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2-BROMOPROPANE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) 2-Bromopropane is a halogenated organic solvent.

Specific Substances

    1) 2-BP
    2) 2-Bromopropane
    3) iPB
    4) Isopropyl bromide
    5) Isopropylbromide
    6) Propane, 2-bromo-
    7) sec-Propyl bromide
    8) Molecular Formula: C3H7Br
    9) CAS #: 75-26-3
    10) BROMOPROPANES
    1.2.1) MOLECULAR FORMULA
    1) C3H7Br
    2) (CH3)2-CH-Br

Available Forms Sources

    A) FORMS
    1) 2-Bromopropane exists as a colorless liquid (HSDB, 2004).
    B) SOURCES
    1) 2-Bromopropane is produced by heating isopropyl alcohol with hydrogen bromide (HSDB, 2004; Merck & Co., 2003; Ashford, 2001).
    C) USES
    1) As an alternative to ozone-depleting solvents, 2-Bromopropane gained increased industrial use in cleaning and spray adhesive applications. However, as its toxic effects were identified, 1-bromopropane was almost entirely substituted for 2-bromopropane in these applications. Currently, the US Environmental Protection Agency restricts the presence of 2-bromopropane in commercial bromopropane solvents in certain end-use applications to 0.05% (68 FR 33284, 2003).
    2) It is also used in chemical processes for the synthesis of pharmaceuticals, dyes, and other organic compounds (HSDB, 2004).

Overview

Laboratory Monitoring

    A) Monitor vital signs, electrocardiogram, and adequacy of respirations. Monitor CBC after chronic excessive exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    C) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: 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, the patient should be seen in a healthcare facility.
    B) CAUSTIC EYE DECONTAMINATION: Immediately irrigate each affected eye with copious amounts of water or sterile 0.9% saline for about 30 minutes. Irrigating volumes up to 20 L or more have been used to neutralize the pH. After this initial period of irrigation, the corneal pH may be checked with litmus paper and a brief external eye exam performed. Continue direct copious irrigation with sterile 0.9% saline until the conjunctival fornices are free of particulate matter and returned to pH neutrality (pH 7.4). Once irrigation is complete, a full eye exam should be performed with careful attention to the possibility of perforation.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

Range Of Toxicity

    A) At the time of review, minimum lethal and maximum tolerated exposure levels for 2-bromopropane have not been determined.

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) WITH POISONING/EXPOSURE
    1) Occupational exposure may occur through inhalation, ingestion, and skin. Hematological or reproductive toxicity may occur following exposure to more than 10 ppm for a prolonged period. Ovarian failure, amenorrhea, high follicle-stimulating hormone levels, irregular menstrual periods, hot flashes, azoospermia, and oligospermia have been reported following inhalational exposure to 2-bromopropane. Headache, dizziness, weakness, anemia, and leukopenia have also been reported.
    0.2.20) REPRODUCTIVE
    A) Reproductive toxicity may occur following exposure to more than 10 ppm for a prolonged period. Ovarian dysfunction with amenorrhea, and high follicle-stimulating hormone levels have been reported in humans following exposure to 2-bromopropane. In addition, azoospermia, oligospermia, or reduced sperm motility have been reported in humans following exposure to 2-bromopropane.
    B) Although one woman developed ovarian failure following exposure to 2-bromopropane for 16 months, she eventually became pregnant and delivered a healthy full-term baby.

Clinical Effects

Summary Of Exposure

    A) WITH POISONING/EXPOSURE
    1) Occupational exposure may occur through inhalation, ingestion, and skin. Hematological or reproductive toxicity may occur following exposure to more than 10 ppm for a prolonged period. Ovarian failure, amenorrhea, high follicle-stimulating hormone levels, irregular menstrual periods, hot flashes, azoospermia, and oligospermia have been reported following inhalational exposure to 2-bromopropane. Headache, dizziness, weakness, anemia, and leukopenia have also been reported.

