BENZENE
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
 -IDENTIFICATION
SYNONYMS
- CONSTITUENTS OF THE GROUP
IDENTIFIERS
SYNONYM REFERENCE
- (Budavari, 2000; CHRIS , 2001; Howard, 1990; HSDB , 2001; ITI, 1995; Lewis, 1998; NIOSH , 2001; RTECS , 2001)
USES/FORMS/SOURCES
Benzene is used as solvent, as a gasoline additive, and to make other industrial chemicals including polymers, detergents, pesticides, pharmaceuticals, dyes, plastics and resins. It is also used as a solvent for waxes, resins, oils and natural rubber (AAR, 2000) (Budavari, 2000). Benzene is added to gasoline and other fuels to act as an octane booster (Lewis, 1998). Benzene is used for printing, lithography and dry cleaning, and in paint, rubber, adhesives and coatings, and in detergents (HSDB , 2001). Benzene has been used extensively in shoe factories and in the tire industry. It has also been used as a disinfectant (HSDB , 2001). The production of ethylbenzene, cumene and cyclohexane constitute the main uses of benzene (ATSDR, 1993).
Benzene has a characteristic aromatic odor. It is a clear, colorless liquid that is lighter than water (AAR, 2000). The nitration grade of benzene is greater than 99% pure. 'Benzol 90' contains 80 to 85% benzene, 13 to 15% toluene and 2 to 3% xylene (HSDB , 2001). Benzene's odor has been described as gasoline-like and pleasantly aromatic (HSDB , 2001).
Natural sources of benzene include volcanoes and forest fires. Benzene is also a natural constituent of crude oil (Howard, 1990). Benzene is the 16th-highest-volume chemical produced in the United States, according to 1995 data. More than 7 million tons are produced annually (Lewis, 1997; Lewis, 1998). Benzene can be recovered from coal tar and produced from the hydrodemethylation of toluene under catalytic or thermal conditions (HSDB , 2001). A chief source of benzene is catalytic reformat, wherein the naphthenes and paraffins contained in naphtha are converted to aromatic hydrocarbons. Solvent extraction is then used to recover the benzene (ATSDR, 1993). Most of the benzene produced in the United States is derived from the petrochemical and petroleum-refining industries (ATSDR, 1993). HOOKAH SMOKE: According to a study that measured urinary S-phenylmercapturic acid (SPMA; a metabolite of benzene) levels in hookah smokers (n=105) and non-smokers (n=103) who attended hookah social events at a hookah lounge or in a private home, the urinary SPMA levels were significantly higher in daily hookah smokers than non-smokers after hookah lounge events (27.4 times higher; median 3.56 pmol/mg vs 0.13 pmol/mg, p<0.001) and after home events (7.8 times higher; 1.24 pmol/mg vs 0.16 pmol/mg, p<0.001). In all hookah smokers (daily or occasional smokers), SPMA levels increased 4.2 times and 1.9 times after hookah lounge and home events, respectively, than before the event. In non-smokers, there was no significant change from pre- to post-home event in the urinary SPMA levels (median, 0.14 pmol/mg to 0.16 pmol/mg, p=0.993); however, there was an increase of 2.6 times after hookah lounge events (median, 0.05 pmol/mg to 0.13 pmol/mg, p=0.055), suggesting that secondhand hookah smoke can also be a source of benzene exposure (Kassem et al, 2014).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- USES: Most commonly used as an intermediate in the production of other chemicals. Many benzene derivatives, such as styrene and phenol, are used to make a variety of other compounds, such as polymers, plastics, resins, and adhesives.
- TOXICOLOGY: Human metabolism of benzene to its principal metabolites (ie, hydroquinone, catechol, and phenol) occurs via cytochrome P450 enzyme 2E1 and quinone oxidoreductase NQ01. It is proposed that these metabolites are responsible for much of the systemic toxicity observed after benzene exposure. Benzene affects many organ systems. Specifically, benzene causes bone marrow suppression and, through its metabolites, disruptions in the cell cycle which can lead to mutagenesis. This effect is further exacerbated by chromosomal aberrations caused by benzene in lymphocytes. As with other solvents, large exposures cause CNS effects.
- EPIDEMIOLOGY: Acute exposure is very rare. Found to be an air pollutant found at low levels. Levels have also been found to be higher in smokers than in nonsmokers. Typically patients who present to medical care with symptoms have been exposed chronically.
MILD TO MODERATE TOXICITY: Benzene is a local irritant. Benzene exposure to the skin causes the development of erythema, burning, and edema. In the gastrointestinal tract, benzene produces a burning sensation of the oral mucous membranes, esophagus, and stomach after ingestion, with associated nausea, vomiting, and abdominal pain. Inhalational exposure causes bronchial irritation, cough, hoarseness, pulmonary edema, and chemical pneumonitis. Exposure to the eyes can cause reversible corneal injury. SEVERE TOXICITY: Inhalation at moderate concentrations may cause pallor, dizziness and excitation, followed by flushing, dyspnea, chest constriction, headache, and weakness. Higher concentrations may cause euphoria and excitation, followed by fatigue, cardiac dysrhythmias, seizures, coma, and death. Ingestion of benzene can cause vomiting, tachycardia, ataxia, somnolence, loss of consciousness, delirium, chemical pneumonitis with initial excitatory symptoms followed by abrupt CNS and respiratory depression. Transverse myelitis has been reported following occupational exposure. Dermal exposure can cause burns and systemic toxicity. CHRONIC EXPOSURE: Has been associated with paroxysmal nocturnal hemoglobinuria, various types of leukemia, myeloid metaplasia, aplastic anemia, menstrual cycle disruption, spontaneous abortion, stillbirth, and an increased likelihood of the development of diabetes.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 130 (ERG, 2004)
May cause toxic effects if inhaled or absorbed through skin. Inhalation or contact with material may irritate or burn skin and eyes. Fire will produce irritating, corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff from fire control or dilution water may cause pollution.
ACUTE CLINICAL EFFECTS
TOXICOLOGY: Human metabolism of benzene to its principal metabolites (ie, hydroquinone, catechol, and phenol) occurs via cytochrome P450 enzyme 2E1 and quinone oxidoreductase NQ01. It is proposed that these metabolites are responsible for much of the systemic toxicity observed after benzene exposure. Benzene affects many organ systems. Specifically, benzene causes bone marrow suppression and, through its metabolites, disruptions in the cell cycle which can lead to mutagenesis. This effect is further exacerbated by chromosomal aberrations caused by benzene in lymphocytes. As with other solvents, large exposures cause CNS effects. EPIDEMIOLOGY: Acute exposure is very rare. Found to be an air pollutant found at low levels. Levels have also been found to be higher in smokers than in nonsmokers. Typically patients who present to medical care with symptoms have been exposed chronically. MILD TO MODERATE TOXICITY: Benzene is a local irritant. Benzene exposure to the skin causes the development of erythema, burning, and edema. In the gastrointestinal tract, benzene produces a burning sensation of the oral mucous membranes, esophagus, and stomach after ingestion, with associated nausea, vomiting, and abdominal pain. Inhalational exposure causes bronchial irritation, cough, hoarseness, pulmonary edema, and chemical pneumonitis. Exposure to the eyes can cause reversible corneal injury. SEVERE TOXICITY: Inhalation at moderate concentrations may cause pallor, dizziness and excitation, followed by flushing, dyspnea, chest constriction, headache, and weakness. Higher concentrations may cause euphoria and excitation, followed by fatigue, cardiac dysrhythmias, seizures, coma, and death. Ingestion of benzene can cause vomiting, tachycardia, ataxia, somnolence, loss of consciousness, delirium, chemical pneumonitis with initial excitatory symptoms followed by abrupt CNS and respiratory depression. Transverse myelitis has been reported following occupational exposure. Dermal exposure can cause burns and systemic toxicity.
