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1-BROMOPROPANE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) 1-Bromopropane is a halogenated organic solvent. Commercial grades may contain a very small percentage of the 2-bromopropane isomer.

Specific Substances

    1) Bromopropane, 1-
    2) 1-Bromopropane
    3) nPB
    4) n-Propyl bromide
    5) n-Propylbromide
    6) Propane, 1-Bromo-
    7) Propyl bromide
    8) Molecular Formula: C3H7Br
    9) CAS 106-94-5
    1.2.1) MOLECULAR FORMULA
    1) C3H7Br
    2) CH3CH2CH2Br

Available Forms Sources

    A) FORMS
    1) 1-Bromopropane is a colorless liquid that is slightly denser than, and slightly soluble in, water (CHRIS, 2004; HSDB, 2004; AAR, 2002).
    B) SOURCES
    1) 1-Bromopropane is synthesized via an alcohol bromination process using n-propanol + hydrobromic acid (Ashford, 2001).
    C) USES
    1) 1-Bromopropane is used as a chemical intermediate in the production of a wide range of products including pharmaceuticals, insecticides, quaternary ammonium compounds, flavoring agents, and fragrances. It is also used as a solvent for fats, waxes, and resins (HSDB, 2004).
    2) The US Environmental Protection Agency has proposed 1-bromopropane as a substitute for ozone-depleting solvents in a number of different industrial sectors, subject to use conditions. 1-Bromopropane use in these categories is as follows:
    IndustryEnd UseSubstitute for these Substances
    CFC-113methyl chloroformHCFC-141b
    Solvents CleaningMetals CleaningXX.
    Solvents CleaningElectronics CleaningXX.
    Solvents CleaningPrecision CleaningXX.
    AerosolsAerosol SolventsXXX
    Adhesives, Coatings, and InksAdhesivesXXX