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) Headache, dizziness, or weakness have been reported in workers exposed to a cleaning solution containing 97.4% 2-bromopropane for an average duration of 10 months (range 2 to 14 months). The ambient levels of 2-bromopropane measured under simulated work conditions were 9.2 to 19.6 ppm in 14 stationary samples from the tactile switch assembling room (Kim et al, 1999; Kim et al, 1996).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CENTRAL NERVOUS SYSTEM FINDING
    a) Peripheral neuropathy has been reported in rats following long-term exposure to 1000 ppm of 2-bromopropane (Yu et al, 1999b). In one study, significant decreases in body weight and motor nerve conduction velocity (MCV) and elongation in distal latency (DL) were observed in animals following exposure to 1000 ppm of 2-bromopropane. In addition, a ball-like enlargement of myelin sheaths was noted (Yu et al, 2001).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) OVARIAN FAILURE
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES - In one report, ovarian dysfunction with amenorrhea, high follicle-stimulating hormone levels, normal prolactin levels, and hot flashes developed in 17 of 25 female workers exposed to a cleaning solution containing 97.4% 2-bromopropane for an average duration of 10 months (range 2 to 14 months). The ambient levels of 2-bromopropane measured under simulated work conditions were 9.2 to 19.6 ppm in 14 stationary samples from the tactile switch assembling room (Kim et al, 1999; Yu et al, 1999; Kim et al, 1996).
    b) CASE SERIES - In another study, 26 female workers exposed to 2-bromopropane (solvent #5200) for 4 to 16 months developed amenorrhea and irregular menstrual periods. Sixteen of 26 workers were diagnosed with primary ovarian failure. Elevated serum luteinizing hormone (LH) and follicle-stimulating hormone (greater than 30 mIU(International Units)/mL) with low estradiol (less than 30 pg/mL) were observed. During the follow-up of 24 months, most cases still had amenorrhea although 2 patients spontaneously recovered from primary ovarian failure (Koh et al, 1998). In another case series, amenorrhea or polymenorrhea was observed only in older females (39 to 54 years) following exposure to 2-bromopropane (Ichihara et al, 1999).
    c) CASE REPORT - A female worker developed an irregular menstrual cycle after exposure to 4.14 ppm of 2-bromopropane for 5 years (Yu et al, 1999).
    B) AZOOSPERMIA
    1) WITH POISONING/EXPOSURE
    a) Eight 8 workers were exposed to a cleaning solution containing 97.4% 2-bromopropane for an average duration of 10 months. Two developed azoospermia and 4 developed some degree of oligospermia (sperm count less than 20 million/mL) or reduced sperm motility. The ambient levels of 2-bromopropane measured under simulated work conditions were 9.2 to 19.6 ppm in 14 stationary samples from the tactile switch assembling room (Kim et al, 1999; Yu et al, 1999; Kim et al, 1996).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) OVARIAN DYSFUNCTION
    a) One animal study reported that 2-bromopropane may damage primordial follicles and their oocytes in female rats resulting in ovarian dysfunction. This cell damage was due to wide-scale apoptosis in these follicles (Yu et al, 1999a).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) HEMATOLOGY FINDING
    1) WITH POISONING/EXPOSURE
    a) Hematological toxicity may occur following exposure to more than 10 ppm for a prolonged period (Ichihara et al, 1999; Yu et al, 1999).
    b) In one report, ovarian dysfunction with amenorrhea developed in 17 of 25 female workers exposed to a cleaning solution containing 97.4% 2-bromopropane for an average duration of 10 months (range 2 to 14 months). In addition, 8 workers with amenorrhea had pancytopenia. The bone marrow biopsy of 2 patients revealed marked hypoplastic marrow (15% and 25% cellularity, respectively). Other women experienced mild anemia or mild leukopenia. The ambient levels of 2-bromopropane measured under simulated work conditions were 9.2 to 19.6 ppm in 14 stationary samples from the tactile switch assembling room (Kim et al, 1999; Yu et al, 1999; Kim et al, 1996).
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) In one animal study, exposure to 1000 ppm of 2-bromopropane caused significant reductions in the number of erythrocytes, platelets, and leukocytes (Jeong & Lee, 2002; Yu et al, 2001).
    2) In one study, repeated doses of 2-bromopropane (125, 250, and 500 mg/kg) were injected into the peritoneum of male Sprague Dawley rats for a 28-day period. Following the high dose, reduction in the red blood cells, hemoglobin, hematocrit, the mean platelet volume, the number of white blood cells, and the number of lymphocytes were observed. The number of granulocytes and monocytes decreased depending on the dose of 2-bromopropane (Yu et al, 1999; Yu et al, 1997). 2-Bromopropane may induce leukopenia and normocytic anemia (Yu et al, 1997).