Cardiac dysrhythmias, including ventricular fibrillation, can occur due to epinephrine sensitization as well as from direct myocardial effects (Kaye, 1978; Nahum & Hoff, 1934). CASE SERIES: Three people died of ventricular fibrillation after acute benzene poisoning resulting from an industrial accident aboard a chemical cargo ship (Gist & Burg, 1997).
DERMATITIS: It is a strong irritant of the eyes, skin and respiratory tract, and can cause dermatitis and dehydration, defatting, edema, burning and blistering of the skin (Bingham et al, 2001; Harbison, 1998; Lewis, 1998). CHEMICAL BURN: Second degree chemical burns to the face, trunk, and extremities were noted on the autopsy reports of 3 crew members who died following exposure to benzene fumes and dermal contact while on a chemical cargo ship (Avis & Hutton, 1993a).
ESOPHAGITIS: A burning sensation in the mouth and stomach can occur following ingestion (Bingham et al, 2001; Lewis, 1998). VOMITING: Stomach pain, nausea and vomiting occur early in intoxication (Drozd & Bockowski, 1967).
HEMOGLOBINURIA: Paroxysmal nocturnal hemoglobinuria (PNH) has been reported in patients occupationally exposed to benzene. PNH is often associated with aplastic anemia and rarely with acute leukemia (Kwong & Chan, 1993). KIDNEY DISEASE: Reports of miscellaneous kidney diseases have been associated with benzene exposure, such as Goodpasture syndrome, antiglomerular basement membrane antibody, and anuric acute renal failure (Gist & Burg, 1997; Winek & Collom, 1971). ABNORMAL SEXUAL FUNCTION: Sexual dysfunction, including erectile abnormalities, decreased libido, and Peyronie's disease, has been reported following occupational exposure to varying amounts of benzene and toluene, and may not occur until several months post-exposure (Leikin et al, 2000).
Splash contact causes a moderate burning sensation, with slight transient epithelial cell injury and rapid recovery (Grant, 1986). BLURRED VISION may occur with acute exposure (Kaye, 1978). CASE REPORT: The autopsy of an 18-year-old man, who died following inhalation of reagent grade benzene, revealed evidence of acute granular tracheitis, laryngitis, and bronchitis (Winek & Collom, 1971).
White blood cell and platelet counts were significantly lower in 250 benzene exposed Chinese shoe workers than 140 controls. This was a persistent finding across all exposure levels from <1 ppm, 1 to <10 ppm, greater than equal 10 ppm. CD4+ counts, CD4+/CD8+ ratio, and B cells were also decreased across all exposure ranges. Hemoglobin was only decreased in workers exposed to 10 ppm or greater air concentrations of benzene. Individuals with two specific genetic variants in two key enzymes (CYP2E1 and myeloperoxidase) that metabolize benzene to toxic quinones and free radicals were more susceptible to benzene induced effects than other genetic subtypes (Lan et al, 2004). Blood diseases that have been associated with benzene exposure include pancytopenia, leukopenia, bone marrow hypoplasia or aplasia, thrombocytopenia, granulocytopenia, and lymphocytopenia (NTP, 1986). Associations have also been made with benzene exposure (especially chronic exposure) and a reduction in T lymphocytes (Moszczynsky & Lisiewicz, 1984). MYELOTOXICITY: Exposures producing acute myelotoxicity can result in delayed hematopoietic changes (Gosselin et al, 1984). Chronic exposure can produce suppression of hematopoiesis, resulting in spontaneous bleeding, anemia and leukopenia. Large single-dose exposure has been postulated to produce acute myelotoxicity or leukemia (Gerarde, 1960). APLASTIC ANEMIA: Aplastic anemia and leukemia can occur (Aksoy, 1985a; Aksoy, 1985b; Kuang & Liang, 2005). Work exposure to 100 ppm resulted in 140 excess deaths from leukemia per 1,000 exposed; 10 ppm resulted in 14 excess deaths (Landrigan & Rinsky, 1984). Bone marrow toxicity in exposed individuals may be triggered by individual susceptibility (pregnancy, infection and alcoholism), and affects women more than men. All elements of the marrow are affected. LEUKOCYTOSIS: One study showed leukocytosis in a 10-year chronically exposed worker with an average benzene exposure level of 0.9 ppm. He also had erythropoietin-independent growth of red cell progenitor colonies on peripheral blood smear. Both conditions began to normalize after benzene exposure was terminated (Froom et al, 1994). PANCYTOPENIA: CHRONIC EXPOSURE: Low RBC, WBC, hemoglobin, and platelet counts have been observed in severe cases of chronic benzene poisoning; bone marrow smear and biopsy examinations were not hypocellular. Aplastic anemia, myelodysplastic syndrome, and leukemia have also been reported (Kuang & Liang, 2005).
EUPHORIA: Initially euphoria is seen, followed by headache, giddiness, vertigo and ataxia (Kaye, 1978; Drozd & Bockowski, 1967; Harrington, 1917). CENTRAL NERVOUS SYSTEM DEFICIT: High doses can result in confusion, seizures and coma (Barbera et al, 1998; Kaye, 1978; Drozd & Bockowski, 1967). CASE REPORT: Depression, concentration and short-term memory impairment, decreased appetite, headaches, fatigue, decreased libido, and sleep disturbances were reported in seven male boilermakers following occupational exposure to varying amounts of benzene, toluene, and tetraethylene glycol (Leikin et al, 2000).
HEADACHE: Headaches have been reported following inhalation (Drozd & Bockowski, 1967). TRANSVERSE MYELOPATHY SYNDROME: CASE REPORT: A 25-year-old man, working at a wholesale supplier of chemicals, presented to the hospital with progressive paresis of his upper and lower extremities, bladder and bowel dysfunction, and paresthesias and sensory distortion. Lumbar punctures revealed no abnormalities of the cerebrospinal fluid, and viral tests were normal. A toxicological examination indicated a high urinary phenol concentration (28 mg/L; normal less than 10 mg/L). With supportive care, the patient's condition gradually improved over the next several months, with normal muscle strength in his upper and lower extremities, and the ability to walk without crutches, although bladder dysfunction continued to persist. The urinary phenol level had decreased to 4 mg/L. The patient was subsequently diagnosed with transverse myelitis postulated to be secondary to occupational exposure of benzene (Herregods et al, 1984). CEREBRAL EDEMA: CASE REPORT: The autopsy of an 18-year-old man, who died after inhaling reagent grade benzene, revealed the presence of cerebral edema (Winek & Collom, 1971).
Respiratory tract irritation may occur after inhalation (Drozd & Bockowski, 1967). Symptoms after ingestion include chest pain/constriction, coughing, breathlessness, and chemical pneumonitis (Bingham et al, 2001; Lewis, 1998). Death can occur due to respiratory failure (Kaye, 1978). ACUTE LUNG INJURY: Pulmonary edema and hemorrhages of the lungs may occur (Barbera et al, 1998; Winek & Collom, 1971).
After inhalation of 25 ppm for 480 minutes, benzene can be detected in the blood. At 50 to 100 ppm for 300 minutes, headache and fatigue develop. Inhalation of 250 to 500 ppm may induce vertigo, headache, dizziness, drowsiness and nausea (Hathaway et al, 1996). Exposure to 1,500 ppm for 60 minutes produces overt illness, and more than 3,000 ppm results in CNS depression and anesthesia. The latter concentration can be tolerated for 0.5 to 1 hour. Approximately 20,000 ppm is lethal in 5 to 10 minutes (Bingham et al, 2001; Hathaway et al, 1996).
CHRONIC CLINICAL EFFECTS
- SUMMARY: Has been associated with paroxysmal nocturnal hemoglobinuria, various types of leukemia, myeloid metaplasia, aplastic anemia, menstrual cycle disruption, spontaneous abortion, stillbirth, and an increased likelihood of the development of diabetes.