    3) Occupational exposure to a furniture glue containing 70% 1-bromopropane in 4 patients resulted in gastrointestinal symptoms (nausea, anorexia, weight loss) and peripheral and central nervous system signs and symptoms (dizziness, fatigue/lethargy, headache, paresthesia, dysesthesia, weakness, and ataxia) (Raymond & Ford, 2007).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: 1-Bromopropane is used as a chemical intermediate in the production of a wide range of products including pharmaceuticals, insecticides, quaternary ammonium compounds, flavoring agents, and fragrances. It is also used as a solvent for fats, waxes, and resins, and as an alternative to ozone-depleting solvents (eg, chlorofluorocarbons).
    B) TOXICOLOGY: Primary routes of exposure are inhalational and dermal, with systemic absorption primarily affecting the peripheral and the central nervous systems.
    C) EPIDEMIOLOGY: Occupational exposure has been infrequently reported.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Mild to moderate toxic effects may include dermatitis, nausea and vomiting, diarrhea, dysphagia, anorexia, urinary difficulties, and irritation of eyes, nose, and throat.
    2) SEVERE TOXICITY: Malaise, dizziness, lightheadedness, headache, trouble concentrating, paresthesias, hypo- and hyperreflexia, ataxia, and weakness of the lower extremities have been reported following inhalational exposure to 1-bromopropane. Liver and lung damage have occurred with repeated, long-term exposure to 1-bromopropane.
    0.2.20) REPRODUCTIVE
    A) Decreased fetal weight and increased incidence of skeletal variations have been reported in rats exposed to 1-bromopropane by inhalation. In animal studies, decreased fertility, decreased numbers of implantation sites and litter size, and increased precoital interval were observed after exposure to 1-bromopropane. In addition, reduced prostate weight, and effects on seminal vesicle weight and sperm quality at higher levels were observed.
    0.2.21) CARCINOGENICITY
    A) No information could be found on the potential carcinogenicity of 1-bromopropane in humans.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor arterial blood gas, pulse oximetry, and chest x-ray in patients with hypoxia or respiratory distress.
    C) Monitor fluid and electrolyte status in patients with significant vomiting and/or diarrhea.
    D) Evaluate for signs/symptoms of muscle weakness, paresthesias, and ataxia.
    E) Monitor liver function as indicated in symptomatic patients.
    F) Urinary measurement of N-acetyl-S-(n-propyl)-L-cysteine (AcPrCys), a urinary specific 1-bromopropane metabolite, may be a useful biomarker of 1-bromopropane exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) DECONTAMINATION
    1) PREHOSPITAL: Toxicity after an acute ingestion is unlikely. Prehospital gastrointestinal decontamination is generally unnecessary. Primary routes of exposure are inhalational and dermal.
    2) HOSPITAL: Toxicity after an acute ingestion is unlikely. Gastrointestinal decontamination is generally unnecessary. Consider activated charcoal only if coingestants with significant toxicity are involved.
    0.4.3) INHALATION EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. Correct any significant fluid and/or electrolyte abnormalities in patients with severe diarrhea and/or vomiting.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Monitor mental status and evaluate for signs/symptoms of muscle weakness, paresthesias, and ataxia.
    C) DECONTAMINATION
    1) PREHOSPITAL: Monitor for respiratory distress. If cough or difficulty breathing develops, administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    2) HOSPITAL: Monitor for respiratory distress. If cough or difficulty breathing develops, administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    D) AIRWAY MANAGEMENT
    1) Ensure adequate ventilation and perform endotracheal intubation early in patients with significant respiratory distress.
    E) ANTIDOTE
    1) There is no specific antidote available.
    F) ENHANCED ELIMINATION PROCEDURE
    1) It is unknown if enhanced elimination techniques are likely to be useful following a 1-bromopropane exposure.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients who are asymptomatic or with minimal symptoms after exposure to 1-bromopropane and are otherwise improving may be managed at home.
    2) OBSERVATION CRITERIA: Patients who are symptomatic need to be monitored until they are clearly improving and clinically stable.
    3) ADMISSION CRITERIA: Only patients with systemic toxicity may require admission.
    4) CONSULT CRITERIA: Consult a regional poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    H) PITFALLS
    1) Failure to obtain adequate history of exposure.
    I) TOXICOKINETICS
    1) 1-Bromopropane is absorbed rapidly by dermal, oral or inhalation routes. 1-Bromopropane metabolism occurs through the mixed function oxidase system (MFO; slow and easily saturable) and via conjugation with glutathione. Enzymatic or non-enzymatic conjugation with glutathione produces several cysteine conjugates that are excreted in the urine.
    J) DIFFERENTIAL DIAGNOSIS
    1) Other chemicals or drugs that cause muscle weakness, paresthesias, or ataxia.
    0.4.4) EYE EXPOSURE
    A) For eye exposures, remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) For dermal exposures, remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists after washing.

Range Of Toxicity

    A) TOXICITY: A specific minimum toxic concentration has not been established. Time-weighted average (TWA) exposure concentrations were 0 to 170.5 parts per million (ppm) in workers occupationally exposed to 1-bromopropane and reported symptoms of dizziness, light- or heavy-headedness, headache, feelings of intoxication, and irritation of mucous membranes. The ambient air concentrations of 1-bromopropane were 3.3 to 90.2 ppm. The American Conference of Governmental Industrial Hygienists (ACGIH) has recommended the TLV-TWA occupational exposure limit of 10 ppm.

