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BUTADIENE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) 1,3-Butadiene is an alkene whose principle uses are in the manufacture of butadiene-styrene rubber and foams, chemicals, and resins. It is a colorless gas. It is a confirmed animal carcinogen.
    1) In 1984, NIOSH estimated that 65,000 workers were exposed to this chemical in the United States (MMWR, 1984).
    2) A more recent estimate by the Office of Toxic Substances in the USEPA has estimated a maximum of 10,000 workers exposed to this substance (EPA, 1985a).
    B) Furan is a related compound which is thought to have similar toxicity.

Specific Substances

    1) Alpha-gamma-butadiene
    2) Biethylene
    3) Bivinyl
    4) Buta-1,3-diene
    5) Divinyl
    6) Erythrene
    7) Pyrrolylene
    8) Vinylethylene
    9) 1,3,Butadiene
    10) CAS 106-99-0
    11) BUTADIEEN (DUTCH)
    12) BUTADIEN (POLISH)
    13) BUTADIENE, INHIBITED
    14) PYRROYLENE
    1.2.1) MOLECULAR FORMULA
    1) C4-H6

Available Forms Sources

    A) FORMS
    1) 1,3-Butadiene is a very reactive colorless gas with a mild aromatic odor (Lewis, 1996). It is available commercially as a 98.0% technical grade, 99.0% CP grade, 99.4% instrument grade, and 99.8% research grade (Sax & Lewis, 1987).
    B) SOURCES
    1) Butadiene has not been found to occur naturally (Harbison, 1998). It occurs in urban air and in drinking water as a pollutant (IARC, 1986).
    C) USES
    1) Butadiene is formed mainly for the production of thermogenic resins and rubber. It is used in the manufacture of butadiene-styrene copolymer elastomer, various synthetic rubber products and chemicals such as adiponitrile and thermoplastic elastomers as well as the food wrapping and latex paint industries (Harbison, 1998; Ackley, 1987). Occupational exposure is most likely to occur during production and polymerization of the monomer (Harbinson, 1998).
    2) It is also used as a copolymer latex for carpet backing and paper coatings as well as a resin for pipes, and automobile and appliance parts.
    3) Butadiene is also used in the production of fungicides.
    4) Furan is a related compound which is thought to have similar toxicity.
    5) Inhibitors generally used in commercial products are di-n-butylamine or phenyl-beta-naphthylamine (Sax & Lewis, 1987). It can also be stabilized with o-dihydroxybenzene or aliphatic mercaptans (Budavari, 1996).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) No serious human exposure cases have been reported. Animal poisonings generally progress from light anesthesia to running movements and tremors, and then to deep anesthesia, respiratory paralysis and death. Asphyxiation can occur.
    B) DERMAL EXPOSURE - Splash contact may cause mild to moderate skin irritation and rapid liquid evaporation may cause frostbite.
    C) INHALATION EXPOSURE - Butadiene is an eye and mucous membrane irritant. Coughing and upper respiratory tract irritation may occur.
    D) Butadiene is a SUSPECT HUMAN CARCINOGEN.
    0.2.4) HEENT
    A) Exposures of industrial workers to concentrations of 2,000 to 8,000 ppm have been reported to cause eye, skin, and nasal irritation.
    B) Headache and blurred vision can occur with CNS depression.
    C) Prickling and dryness of the nose, mouth and throat may occur.
    0.2.5) CARDIOVASCULAR
    A) Bradycardia and hypotension can occur with CNS depression.
    0.2.6) RESPIRATORY
    A) Respiratory paralysis resulting in death has occurred in animals. Coughing has been reported from higher but unspecified exposure concentrations in humans.
    B) Asphyxiation can occur.
    0.2.7) NEUROLOGIC
    A) Animal studies have shown mild anesthesia at 150,000 to 200,000 ppm. 250,000 ppm has caused death by respiratory paralysis. Drowsiness and fatigue have been reported in workers exposed to high concentrations. This agent is a CNS depressant.
    0.2.10) GENITOURINARY
    A) Animal studies have found increased kidney weight and nephrotoxicity in male rats.
    0.2.14) DERMATOLOGIC
    A) Splash contact may cause mild to moderate skin irritation or frostbite.
    0.2.18) PSYCHIATRIC
    A) Hallucinations and distorted perceptions have been reported after prolonged inhalation.
    0.2.20) REPRODUCTIVE
    A) Malformations have been seen in rats.
    0.2.21) CARCINOGENICITY
    A) Butadiene chronic inhalation studies in animals indicate it is carcinogenic at various sites. Mortality studies done on workers showed higher than normal but not statistically significant mortality ratios.