- Although it can cause permanent CNS effects and sudden deaths, possibly due to ventricular fibrillation or other non-perfusing cardiac arrhythmias due to a lowered myocardial threshold to the arrhythmogenic effects of epinephrine, the overwhelming concern with chronic benzene exposure is its effect on the blood-forming system, and its related ability to induce leukemia in humans (Bingham et al, 2001).
- General signs and symptoms of chronic overexposure to low concentrations of benzene include fatigue, headache, dizziness, anorexia, diarrhea, dyspnea, pallor, vertigo, visual changes, enlarged liver and spleen, bone pain, fever, hemorrhage and bleeding gums (Bingham et al, 2001; Harbison, 1998).
- The effects on hematopoiesis begin with blood-clotting defects, followed by hyper- then hypoplastic bone marrow, with internal hemorrhaging, and finally, bone marrow aplasia occurs (Bingham et al, 2001). After a possible initial increase, total polymorphonuclear leucocyte levels decrease to less than 4,000/mm(3); lymphocytosis, macrocytic, normochromic, or slightly hyperchromic anemia, and/or thrombocytopenia can develop (ILO, 1983).
The myelotoxicant effects of suppression of bone marrow cell proliferation can result in aplastic anemia with leukopenia, anemia, thrombocytopenia, or pancytopenia, with accompanying bleeding disorders; symptoms include weakness, purpura and hemorrhage (ACGIH, 1991). Vaginal bleeding, heavy menstrual bleeding, and hemorrhagic complications of pregnancy have been reported in severe cases with aplastic anemia, with former high-level exposures (Barlow & Sullivan, 1982). The effects on hematopoiesis may be permanent if left untreated, and are a consequence of the direct toxicity of benzene or its metabolites on the bone marrow (Bingham et al, 2001; ILO, 1983). The actual effects seen may vary from one individual to another (ILO, 1983). One or all of the types of precursor cells in the blood-forming system may be damaged.
- In a group of 44 Chinese workers, changes in absolute lymphocyte counts was the most sensitive hematologic parameter for benzene exposure (Rothman et al, 1996). Results of hematologic screening for 35 years in a rubber factory also showed a much stronger dose-response for white blood cells than for erythrocytes, and there was no evidence of a threshold for this response (Ward et al, 1996).
- A sclerodermatous syndrome occurring with peripheral neuropathy and Raynaud's phenomenon was noted in an isolated case report of a 50-year-old man with a 32-year occupational exposure to benzene, other aromatics and ethanolamine (Bottomley et al, 1993). Because of the mixed exposures, these effects could not be attributed solely to benzene. Scleroderma-like changes have been linked with exposure to various solvents.
- F344 rats given a mixture of low concentrations of benzene along with arsenic, phenol, chloroform, chromium, lead and trichloroethylene, showed hepatic proliferation after treatments up to 1 month (Constan et al, 1995).
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
- Prehospital GI decontamination is not recommended because of the risk of abrupt onset decreased mental status or seizures and aspiration.
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 130 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Wash skin with soap and water. Keep victim warm and quiet. In case of burns, immediately cool affected skin for as long as possible with cold water. Do not remove clothing if adhering to skin. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
FIRST AID EYE EXPOSURE: Immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Primary eye protection (spectacles or goggles), as defined by the Occupational Safety and Health Administration (OSHA), should be used when working with this chemical. Face shields should only be worn over primary eye protection. DERMAL EXPOSURE: Immediately wash the contaminated skin with soap and water. If this chemical penetrates the clothing, immediately remove the clothing, wash the skin with soap and water, and get medical attention promptly. INHALATION EXPOSURE: Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible. ORAL EXPOSURE: If this chemical has been swallowed, get medical attention immediately. TARGET ORGANS: Eyes, skin, respiratory system, blood, central nervous system, and bone marrow (National Institute for Occupational Safety and Health, 2007; OSHA, 2000).
INHALATION EXPOSURE 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. SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue). Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years). Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
Toxic effects of benzene are produced chiefly by inhalation of the vapor. Monitor patient for respiratory depression. If a cough or difficulty in breathing develops, evaluate for respiratory tract irritation, bronchitis, and pneumonia.
DERMAL EXPOSURE 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). Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
EYE EXPOSURE 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.
ORAL EXPOSURE Because of the potential for gastrointestinal tract irritation, CNS depression, or seizures, DO NOT induce emesis. PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION 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). 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. 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).
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. SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue). Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years). Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
Monitor EKG for cardiac arrhythmias. Avoid administration of epinephrine as benzene may decrease the myocardial threshold to the arrhythmogenic effects of catecholamines.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
- Oral doses from 9 to 30 grams have proven fatal (HSDB , 2001).
- It is estimated that the probable human oral lethal dose is 50 to 500 mg/kg (HSDB , 2001).
- It has been estimated that 10 mL benzene is a lethal dose for humans (ATSDR, 1993).
- Inhalation of approximately 20,000 ppm (2 percent in air) was fatal in 5 to 10 minutes (Wilbur et al, 2008; HSDB , 2001; ATSDR, 1993; Paustenbach et al, 1993) .
- Exposure to benzene is lethal in humans by means of asphyxiation, respiratory arrest, central nervous system depression or cardiac collapse (ATSDR, 1993).
MAXIMUM TOLERATED EXPOSURE
- The maximum tolerated human exposure to this agent has not been delineated.
- CNS effects, including drowsiness, dizziness, headache, vertigo, tremor, delirium, and coma, may occur following inhalation at levels of 300 to 3000 ppm (Wilbur et al, 2008).
- Listlessness and confusion were reported following inhalation of approximately 4,700 ppm for 30 minutes (Paustenbach et al, 1993).
- One study concluded that a TWA exposure of 3.2 mg/m(3) (1 ppm) for a 40 year working career does not show any statistical increase of leukemia. However, because benzene is a carcinogen, exposure should be limited to the lowest level technically feasible (WHO, 1993).
- A study of workers in a Texas refinery indicated that very low levels of benzene exposure (0.5 ppm for 1 to 21 years) resulted in no hematological changes to the workers (ATSDR, 1993).
- Two additional studies of workers exposed to low levels of benzene showed that the workers experienced slight decreases in red blood cell counts (ATSDR, 1993).
- Headache, lassitude, and fatigue occurred following inhalation of 50 to 150 ppm for 5 hours (Paustenbach et al, 1993).
- Carcinogenicity Ratings for CAS71-43-2 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A1 ; Listed as: Benzene EPA (U.S. Environmental Protection Agency, 2011): A ; Listed as: Benzene EPA (U.S. Environmental Protection Agency, 2011): A ; Listed as: Benzene 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: Benzene 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.