Clinical Effects

Summary Of Exposure

    A) USES: 1-Bromopropane is used as a chemical intermediate in the production of a wide range of products including pharmaceuticals, insecticides, quaternary ammonium compounds, flavoring agents, and fragrances. It is also used as a solvent for fats, waxes, and resins, and as an alternative to ozone-depleting solvents (eg, chlorofluorocarbons).
    B) TOXICOLOGY: Primary routes of exposure are inhalational and dermal, with systemic absorption primarily affecting the peripheral and the central nervous systems.
    C) EPIDEMIOLOGY: Occupational exposure has been infrequently reported.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Mild to moderate toxic effects may include dermatitis, nausea and vomiting, diarrhea, dysphagia, anorexia, urinary difficulties, and irritation of eyes, nose, and throat.
    2) SEVERE TOXICITY: Malaise, dizziness, lightheadedness, headache, trouble concentrating, paresthesias, hypo- and hyperreflexia, ataxia, and weakness of the lower extremities have been reported following inhalational exposure to 1-bromopropane. Liver and lung damage have occurred with repeated, long-term exposure to 1-bromopropane.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Painful eyes (9 of 24 women and 2 of 13 men) and dim eyesight (2 of 24 women and 3 of 13 men) have been reported in factory workers exposed to 1-bromopropane (equal or less than 170 ppm) (Ichihara et al, 2004).
    2) CASE SERIES: In one study, blurred vision was reported in 6 (50%; n=12) individuals exposed to 1-bromopropane and 1 (6%; n=18) person in the comparison group (NIOSH, 2002).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) Irritation of nose (10 of 24 women and 6 of 13 men) has been reported in factory workers exposed to 1-bromopropane (equal or less than 170 ppm) (Ichihara et al, 2004).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) Sore throat (9 of 24 women and 3 of 13 men) has been reported in factory workers exposed to 1-bromopropane (equal or less than 170 ppm) (Ichihara et al, 2004).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) RESPIRATORY FINDING
    1) WITH POISONING/EXPOSURE
    a) Lung damage may occur following repeated long-term exposure to high levels of 1-bromopropane (Pohanish, 2002).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PULMONARY EDEMA
    a) Following acute exposure to lethal levels of 1-bromopropane (greater than 30,200 mg/m(3) or 6003 ppm), pulmonary edema was noted in animal studies (Anon, 2004).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 19-year-old man developed weakness of the lower extremities and right hand, numbness, dysphagia, and urinary difficulties following a 2-month exposure to a degreasing and cleaning solvent containing 1-bromopropane (95.5%), butylene oxide (less than 0.5%), 1,3-dioxolane (less than 2.5%), and nitromethane (less than 0.25%). Nerve conduction tests showed a primary, symmetric demyelinating polyneuropathy. MRI scans revealed patchy areas of increased T2 signal in the periventricular white matter and root enhancement in the lumbar region of the spinal cord. The authors concluded that this patient was suffering from a symmetric demyelinating polyneuropathy with CNS involvement. However, it is difficult to confirm that these effects were due to exposure to 1-bromopropane (Sclar, 1999; Anon, 2004; 68 FR 33284, 2003).
    b) CASE SERIES: Three women developed signs of peripheral and central nervous system toxicity (eg; stumbling, numbness, urinary incontinence, diarrhea, nausea, difficulty in concentrating, dizziness, and headache) following 1-bromopropane exposure(68 FR 33284, 2003).
    c) CASE SERIES: Malaise, dizziness, lightheadedness, heavy headedness, and headache have been reported in factory workers exposed to 1-bromopropane (equal or less than 170 ppm) (Ichihara et al, 2004; Pohanish, 2002).
    d) CASE SERIES: One study evaluated the neurologic function and other health-related changes in female workers (n=23) exposed to 1-bromopropane, compared with an unexposed control group. Tests with a tuning fork revealed reduced vibration sensation of the foot in 15 workers exposed to 1-bromopropane but in none of the controls (n=23). When compared with controls, 1-bromopropane-exposed workers had a significantly longer distal latency in the tibial nerve, and lower values in sensory nerve conduction velocity in the sural nerve, backward recalled digits, Benton visual memory test scores, pursuit aiming test scores, and give items of the Profile of Mood States (POMS) test (tension, depression, anxiety, fatigue, and confusion). For exposed workers, time-weighted average exposure concentration were 0.34 to 49.19 ppm. The authors concluded that 1-bromopropane exposure could adversely affect peripheral nerves and/or the central nervous system (Ichihara et al, 2004a).
