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

H2

H2

C

Br

CH3

Carcinogenicity

1-Bromopropane is reasonably anticipated to be a human carcinogen

based on sufficient evidence of carcinogenicity from studies in experimental animals. 1-Bromopropane, either directly or via reactive metabolites, causes molecular alterations that typically are associated 

with carcinogenesis, including genotoxicity, oxidative stress, and glutathione 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 studies in experimental animals to human carcinogenicity.

Cancer Studies in Experimental Animals

Inhalation exposure to 1-bromopropane caused tumors in two rodent 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 increases in the incidences of several types of benign and/or malignant 

skin tumors (keratoacanthoma; keratoacanthoma and squamous-cell 

carcinoma combined; and keratoacanthoma, squamous-cell carcinoma, 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, including inhalation exposure. In males, the incidence of large-intestine 

adenoma was not significantly increased, but exceeded the historical 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 controls). 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 combined (alveolar/bronchiolar adenoma and carcinoma). 

These findings are supported by the observation of additional tumors in rats that may have been related to 1-bromopropane exposure, 

including malignant mesothelioma of the abdominal cavity and pancreatic islet tumors in males and skin tumors (squamous-cell papilloma, 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 inhalation and dermal contact. Unmetabolized 1-bromopropane has been 

detected in the urine of exposed workers at levels significantly correlated with exposure to 1-bromopropane in air (Kawai et al. 2001, 

Ichihara et al. 2004). 

1-Bromopropane is metabolized via several pathways; 16 urinary 

metabolites have been detected in rodents, and several other metabolites have been proposed (Jones and Walsh 1979, Ishidao et al. 

2002, Garner et al. 2006). The primary metabolic pathways in rodents are oxidation reactions catalyzed by cytochrome P450 (primarily 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 observed 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-bromopropane 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 genotoxicity (mutations and DNA damage), oxidative stress, glutathione 

depletion, and immunomodulation. 

Studies have shown that 1-bromopropane can bind to macromolecules; it formed S-propylcysteine–globin adducts in exposed animals and humans (Valentine et al. 2007). Although 1-bromopropane 

did not induce mutations in bacteria under standard assay conditions, it did induce mutations in bacteria both with and without exogenous 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 mammalian cells with or without mammalian metabolic activation (Elf Atochem 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 micronucleus 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 regarded 

as 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 genotoxicity and toxicity of 1-bromopropane. Several reactive metabolites (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 compounds cause genotoxic effects in vitro, including DNA adduct formation, 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 animals, 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-bromopropane, 

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 oxidative 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 carcinogenicity. 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 synthesis inhibitor showed that this metabolic activation pathway is 

involved in 1-bromopropane–induced toxicity, including neurological and reproductive effects, hepatotoxicity, and immunosuppression (NTP 2003, 2011, Lee et al. 2007, 2010a,b). Neurological effects 

of 1-bromopropane exposure have also been reported in humans (Li 

et al. 2010, Ichihara et al. 2012).

It is unclear whether induction of immunotoxicity by 1-bromopropane plays a role in tumor development. Recent studies have 

shown that 1-bromopropane causes immunosuppression in rodents 

(Lee et al. 2007, Anderson et al. 2010). In particular, it reduced the 

numbers of T cells and T-cell subpopulations. In addition, there is 

evidence that 1-bromopropane causes an inflammatory response. 

It induced dose-related increases in gene expression and production 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 associated 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 evaluated the relationship between human cancer and exposure specifically to 1-bromopropane.

Properties

1-Bromopropane is a halogenated alkane that exists at room temperature as a colorless to pale-yellow, volatile liquid with a strong, characteristic odor (NTP 2011). It is slightly soluble in water and in most 

organic solvents, including acetone, ethanol, ether, benzene, chloroform, 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 compounds and with water to produce acids. Physical and chemical properties of 1-bromopropane are listed in the following table.

Property Information

Molecular weight 123.0a

Specific gravity 1.353 at 20°C/20°Cb

Melting point –110°Ca

Boiling point 64.7°Ca

Log Kow 2.10b

Water solubility 2.45 g/L at 20°Cb

Vapor pressure 110.8 mm Hg at 20°Ca

Vapor density relative to air 4.25b

Sources: aNTP 2003, bHSDB 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-bromopropane to be unacceptable for these uses (see Regulations). In recent 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 tetrachloroethylene 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 substitute for trichloroethylene concluded that chronic toxicity data were 

insufficient, and use of 1-bromopropane was not recommended until more data were available (Mirza et al. 2000). In the past, 1-bromopropane 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 generally 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 worldwide, 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 + importsa 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: aEPA 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 industrial 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-bromopropane 

in air (8- to 12-hour time-weighted averages [TWAs]) from all studies identified across several U.S. industrial sectors ranged from not 

detected to 380 ppm, with the highest concentrations being for adhesive use and the lowest for vapor degreasing. Sprayers in the adhesive 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. Manufacturing exposure reported from China (Ichihara et al. 2004) ranged 

from not detectable to 170.5 ppm for processes that included adding materials to large reaction pots. However, production methods 

reported in a patent application by a U.S. manufacturer included numerous 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; 

Ichihara et al. 2004), drycleaning (Eisenberg and Ramsey 2010), aerosol solvent use (Graul 2012), vapor degreasing (Hanley et al. 2010), 

and cleaning and painting in workshops using 1-bromopropane solvents (Kawai et al. 2001).

0	 25	 50	 75	 100	 125	 150	 175	 200

	Time-weighted average (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 manufacturing facilities, geometric mean values for daily urinary bromide excretion and urinary N-acetyl-S-propylcysteine concentrations 

were approximately 4 times as high for adhesive sprayers as for nonsprayers (Hanley et al. 2006, 2009). Concentrations of 1-bromopropane in exhaled breath also were consistently higher among 

sprayers than among workers performing other jobs. A National Institute 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-bromopropane air concentrations (TWAs) could be reduced by 80% or more 

through implementation of NIOSH recommendations for engineering controls, such as ventilation improvements and enclosure of spray 

tables (Reh et al. 2002).

The general population may be exposed to 1-bromopropane 

through inhalation of ambient air in the vicinity of industrial facilities 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 estimated concentrations were 0.138 mg/m3

 [0.0274 ppm] for facilities 

with average adhesive use and 1.38 mg/m3

 [0.274 ppm] for facilities 

with high adhesive use (Morris and Wolf 2003). EPA also estimated 

daily inhalation uptake of 1-bromopropane for a person living 100 m 

from a model facility to be 0.0537 mg/kg for average-adhesive-use facilities and 0.537 mg/kg for high-adhesive-use facilities. 

Based on its production levels and industrial uses, 1-bromopropane 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 algae to the marine environment (HSDB 2006). No data were found 

on levels of 1-bromopropane in ambient air, drinking water, surface 

water, soil, food, or consumer products or on non-occupational exposure 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.

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