Laboratory Monitoring

    A) No toxic serum levels have been established.
    B) A NIOSH analytical method exists for 1,3-butadiene.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    B) 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.
    C) Butadiene is only a mild irritant and its primary toxicity is CNS depression and anesthesia in high concentrations (shown in animal studies). Treatment of serious cases would involve support of respiratory function.
    1) No serious human exposures have yet been reported.
    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.
    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).

Range Of Toxicity

    A) Human volunteers exposed to 2,000 to 8,000 ppm for six to eight hours developed slight smarting of the eyes, difficulty in focusing and transient objection to the odor.

Clinical Effects

Summary Of Exposure

    A) No serious human exposure cases have been reported. Animal poisonings generally progress from light anesthesia to running movements and tremors, and then to deep anesthesia, respiratory paralysis and death. Asphyxiation can occur.
    B) DERMAL EXPOSURE - Splash contact may cause mild to moderate skin irritation and rapid liquid evaporation may cause frostbite.
    C) INHALATION EXPOSURE - Butadiene is an eye and mucous membrane irritant. Coughing and upper respiratory tract irritation may occur.
    D) Butadiene is a SUSPECT HUMAN CARCINOGEN.

Heent

    3.4.1) SUMMARY
    A) Exposures of industrial workers to concentrations of 2,000 to 8,000 ppm have been reported to cause eye, skin, and nasal irritation.
    B) Headache and blurred vision can occur with CNS depression.
    C) Prickling and dryness of the nose, mouth and throat may occur.
    3.4.3) EYES
    A) Exposure of industrial workers to concentrations of 2000 to 8000 ppm has been reported to cause irritation of skin, eyes, nose, and throat (NIOSH, 1984).
    B) Human volunteers exposed to 2000, 4000, and 6000 ppm for 6 to 8 hours developed difficulty in focusing and smarting of the eyes (ACGIH, 1980).
    C) Blurred vision is part of the pattern of CNS depression (EPA, 1985).
    D) Following exposure of butadiene to photo-oxidation with ozone and nitrogen dioxide (formation of smog), it is an exceptionally potent precursor of products that are irritating to the human eye, producing both formaldehyde and acrolein (Grant & Schuman, 1993).
    3.4.5) NOSE
    A) IRRITATION - Exposure of industrial workers to concentrations of 2000 to 8000 ppm has been reported to cause irritation of skin, eyes, nose, and throat (NIOSH, 1984).
    B) Odor threshold is 1.33 ppm (NIOSH, 1984).
    C) Prickling and dryness of the nose may occur.
    3.4.6) THROAT
    A) IRRITATION - Exposure of industrial workers to concentrations of 2000 to 8000 ppm has been reported to cause irritation of skin, eyes, nose, and throat (Harbison, 1998; NIOSH, 1984).
    B) Rats subchronically exposed to 4000 to 8000 ppm daily for 3 months experienced moderate increases in salivation (NIOSH, 1984).

Cardiovascular

    3.5.1) SUMMARY
    A) Bradycardia and hypotension can occur with CNS depression.
    3.5.2) CLINICAL EFFECTS
    A) BRADYCARDIA
    1) Bradycardia is part of the pattern of CNS depression (EPA, 1985).
    B) HYPOTENSIVE EPISODE
    1) Hypotension can occur with CNS depression (EPA, 1985).