    e) CASE SERIES: One study reported symptoms among 1-bromopropane exposed (n=12) and comparison groups (n=18). The following symptoms were reported: anxiety [2 (17%) exposed vs 2 (11%) control], trouble concentrating [1 (8%) vs 0 (0%)], depression [3 (25%) vs 1 (6%)], dizziness [6 (50%) vs 1 (6%)], felt drunk [1 (8%) vs 0 (0%)], headache [7 (58%) vs 7 (39%)], memory loss [2 (17%) vs 2 (11%)], numbness in hands [3 (25%) vs 3 (17%)], numbness in feet [4 (33%) vs 1 (6%)], sleeping too much [2 (17%) vs 1 (6%)], trouble falling asleep or staying asleep [5 (42%) vs 3 (17%)], tremor or shakiness [2 (17%) vs 1 (6%)], weakness/clumsiness in hands [1 (8%) vs 2(11%)], weakness in arms [3 (25%) vs 3 (17%)], weakness in feet [2 (17%) vs 0 (0%)], weakness in legs [3 (25%) vs 1 (6%)], walking problems [1 (8%) vs 0 (0%)], weight loss [1 (8%) vs 1 (6%)] (NIOSH, 2002).
    f) CASE SERIES: Dizziness, fatigue/lethargy, headache, paresthesia, ataxia, weakness, dysesthesia, hypesthesia, hyperreflexia, and sleep disturbances were reported in 4 furniture makers following 2 to 3 weeks of occupational exposure to a glue containing 70% 1-bromopropane. Serum bromide concentrations ranged from 3 to 12.5 mEq/L and urinary arsenic levels ranged from 200 to 318 mcg/L (normal less than 100 mcg/L). Despite supportive treatment, including succimer administration, and a decline in the serum bromide and urinary arsenic levels, all 4 patients continued to experience persistent symptoms, including ataxia, numbness, paresthesia, and dysesthesia (Raymond & Ford, 2007). The source of arsenic exposure in the patients has not been delineated and it is suspected that arsenic may have been a contributory factor to their symptoms.
    g) CASE SERIES: Daily occupational exposure to 1-bromopropane (1-BP), for 3 to 10 months, in 6 workers in a golf-club cleaning factory resulted in a variety of neurologic effects including paresthesia, lower extremity spasticity and weakness, lower extremity hypo- and hyperreflexia, and an unstable gait. Analysis of the workers urine samples, collected 1 to 26 days post-1-BP exposure, detected and quantified the presence of N-acetyl-S-(n-propyl)-L-cysteine (AcPrCys), a 1-BP metabolite. The urinary AcPrCys concentrations ranged from 0.171 to 2.708 mg/g-Cr, confirming the exposure to 1-BP. It is suggested that AcPrCys, as a urinary specific metabolite of 1-BP, may be a useful and valid urinary biomarker for detection of exposure to 1-bromopropane (Wang et al, 2015).
    h) CASE REPORT: A 43-year-old metal cleaner presented with a 2-month history of progressive weakness and numbness of upper and lower extremities, and gait disturbance. A neurological exam demonstrated mild weakness of distal extremities and decreased ankle reflex bilaterally, decreased pain and temperature sensation in distal lower extremities, and an inability to walk due to severe ataxia. A brain MRI revealed mild brain atrophy with no evidence of lesions and a spinal cord MRI indicated cervical spondylosis without significant compression of the spinal cord. Sural nerve sensory conduction studies indicated a decrease in the sensory nerve action potential and a biopsy of the sural nerve revealed axonal damage. Extensive interview of the patient revealed that he had been using 1-bromopropane (1-BP) as a cleaning agent up to 9.5 hours per day 5 to 6 days per week for 18 months, and the patient had not used a protective mask for the first year of 1-BP exposure. At 2 months after the last exposure, his measured serum bromide concentration was 58 mcg/mL (normal, less than 5 mcg/mL). The estimated level of exposure to 1-BP was a mean time-weighted average of 553 parts per million (ppm) (range, 353 to 663 ppm), confirming a diagnosis of neurotoxicity secondary to 1-BP exposure. Over the next several months, the patient's mobility significantly improved with normalization of his serum bromide concentration (Samukawa et al, 2012).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CENTRAL NERVOUS SYSTEM FINDING
    a) In one animal study, 44 Wistar male rats were randomly divided into 4 groups and were exposed to 200, 400, 800 ppm of 1-bromopropane or only fresh air 8 hours daily for 12 weeks. This study showed that 1-bromopropane induced weakness in the muscle strength of rat limbs and deterioration of maximum motor nerve conduction velocity (MCV), and distal latency (DL), in a concentration-dependent and exposure period-dependent manner. Histopathological studies revealed ovoid or bubble-like debris of myelin in the peripheral nerve, preterminal swelling in the gracile nucleus, and irregular banding of muscle fibers in soleus muscle (Ichihara et al, 2000). In another similar animal study, 1-bromopropane (1000 ppm) caused severe paralysis of hind limbs, decreased MCV, and increased DL after 5 to 7 weeks of exposure (Yu et al, 2001).
