cluding inhalation exposure. In males, the incidence of large-intestine adenoma was not significantly increased, but exceeded the histori cal control range for inhalation-exposure studies, and its occurrence was considered to be biologically significant because of the rarity of these tumors (which occurred in less than 0.2% of the historical con trols). Although no carcinoma of the large intestine was observed in male or female rats in this study, adenoma of the large intestine has been shown to progress to carcinoma in other studies, and forms a morphologic continuum with carcinoma (Deschner 1983, Chang 1984, Nigro 1985). In female mice, 1 - bromopropane caused significant dose-related increases in the incidence of benign and malignant lung tumors com bined (alveolar/bronchiolar adenoma and carcinoma). These findings are supported by the observation of additional tu mors in rats that may have been related to 1 - br omopropane exposure, including malignant mesothelioma of the abdominal cavity and pan creatic islet tumors in males and skin tumors (squamous-cell pap illoma, keratoacanthoma, and basal-cell adenoma or carcinoma) in females. Other Relevant Data 1-Bromopropane is well absorbed following ingestion, inhalation, or dermal exposure. Occupational exposure occurs primarily by inhala tion and dermal contact. Unmetabolized 1 - bromopropane has been detected in the urine of exposed workers at levels significantly cor related with exposure to 1 - bromopropane in air (Kawaiet al. 2001, Ichiharaet al. 2004). 1 - Bromopropane is metabolized via several pathways; 16 urinary metabolites have been detected in rodents, and several other me tabolites have been proposed (Jones and Walsh 1979, Ishidao et al. 2002, Garner et al. 2006). The primary metabolic pathways in ro dents are oxidation reactions catalyzed by cytochrome P450 (pri marily CYP2E1) and glutathione conjugation. The available data on human metabolism of 1-bromopropane, although limited, suggest that some of its metabolic pathways in humans are similar to those ob served in rodents. Four mercapturic conjugates identified in the urine of rodents were also identified in the urine of workers exposed to 1 - bromopropane (Hanley et al. 2009). The major metabolite, N-acetylS -( n -propyl)- l -cysteine, has been detected in the urine of exposed workers at levels that increased with increasing levels of 1 - bromo propane in ambient air (Hanley and Dunn 2006, Valentine et al. 2007, Hanley et al. 2009, 2010). This metabolite is produced in humans by conjugation of 1 - bromopropane with glutathione, and that reaction also releases free bromide ions, another useful biomarker for human exposure to 1 - bromopropane (Jones and Walsh 1979, Hanley et al. 2006). No studies were identified that tested for the occurrence in humans of the oxidative metabolites that are obligate intermediates to the measured conjugates. Studies on Mechanisms of Carcinogenesis The mechanism(s) by which 1-bromopropane causes cancer is not known. However, exposure to 1-bromopropane has been shown to cause molecular alterations related to carcinogenicity, including geno toxicity (mutations and DNA damage), oxidative stress, glutathione depletion, and immunomodulation. Studies have shown that 1-bromopropane can bind to macromol ecules; it formed S - propylcysteine–globin adducts in exposed ani mals and humans (Valentine et al. 2007). Although 1 - br omopropane did not induce mutations in bacteria under standard assay condi tions, it did induce mutations in bacteria both with and without ex ogenous mammalian metabolic activation in the only reported study whose design was appropriate for testing a highly volatile chemical (Barber et al. 1981). It also caused mutations in cultured mamma lian cells with or without mammalian metabolic activation (Elf Ato chem 1996, as reviewed in NTP 2003) and DNA damage in cultured human cells without metabolic activation (Toraason et al. 2006). In addition, there is limited evidence of DNA damage in leukocytes from 1-bromopropane–exposed workers (Toraason et al. 2006). In rodents exposed in vivo , 1 - bromopropane did not increase micro nucleus formation in bone marrow (Kim et al. 1998, as reviewed in NTP 2003) or peripheral blood erythrocytes (Elf Atochem 1996, cited in NTP 2003, NTP 2011) or cause dominant lethal mutations. However, the dominant lethal mutation assay is generally regardedas relatively insensitive for the detection of mutagenic agents (SaitoSuzuki et al. 1982, Yu et al. 2008). There is evidence that metabolic activation plays a role in the geno toxicity and toxicity of 1 - bromopropane. Several reactive metabo lites (or intermediates) of 1 - bromopropane have been identified in rodents, including glycidol and α-bromohydrin, and propylene oxide has been proposed as a metabolite (Garner et al. 2006). These com pounds cause genotoxic effects in vitro, including DNA adduct for mation, mutations, and DNA or chromosome damage (Stolzenberg and Hine 1979, IARC 1994, 2000). Glycidol and propylene oxide cause cytogenetic effects in vivo and are carcinogenic in experimental an imals, and both substances are listed in the Report on Carcinogens as reasonably anticipated to be human carcinogens . These reactive and genotoxic metabolites may be responsible for at least some of the

