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DIBROMOCHLOROPROPANE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Dibromochloropropane is used as a nematocide and soil fumigant. It has been banned from production or application in the United States since 1977 (Sittig, 1991). It is still used in other parts of the world (Clayton & Clayton, 1981).

Specific Substances

    1) DBCP
    2) 1,2-dibromo-3-chloropropane
    3) 3-chloro-1, 2-dibromopropane
    4) Molecular Formula: C3-H5-Br2-Cl
    5) NIOSH/RTECS TX 8750000
    6) CAS 96-12-8
    7) DBCP (DIBROMOCHLOROPROPANE)
    8) NEMAGON SOIL FUMAGANT
    9) NEMAPAX
    1.2.1) MOLECULAR FORMULA
    1) C3-H5-Br2-Cl

Available Forms Sources

    A) FORMS
    1) Dibromochloropropane is a dense yellow, amber or brown liquid (technical grade) with a pungent odor at high concentrations (Budavari, 1996; NIOSH , 1998). When pure, dibromochloropropane is a colorless liquid (HSDB , 1998).
    2) Some trade names include: Fumazone, Nemagon, Nemafume, Nemaset, and Nematox (Budavari, 1996; RTECS , 1998).
    B) USES
    1) Dibromochloropropane was used as a soil fumigant and nematocide in the United States until 1977 and has been used as a intermediate in organic synthesis (HSDB , 1998) US Dept Health & Human Services, 1989).
    2) Dibromochloropropane was first produced commercially in the United States in 1955. It was banned for agricultural use in 1977 except for restricted use on pineapple in Hawaii. In 1985, this exception was revoked (US Dept Health & Human Services, 1989).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) DBCP is a testicular toxicant in experimental animals and humans. It is a mild eye and mucous membrane irritant and CNS depressant, and liver and renal toxicant.
    B) DBCP has been shown to be carcinogenic in experimental animals.
    0.2.4) HEENT
    A) DBCP is an eye irritant, but is not caustic.
    0.2.7) NEUROLOGIC
    A) CNS depression has been reported in experimental animal studies.
    0.2.9) HEPATIC
    A) Liver injury has been noted in experimental animal studies.
    0.2.14) DERMATOLOGIC
    A) Repeated exposure may cause skin necrosis; single one-time exposure appears to have little effect.
    0.2.20) REPRODUCTIVE
    A) No teratogenic effects have been found in rat studies. Placental transfer has been documented in rats.
    B) No increased risk of spontaneous abortion or fetal malformation was reported in a study of conceiving couples when the father had been exposed to DBCP.

Laboratory Monitoring

    A) No toxic levels have been established.

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.
    B) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    C) TESTICULAR FUNCTION - Men exposed to DBCP should have baseline and regular sperm counts.
    D) Chronic DBCP exposure may cause liver and kidney damage.
    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.
    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.
    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) The no-effect level in the rabbit via inhalation is 0.1 ppm, and orally is 0.05 mg/kg. CNS depression occurs at about 60 ppm.
    B) Toxic levels for humans have not been established.

Clinical Effects

Summary Of Exposure

    A) DBCP is a testicular toxicant in experimental animals and humans. It is a mild eye and mucous membrane irritant and CNS depressant, and liver and renal toxicant.
    B) DBCP has been shown to be carcinogenic in experimental animals.

Heent

    3.4.1) SUMMARY
    A) DBCP is an eye irritant, but is not caustic.
    3.4.3) EYES
    A) IRRITATION - DBCP is an eye irritant but is not caustic. The liquid applied undiluted to rabbit eyes caused transient irritation (Torkelson & Sadek, 1961).
    B) CHRONIC - Permanent eye damage may occur from repeated vapor exposure (Gosselin et al, 1984).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) ACUTE LUNG INJURY
    1) Non-cardiogenic pulmonary edema may result following acute ingestion of DBCP (Gosselin et al, 1984).

Neurologic

    3.7.1) SUMMARY
    A) CNS depression has been reported in experimental animal studies.
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CNS DEPRESSION
    a) CNS depression has been reported in experimental animal studies with acute exposure to high concentrations. Similar exposures or symptoms have not been reported in humans (Clayton & Clayton, 1981).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTRITIS
    1) Gastrointestinal distress may occur following acute ingestion of DBCP (Gosselin et al, 1984).