    b) In a 28-day inhalation study in rats, microscopic findings of vacuolization of white and gray matter in the central nervous system and decreased brain weight were reported with 1-bromopropane doses of 2 mg/L (400 ppm), 5 mg/L (1,000 ppm), and 8 mg/L (1,600 ppm) 6 hours/day for 5 days/week. However, another 13-week inhalation study did not observe lesions observed in the 28-day study. Another 12-week inhalation study in rats showed that the most sensitive functional neurologic effect of 1-bromopropane was decreased hind limb grip strength with the lowest occupational exposure limit (LOEL) of 200 ppm at 4 weeks into dosing (Rozman & Doull, 2002).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting have been reported following exposure to 1-bromopropane (Ichihara et al, 2004).
    b) CASE SERIES: In one study, nausea was reported in 4 (33%; n=12) subjects exposed to 1-bromopropane and 2 (11%; n=18) subjects in the comparison group (NIOSH, 2002).
    c) Nausea was reported in 3 of 4 furniture makers following occupational exposure to glue containing 70% 1-bromopropane. Serum bromide concentrations, in the 3 patients, ranged from 3 to 9.6 mEq/L (Raymond & Ford, 2007).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In one study, diarrhea was reported in 1 (8%; n=12) individual exposed to 1-bromopropane and 1(6%; n=18) person in the comparison group (NIOSH, 2002).
    b) Watery diarrhea occurred in one patient following 2 weeks of occupational exposure to a furniture glue containing 70% 1-bromopropane (Raymond & Ford, 2007).
    C) DYSPHAGIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 19-year-old man developed weakness of the lower extremities and right hand, numbness, dysphagia, and urinary difficulties following a 2-month exposure to a degreasing and cleaning solvent containing 1-bromopropane (95.5%), butylene oxide (less than 0.5%), 1,3-dioxolane (less than 2.5%), and nitromethane (less than 0.25%). However, it is difficult to confirm that these effects were due to exposure to 1-bromopropane (Sclar, 1999; Anon, 2004; 68 FR 33284, 2003).
    D) WEIGHT LOSS FINDING
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: Anorexia and weight loss of 10 to 25 pounds were reported in 3 of 4 furniture makers who were occupationally exposed to 70% 1-bromopropane (Raymond & Ford, 2007).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER DAMAGE
    1) WITH POISONING/EXPOSURE
    a) Liver damage may occur following repeated long-term exposure to high levels of 1-bromopropane (Pohanish, 2002).
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) In a 13-week inhalation study in rats, vacuolization of the liver and liver enlargement were reported with 1-bromopropane doses of 2 mg/L (400 ppm) and 3 mg/L (600 ppm); a NOEL of 1 mg/L (200 ppm) was estimated for this effect (Rozman & Doull, 2002).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) DISORDER OF MENSTRUATION
    1) WITH POISONING/EXPOSURE
    a) In one study, disruption or failure of menstruation were observed in 4 of 24 female factory workers exposed to 1-bromopropane (equal or less than 170 ppm). Workers with amenorrhea had high gonadotropin levels; moderate estradiol levels were observed in women with irregular menses (Ichihara et al, 2004). However, the authors could not confirm that these effects were due to exposure to 1-bromopropane because of the small number of subjects and the lack of appropriate controls.
    B) FINDING OF URINARY TRACT PROPER
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 19-year-old man developed weakness of the lower extremities and right hand, numbness, dysphagia, and urinary difficulties following a 2-month exposure to a degreasing and cleaning solvent containing 1-bromopropane (95.5%), butylene oxide (less than 0.5%), 1,3-dioxolane (less than 2.5%), and nitromethane (less than 0.25%). However, it is difficult to confirm that these effects were due to exposure to 1-bromopropane (Sclar, 1999; Anon, 2004; 68 FR 33284, 2003).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) HEMATOLOGY FINDING
    1) WITH POISONING/EXPOSURE
    a) In one study, low values of red blood cells, hemoglobin, or hematocrit were observed in 10 of 24 female and 4 of 13 male factory workers exposed to 1-bromopropane (equal or less than 170 ppm) (Ichihara et al, 2004). However, the authors could not confirm that these effects were due to exposure to 1-bromopropane because of the small number of subjects and the lack of appropriate controls.
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) In a 28-day inhalation study in rats, severe toxicity (low values of red blood cells, hemoglobin, or hematocrit) occurred with 1-bromopropane doses of 5 mg/L (1,000 ppm), and 8 mg/L (1,600 ppm). Death occurred when rats were exposed to 1-bromopropane 8 mg/L (1,600 pm) 6 hours/day for 5 days/week (Rozman & Doull, 2002).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Dermatitis has been reported following exposure to 1-bromopropane (Pohanish, 2002).