### Report on Carcinogens, Thirteenth Edition

National Toxicology Program, Department of Health and Human Services 2 carcinogenic effects of 1 - bromopropane. As with 1-bromo prop ane, oral exposure to glycidol caused rare tumors of the large intestine in rats, as did oral exposure to two halogenated alkane analogues of 1-bromopropane, tribromomethane and bromodichloromethane (NTP 1987, 1989, 1990). Chronic exposure to 1 - bromopropane may produce levels of ox idative metabolites that exceed the glutathione-conjugating capacity or may inhibit enzymes required for glutathione synthesis. Because glutathione is an important cellular defense mechanism, reduced levels can lead to oxidative stress, increased toxicity, and carcinoge nicity. Numerous studies have shown that 1 - bromopropane induces both oxidative stress and glutathione depletion (Lee et al. 2005, 2007, 2010a, Liu et al. 2009, 2010, Huang et al. 2011). Studies with Cyp2e1 -/ - knockout mice, cytochrome P450 inhibitors, or a glutathione syn thesis inhibitor showed that this metabolic activation pathway is involved in 1 - bromopropane–induced toxicity, including neurolog ical and reproductive effects, hepato to xicity, and immunosuppres sion (NTP 2003, 2011, Lee et al. 2007, 2010a,b). Neurological effects of 1 - bromo prop ane exposure have also been reported in humans (Li et al. 2010, Ichihara et al. 2012). It is unclear whether induction of immunotoxicity by 1-bromo propane plays a role in tumor development. Recent studies have shown that 1-bromopropane causes immunosuppression in rodents (Lee et al. 2007, Andersonet al. 2010). In particular, it reduced the numbers of T cells and T-cell subpopulations. In addition, there is evidence that 1-bromo prop ane causes an inflammatory response. It induced dose-related increases in gene expression and produc tion of proinflammatory cytokines in mouse macrophages (Han et al. 2008) and an inflammatory response in rats (NTP 2011). However, chronic respiratory inflammation and lung tumors were not associ ated in rodents; respiratory inflammation occurred in rats but not mice, whereas lung tumors occurred in mice but not rats. Cancer Studies in Humans No epidemiological studies or case reports were identified that eval uated the relationship between human cancer and exposure specifi cally to 1 - bromopropane. 

### Properties 1-Bromopropane is a halogenated alkane that exists at room temper ature as a colorless to pale-yellow, volatile liquid with a strong, char acteristic odor (NTP 2011). It is slightly soluble in water and in most organic solvents, including acetone, ethanol, ether, benzene, chloro form, and carbon tetrachloride. It is less flammable than many other halogenated alkanes at room temperature. Thermal decomposition of 1 - bromopropane produces hydrogen bromide. 1 - Bromopropane can react with oxidizing agents to form hazardous flammable com pounds and with water to produce acids. Physical and chemical prop erties of 1-bromopropane are listed in the following table. Property Information Molecular weight 123.0 a Specific gravity 1.353 at 20°C/20°C b Melting point –110°C a Boiling point 64.7°C a Log K ow 2.10 b Water solubility 2.45 g/L at 20°C b Vapor pressure 110.8 mm Hg at 20°C a Vapor density relative to air 4.25 b Sources: a NTP 2003, b HSDB 2006. 