Respiratory

    3.6.1) SUMMARY
    A) Respiratory paralysis resulting in death has occurred in animals. Coughing has been reported from higher but unspecified exposure concentrations in humans.
    B) Asphyxiation can occur.
    3.6.2) CLINICAL EFFECTS
    A) COUGH
    1) Coughing has been reported from higher (unspecified) exposure concentrations (NIOSH, 1984). 8000 ppm for 8 hours caused upper respiratory tract irritation in human volunteers (Proctor et al, 1988).
    B) SEQUELA
    1) Recovery is likely if persons accidentally anesthetized are rescued while respiration is still strong; if anesthesia is deep, fatal outcome is more likely (Carpenter et al, 1944).
    C) INJURY DUE TO ASPHYXIATION
    1) Butadiene can displace oxygen from the breathing atmosphere, causing hypoxia and asphyxiation (HSDB , 2001; AAR, 1987). The lungs are the target organ for acute effects of butadiene inhalational exposure (Harbison, 1998).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) APNEA
    a) Respiratory paralysis resulting in death occurred in animals exposed to 200,000 to 250,000 ppm for 30 to 35 minutes (Proctor et al, 1988).

Neurologic

    3.7.1) SUMMARY
    A) Animal studies have shown mild anesthesia at 150,000 to 200,000 ppm. 250,000 ppm has caused death by respiratory paralysis. Drowsiness and fatigue have been reported in workers exposed to high concentrations. This agent is a CNS depressant.
    3.7.2) CLINICAL EFFECTS
    A) DROWSY
    1) Drowsiness, lightheadedness and fatigue were reported in workers exposed to higher, but unspecified concentrations (HSDB , 2001; Harbison, 1998; NIOSH, 1984).
    B) CENTRAL NERVOUS SYSTEM DEFICIT
    1) A typical pattern of CNS depression including blurred vision, fatigue, headache, vertigo, hypotension and bradycardia, unconsciousness and respiratory paralysis may occur (EPA, 1985). High concentrations result in an anesthetic effect (Harbison, 1998). Unconsciousness and death may result following exposure to very high concentrations (HSDB , 2001).
    C) HEADACHE
    1) Headache is part of the pattern of CNS depression and may indicate unsafe concentrations in the atmosphere (HSDB , 2001; EPA, 1985).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CNS DEPRESSION
    a) Animal studies have shown mild anesthesia to occur at 150,000 to 200,000 ppm and 200,000 to 250,000 ppm to cause death by way of respiratory paralysis within 35 minutes (ACGIH, 1986).

Genitourinary

    3.10.1) SUMMARY
    A) Animal studies have found increased kidney weight and nephrotoxicity in male rats.
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NEPHROPATHY TOXIC
    a) Increased kidney weight associated with increased severity of nephropathy was seen in male but not female rats chronically exposed to 8000 ppm butadiene for 111 weeks (Owen et al, 1987).

Hematologic

    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) MARROW DEPRESSION
    a) It has been shown in mouse studies that mouse bone marrow cells, in the presence of peroxide (but not NADPH), produced butadiene monoepoxide (BMO) from butadiene (BD) with resultant bone marrow toxicity. The authors suggest that the conversion of BD to BMO may occur in the liver via cytochrome P450 oxidation prior to its uptake into bone marrow. Alternatively, other routes of BD oxidation may be responsible for BD oxidation within the bone marrow, resulting in elevated levels of BMO in bone marrow (Genter & Recio, 1994).

Dermatologic

    3.14.1) SUMMARY
    A) Splash contact may cause mild to moderate skin irritation or frostbite.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) SPLASH CONTACT may cause mild to moderate skin irritation, or its rapid evaporation may cause frostbite (Lewis, 1996) ACGIH, 1980).
    B) FROSTBITE
    1) Frostbite might occur if the liquid contacts the skin due to rapid vaporization (AAR, 1987; CHRIS , 1989; Lewis, 1996).