Reproductive

    3.20.1) SUMMARY
    A) Decreased fetal weight and increased incidence of skeletal variations have been reported in rats exposed to 1-bromopropane by inhalation. In animal studies, decreased fertility, decreased numbers of implantation sites and litter size, and increased precoital interval were observed after exposure to 1-bromopropane. In addition, reduced prostate weight, and effects on seminal vesicle weight and sperm quality at higher levels were observed.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) In prenatal developmental toxicity Crl:CD rats studies, decreased fetal weight and increased incidence of skeletal variations were observed in rats exposed to 1-bromopropane by inhalation on a daily basis during the period of in utero development. These reversible skeletal effects were reported in pups whose dams were exposed to levels of 503 ppm (2530 mg/m(3)) or higher for 6 hours daily (Anon, 2004).
    3.20.5) FERTILITY
    A) ANIMAL STUDIES
    1) In a two-generation inhalation study in Crl:CD rats, decreased fertility, decreased numbers of implantation sites and litter size and increased precoital interval were observed after exposure at levels of 500 ppm (2514 mg/m(3)) and higher, effecting either the male or female parents (Anon, 2004).
    2) Prostate weight was decreased at levels of 250 ppm (1257 mg/m(3)) and higher. In addition, effects on seminal vesicle weight and sperm quality and count at higher levels were observed (Anon, 2004).
    3) In females, an increase in ovarian follicular cysts at 750 ppm (3771 mg/m(3)) was observed. In addition, an increase in estrous cycle length with levels of 250 ppm (1257 mg/m(3)) and higher were noted (Anon, 2004).
    4) In subchronic inhalation study in male Wistar rats, effects on reproductive organ weights were observed at the lowest levels tested (200 ppm [1006 mg/m(3)]). In histopathologic tests, inhibited spermiation was noted at levels of 400 ppm (2012 mg/m(3)) and higher (Anon, 2004).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS106-94-5 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) No information could be found on the potential carcinogenicity of 1-bromopropane in humans.

Genotoxicity

    A) In studies, 1-bromopropane was an extremely weak genotoxic agent (Rozman & Doull, 2002).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Monitor arterial blood gas, pulse oximetry, and chest x-ray in patients with hypoxia or respiratory distress.
    C) Monitor fluid and electrolyte status in patients with significant vomiting and/or diarrhea.
    D) Evaluate for signs/symptoms of muscle weakness, paresthesias, and ataxia.
    E) Monitor liver function as indicated in symptomatic patients.
    F) Urinary measurement of N-acetyl-S-(n-propyl)-L-cysteine (AcPrCys), a urinary specific 1-bromopropane metabolite, may be a useful biomarker of 1-bromopropane exposure.
    4.1.2) SERUM/BLOOD
    A) Monitor liver function as indicated in symptomatic patients.
    B) Monitor fluid and electrolyte status in patients with significant vomiting and/or diarrhea.
    4.1.3) URINE
    A) One study showed that the urinary excretion of 1-bromopropane correlated significantly with the exposure level measured on the same day. The authors concluded that the urine concentration of 1-bromopropane may be a reliable biomarker of acute 1-bromopropane exposure (Ichihara et al, 2004).
    B) Daily occupational exposure to 1-bromopropane (1-BP), for 3 to 10 months, in 6 workers in a golf-club cleaning factory resulted in a variety of neurologic effects including paresthesia, lower extremity spasticity and weakness, lower extremity hypo- and hyperreflexia, and an unstable gait. Analysis of the workers urine samples, collected 1 to 26 days post 1-BP exposure, detected and quantified the presence of N-acetyl-S-(n-propyl)-L-cysteine (AcPrCys), a 1-BP metabolite. The urinary AcPrCys concentrations ranged from 0.171 to 2.708 mg/g-Cr, confirming the exposure to 1-BP. It is suggested that AcPrCys, as a urinary specific metabolite of 1-BP, may be a useful and valid urinary biomarker for detection of exposure to 1-bromopropane, because there may be less occupational interference and AcPrCys levels appear to increase with increasing 1-BP ambient exposure (Wang et al, 2015).
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor vital signs and mental status.
    b) Monitor arterial blood gas, pulse oximetry, and chest x-ray in patients with hypoxia or respiratory distress.
    c) Evaluate for signs/symptoms of muscle weakness, paresthesias, and ataxia.