### Use 1-Bromopropane is used primarily as a solvent cleaner in vapor and immersion degreasing operations to clean optics, electronics, and metals and as a solvent vehicle in industries using aerosol-applied adhesives, such as foam cushion manufacturing. However, its use as an aerosol solvent or adhesive could be affected by the proposed U.S. Environmental Protection Agency (EPA) rule that finds 1 - bromo propane to be unacceptable for these uses (see Regulations). In re cent years, 1-bromopropane usage has increased as a result of new industrial and commercial uses as a substitute for ozone-depleting chemicals or suspected carcinogens (e.g., as an alternative to tetra chloroethylene in the drycleaning industry) (Blando et al. 2010). 1 - Bromopropane also has potential for use as a spot remover in the textile industry; however, an evaluation of 1 - bromopropane as a sub stitute for trichloroethylene concluded that chronic toxicity data were insufficient, and use of 1 - bromopropane was not recommended un til more data were available (Mirzaet al. 2000). In the past, 1 - bromo propane was used primarily as a solvent for fats, waxes, and resins and as an intermediate in the synthesis of pharmaceuticals, insecticides, quaternary ammonium compounds, flavors, and fragrances in gener ally well-controlled, closed processes (Hanley et al. 2006, NTP 2003). 

### Production 1-Bromopropane is a high-production-volume chemical. In 2012, 1-bromopropane was manufactured by at least 21 companies world wide, including at least one company in the United States (SRI 2012). Reported recent and historical volumes of U.S. production, imports, and exports of 1-bromopropane are listed in the following table. Category Year Quantity (lb) Production + imports a 2012 1998–2006 1994 1986, 1990 15.3 million 1 million to < 10 million > 500K to 1 million 10K to 500K U.S. imports: b recent historical 2013 2007 9.2 million 10.9 million U.S. exports: b recent historical 2013 2007 15.6 million 8.8 million Sources: a EPA 2014 (EPA Chemical Data Reporting Rule, formerly the Inventory Update Rule), b USITC 2014 (reported as “brominated derivatives of acyclic hydrocarbons”). 

### Exposure A significant number of people in the United States are exposed to 1-bromopropane as a result of widespread usage, high production volume, and high levels of 1-bromopropane in commercial and in dustrial settings. Occupational exposure to 1-bromopropane may occur through inhalation or dermal contact at workplaces where 1-bromopropane is produced or used (HSDB 2006). Concentrations of 1 - br omo pr opane in air (8- to 12-hour time-weighted averages [TWAs]) from all stud ies identified across several U.S. industrial sectors ranged from not detected to 380 ppm, with the highest concentrations being for ad hesive use and the lowest for vapor degreasing. Sprayers in the ad hesive industry had the highest exposure, which ranged from 18 to 380 ppm across several studies. Exposure data for 1 - bromopropane manufacturing were not available for the United States. Manufac turing exposure reported from China (Ichihara et al. 2004) ranged from not detectable to 170.5 ppm for processes that included add ing materials to large reaction pots. However, production methods reported in a patent application by a U.S. manufacturer included nu merous control processes to contain 1 - bromopropane, which would likely reduce potential exposure substantially. The graph below shows

### Report on Carcinogens, Thirteenth Edition

National Toxicology Program, Department of Health and Human Services 3 TWA 1 - bromopropane exposure levels from representative studies of adhesive application (Hanley et al. 2006), manufacturing (in China; Ichiharaet al. 2004), drycleaning (Eisenberg and Ramsey 2010), aero sol solvent use (Graul 2012), vapor degreasing (Hanley et al. 2010), and cleaning and painting in workshops using 1-bromopropane sol vents (Kawai et al. 2001).