NIOSH (National Institute for Occupational Safety and Health, 2007): Ca ; Listed as: Benzene MAK (DFG, 2002): Category 1 ; Listed as: Benzene NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS71-43-2 (U.S. Environmental Protection Agency, 2011):
Oral: Inhalation: Drinking Water: Oral: Inhalation: Drinking Water:
References: Clayton & Clayton, Vol. 2B, 1994; Lewis, 2000; RTECS, 2001; WHO, 1993 LC50- (INHALATION)MOUSE: LC50- (INHALATION)RAT: 10,000 ppm for 7H 44,660 mg/m(3) for 4H (WHO, 1993) 32,600 mg/m(3) for 7H (WHO, 1993)
LCLo- (INHALATION)CAT: LCLo- (INHALATION)DOG: LCLo- (INHALATION)HUMAN: LCLo- (INHALATION)RABBIT: LD50- (SKIN)GUINEA_PIG: LD50- (INTRAPERITONEAL)MOUSE: LD50- (ORAL)MOUSE: LD50- (SKIN)MOUSE: LD50- (SUBCUTANEOUS)MOUSE: LD50- (SKIN)RABBIT: LD50- (INTRAPERITONEAL)RAT: LD50- (ORAL)RAT: <1.0-5 g/kg (Clayton & Clayton, 1994) 3.4 g/kg (Clayton & Clayton, 1994) 5.6 g/kg (Clayton & Clayton, 1994) 3306 mg/kg (Lewis, 2000) 14 days old, 3000 mg/kg (WHO, 1993) young adult, 3300 mg/kg (WHO, 1993) old adult, 4900 mg/kg (WHO, 1993) 8100 mg/kg (WHO, 1993) 930 mg/kg -- tremors; affected seizure threshold; convulsions
LDLo- (ORAL)DOG: LDLo- (INTRAPERITONEAL)GUINEA_PIG: LDLo- (ORAL)HUMAN: LDLo- (INTRAVENOUS)RABBIT: TCLo- (INHALATION)HUMAN: 100 ppm -- depressed activity; nausea or vomiting; dermatitis 10 ppm for 8H/10Y - intermittent -- carcinogenic; leukemia 150 ppm for 1 Y-intermittent -- blood changes and body temperature increase 200 mg/m(3) for 78W - intermittent -- carcinogenic; leukemia; thrombocytopenia
TCLo- (INHALATION)MOUSE: Female, 500 ppm for 7H at 6-15D of pregnancy -- fetotoxicity (except death); musculoskeletal system effects Female, 500 mg/m(3) for 12H at 6-15D of pregnancy -- fetotoxicity (except death); musculoskeletal system effects Female, 20 ppm for 6H at 6-15D of pregnancy -- affected blood and lymphatic system Female, 5 ppm at 6-15D of pregnancy -- cytological changes in embryo; blood and lymphatic system changes 300 ppm for 6H/16W - intermittent -- tumorigenic agent; lymphomas including Hodgkin's disease 300 ppm for 6H/13W - intermittent -- blood changes and changes in testicular weight 300 ppm for 6H/16W - intermittent -- changes in blood; death 25 ppm for 6H/5D - intermittent -- changes in spleen weight and WBC count 10 ppm for 6H/26W - intermittent -- changes in spleen, cell count, and RBC count 48 ppm for 6H/14D - intermittent -- leukopenia; changes in spleen weight; humoral immune responses decrease 10 ppm for 6H/10W - intermittent -- changes in spleen weight and spleen 100 ppm for 6H/72W - intermittent -- normocytic anemia; leukopenia; death
TCLo- (ORAL)MOUSE: TCLo- (INHALATION)PIG: TCLo- (INHALATION)RABBIT: 500 mg/m(3) for 3H/13W - intermittent -- hemorrhage; other blood changes; changes in lung, thorax, or respiration Female, 1 g/m(3) for 24H at 7-20D of pregnancy -- fetotoxicity (except death); developmental abnormalities Female, 1 g/m(3) for 24H at 7-20D of pregnancy -- post-implantation mortality; abortion; fetal death Female, 500 ppm for 7H at 6-18D of pregnancy -- maternal effects
TCLo- (INHALATION)RAT: 1200 ppm for 6H/10W - intermittent -- equivocal tumorigenic agent; sense organ tumors 300 ppm for 6H/13W - intermittent -- leukopenia 1000 ppm for 7H/28W - intermittent -- unspecified changes in cell count 500 ppm for 6H/3W - intermittent -- red blood cells pigmented or nucleated; bone marrow changes; WBC changes 300 ppm for 6H/99W - intermittent -- leukopenia; bone marrow changes; death 23 mg/m(3) for 4H/8D - intermittent -- changes in liver and pituitary weight Female, 56,600 mcg/m(3) for 24H at 1-22D of pregnancy -- biochemical and metabolic effects on newborn Female, 670 mg/m(3) for 24H At 15D prior to mating and 1-22D of pregnancy -- affected female fertility index Female, 50 ppm for 24H at 7-14D of pregnancy -- extra embryonic structures; fetotoxicity (except death) Female, 150 ppm for 24H at 7-14D of pregnancy -- effects on fertility; musculoskeletal system abnormalities
TD- (ORAL)MOUSE: TD- (ORAL)RAT: TDLo- (INTRAPERITONEAL)MOUSE: Female, 219 mg/kg at 14D of pregnancy -- blood, lymphatic system, and hepatobiliary system abnormalities Male, 5 mg/kg at 1D prior to mating -- pre-implantation mortality; fetal death 1200 mg/kg for 8W-intermittent -- neoplastic; tumors
TDLo- (INTRAVENOUS)MOUSE: Female, 13,200 mcg/kg at 13-16D of pregnancy -- cytological changes in embryo or fetus Female, 4 g/kg at 12D of pregnancy -- effects on weaning or lactation index 670 mg/kg for 19W - intermittent -- equivocal tumorigenic agent; leukemia; lymphomas including Hodgkin's disease
TDLo- (ORAL)MOUSE: Female, 16,880 mg/kg at 6-15D of pregnancy -- fetotoxicity (except death); fetal death Female, 6500 mg/kg at 8-12D of pregnancy -- reduced weight gain in newborn Female, 9 g/kg at 6-15D of pregnancy -- fetotoxicity (except death) Female, 12 g/kg at 6-15D of pregnancy -- post-implantation mortality 18,250 mg/kg for 2Y-continuous -- carcinogenic; tumors; lymphomas including Hodgkin's disease 4250 mg/kg for 17W - intermittent -- blood changes; changes in WBC count
TDLo- (SKIN)MOUSE: TDLo- (SUBCUTANEOUS)MOUSE: Female, 7030 mg/kg at 12-13D of pregnancy -- extra embryonic structures; fetotoxicity (except death); musculoskeletal system affected Female, 1100 mg/kg at 12D of pregnancy -- embryo affected 600 mg/kg for 17W-intermittent -- equivocal tumorigenic agent; leukemia; lymphomas including Hodgkin's disease 2197 mg/kg for 5D-intermittent -- changes in spleen and thymus weight; changes in WBC count
TDLo- (INTRAPERITONEAL)RAT: TDLo- (ORAL)RAT: 52 g/kg for 52W-intermittent -- carcinogenic; tumors; leukemia 6600 mg/kg for 27W - intermittent -- leukopenia; changes in RBC count 17 g/kg for 17W-intermittent -- changes in spleen and WBC count
TDLo- (SUBCUTANEOUS)RAT: 18 mg/kg for 21D-intermittent -- changes in RBC and WBC count; weight loss or decreased weight gain 13,536 mg/kg for 12W-intermittent -- liver changes; urine composition changes; biochemical changes 2197 mg/kg for 5D-intermittent -- pigmented or nucleated red blood cells; changes in WBC count; weight loss or decreased weight gain 12 g/kg for 6W-intermittent -- changes in bone marrow; changes in cell count; changes in WBC count
CALCULATIONS
1 ppm = 3.26 mg/m(3) (HSDB , 2001) 1 ppm = 3.19 mg/m(3) (at 68 degrees F and 760 mmHg) (NIOSH , 2001)
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS71-43-2 (American Conference of Governmental Industrial Hygienists, 2010):
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.
- AIHA WEEL Values for CAS71-43-2 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS71-43-2 (National Institute for Occupational Safety and Health, 2007):
Listed as: Benzene REL: IDLH:
- OSHA PEL Values for CAS71-43-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
Listed as: Benzene; see 29 CFR 1910.1028; see Table Z-2 for the limits applicable in the operations or sectors excluded in 1910.1028 Table Z-1 for Benzene; see 29 CFR 1910.1028; see Table Z-2 for the limits applicable in the operations or sectors excluded in 1910.1028: 8-hour TWA: ppm: mg/m3: Ceiling Value: Skin Designation: No Notation(s): (d): The final benzene standard in 1910.1028 applies to all occupational exposures to benzene except in some circumstances the distribution and sale of fuels, sealed containers and pipelines, coke production, oil and gas drilling and production, natural gas processing, and the percentage exclusion for liquid mixtures; for the excepted subsegments, the benzene limits in Table Z-2 apply. See 1910.1028 for specific circumstances.