Reproductive

    3.20.1) SUMMARY
    A) Malformations have been seen in rats.
    3.20.2) TERATOGENICITY
    A) FETOTOXICITY
    1) RATS - Butadiene has been a maternal and fetotoxic agent in rats exposed to 1000 to 8000 ppm for 6 hours/day during susceptible periods of their pregnancies (ACGIH, 1980).
    B) SKELETAL MALFORMATION
    1) RATS - It induced musculoskeletal abnormalities in rats at 8000 ppm for 6 hours when given during days 6-15 of gestation (RTECS , 2001).
    C) TESTIS NEOPLASM MALIGNANT
    1) MICE - NIOSH regards butadiene as a potential reproductive hazard, based on testicular and ovarian atrophy in chronic studies in mice (NIOSH, 1984).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS106-99-0 (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: 1,3-Butadiene
    b) Carcinogen Rating: 1
    1) The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.
    3.21.2) SUMMARY/HUMAN
    A) Butadiene chronic inhalation studies in animals indicate it is carcinogenic at various sites. Mortality studies done on workers showed higher than normal but not statistically significant mortality ratios.
    3.21.3) HUMAN STUDIES
    A) CASE SERIES
    1) Mortality studies done among workers from 1943 to 1979 showed higher than normal but NOT statistically significant site mortality ratios. These studies were complicated by mixed exposures (Downs et al, 1987).
    2) A more recent mortality study on male workers involved in the manufacture of butadiene found significantly increased deaths from lymphosarcoma and reticulum cell sarcoma, and elevated but not significant excesses from non-Hodgkin's lymphoma, in all exposure groups; however, the deaths were not clearly dose-related (Downs et al, 1987).
    a) This study was admitted by the authors to be flawed in that no racial discriminations were made, no exposure data were available, and almost half of the exposed cohort had less than five years exposure.
    3) LEUKEMIA
    a) A study of 16,579 synthetic rubber industry workers found that cumulative exposure to 1,3-butadiene was positively associated with leukemia. Chronic lymphocytic leukemia was weakly, but most consistently associated with butadiene; chronic myelogenous leukemia was more consistently and strongly associated with butadiene than other forms of leukemia (Graff et al, 2005).
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Butadiene chronic inhalation studies in experimental animals indicate that it is carcinogenic at various sites (ACGIH, 1980; (Huff et al, 1985). There is limited evidence for carcinogenicity in humans (HSDB , 2001).
    a) In a National Toxicology Program bioassay, malignant lymphomas, hemangiosarcomas, and alveolar-bronchiolar neoplasms were increased in male and female B6C3F1 mice exposed to 625 or 1250 ppm for 60 and 61 weeks, respectively. Tumors of the forestomach, mammary gland, ovary and liver were also elevated in females (NTP, 1989).
    2) In a second inhalation study at intermediate doses over a longer exposure period, lymphocytic lymphomas and hemangiosarcomas were again elevated in male mice exposed to 625 or 200 ppm for approximately 60 or 100 weeks, respectively.
    a) Females were at increased risk for lymphocytic lymphoma and alveolar-bronchiolar neoplasms (NTP, 1989).
    3) In an independent chronic inhalation study in rats, increased incidence was seen for pancreatic exocrine adenoma in males, uterine sarcoma in females, Zymbal gland carcinoma in females, mammary tumors in females, thyroid follicular cell tumors, and testis Leydig-cell tumors.
    a) The authors concluded that butadiene is a weak carcinogen in rats (Owen et al, 1987).
    4) NTP Toxicology and Carcinogenesis Study (US Dept Health & Human Services, 1993)
    a) CONCLUSIONS - The previous inhalation studies of 1,3-butadiene in male and female B6C3F1 mice provided clear evidence of carcinogenicity at exposure concentrations of 625 or 1,250 ppm. The present inhalation studies - 2-year exposures of 6.25, 20, 62.5, 200, or 625 ppm or shorter duration exposures of 200, 312, or 625 ppm - provide a better characterization of the concentration-dependent responses for 1,3-butadiene-induced neoplasms and non-neoplastic lesions. The present studies confirmed the clear evidence of carcinogenicity of 1,3-butadiene in male B6C3F1 mice based on increased incidences of neoplasms in the hematopoietic system, heart, lung, forestomach, liver, harderian gland, preputial gland, brain, and kidney. There was clear evidence of carcinogenicity of 1,3-butadiene in female B6C3F1 mice based on increased incidences of neoplasms in the hematopoietic system, heart, lung, forestomach, liver, harderian gland, ovary, and mammary gland.
    B) SKIN CARCINOMA
    1) Butadiene diepoxide (1,2:3,4-diepoxybutane), a probable metabolite of butadiene, has been shown to be a mild skin tumorigen in mice (ACGIH, 1980).