0	 25	 50	 75	 100	 125	 150	 175	 200 Time-weighted av erage (ppm) Occupational exposure to 1-bromopropane, by industry Time-weighted-average 1-bromopropane exposure levels as geometric means (adhesives, vapor degreasing, and other); arithmetic mean (drycleaning); or not reported (manufacturing and aerosol solvents). The dashed vertical line represents the American Conference of Governmental Industrial Hygienists threshold limit value – time-weighted average (TLV-TWA) of 10 ppm. Among workers at polyurethane foam furniture cushion man ufacturing facilities, geometric mean values for daily urinary bro mide excretion and urinary N -acetyl- S-propylcysteine concentrationswere approximately 4 times as high for adhesive sprayers as for nonsprayers (Hanley et al. 2006, 2009). Concentrations of 1 - bromo propane in exhaled breath also were consistently higher among sprayers than among workers performing other jobs. A National In stitute for Occupational Safety and Health (NIOSH) Health Hazard Evaluation (HHE) of a furniture foam cushion manufacturing facility found the average difference between end-of-week and start-of-week serum bromide concentrations to be 23 mg/L for exposed workers, compared with 3 mg/L for unexposed workers (Harney et al. 2003). NIOSH HHEs and follow-ups at two facilities showed that 1 - bromo propane air concentrations (TWAs) could be reduced by 80% or more through implementation of NIOSH recommendations for engineer ing controls, such as ventilation improvements and enclosure of spray tables (Rehet al. 2002). The general population may be exposed to 1-bromopropane through inhalation of ambient air in the vicinity of industrial facil ities where 1-bromopropane is used as an adhesive. EPA used air dispersion modeling to estimate 1 - bromopropane concentrations in ambient air at a distance of 100 m from model facilities. The esti mated concentrations were 0.138 mg/m 3[0.0274 ppm] for facilities with average adhesive use and 1.38 mg/m 3[0.274 ppm] for facilities with high adhesive use (Morris and Wolf 2003). EPA also estimated daily inhalation uptake of 1 - bro mopropane for a person living 100 m from a model facility to be 0.0537 mg/kg for average-adhesive-use fa cilities and 0.537 mg/kg for high-adhesive-use facilities. Based on its production levels and industrial uses, 1-bromo propane may be released to the environment through various waste streams. 1-Bromopropane has been detected in temperate marine macroalgal tissue and is believed to be transported from these al gae to the marine environment (HSDB 2006). No data were found on levels of 1-bromo propane in ambient air, drinking water, surface water, soil, food, or consumer products or on non-occupational ex posure to 1 - bromopropane. 

### Regulations California Occupational Safety and Health Standards Board (OSHSB) Permissible exposure limit (PEL) = 5 ppm. Potential for dermal absorption. Department of Transportation (DOT) Bromopropanes are considered hazardous materials, and special requirements have been set for marking, labeling, and transporting these materials. Environmental Protection Agency (EPA) Significant New Alternatives Policy (SNAP) Program The EPA SNAP program reviews alternatives to ozone-depleting substances and approves the use of alternatives that do not present substantially greater risk to the public health and environment than the substance they replace or other available substitutes. The EPA SNAP program has made the following determinations regarding various end uses of 1

- bromopropane: Solvent in industrial equipment for metals cleaning, electronics cleaning, or precision cleaning as a substitute for CFC-113 and methyl chloroform: acceptable (final rule). Coatings as a substitute for CFC-113, HCFC-141b, and methyl chloroform: acceptable subject to the condition that use is limited to coatings facilities that have provided EPA data which demonstrate their ability to maintain acceptable workplace exposures (proposed rule). Aerosol solvents as a substitute for CFC-113, HCFC-141b, and methyl chloroform: unacceptable (proposed rule). Adhesives as a substitute for CFC-113, HCFC-141b, and methyl chloroform: unacceptable (proposed rule). 

### Guidelines American Conference of Governmental Industrial Hygienists (ACGIH) Threshold limit value – time-weighted average (TLV-TWA) = 0.1 ppm. Environmental Protection Agency (EPA) Acceptable exposure limit (8-hour time-weighted average) = 25 ppm. 