Immunologic

    3.19.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IMMUNOTOXICITY
    a) In one study, mice were treated orally with either 2-bromopropane at 2000 and 4000 mg/kg or 1,2-dibromopropane (2-bromopropane analog) at 300 and 600 mg/kg. The mice were immunized intraperitoneally with sheep red blood cells (SRBCs) 4 days before necropsy. It was determined that the antibody response was significantly suppressed by treatment with 2-bromopropane (Kim et al, 2003).
    b) Following a 28-day exposure of male Sprague-Dawley rats to 2-bromopropane (100, 330, or 1000 mg/kg), a significant suppression of antibody response to sheep red blood cells (SRBCs) was observed. Following treatment with 1000 mg/kg, the numbers of most cell types were significantly decreased in the spleen (Jeong & Lee, 2002). Another study showed that the number of white blood cells decreased significantly when rats were exposed to 2-bromopropane (Yu et al, 1997).

Reproductive

    3.20.1) SUMMARY
    A) Reproductive toxicity may occur following exposure to more than 10 ppm for a prolonged period. Ovarian dysfunction with amenorrhea, and high follicle-stimulating hormone levels have been reported in humans following exposure to 2-bromopropane. In addition, azoospermia, oligospermia, or reduced sperm motility have been reported in humans following exposure to 2-bromopropane.
    B) Although one woman developed ovarian failure following exposure to 2-bromopropane for 16 months, she eventually became pregnant and delivered a healthy full-term baby.
    3.20.2) TERATOGENICITY
    A) LACK OF EFFECT
    1) Although one woman developed ovarian failure following exposure to 2-bromopropane for 16 months, she eventually became pregnant and delivered a healthy full-term baby (Koh et al, 1998).
    B) ANIMAL STUDIES
    1) One animal study evaluated the potential adverse effects of 2-bromopropane (0, 250, 500, and 1000 mg/kg/day subcutaneously) on pregnant dams and embryo-fetal development after maternal exposure on gestational days 6 through 19 in Sprague-Dawley rats. All fetuses were examined for external, visceral and skeletal abnormalities on gestational day 20. A suppression in the body weight and body weight gain, and a decrease in the food intake indicating maternal toxicity were observed following the 1000 mg/kg/day dose. An increase in the fetal deaths, a decrease in the litter size, a reduction in the fetal body weight, and an increase in the incidence of fetal external, visceral, and skeletal abnormalities were also seen. Although no adverse effects on either pregnant dams or embryo-fetal development were observed in the 250 mg/kg group, minimal developmental toxicity such as decreased fetal body weight and increased fetal ossification delay were observed in the 500 mg/kg group. The authors concluded that 2-bromopropane was embryotoxic at a nonmaternotoxic dose (500 mg/kg/day) and was embryolethal and teratogenic at a maternotoxic dose (1000 mg/kg/day) in pregnant rats. In addition, the no-observed-adverse-effect level (NOAEL) of 2-bromopropane was 500 mg/kg/day for dams and 250 mg/kg/day for embryo-fetal development (Kim et al, 2004).
    3.20.3) EFFECTS IN PREGNANCY
    A) REPRODUCTIVE EFFECTS
    1) Reproductive toxicity may occur following exposure to more than 10 ppm for a prolonged period (Ichihara et al, 1999; Yu et al, 1999).
    2) Although one woman developed ovarian failure following exposure to 2-bromopropane for 16 months, she eventually became pregnant and delivered a healthy full-term baby (Koh et al, 1998).
    B) ANIMAL STUDIES
    1) In one animal study, Sprague-Dawley rats were exposed by inhalation to 2-bromopropane (0 [control], 125, 250, 500, or 1000 ppm) for 6 hours per day, 7 days per week during 2 weeks of the pre-mating period, during the mating period until copulation and during the period of gestation days 0 to 19. Although no maternal toxicity was noted, exposure to 1000 ppm markedly reduced the number of pups born; however, the number of implantations did not decrease. 2-Bromopropane exposure did not effect pups weights or survival until postnatal day 4. It was concluded that the repeated inhalation exposure of rats to 1000 ppm 2-bromopropane induced fetal lethality during the post-implantation period (Takeuchi et al, 2004).