Methods

    A) CHROMATOGRAPHY
    1) Urinary 1-bromopropane levels were measured using gas chromatography (Ichihara et al, 2004).
    2) Gas chromatography and thin liquid chromatography were used to detect 1-bromopropane metabolites in rat studies (Anon, 2004) .
    3) Liquid chromatography/mass spectrometry was used to detect a urinary specific 1-bromopropane metabolite, N-acetyl-S-(n-propyl)-L-cysteine (AcPrCys), in urine samples of workers occupationally exposed to 1-bromopropane (Wang et al, 2015).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.1) ADMISSION CRITERIA/INHALATION
    A) Only patients with systemic toxicity may require admission.
    6.3.3.2) HOME CRITERIA/INHALATION
    A) Patients who are asymptomatic or with minimal symptoms after exposure to 1-bromopropane and are otherwise improving may be managed at home.
    6.3.3.3) CONSULT CRITERIA/INHALATION
    A) Consult a regional poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Patients who are symptomatic need to be monitored until they are clearly improving and clinically stable.

Monitoring

    A) Monitor vital signs and mental status.
    B) Monitor arterial blood gas, pulse oximetry, and chest x-ray in patients with hypoxia or respiratory distress.
    C) Monitor fluid and electrolyte status in patients with significant vomiting and/or diarrhea.
    D) Evaluate for signs/symptoms of muscle weakness, paresthesias, and ataxia.
    E) Monitor liver function as indicated in symptomatic patients.
    F) Urinary measurement of N-acetyl-S-(n-propyl)-L-cysteine (AcPrCys), a urinary specific 1-bromopropane metabolite, may be a useful biomarker of 1-bromopropane exposure.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Toxicity after an acute ingestion is unlikely. Gastrointestinal decontamination is generally unnecessary.
    B) Primary routes of exposure are inhalational and dermal.
    1) INHALATION EXPOSURE: Monitor for respiratory distress. If cough or difficulty breathing develops, administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    2) DERMAL EXPOSURE: Remove contaminated clothing and wash exposed area extremely thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists after washing.
    C) EYE EXPOSURE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed.
    6.5.2) PREVENTION OF ABSORPTION
    A) Toxicity after an acute ingestion is unlikely. Gastrointestinal decontamination is generally unnecessary. Consider activated charcoal only if coingestants with significant toxicity are involved.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) Refer to INHALATION EXPOSURE section for treatment recommendations.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive. Correct any significant fluid and/or electrolyte abnormalities in patients with severe diarrhea and/or vomiting.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. Monitor mental status and evaluate for signs/symptoms of muscle weakness, paresthesias, and ataxia.
    B) MONITORING OF PATIENT
    1) Monitor vital signs and mental status.
    2) Monitor arterial blood gas, pulse oximetry, and chest x-ray in patients with hypoxia or respiratory distress.
    3) Monitor fluid and electrolyte status in patients with significant vomiting and/or diarrhea.
    4) Evaluate for signs/symptoms of muscle weakness, paresthesias, and ataxia.
    5) Monitor liver function as indicated in symptomatic patients.
    6) Urinary measurement of N-acetyl-S-(n-propyl)-L-cysteine (AcPrCys), a urinary specific 1-bromopropane metabolite, may be a useful biomarker of 1-bromopropane exposure.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

    A) HEMODIALYSIS
    1) It is unknown if hemodialysis or other enhanced elimination techniques are likely to be useful following a 1-bromopropane exposure.