Table Z-2 for Benzene (Z37.40-1969):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS71-43-2 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS71-43-2 (U.S. Environmental Protection Agency, 2010):
Listed as: Benzene (D018) Final Reportable Quantity, in pounds (kilograms): Additional Information: Unlisted Hazardous Wastes Characteristic of Toxicity Listed as: Benzene Final Reportable Quantity, in pounds (kilograms): Additional Information:
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS71-43-2 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS71-43-2 (U.S. Environmental Protection Agency, 2010b):
Listed as: Benzene P or U series number: U019 Footnote: Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.
- EPA SARA Title III, Extremely Hazardous Substance List for CAS71-43-2 (U.S. Environmental Protection Agency, 2010):
- EPA SARA Title III, Community Right-to-Know for CAS71-43-2 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS71-43-2 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS71-43-2 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions for UN/NA Number 1114 (49 CFR 172.101, 2005):
- ICAO International Shipping Name for UN1114 (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS71-43-2 (NFPA, 2002):
Listed as: Benzene Hazard Ratings: Health Rating (Blue): 1 Flammability Rating (Red): 3 (3) Flammable. Liquids and solids that can be ignited under almost all ambient temperature conditions. Including liquids with a flash point below 73 degrees F and a boiling point above 100 degrees F, solid materials which form coarse dusts that burn rapidly without becoming explosive, materials which burn rapidly by reason of self-contained oxygen (ie, organic peroxides), and materials which ignite spontaneously when exposed to air.
Instability Rating (Yellow): 0 Oxidizer/Water-Reactive Designation: Not Listed
-HANDLING AND STORAGE
HANDLING
- When handling benzene, avoid all potential sources of ignition (OHM/TADS , 2001).
- Use spark resistant tools and protect containers against physical damage (ITI, 1995).
STORAGE
Containers of benzene should be kept well-closed and away from fire (Budavari, 2000). Benzene is normally shipped in the following containers: Glass bottles, cans, drums, and tanks on trucks, rail cars, and barges (NFPA, 1997). Containers of benzene should be kept separate from oxidizing materials (NFPA, 1997).
- ROOM/CABINET RECOMMENDATIONS
Rooms used to store benzene should be kept cool (Budavari, 2000). Benzene should be kept in either outside or detached storage areas. If kept indoors, standard flammable liquids storage warehouse, room, or cabinet should be used (NFPA, 1997). Rooms containing benzene should have adequate ventilation (Lewis, 2000).
Benzene will react with oxidizing materials (NFPA, 1997). Benzene is incompatible with strong oxidizers, nitric acid, oxygen, ozone, and perchlorates (Pohanish & Greene, 1997). Benzene will attack some forms of plastics, coatings, and rubber (Pohanish & Greene, 1997).
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 130 (ERG, 2004)
- Keep upwind; avoid breathing vapors. Wear full protective clothing and positive pressure self-contained breathing apparatus (SCBA). Do not handle broken containers unless wearing appropriate protective clothing. Wash away benzene which may have contacted the body with copious amounts of water or soap and water (AAR, 2000; (NFPA, 1997).
EYE/FACE PROTECTION
- Wear chemical safety goggles, face shield, and a self-contained breathing apparatus (ITI, 1995).
RESPIRATORY PROTECTION
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 71-43-2.
ENGINEERING CONTROLS
- Refer to 29 CFR 1910.1028 for OSHA engineering controls.
-PHYSICAL HAZARDS
FIRE HAZARD
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 130 (ERG, 2004) HIGHLY FLAMMABLE: Will be easily ignited by heat, sparks or flames. Vapors may form explosive mixtures with air. Vapors may travel to source of ignition and flash back. Most vapors are heavier than air. They will spread along ground and collect in low or confined areas (sewers, basements, tanks). Vapor explosion hazard indoors, outdoors or in sewers. Those substances designated with a "P" may polymerize explosively when heated or involved in a fire. Runoff to sewer may create fire or explosion hazard. Containers may explode when heated. Many liquids are lighter than water.
Benzene is a dangerous fire hazard when exposed to heat or flame (Lewis, 2000). Approach fire from upwind to avoid hazardous vapors. Vapors are heavier than air and may travel to a source of ignition and flash back. Liquid floats on water and may travel to a source of ignition and spread fire. Benzene may accumulate static electricity (AAR, 2000; (NFPA, 1997). Benzene is extremely flammable (AAR, 2000).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS71-43-2 (NFPA, 2002):
Listed as: Benzene Flammability Rating: 3 (3) Flammable. Liquids and solids that can be ignited under almost all ambient temperature conditions. Including liquids with a flash point below 73 degrees F and a boiling point above 100 degrees F, solid materials which form coarse dusts that burn rapidly without becoming explosive, materials which burn rapidly by reason of self-contained oxygen (ie, organic peroxides), and materials which ignite spontaneously when exposed to air.
- INITIATING OR CONTRIBUTING PROPERTIES
Benzene has a flash point of 12 degrees F (-11 degrees C) (NFPA, 1997). Benzene vapors may travel a considerable distance to ignition source, and then flash back (OHM/TADS , 2001).
- FIRE CONTROL/EXTINGUISHING AGENTS
- FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 130 (ERG, 2004)
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 130 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 130 (ERG, 2004)
Water spray, fog or regular foam. Do not use straight streams. Move containers from fire area if you can do it without risk.
- TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 130 (ERG, 2004)
Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.
- NFPA Extinguishing Methods for CAS71-43-2 (NFPA, 2002):
- Benzene vapors burn with a smokey flame (ITI, 1995). To fight fire, use water spray, dry chemical, foam or CO2. Apply water from as far a distance as possible. Use water spray to keep fire-exposed containers cool (AAR, 2000; (NFPA, 1997).
- Use foam, carbon dioxide, and dry chemicals to fight a fire caused by benzene (Lewis, 2000).
- Water may be ineffective as an extinguishing method (OHM/TADS , 2001)
EXPLOSION HAZARD
- Benzene explodes on contact with diborane, bromine pentafluoride, permanganic acid, peroxomonosulfuric acid, and peroxodisulfuric acid. It forms sensitive, explosive mixtures with iodine pentafluoride, silver perchlorate, nitryl perchlorate, nitric acid, liquid oxygen, and ozone (Lewis, 2000) Urben, 1999).
An explosive mixture is created by the interaction of arsenic pentafluoride + potassium methoxide when benzene is used as the solvent (explodes above 30 degrees C) (Lewis, 2000) Urben, 1999). Interaction of benzene with iodine pentafluoride becomes violent above 50 degrees C (Urben, 1999).
- Benzene ignites on contact with sodium peroxide + water, dioxygenyl tetrafluoroborate, iodine heptafluoride, and dioxygen difluoride (Lewis, 2000) Urben, 1999).
- Benzene forms a vigorous or incandescent reaction with uranium hexafluoride, and bromine trifluoride. It can react vigorously with oxidizing materials such as chlorine, chromium trioxide, oxygen, sodium perchlorate, ozone, perchlorates, (aluminum chloride + fluorine perchlorate), (sulfuric acid + permanganates), potassium peroxide, (silver (I) perchlorate + acetic acid), and sodium peroxide (Lewis, 2000) Urben, 1999).
A vigorous reaction which bulged a reactor wall was observed during hydrogenation of benzene at temperatures above 210 degrees C (Lewis, 2000) Urben, 1999). An explosion occurred during the ozonization of rubber dissolved in benzene. Since the solution remained clear, it is unlikely that the explosion was caused by the formation of benzene triozonide. A rubber ozonide may have been involved, but the benzene-oxygen system itself has high potential for hazard (Urben, 1999).