    2) One animal study evaluated the potential adverse effects of 2-bromopropane (0, 250, 500, and 1000 mg/kg/day subcutaneously) on pregnant dams and embryo-fetal development after maternal exposure on gestational days 6 through 19 in Sprague-Dawley rats. All fetuses were examined for external, visceral and skeletal abnormalities on gestational day 20. A suppression in the body weight and body weight gain, and a decrease in the food intake indicating maternal toxicity were observed following the 1000 mg/kg/day dose. An increase in the fetal deaths, a decrease in the litter size, a reduction in the fetal body weight, and an increase in the incidence of fetal external, visceral, and skeletal abnormalities were also seen. Although no adverse effects on either pregnant dams or embryo-fetal development were observed in the 250 mg/kg group, minimal developmental toxicity such as decreased fetal body weight and increased fetal ossification delay were observed in the 500 mg/kg group. The authors concluded that 2-bromopropane was embryotoxic at a nonmaternotoxic dose (500 mg/kg/day) and was embryolethal and teratogenic at a maternotoxic dose (1000 mg/kg/day) in pregnant rats. In addition, the no-observed-adverse-effect level (NOAEL) of 2-bromopropane was 500 mg/kg/day for dams and 250 mg/kg/day for embryo-fetal development (Kim et al, 2004).
    3.20.5) FERTILITY
    A) AZOOSPERMIA
    1) CASE SERIES - After 8 workers were exposed to a cleaning solution containing 97.4% 2-bromopropane for an average duration of 10 months, 2 developed azoospermia and 4 developed some degree of oligospermia (sperm count less than 20 million/mL) or reduced sperm motility. The ambient levels of 2-bromopropane measured under simulated work conditions were 9.2 to 19.6 ppm in 14 stationary samples from the tactile switch assembling room (Kim et al, 1999; Yu et al, 1999; Kim et al, 1996).
    B) OVARIAN DYSFUNCTION
    1) CASE SERIES - In one report, ovarian dysfunction with amenorrhea, high follicle-stimulating hormone levels, normal prolactin levels, and hot flashes developed in 17 of 25 female workers exposed to a cleaning solution containing 97.4% 2-bromopropane for an average duration of 10 months (range 2 to 14 months). The ambient levels of 2-bromopropane measured under simulated work conditions were 9.2 to 19.6 ppm in 14 stationary samples from the tactile switch assembling room (Kim et al, 1999; Yu et al, 1999; Kim et al, 1996).
    C) ANIMAL STUDIES
    1) In one animal study, exposure to 1000 ppm of 2-bromopropane resulted in testicular germ cell loss, and seminiferous atrophy (Yu et al, 2001).
    2) In another study, repeated doses of 2-bromopropane (125, 250, and 500 mg/kg) were injected into the peritoneum of male Sprague Dawley rats for a 28-day period. Following the middle and high 2-bromopropane doses, the histopathology of the testes revealed a typical patch appearance with severely depleted atrophic tubules, exhibiting germ cell necrosis of spermatogonia and spermatocytes in the seminiferous tubules. In addition, Leydig cell hyperplasia or hypertrophy in the interstitial tissue was observed. The epididymis revealed some degree of atrophy with vacuolization of the epididymal epithelium (Yu et al, 1997).
    3) In one animal study, Sprague-Dawley rats were exposed by inhalation to 2-bromopropane (0 [control], 125, 250, 500, or 1000 ppm) for 6 hours per day, 7 days per week during 2 weeks of the pre-mating period, during the mating period until copulation and during the period of gestation days 0 to 19. It was found that the ability of females to copulate and become pregnant was normal following inhalation exposure to 2-bromopropane at 4 different concentrations at least for 2 weeks. In addition, 2-bromopropane did not affect the ability of the exposed males to copulate and impregnate the females exposed to 2-bromopropane at the same levels (Takeuchi et al, 2004).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS75-26-3 (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