Genotoxicity

    A) Butadiene has induced mutations in bacteria and chromosome aberrations, micronuclei and sister chromatid exchanges in mice.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No toxic serum levels have been established.
    B) A NIOSH analytical method exists for 1,3-butadiene.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) No toxic levels have been established in serum.
    2) Blood glucose levels should be determined if signs of CNS depression are apparent (Proctor & Hughes, 1978).
    4.1.3) URINE
    A) Urine and blood 1,3-butadiene concentrations and urine concentrations of two different mercapturic acids were measured in 42 occupationally exposed and 43 control workers at a petrochemical plant. Only 1,3-butadiene urine and blood levels correlated with environmental exposure. Because of the ease of urine sampling compared to blood, the authors concluded that urine 1,3-butadiene measurements provided the best index of exposure (Fustinoni et al, 2004).
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) A complete neurological examination with possible further specific neurological examinations may be indicated if signs of CNS depression are apparent (Proctor & Hughes, 1978).
    2) OTHER
    a) BIOLOGICAL MARKER - An adenine adduct of DNA formed by diepoxybutane, a mutagenic metabolite of butadiene, and detected by (32)P-postlabeling analysis, is a candidate biomarker for butadiene exposure (Leuratti et al, 1994).

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) If respiratory tract irritation is present, monitor chest x-ray.

Methods

    A) CHROMATOGRAPHY
    1) 1,3-Butadiene can be analyzed in ambient air using NIOSH analytical method 1024: charcoal adsorption, workup with carbon disulfide, and gas chromatography. The range of detection is 1065-4590 mg/m(3) (RTECS , 1989; Sittig, 1985; HSDB , 1989).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) No toxic serum levels have been established.
    B) A NIOSH analytical method exists for 1,3-butadiene.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED -
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression.
    B) 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) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    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) No serious human exposures have yet been reported. Extrapolation of animal data would indicate primary treatment should be respiratory support during periods of anesthesia.

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.

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) FROSTBITE
    1) PREHOSPITAL
    a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).
    2) REWARMING
    a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
    b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
    c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
    d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).
    3) WOUND CARE
    a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
    b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
    c) The injured extremities should be elevated and should not be allowed to bear weight.
    d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
    e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
    f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
    g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
    h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
    i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
    j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
    k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
    l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
    m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
    n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) Human volunteers exposed to 2,000 to 8,000 ppm for six to eight hours developed slight smarting of the eyes, difficulty in focusing and transient objection to the odor.

Minimum Lethal Exposure

    A) ANIMAL DATA
    1) LCLo (INHL) RABBIT - 25 pph/23 minutes (RTECS , 2001)

Maximum Tolerated Exposure

    A) ADULT
    1) Volunteers exposed to 2000, 4000 and 8000 ppm for 6 to 8 hours developed slight smarting of the eyes, difficulty in focusing and transient objection to the odor (ACGIH, 1980).
    2) TOLERANCE may develop after a single exposure (Carpenter et al, 1944).
    B) ANIMAL DATA
    1) Inhaled concentrations of 600, 2300 and 6700 ppm for 7.5 hours/day, 6 days/week for 8 months produced no significant toxicity in guinea pigs, rats, rabbits and one dog (ACGIH, 1980).
    2) Deep anesthesia was induced in rabbits within 8 to 10 minutes of exposure to 200,000 to 250,000 ppm. 25 to 35 minutes of exposure to these concentrations resulted in death due to respiratory paralysis (ACGIH, 1980). Recovery from anesthesia occurred within two minutes.
    3) Another study on mice showed no anesthesia at 100,000 ppm, light narcosis at 150,000 ppm and some excitement and then narcosis at 200,000 ppm within 6 to 12 minutes.
    C) ACUTE
    1) TCLo - (INHL) HUMAN: 8000 ppm (RTECS , 2001)