- Benzene presents a moderate explosion hazard when exposed to heat or flame; use with adequate ventilation (Lewis, 2000).
- Explosions have occurred when benzene was mixed with peroxomonosulfuric acid (HSDB , 2001).
- Light initiated an explosion of benzene vapors which were inadvertently mixed with chlorine (HSDB , 2001).
- Benzene vapors will form explosive mixtures with air (OHM/TADS , 2001).
DUST/VAPOR HAZARD
- Light initiated an explosion of benzene vapors which were inadvertently mixed with chlorine (HSDB , 2001).
- Benzene vapors will form explosive mixtures with air (OHM/TADS , 2001).
- Benzene vapors may travel a considerable distance to ignition source, and then flash back (OHM/TADS , 2001).
REACTIVITY HAZARD
- Benzene will react violently with iodine pentafluoride. It will ignite in contact with iodine heptafluoride gas. The interaction with iodine pentafluoride will become violent at temperatures above 50 degrees C (HSDB , 2001) Urben, 1999).
- Benzene is incompatible with strong oxidizers, many fluorides and perchlorates, and nitric acid (NIOSH , 2001) Urben, 1999).
- Refer to the "Explosion Hazard" Section of the Benzene HAZARDTEXT(R) Document for detailed information.
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- LARGE SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 130 (ERG, 2004)
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 130 (ERG, 2004)
If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 130 (ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering.
- If a fire involving benzene becomes uncontrollable or a container of benzene is exposed to direct flame, consider an evacuation of a one-third (1/3) mile radius. If benzene is leaking (not on fire), consider an evacuation from the downwind area based on the amount of material spilled, location, and weather conditions (AAR, 2000).
- AIHA ERPG Values for CAS71-43-2 (AIHA, 2006):
Listed as Benzene ERPG-1 (units = ppm): 50 ERPG-2 (units = ppm): 150 ERPG-3 (units = ppm): 1000 Under Ballot, Review, or Consideration: Yes Definitions: ERPG-1: The ERPG-1 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing more than mild, transient adverse health effects or perceiving a clearly defined objectionable odor. ERPG-2: The ERPG-2 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing irreversible or other serious health effects or symptoms that could impair an individual's ability to take protective action. ERPG-3: The ERPG-3 is the maximum airborne concentration below which it is believed nearly all individuals could be exposed for up to one hour without experiencing or developing life-threatening health effects.
- DOE TEEL Values for CAS71-43-2 (U.S. Department of Energy, Office of Emergency Management, 2010):
- AEGL Values for CAS71-43-2 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
- NIOSH IDLH Values for CAS71-43-2 (National Institute for Occupational Safety and Health, 2007):
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 130 (ERG, 2004) ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). All equipment used when handling the product must be grounded. Do not touch or walk through spilled material. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. A vapor suppressing foam may be used to reduce vapors. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. Use clean non-sparking tools to collect absorbed material.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 130 (ERG, 2004) To contain benzene spilled on land, dig a pit, pond, lagoon, or holding area. Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash, cement powder, or commercial sorbents. Apply appropriate foam to diminish vapor and fire hazard (AAR, 2000). To contain benzene spilled on water, natural barriers or booms should be used to limit spill travel. Surfactants that have been approved by EPA may be used. The spill may be solidified by using gelling agents. Activated carbon, applied at ten times the amount spilled, may be used if the concentration of dissolved benzene is 10 ppm or greater. Suction hoses, mechanical dredges, and/or lifts may be used to remove spilled material (AAR, 2000). To contain benzene in the air, water spray or mist should be applied to knock down vapors (AAR, 2000).
Three systems for removing benzene, toluene and xylene (BTX) from contaminated water were evaluated. System one used granular activated charcoal (GAC), system two used GAC in conjunction with biological removal, and system three used microbial growth without adsorption. The results showed that system two gave the best combination of BTX removal and stable operation (Voice et al, 1992). Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.
Chemical reactions can be used to destroy benzene. Treating benzene with dichromate in strong sulfuric acid for 2 days resulted in total destruction (ATSDR, 1993). When chelated to such compounds as ethylenediamine tetraacetic acid (EDTA), N-methyliminodiacetic acid, ethanol diglycine, humic acids, and phosphates, Fe(III) stimulated benzene oxidation coupled to Fe(III) reduction in anaerobic sediments from a petroleum-contaminated aquifer as effectively as, or more effectively than nitrilotriacetic acid. These results indicate that many forms of chelated Fe(III) may be applicable to aquifer remediation (Lovley et al, 1996). Disposal of benzene wastes, including commercial chemical products, manufacturing chemical intermediates, and spent solvents, must be in accordance with applicable state and/or federal regulations (ATSDR, 1993). Incineration is one recommended method of disposal. Solvent mixtures and sludges should be incinerated at temperatures high enough to ensure complete combustion (ATSDR, 1993). Benzene is a good candidate for incineration using appropriate temperatures and residence times (HSDB , 2001).
Aeration or activated sludge processing, as well as the use of activated carbon, has been shown to be one method of processing waste water containing benzene (ATSDR, 1993). Full scale activated carbon column treatment resulted in a 48-80% removal of benzene (HSDB , 2001). In-situ bioremediation of benzene, toluene, ethylbenzene and the xylenes (BTEX) was conducted in a fuel-contaminated, oxygen-poor aquifer. Extracted groundwater was enriched with ammonium polyphosphate as nutrient and potassium nitrate as the electron acceptor. It was then piped to an infiltration gallery over the contaminated site. BTEX measurements declined by 78% in the most contaminated well and by nearly 99% in another well. Final data indicated that the BTEX was biodegraded in-situ in the nitrate-enriched aquifer under denitrifying conditions (Gersberg et al, 1995). Data from continuous activated sludge biological treatment simulators indicate that the removal percentages of benzene range from 44% to 100% (Howard et al, 1991).
Air stripping, steam stripping, and solvent extraction can be used to process wastewater that contains benzene (ATSDR, 1993). Air stripping, useful for the removal of volatile organic compounds from water or aqueous waste streams, can be applied to solvents, including benzene, at ambient temperatures. Air stripping has found its widest application in the remediation of aquifers contaminated with solvents (Freeman, 1989).
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- Benzene is a common air contaminant (Lewis, 1998).
- Benzene will enter the atmosphere primarily from fugitive emissions and exhaust connected with its use in gasoline. Another important source is emissions associated with its production and use as an industrial intermediate. In addition, there are discharges into water from industrial effluents and losses during spills. Naturally occurring sources of benzene include volcanoes, crude oil of which it is a natural constituent, forest fires, and plants (HSDB, 2004).
- Inhalation of air containing benzene is the primary route of human exposure to benzene. Areas of particular concern are areas with heavy traffic and near filling stations, as well as industrial zones. Exposure to tobacco smoke is another route of exposure (HSDB, 2004).
- Benzene occurs in both groundwater and surface public water supplies with higher levels occurring in groundwater supplies. Based upon federal drinking water surveys, approximately 1.3% of all groundwater systems are estimated to contain benzene at levels greater than 0.5 mcg/L (HSDB, 2004).