Hepatic

    3.9.1) SUMMARY
    A) Liver injury has been noted in experimental animal studies.
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATITIS
    a) Cloudy swelling of the liver has been seen in experimental animal studies. Most such studies indicate significant acute and chronic hepatic injury. The effects have not been seen in humans (Clayton & Clayton, 1981).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) NEPHRITIS
    1) Nephritis has been seen both in chronic and acute experimental animal studies (Clayton & Clayton, 1981).
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) TESTIS DISORDER
    a) Testicular necrosis, atrophy of seminiferous tubules, and decreased testicular weights were noted in guinea pigs and rats administered single intraperitoneal doses of 40 mg/kg (170 micromoles/kg) of DBCP (Lag et al, 1989).
    b) Minor testicular damage was observed in mice following single intraperitoneal doses of 80 and 120 mg/kg (340 and 510 micromoles/kg) of DBCP (Lag et al, 1989).
    c) Necrosis nor atrophy of the testicle was noted in hamsters given intraperitoneal doses of 160 mg/kg (680 micromoles/kg) of DBCP (Lag et al, 1989).

Hematologic

    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PANCYTOPENIA
    a) EXPERIMENTAL ANIMALS - Rats exposed chronically to DBCP developed pancytopenia (Gosselin et al, 1984).

Dermatologic

    3.14.1) SUMMARY
    A) Repeated exposure may cause skin necrosis; single one-time exposure appears to have little effect.
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SKIN NECROSIS
    a) Single applications to rabbit skin appear to do little. Repeated exposure, in one animal, caused extensive necrosis to the dermis even though the epidermis showed only slight crustiness (Clayton & Clayton, 1981; NIOSH, 1978).

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) DISORDER OF ENDOCRINE SYSTEM
    1) Follicle stimulating hormone (FSH) level appeared to be associated with azoospermia (as well as the likelihood of return to normospermia) after exposure ended among azoospermic males exposed to dibromochloropropane (DBCP) (Olsen et al, 1990).
    2) Increased levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) have been noted in men exposed for 3 years or more to airborne DBCP levels of 0.4 to 0.6 ppm (Glass et al, 1979).

Reproductive

    3.20.1) SUMMARY
    A) No teratogenic effects have been found in rat studies. Placental transfer has been documented in rats.
    B) No increased risk of spontaneous abortion or fetal malformation was reported in a study of conceiving couples when the father had been exposed to DBCP.
    3.20.2) TERATOGENICITY
    A) LACK OF EFFECT
    1) RATS - No embryo-lethal or teratogenic effects were noted with doses up to 50 mg/kg in rats (Barlow & Sullivan, 1982).
    2) RATS - Ruddick & Newsome (1979) noted no teratogenic effects from dibromochloropropane (DBCP) exposure in rats.
    3.20.3) EFFECTS IN PREGNANCY
    A) PLACENTAL BARRIER
    1) RATS - Placental transfer has been documented in rats (Barlow & Sullivan, 1982).
    B) LACK OF EFFECT
    1) No increased risk of spontaneous abortion or fetal malformation was reported in a study of conceiving couples when the father had been exposed to DBCP (Potashnik & Yanai-Inbar, 1987).
    3.20.5) FERTILITY
    A) FERTILITY DECREASED MALE
    1) Infertility and azoospermia have been seen among factory workers. Sperm count reduction was also seen in DBCP appliers, related to duration of exposure in the year of application, but not to previous years' exposures (Glass et al, 1979; Harbison, 1998). In severe exposure, there is total loss of spermatogonial stem cells, with no recovery after several years.
    B) FERTILITY DECREASED FEMALE
    1) The rate of male births among offspring conceived during paternal exposure to DBCP was decreased (Potashnik & Yanai-Inbar, 1987).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS96-12-8 (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) IARC Classification
    a) Listed as: 1,2-Dibromo-3-chloropropane
    b) Carcinogen Rating: 2B
    1) The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) Studies attempting to demonstrate DBCP's carcinogenicity in humans have been contradictory (Hathaway et al, 1996; Hearn et al, 1984).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) DBCP's carcinogenic potential has been shown in experimental animals, with the projected target organs being stomach, liver, kidney, lung, testes and skin (Hearn et al, 1984; Clayton & Clayton, 1981; Hathaway et al, 1996).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No toxic levels have been established.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) No specific lab work (CBC, electrolytes) is needed unless otherwise clinically indicated.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) OCCUPATIONAL MONITORING - Serum testosterone, follicle stimulating hormone (FSH), and luteinizing hormone (LH) serum levels may be useful for monitoring workers exposed to dibromochloropropane (Sittig, 1991).
    b) Potashnik & Yanai-Inbar (1987) demonstrated a direct relationship between normal follicle stimulating hormone concentrations and reversibility of the DBCP-induced spermatogenic suppression. Severity of damage is believed to be reflected by an increased follicle stimulating hormone concentration.
    c) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.