### References Anderson SE, Munson AE, Butterworth LF, Germolec D, Morgan DL, Roycroft JA, Dill J, Meade BJ. 2010. Whole-body inhalation exposure to 1-bromopropane suppresses the IgM response to sheep red blood cells in female B6C3F 1 mice and Fisher 344/N rats. Inhal Toxicol 22(2): 125-132. Barber ED, Donish WH, Mueller KR. 1981. A procedure for the quantitative measurement of the mutagenicity of volatile liquids in the Ames Salmonella/microsome assay. Mutat Res90(1): 31-48. Blando JD, Schill DP, de la Cruz MP, Zhang L, Zhang J. 2010. Preliminary study of propyl bromide exposure among New Jersey dry cleaners as a result of a pending ban on perchloroethylene. J Air Waste Manag Assoc 60(9): 1049-1056. Chang WW. 1984. Histogenesis of colon cancer in experimental animals. Scand J Gastroenterol Suppl 104: 27-43. Deschner EE. 1983. Adenomas: preneoplastic events, growth and development in man and experimental systems. Pathol Annu18(Pt 1): 205-219. Eisenberg J, Ramsey J. 2010. Evaluation of 1-Bromopropane Use in Four New Jersey Commercial Dry Cleaning Facilities. Health Hazard Evaluation Report HETA 2008-0175-3111. National Institute for Occupational Safety and Health. 28 pp. Elf Atochem. 1996. In Vitro Mammalian Cell Gene Mutation Test in L5178Y TK+/- Mouse Lymphoma Cells of n -Propyl Bromide. Study No. 13293. Miserey, France: Centre International de Toxicologie. EPA. 2014. Non-confidential 2012 Chemical Data Reporting (CDR) Database. U.S. Environmental Protection Agency. http://java.epa.gov/oppt_chemical_search and select CDR and search on CAS no. Last accessed: 7/10/14. Garner CE, Sumner SC, Davis JG, Burgess JP, Yueh Y, Demeter J, et al. 2006. Metabolism and disposition of 1-bromopropane in rats and mice following inhalation or intravenous administration. Toxicol Appl Pharmacol 215(1): 23-36. Graul F. 2012. Summary of Data on Workplace Exposure to n -Propyl Bromide. Public comment submitted by F. Graul, Executive Director, Halogenated Solvents Industry Association, Arlington VA, to R. Lunn, NTP, Research Triangle Park, NC, February 28, 2012. 8 pp. http://ntp.niehs.nih.gov/go/37663. Han EH, Hwang YP, Lee KJ, Jeong TC, Jeong HG. 2008. 1-Bromopropane induces macrophage activation via extracellular signal-regulated kinase 1/2 MAPK and NF-κB pathways. Cancer Lett 262(1): 28-36. Hanley KW, Dunn K. 2006. Workers’ Exposures to n -Propyl Bromide at a Helicopter Transmission Factory. Report no. IWSB 232.11. Cincinnati, OH: National Institute for Occupational Safety and Health. 21 pp. Hanley KW, Dunn K, Sollberger R. 2006. Workers’ Exposures to n -Propyl Bromide at an Aerospace Components Manufacturer. Report no. IWSB 232.12. Cincinnati, OH: National Institute for Occupational Safety and Health. 26 pp. Hanley KW, Petersen MR, Cheever KL, Luo L. 2009. N-acetyl-S-( n -propyl)- l -cysteine in urine from workers exposed to 1-bromopropane in foam cushion spray adhesives. Ann Occup Hyg53(7): 759-769. Hanley KW, Petersen MR, Cheever KL, Luo L. 2010. Bromide and N-acetyl- S-( n -propyl)- l -cysteine in urine from workers exposed to 1-bromopropane solvents from vapor degreasing or adhesive manufacturing. Int Arch Occup Environ Health 83(5): 571-584. Adhesives Sprayers Non-sprayers Manufacturing

Operators Drycleaning

Operators Aerosol solvents Exposed workers Vapor degreasing Exposed workers Other Cleaners & painters