ENVIRONMENTAL FATE AND KINETICS
Benzene will exist solely as a vapor in the atmosphere, and it can be removed from the atmosphere by rain (HSDB, 2004). Vapor-phase benzene in the atmosphere is degraded when it reacts with hydroxyl radicals. It is estimated that the half-life for this reaction is 13 days (HSDB, 2004). Photochemical reactions occur in the atmosphere with benzene. Benzene's estimated lifetime is 28 hours under photochemical smog conditions in SE England (Verschueren, 2001). Atmospheric half-life for reaction with hydroxyl radicals: 5.7D (Verschueren, 2001) Atmospheric half-life for reaction with ozone: 170,000D (Verschueren, 2001) The photooxidation half-life of benzene in air ranges from 50.1 hours (2.09 days) to 501 hours (20.9 days), based on the measured rate data for reaction with hydroxyl radicals in air (Howard et al, 1991). Scientific judgement of the atmospheric photolysis half-life of benzene is from 2808 hours (117 days) to 16,152 hours (673 days) based on measured photolysis half-lives in deionized water (Howard et al, 1991). The lambda maximum light absorption of benzene in cyclohexane is approximately 239 nm, 244 nm, 249 nm, 255 nm, 261 nm, and 268 nm. Absorption in cyclohexane extends to approximately 285 nm; absorption in the gas phase extends to approximately 275 nm (Howard et al, 1991).
Benzene has the following half-lives in air: 20.9 days (high); 2.09 days (low) (Howard, 1991).
SURFACE WATER It is expected that volatilization from water surfaces will be an important fate process. This is based on benzene's Henry's Law Constant of 5.56x10(-3) atm-m(3)/mole (HSDB, 2004). Using estimation methods and modeling techniques, benzene will likely volatilize from water surfaces. The volatilization half-life for a model river is 1 hour, and the volatilization half-life for a model lake is 3.5 days (HSDB, 2004). Evaporation half-lives in water at 25 degrees C and 1 m depth are 4.81H, based on an evaporation rate of 0.144 m/H, and 5.03H, based on an evaporation rate of 0.137 m/H (Verschueren, 2001).
Benzene is not expected to adsorb to sediment or suspended solids in water. This is based on benzene's Koc value of 85 (HSDB, 2004). Scientific judgement of the aqueous photolysis half-life range for benzene is from 2808 hours (117 days) to 16,152 hours (673 days) based on measured photolysis half-lives in deionized water (Howard et al, 1991). The half-life just below the surface is approximately 80D based on reaction with hydroxyl radicals. Linear increases in the half-life occur with increasing depth due to decreasing light intensity (Verschueren, 2001). Benzene levels from 6-24 mcg/L in estuaries had a half-life of 15-38D (Verschueren, 2001). In a sea mesocosm at a depth of 5.5 ft and concentration range of 0.2-4 mcg/L, benzene half-lives were (Verschueren, 2001): - 13D at 3-7 degrees C;
- 23D at 6-16 degrees C; and
- 3.1D at 20-22 degrees C.
Benzene will react with hydroxyl radicals at a rate of 7.8X10(9) L/mol sec in aqueous solutions. The half life of benzene is estimated to be 103 days (HSDB, 2004). The photooxidation half-life of benzene in water ranges from 8021 hours (334 days) to 3.21 x 10(5) hours (36.6 years) based on the measured rate data for hydroxyl radicals in aqueous solution (Howard et al, 1991). Benzene has the following half-life in surface water: 16 days (high); 5 days (low) (Howard, 1991). Degradation of benzene in water involves biotic transformation processes (Verschueren, 2001).
GROUND WATER
TERRESTRIAL It is expected that benzene will be very mobile if it is released to soil (HSDB, 2004). It is possible that benzene will volatilize from dry soil (HSDB, 2004). Adsorption of benzene vapor on the surface of soils was less than 4% of the total adsorption. This result indicates that uptake was due mainly to condensation, rather than to partitioning or monolayer sorption. Uptake was greater for soils with higher organic carbon content (Li & Voudrias, 1993). The diffusive transport of benzene was measured in air-dry soils to test the effect of non-linear sorption. The chemical followed the BET type sorption model. The increase of diffusivity with high initial chemical concentration produced higher-than-predicted emission rates (Shonnard et al, 1993). Volatilization of benzene from moist soil surfaces is expected to be an important fate process, based on a Henry's Law constant of 5.56x10(-3) atm-m(3)/mole (HSDB, 2004). Benzene administered in aqueous solution or as a vapor is translocated and metabolized in higher plants (Verschueren, 2001). Benzene has the following half-life in soil: 16 days (high); 5 days (low) (Howard, 1991). Benzene will biodegrade in some soils (Verschueren, 2001).
ABIOTIC DEGRADATION
- Benzene is highly mobile in soil. It volatilizes from soil and water surfaces, and exists as a vapor in the atmosphere. Photooxidation and photolysis contribute to the fate of benzene in air and water. Vapors react with hydroxyl radicals and ozone, to a lesser extent. Adsorption in soil is not significant. Biodegradation may occur in water and soil systems, leading to biotransformation of the material (HSDB, 2004; Verschueren, 2001; Howard, 1991; Howard et al, 1991).
BIODEGRADATION
- The biodegradation half-life is 27 weeks in a methanogenic aquifer at 17 degrees C and an initial benzene concentration of 613 mcg/L (Verschueren, 2001).
- Biodegradation half-lives in non-adapted aerobic subsoil (Verschueren, 2001):
12D (Florida groundwater system); 24D (Oklahoma river system); 48D (Ontario sand system); and >161D (Texas sand system).
- A biodegradation study in a base-rich para-brownish soil indicated that benzene should biodegrade in soil. The soil had a 20 ppm concentration of benzene. 24% degraded in 1 week, 44% degraded in 5 weeks, and 47% degraded in 10 weeks (HSDB, 2004).
- It is expected that benzene will biodegrade in water. An experiment showed almost complete degradation of benzene from an aqueous solution within 90 hours (HSDB, 2004).
- The white rot fungus, Phanerochaete chrysosporium, degraded benzene either alone or in a mixture with toluene, xylene, and ethylbenzene, with substantial mineralization to carbon dioxide (Yadav & Reddy, 1993).
- Benzene resisted biodegradation under anaerobic, denitrifying conditions, in both field and laboratory tests (Barbaro et al, 1992).
- The transport and biodegradation of benzene and toluene in the subsurface environment was simulated with a one-dimensional numerical model. The governing equations included five nonlinear partial differential equations describing component transport, five nonlinear algebraic equations simulating interphase mass exchange, and two ordinary differential equations simulating microbial growth. The model was tested against actual lab and field results and found to be in reasonable agreement with experimental data. Microbial parameters dominated the sensitivity analyses and emphasized the importance of accurate estimates of these data (Chen et al, 1992).
- Bacterial strains isolated from contaminated soils and groundwater were tested and shown to degrade up to 54% of chlorobenzene in 7 days with no accumulation of 3-chlorocatechol. Other isolates grew on benzene, p-cresol, phenol and p-dichlorobenzene and suggested the indigenous microbial community at a contaminated site might provide the appropriate degrading organism to degrade aromatic compounds if cultured properly (Nishino et al, 1992).
- Summary of reported biodegradation rates for benzene (Dragun, 1988):
In a static-culture flask biodegradation test (original culture) using settled domestic wastewater as the microbial inoculum, 43% of the benzene degraded in 7 days. Benzene had an estimated half-life of 110 days based on field observation in a naturally occurring soil-groundwater system. Another field observation under similar conditions estimated a half-life of 68 days. Benzene had a half-life of 48 days in a groundwater incubation study using natural microbial flora as the inoculum. In a soil incubation study using natural microbial flora as the inoculum, 20% to 90% of the benzene degraded in 80 days. It was estimated that in a naturally occurring soil-groundwater system, 100% of the benzene was degraded based on field observation. In a soil incubation study using natural microbial flora as the inoculum, greater than 99% of the benzene degraded in 120 weeks.
BIOACCUMULATION
TERRESTRIAL In a laboratory soil-plant system, biouptake of benzene occurred in barley and cress at 0.065% and 0.24%, respectively. Approximately 62% of the benzene in the system was mineralized, 0.25% was volatilized, and 0.93% remained as soluble soil metabolites (Verschueren, 2001).