Range Of Toxicity

Summary

    A) TOXICITY: A specific minimum toxic concentration has not been established. Time-weighted average (TWA) exposure concentrations were 0 to 170.5 parts per million (ppm) in workers occupationally exposed to 1-bromopropane and reported symptoms of dizziness, light- or heavy-headedness, headache, feelings of intoxication, and irritation of mucous membranes. The ambient air concentrations of 1-bromopropane were 3.3 to 90.2 ppm. The American Conference of Governmental Industrial Hygienists (ACGIH) has recommended the TLV-TWA occupational exposure limit of 10 ppm.

Maximum Tolerated Exposure

    A) HUMAN
    1) Female factory workers from a 1-bromopropane production facility in China exhibited signs suggesting 1-bromopropane neurotoxicity. Exposed workers had significantly increased distal latency in tibial nerves, lower values in sensory nerve conduction velocity in sural nerves, and lower scores on neurological function tests, as compared with controls. Time weighted average exposure concentrations of 1-bromopropane ranged from 0.34 parts per million (ppm) to 49.19 ppm (Ichihara et al, 2004a).
    2) Workers exposed to 1-bromopropane in a factory setting reported symptoms of dizziness, light- or heavy-headedness, headache, feelings of intoxication, and irritation of mucous membranes. Time-weighted average exposure concentrations and ambient air concentrations of 1-bromopropane were 0 to 170.5 ppm and 3.3 to 90.2 ppm, respectively (Ichihara et al, 2004).
    3) The American Conference of Governmental Industrial Hygienists (ACGIH) has recommended the TLV-TWA occupational exposure limit of 10 ppm (Wang et al, 2015).

Workplace Standards

    A) ACGIH TLV Values for CAS106-94-5 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) 1-Bromopropane
    a) TLV:
    1) TLV-TWA: 10 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): Liver and embryo/fetal dam; neurotoxicity
    d) Molecular Weight: 122.99
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:
    b) Under Study
    1) 1-Bromopropane
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s):
    d) Molecular Weight:
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS106-94-5 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS106-94-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: 1-Bromopropane
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: 1-Bromopropane
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    4) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    6) MAK (DFG, 2002): Not Listed
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS106-94-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (INTRAPERITONEAL)MOUSE:
    1) 1210 mg/kg (RTECS, 2004)
    2) 1350 mg/kg for 5D - intermittent -- degenerative changes to brain (RTECS, 2004)
    B) LD50- (ORAL)MOUSE:
    1) 4700 mg/kg (RTECS, 2004)
    C) LD50- (INTRAPERITONEAL)RAT:
    1) 2950 mg/kg (RTECS, 2004)
    D) LD50- (ORAL)RAT:
    1) 3600 mg/kg (RTECS, 2004)
    E) TCLo- (INHALATION)RAT:
    1) 821 ppm for 8H, male, 12W prior to mating -- affected spermatogenisis (RTECS, 2004)
    2) 200 ppm for 8H, male, 12W prior to mating -- affected prostate, seminal vesicle, Cowper's and accessory glands (RTECS, 2004)
    3) 98408 mg/m(3) for 30min. for 1W - intermittent -- affected respiration; hemorrhages (RTECS, 2004)
    4) 1800 ppm for 6H for 8W - intermittent -- changes in liver weight; weight loss or decreased weight gain (RTECS, 2004)
    5) 400 ppm for 8H for 12W - intermittent -- changes to nerve structure (RTECS, 2004)

Physicochemical

Physical Characteristics

    A) 1-Bromopropane is a colorless liquid that is slightly denser than, and slightly soluble in, water (CHRIS, 2004; HSDB, 2004; AAR, 2002).

Molecular Weight

    A) 122.99

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