Methods

    A) CHROMATOGRAPHY
    1) AIR - An air sample is collected on a tube of Florisil(R) then desorbed with hexane and analyzed via gas chromatography equipment with an electron-capture detector. This method is applicable to air concentrations ranging from 1 to 100 ppb (0.10 to 1 mg/mm(3)) (NIOSH, 1978).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) No toxic levels have been established.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) 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).
    1) 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.
    2) 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).
    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).
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) DBCP is poorly soluble in water, and therefore commercial products are often mixed with a hydrocarbon such as kerosene. Before deciding to perform gastric lavage, check the solvent base for possible aspiration hazard.
    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) MONITORING OF PATIENT
    1) TESTICULAR
    a) Men exposed to DBCP should have sperm count tests for azoospermia and infertility.
    2) LIVER
    a) Liver toxicity has been seen in experimental animals only. Monitor liver function tests.
    3) KIDNEY
    a) Kidney damage and nephritis have occurred in exposed experimental animals. Monitor liver and renal function tests.
    B) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).

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) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    B) 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) 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) NECROSIS
    1) One rabbit, when tested with DBCP, developed dermal layer necrosis with minimal epidermal signs of toxicity. Patients should be monitored for this effect after significant chronic exposures.
    B) 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.
    C) SKIN IRRITATION
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) The no-effect level in the rabbit via inhalation is 0.1 ppm, and orally is 0.05 mg/kg. CNS depression occurs at about 60 ppm.
    B) Toxic levels for humans have not been established.

Minimum Lethal Exposure

    A) GENERAL
    1) When heated to decomposition, dibromochloropropane emits toxic fumes of chlorides and bromides (Lewis, 1996).
    B) ANIMAL DATA
    1) The no-effect level in the rabbit via inhalation is 0.1 part per million and via the oral route 0.05 milligram/kilogram.
    2) Levels which affect male infertility appear to have no effect on the menstrual cycles of females or FSH and LH levels (Barlow & Sullivan, 1982).
    3) DBCP has been shown in experimental animals to be a mucous membrane and lung irritant and a mild CNS depressant (Hathaway et al, 1996).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.
    B) ANIMAL DATA
    1) A dose of 10 grams in the standard Draize test caused severe skin irritation in rabbits (RTECS , 1998).
    2) A dose of 1 percent in the standard Draize test caused mild eye irritation in rabbits (RTECS , 1998).

Workplace Standards

    A) ACGIH TLV Values for CAS96-12-8 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS96-12-8 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: 1,2-Dibromo-3-chloropropane
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix A
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS96-12-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: 1,2-Dibromo-3-chloropropane (DBCP)
    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): 2B ; Listed as: 1,2-Dibromo-3-chloropropane
    a) 2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: 1,2-Dibromo-3-chloropropane
    a) Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    5) MAK (DFG, 2002): Category 2 ; Listed as: 1,2-Dibromo-3-chloropropane
    a) Category 2 : Substances that are considered to be carcinogenic for man because sufficient data from long-term animal studies or limited evidence from animal studies substantiated by evidence from epidemiological studies indicate that they can make a significant contribution to cancer risk. Limited data from animal studies can be supported by evidence that the substance causes cancer by a mode of action that is relevant to man and by results of in vitro tests and short-term animal studies.
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS96-12-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: 1,2-Dibromo-3-chloropropane (DBCP); see 29 CFR 1910.1044
    2) Table Z-1 for 1,2-Dibromo-3-chloropropane (DBCP); see 29 CFR 1910.1044:
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3:
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 1998 Lewis, 1996 HSDB, 1998
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 123 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 257 mg/kg
    3) LD50- (ORAL)RAT:
    a) 170 mg/kg
    4) LD50- (SUBCUTANEOUS)RAT:
    a) 100 mg/kg

Physicochemical

Physical Characteristics

    A) Dibromochloropropane is a dense yellow, amber or brown liquid (technical grade) with a pungent odor at high concentrations (Budavari, 1996; NIOSH , 1998).
    B) Yellow, brown, or amber liquid with pungent odor (Sittig, 1991)
    C) When pure, dibromochloropropane is a colorless liquid (HSDB , 1998).
    D) Taste Threshold: 0.01 mg/L (EPA, 1985)

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) 236.36 (Budavari, 1996)
    B) 236.35 (RTECS , 1998)

Other

    A) ODOR THRESHOLD
    1) Low odor threshold= 0.0965 mg/cu m; High odor threshold= 0.2895 mg/cu m; Irritating concn= 1.93 mg/cu m (HSDB , 2002)

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