Algae (Selenastrum capricornutum): 1.63 (log BCF) (Verschueren, 2001) Anchovy (Engraulis mordex): 5-135 (BCF) (Verschueren, 2001) Atlantic herring (Clupea harengus): 1.0-14 (BCF) (Verschueren, 2001) Bluegill: 1.48 (BCF) (Verschueren, 2001) Goldfish: 4.3 (BCF) (Verschueren, 2001) Green algae (Chlorella fusca): 30 (BCF, wet weight) (Verschueren, 2001) Green algae (Chlorella fusca, var. vacuolata): 30 (BCF) (Verschueren, 2001) Japanese eel (Anguilla japonica): 3.3-3.5 (BCF) (Verschueren, 2001) Pacific herring (Clupea harengus pallasi) (Verschueren, 2001): Rainbow trout: 1.72 (BCF)(Verschueren, 2001) Striped bass (Morone saxatilis): 1.1 (BCF) (Verschueren, 2001) Water flea (Daphnia pulex): 153; 203; 225 (BCFs) (Verschueren, 2001) Benzene has a bioconcentration factor ranging from 1.1 to 20. This BCF indicates that bioconcentration in aquatic organisms is low (HSDB, 2004).
ENVIRONMENTAL TOXICITY
- Benzene inhibited photosynthesis in a freshwater nonaxenic unialgal culture of Selanastrum capricornutum (Verschueren, 2001).
- Herring (Clupea pallasi) and anchovy (Engraulis mordex) larvae exhibited benzene toxicity (Verschueren, 2001):
35-45 ppm caused delay in egg development and abnormal larvae. 10-35 ppm caused delay in larvae development, decreased feeding and growth, and increased respiration.
- Chinook salmon (Onchorhynchus tschawytscha): 5-10 ppm led to an initial increase in respiration (Verschueren, 2001).
- Striped bass (Morone saxatilis): 5-10 ppm led to an initial increase in respiration (Verschueren, 2001).
LC100 - (WATER) CILIATE (Tetrahymena pyriformis): 12.8 mcmole/L for 24H, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) GRASS SHRIMP (Palaemonetes pugio): 27 ppm for 96H, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) CRAB, Larva, stage 1 (Cancer magister): 108 ppm for 96H, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) SHRIMP (Crangon franciscorum): 20 mg/L for 96H, conditions of bioassay not specified(HSDB, 2004) LC50 - (WATER) BASS: Morone saxatilis: 5.8 to 11 mg/L for 96H, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) GUPPY (Poecilia reticulata): 63 mg/L for 14 days, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) BROWN TROUT, Yearlings (Salmo trutta): 12 mg/L for 1H, static bioassay (HSDB, 2004) LC50 - (WATER) MEXICAN AXOLOT (Ambystoma mexicanum): 3 to 4 weeks after hatching, 370 mg/L for 48H, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) CLAWED TOAD, 3 to 4 weeks after hatching: 190 mg/L for 48H, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) GOLDFISH (Carassius auratus): 46 mg/L for 24H, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) BLUEGILL SUNFISH (Lepomis macrochirus): 20 mg/L for 24 to 48H, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) BRINE SHRIMP: 66 - 21 mg/L for 24H - 48H, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) FATHEAD MINNOW (Pimephales promelas): 35 - 33 mg/L for 24H - 96H, soft water, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) FATHEAD MINNOW (Pimephales promelas): 24 to 32 mg/L for 24H - 96H, hard water, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) BLUEGILL: 22 mg/L for 24H - 48H, soft water, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) GOLDFISH (Carassius auratus): 34.4 mg/L for 24H - 96H, soft water, conditions of bioassay not specified (HSDB, 2004) LC50 - (WATER) MOSQUITO FISH (Gambusia affinis): 395 mg/L for 24H - 96H, conditions of bioassay not specified (HSDB, 2004) LD100 - (WATER) BLUEGILL SUNFISH (Lepomis macrochirus): 34 mg/L for 24H, conditions of bioassay not specified (HSDB, 2004) LD100 - (WATER) BLUEGILL SUNFISH (Lepomis macrochirus): 60 mg/L for 2H, conditions of bioassay not specified (HSDB, 2004) TLm - (WATER) GUPPY (Lebistes reticulata): 36 mg/L for 24H - 96H, soft water, conditions of bioassay not specified (HSDB, 2004)
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Benzene is a colorless, watery liquid with a gasoline-like odor (CHRIS , 2001).
- Benzene is a liquid at 15 degrees C and 1 atm (CHRIS , 2001).
- Benzene is a clear, colorless liquid (Budavari, 1996).
- Benzene is a colorless to light-yellow liquid. Below 42 degrees F, it is a solid (HSDB , 2001).
- The taste threshold of benzene in water is 0.5-4.5 mg/L (HSDB , 2001)
VAPOR PRESSURE
- 95.19 mmHg (at 25 degrees C) (Howard, 1990)
- 75 mmHg (at 20 degrees C) (NFPA, 1997)
- 94.8 mmHg (at 25 degrees C) (HSDB , 2001)
- 100 mmHg (at 26.1 degrees C) (Lewis, 2000)
SPECIFIC GRAVITY
- OTHER TEMPERATURE AND/OR PRESSURE
- TEMPERATURE AND/OR PRESSURE NOT LISTED
DENSITY
- OTHER TEMPERATURE AND/OR PRESSURE
FREEZING/MELTING POINT
5.5 degrees C (Budavari, 2000; Howard, 1990) 6 degrees C; 42 degrees F (NFPA, 1997) 5.56 degrees C (OHM/TADS , 2001)
BOILING POINT
- 80.1 degrees C (Budavari, 2000; Howard, 1990)
- 80 degrees C; 176 degrees F (NFPA, 1997)
- 80.093-80.094 degrees C (Lewis, 2000)
FLASH POINT
- -11 degrees C; 12 degrees F (closed cup) (Budavari, 2000)
AUTOIGNITION TEMPERATURE
- 498 degrees C; 928 degrees F (NFPA, 1997)
- 580 degrees C (ATSDR, 1993)
- 1044 degrees F (Lewis, 2000)
- 562 degrees C (ACGIH, 1991)
EXPLOSIVE LIMITS
SOLUBILITY
1791 mg/L (Howard, 1990) 1780 mg/L (at 25 degrees C) (ATSDR, 1993) 820 ppm (at 25 degrees C) (OHM/TADS , 2001) Benzene is not soluble in water (NFPA, 1997). 0.07% (NIOSH , 2001) SOLUBILITY IN LIQUID HYDROCARBON SOLVENTS
Benzene is miscible with alcohol, chloroform, ether, carbon disulfide, acetone, oils, carbon tetrachloride, and glacial acetic acid (Budavari, 2000).
OCTANOL/WATER PARTITION COEFFICIENT
- log Kow=2.13 (Howard, 1990; HSDB , 2001)
HENRY'S CONSTANT
- 5.43X10(-3) atm-m(3)/mole (Howard, 1990)
- 5.56X10(-3) atm-m(3)/mole (at 25 degrees C) (HSDB , 2001)
SPECTRAL CONSTANTS
OTHER/PHYSICAL
4.68 ppm (CHRIS , 2001) 1.5 - 4.7 ppm (ATSDR, 1993) 2.0 mg/L (in water) (ATSDR, 1993) 4.9 ppm (mg/m(3)) (Sittig, 1991) 12 ppm (ACGIH, 1991)
28.22 mN/m (at 25 degrees C) (HSDB , 2001) 28.9 dynes/cm (0.0289 N/m) (at 20 degrees C)est.; 35.0 dynes/cm (0.035 N/m)(at 20 degrees C) (CHRIS , 2001)
-17,460 Btu/lb; -9698 cal/g; -406.0x10(5) J/kg (CHRIS , 2001) -3275.3 kJ/mol (HSDB , 2001)
30.45 cal/g (CHRIS , 2001) 9.95 kJ/mol (HSDB , 2001)
- NUCLEAR MAGNETIC RESONANCE
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