### Report on Carcinogens, Thirteenth Edition

National Toxicology Program, Department of Health and Human Services 4 Harney JM, Nemhauser JB, Reh CM, Trout D. 2003. HHE Report No. HETA 99-0260-2906. Marx Industries, Inc., Sawmills, North Carolina. NIOSH Health Hazard Evaluation Report. Cincinnati, OH: National Institute for Occupational Safety and Health. http://www.cdc.gov/niosh/hhe/reports/pdfs/1999-0260-2906.pdf. HSDB. 2006. Hazardous Substances Data Bank. National Library of Medicine. Last updated: 4/20/06. http:// toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?HSDB and search on CAS number. Huang Z, Ichihara S, Oikawa S, Chang J, Zhang L, Takahashi M, et al. 2011. Proteomic analysis of hippocampal proteins of F344 rats exposed to 1-bromopropane. Toxicol Appl Pharmacol 257(1): 93-101. IARC. 1994. Propylene oxide. In Some Industrial Chemicals. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, vol. 60. Lyon, France: International Agency for Research on Cancer. pp. 181- 213. IARC. 2000. Glycidol. In Some Industrial Chemicals. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, vol. 77. Lyon, France: International Agency for Research on Cancer. pp. 469-486. Ichihara G, Li W, Ding X, Peng S, Yu X, Shibata E, et al. 2004. A survey on exposure level, health status, and biomarkers in workers exposed to 1-bromopropane. Am J Ind Med 45(1): 63-75. Ichihara G, Kitoh J, Li W, Ding X, Ichihara S, Takeuchi Y. 2012. Neurotoxicity of 1

- bromopropane: Evidence from animal experiments and human studies. J Adv Res3(2): 91-98. Ishidao T, Kunugita N, Fueta Y, Arashidani K, Hori H. 2002. Effects of inhaled 1

- bromopropane vapor on rat metabolism. Toxicol Lett 134(1-3): 237-243. Jones AR, Walsh DA. 1979. The oxidative metabolism of 1-bromopropane in the rat. Xenobiotica9(12): 763-772. Kawai T, Takeuchi A, Miyama Y, Sakamto K, Zhang ZW, Higashikawa K, Ikeda M. 2001. Biological monitoring of occupational exposure to 1-bromopropane by means of urinalysis for 1-bromopropane and bromide ion. Biomarkers6(5): 303-312. Kim H, Chung J, Chung Y, Kim K, Maeng S, Hang C, et al. 1998. Toxicological Studies on Inhalation of 1 - Bromopropane Using Rats . Report submitted to the Industrial Health Research Institute, Korea Industrial Safety Corporation. Lee SK, Jo SW, Jeon TW, Jun IH, Jin CH, Kim GH, et al. 2005. Hepatotoxic effect of 1-bromopropane and its conjugation with glutathione in male ICR mice. Arch Pharm Res28(10): 1177-1182. Lee SK, Jeon TW, Kim YB, Lee ES, Jeong HG, Jeong TC. 2007. Role of glutathione conjugation in the hepatotoxicity and immunotoxicity induced by 1-bromopropane in female BALB/c mice. J Appl Toxicol 27(4): 358-367. Lee SK, Kang MJ, Jeon TW, Ha HW, Yoo JW, Ko GS, et al. 2010a. Role of metabolism in 1-bromopropaneinduced hepatotoxicity in mice. J Toxicol Environ Health A 73(21-22): 1431-1440. Lee SK, Lee DJ, Ko GS, Yoo SH, Ha HW, Kang MJ, Jeong TC. 2010b. Role of glutathione conjugation in 1-bromobutane-induced hepatotoxicity in mice. Food Chem Toxicol 48(10): 2707-2711. Li W, Shibata E, Zhou Z, Ichihara S, Wang H, Wang Q, et al. 2010. Dose-dependent neurologic abnormalities in workers exposed to 1-bromopropane. J Occup Environ Med 52(8): 769-777. Liu F, Ichihara S, Mohideen SS, Sai U, Kitoh J, Ichihara G. 2009. Comparative study on susceptibility to 1-bromopropane in three mice strains. Toxicol Sci 112(1): 100-110. Liu F, Ichihara S, Valentine WM, Itoh K, Yamamoto M, Sheik Mohideen S, Kitoh J, Ichihara G. 2010. Increased susceptibility of Nrf2-null mice to 1-bromopropane-induced hepatotoxicity. Toxicol Sci 115(2): 596-606. Mirza T, Gérin M, Bégin D, Drolet D. 2000. A study on the substitution of trichloroethylene as a spot remover in the textile industry. Am Ind Hyg Assoc J 61(3): 431-438. Morris M, Wolf K. 2003. Alternative Adhesive Technologies in the Foam Furniture and Bedding Industries. Prepared for the U.S. Environmental Protection Agency. Los Angeles: Institute for Research and Technical Assistance. 260 pp. Nigro ND. 1985. Animal model for colorectal cancer. Prog Clin Biol Res186: 161-173. NTP. 1987. Toxicology and Carcinogenesis Studies of Bromodichloromethane (CAS No. 75-27-4) in F344/N Rats and B6C3F 1 Mice (Gavage Studies). NTP Technical Report Series no. 321. Research Triangle Park, NC: National Toxicology Program. 185 pp. NTP. 1989. Toxicology and Carcinogenesis Studies of Tribromomethane (Bromoform) (CAS No. 75-25-2) in F344/N Rats and B6C3F 1 Mice (Gavage Studies). NTP Technical Report Series no. 350. Research Triangle Park, NC: National Toxicology Program. 198 pp. NTP. 1990. Toxicology and Carcinogenesis Studies of Glycidol (CAS No. 556-52-5) in F344/N Rats and B6C3F 1 Mice (Gavage Studies). NTP Technical Report Series no. 374. Research Triangle Park, NC: National Toxicology Program. 231 pp. NTP. 2003. NTP-CERHR Monograph on the Potential Human Reproductive and Developmental Effects of 1-Bromopropane. Research Triangle Park, NC: National Toxicology Program, Center for the Evaluation of Risks to Human Reproduction. 88 pp. NTP. 2011. NTP Technical Report on the Toxicology and Carcinogenesis Studies of 1