Workplace Standards

    A) ACGIH TLV Values for CAS106-99-0 (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) 1,3-Butadiene
    a) TLV:
    1) TLV-TWA: 2 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A2
    2) Codes: Not Listed
    3) Definitions:
    a) A2: Suspected Human Carcinogen: Human data are accepted as adequate in quality but are conflicting or insufficient to classify the agent as a confirmed human carcinogen; OR, the agent is carcinogenic in experimental animals at dose(s), by route(s) of exposure, at site(s), of histologic type(s), or by mechanism(s) considered relevant to worker exposure. The A2 is used primarily when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals with relevance to humans.
    c) TLV Basis - Critical Effect(s): Cancer
    d) Molecular Weight: 54.09
    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 CAS106-99-0 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: 1,3-Butadiene
    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:
    a) IDLH: 2000 ppm
    b) Note(s): [10%LEL]
    1) [10%LEL]: The 10%LEL designation is provided where the IDLH was based on 10% of the lower explosive limit. This is used for safety purposes in some cases even though toxicity is not indicative of irreversible health effects or impairment of escape exists only at higher concentrations.

    C) Carcinogenicity Ratings for CAS106-99-0 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A2 ; Listed as: 1,3-Butadiene
    a) A2 :Suspected Human Carcinogen: Human data are accepted as adequate in quality but are conflicting or insufficient to classify the agent as a confirmed human carcinogen; OR, the agent is carcinogenic in experimental animals at dose(s), by route(s) of exposure, at site(s), of histologic type(s), or by mechanism(s) considered relevant to worker exposure. The A2 is used primarily when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals with relevance to humans.
    2) EPA (U.S. Environmental Protection Agency, 2011): Not applicable. This substance was not assessed using the 1986 cancer guidelines (U.S. EPA, 1986). ; Listed as: 1,3-Butadiene
    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): 1 ; Listed as: 1,3-Butadiene
    a) 1 : The agent (mixture) is carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans. This category is used when there is sufficient evidence of carcinogenicity in humans. Exceptionally, an agent (mixture) may be placed in this category when evidence of carcinogenicity in humans is less than sufficient but there is sufficient evidence of carcinogenicity in experimental animals and strong evidence in exposed humans that the agent (mixture) acts through a relevant mechanism of carcinogenicity.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: 1,3-Butadiene
    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 1 ; Listed as: 1,3-Butadiene
    a) Category 1 : Substances that cause cancer in man and can be assumed to make a significant contribution to cancer risk. Epidemiological studies provide adequate evidence of a positive correlation between the exposure of humans and the occurence of cancer. Limited epidemiological data can be substantiated by evidence that the substance causes cancer by a mode of action that is relevant to man.
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): K ; Listed as: 1,3-Butadiene
    a) K : KNOWN = Known to be a human carcinogen

    D) OSHA PEL Values for CAS106-99-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Butadiene (1,3-Butadiene); see 29 CFR 1910.1051; 29 CFR 1910.19(l)
    2) Table Z-1 for Butadiene (1,3-Butadiene); see 29 CFR 1910.1051; 29 CFR 1910.19(l):
    a) 8-hour TWA:
    1) ppm: 1 ppm/5 ppm STEL
    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, 2001
    1) LD50- (ORAL)MOUSE:
    a) 3210 mg/kg
    2) LD50- (ORAL)RAT:
    a) 5480 mg/kg
    3) TCLo- (INHALATION)HUMAN:
    a) 2000 ppm for 7H
    b) 8000 ppm

Pharmacology Toxicology

Toxicologic Mechanism

    A) The genotoxic metabolites are active alkylating agents (Rosenthal, 1985). The diepoxybutane can form interstrand cross-links with DNA (Lawley & Brookes, 1967).

Physicochemical

Physical Characteristics

    A) Butadiene is a colorless gas with a mild aromatic odor which is very reactive (Lewis, 1996; ACGIH, 1986).
    B) non-corrosive, flammable gas (ACGIH, 1986)
    C) 1,3-Butadiene vapor is heavier than air (NFPA, 1986).
    D) 1,3-Butadiene floats on and boils on water. It can produce a visible and flammable vapor cloud (CHRIS , 1989).

Molecular Weight

    A) 54.09 (HSDB , 2001)

Other

    A) ODOR THRESHOLD
    1) 1.3 ppm (ACGIH, 1986)

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