Genotoxicity

    A) 2-Bromopropane did not induce chromosome aberrations in Chinese hamster lung cells with or without metabolic activation in vitro. In addition, it did not induce micronucleus in the rat bone marrow cells in vivo (Maeng & Yu, 1997; Yu et al, 1999).
    B) 2-Bromopropane was mutagenic in reverse mutation assays using Salmonella typhimurium TA 100 and TA 1535, revealing a dose-response relationship. It showed that 2-bromopropane induced the base-pair substitution type mutations in Salmonella strains (Maeng & Yu, 1997; Yu et al, 1999).
    C) One study reported that 2-bromopropane induces DNA damage, impairs functional antioxidant cellular defenses, and enhances the lipid peroxidation in cultured rat Leydig cells (Wu et al, 2002).

Laboratory Monitoring

Methods

    A) GAS CHROMATOGRAPHY
    1) In one study, a static-headspace gas chromatogram equipped with an electron capture detector were used to monitor the levels of 1- and 2-bromopropane in human urine. The limit of detection in urine was 2 ng/mL for 1-bromopropane and 7 ng/mL for 2-bromopropane (Hymer & Cheever, 2005).
    2) One study used a gas chromatographic method to obtain 2-bromopropane levels following percutaneous absorption (Boekelheide et al, 2004).

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs, electrocardiogram, and adequacy of respirations. Monitor CBC after chronic excessive exposure.
    4.1.2) SERUM/BLOOD
    A) URINE
    1) 2-Bromopropane is hydrolyzed to isopropyl alcohol and bromide ion, followed by oxidation of the alcohol to acetone and excretion of bromide and acetone through urine. In one study, urinary concentrations of 2-bromopropane, bromide ion, acetone, and isopropyl alcohol were obtained in 5 Japanese workers exposed to 2-bromopropane (mean area concentration of 3 mg/m(3) (0.6 ppm)). Highest level of 2-bromopropane was obtained in only one worker; his urinary levels of acetone and bromide exceeded levels found in unexposed controls. Concentrations of 2-bromopropane and isopropyl alcohol were not detected in the urine of workers or non-exposed controls (Boekelheide et al, 2004).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

Monitoring

    A) Monitor vital signs, electrocardiogram, and adequacy of respirations. Monitor CBC after chronic excessive exposure.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    1) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    a) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    b) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    B) CHARCOAL DOSE
    1) 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).
    a) 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).
    2) ADVERSE EFFECTS/CONTRAINDICATIONS
    a) 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.
    b) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) 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) OBSERVATION REGIMES
    1) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    B) HOSPITAL ADMISSION
    1) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

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) OBSERVATION REGIMES
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    2) Monitor vital signs, electrocardiogram, and adequacy of respirations.
    B) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    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).
    6.9.2) TREATMENT
    A) SKIN ABSORPTION
    1) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EFFICACY
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.

Range Of Toxicity

Summary

    A) At the time of review, minimum lethal and maximum tolerated exposure levels for 2-bromopropane have not been determined.

Minimum Lethal Exposure

    A) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) The maximum tolerated human exposure to this agent has not been delineated.
    B) ANIMAL
    1) Rats exposed to 1000 ppm 2-bromopropane, 8 hours a day for 12 weeks, showed significant reduction in body weights and evidence of peripheral neuropathy, including significantly decreased motor nerve conduction velocity and prolonged distal latency in tail nerves. However, researchers observed no overt changes in neurobehavior. Significant hematological effects included reductions in number of erythrocytes, platelets, and leukocytes. Testicular germ cell loss and seminiferous atrophy were also observed (Yu et al, 2001).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) URINE - 2-Bromopropane is hydrolyzed to isopropyl alcohol and bromide ion. The alcohol is oxidized to acetone. Both the acetone and bromide ion are excreted in the urine. In one study, urinary concentrations of 2-bromopropane, bromide ion, acetone, and isopropyl alcohol were obtained in 5 Japanese workers exposed to 2-bromopropane (mean area concentration of 3 mg/m(3) (0.6 ppm)). Highest level of 2-bromopropane was obtained in only one worker; his urinary levels of acetone and bromide exceeded levels found in unexposed controls. Concentrations of 2-bromopropane and isopropyl alcohol were not detected in the urine of workers or non-exposed controls (Boekelheide et al, 2004).

Workplace Standards

    A) ACGIH TLV Values for CAS75-26-3 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS75-26-3 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS75-26-3 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) 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
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS75-26-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (INTRAPERITONEAL)MOUSE:
    1) 483.7 mg/kg (RTECS, 2004)
    B) TCLo- (INHALATION)RAT:
    1) 1000 ppm for 6H -- male (RTECS, 2004)
    2) 172 g/m(3) for 30 minutes for 14D, intermittent -- respiratory changes; hemorrhage (RTECS, 2004)
    3) 2000 ppm for 6H for 14D, intermittent -- changes in testicular weight (RTECS, 2004)
    4) 300 ppm for 8H for 9W, intermittent -- changes to the endocrine system (RTECS, 2004)

Physicochemical

Physical Characteristics

    A) 2-Bromopropane exists as a colorless liquid (HSDB, 2004).

Molecular Weight

    A) 122.99

References

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