- Bromopropane (CAS No. 106-94-5) in F344/N Rats and B6C3F 1 Mice (Inhalation Studies). NTP TR 564, NIH Publication No. 11-5906. Research Triangle Park, NC: National Toxicology Program. 195 pp. Reh CM, Mortimer V, Nemhauser JB, Trout D. 2002. HHE Report no. HETA 98-0153-2883. Custom Products, Inc., Mooresville, North Carolina. NIOSH Health Hazard Evaluation Report. Cincinnati, OH: National Institute for Occupational Safety and Health. 46 pp. Saito-Suzuki R, Teramoto S, Shirasu Y. 1982. Dominant lethal studies in rats with 1,2-dibromo-3- chloropropane and its structurally related compounds. Mutat Res101(4): 321-327. SRI. 2012. Directory of Chemical Producers. Menlo Park, CA: SRI Consulting. Database edition. Last accessed: 2/13/12. Stolzenberg SJ, Hine CH. 1979. Mutagenicity of halogenated and oxygenated three-carbon compounds. J Toxicol Environ Health 5(6): 1149-1158. Toraason M, Lynch DW, DeBord DG, Singh N, Krieg E, Butler MA, Toennis CA, Nemhauser JB. 2006. DNA damage in leukocytes of workers occupationally exposed to 1

- bromopropane. Mutat Res603(1): 1-14. USITC. 2014. USITC Interactive Tariff and Trade DataWeb. United States International Trade Commission. http://dataweb.usitc.gov/scripts/user_set.asp and search on HTS no. 2903391550. Last accessed: 7/10/14. Valentine H, Amarnath K, Amarnath V, Li W, Ding X, Valentine WM, Ichihara G. 2007. Globin s -propyl cysteine and urinary N-acetyl- S-propylcysteine as internal biomarkers of 1

- bromopropane exposure. Toxicol Sci 98(2): 427-435. Yu WJ, Kim JC, Chung MK. 2008. Lack of dominant lethality in mice following 1

- b romopropane treatment. Mutat Res652(1): 81-87.