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Biomonitoring Summary


CAS No. 71-43-2

General Information

Benzene is a volatile chemical that is produced commercially from coal and petroleum sources. It is among the most abundantly produced chemicals in the U.S. and is used extensively as an industrial solvent, in the synthesis of numerous chemicals, and as an additive in unleaded gasoline (ATSDR, 2007).

Human exposure occurs primarily by inhaling benzene in ambient air (Hattemer-Frey et al., 1990; Wallace, 1996). Sources of benzene in the air may result from either natural (e.g., forest fires) or industrial sources. Among industrial sources, automobile emissions and vapor around gasoline filling stations contribute to benzene in air (ATSDR, 2007). Tobacco smoke contributes to benzene in indoor air (Duarte-Davidson, et al., 2001), and tobacco smoke is estimated to account for about half of the total estimated exposure to benzene (ATSDR, 2007). Indoor sources for benzene, which include the offgassing of building materials, account for a significant portion of a non-smoker's benzene exposure (Wallace, 1996; Wallace et al., 1987). The consumption of food, drinking water, and beverages are considered negligible sources of exposure unless benzene contamination has occurred, such as from leaking underground fuel storage tanks (ATSDR, 2007; Wallace, 1996). In recent years, less than five percent of domestic wells used for drinking water in the U.S. have been found to contain detectable amounts of benzene (Rowe et al., 2007). Workplace exposure to benzene may result from production, use, or transportation of petroleum products.

Benzene is well absorbed after inhalational, oral, or dermal exposure. In the blood, benzene is distributed rapidly throughout the body, especially into the brain and fatty tissues, and can cross the placenta. Benzene is metabolized in the liver, and some metabolites may be distributed to the bone marrow, where additional metabolism may result in toxic effects on hematopoietic cells (ATSDR, 2007; Ross, 2000). The primary benzene metabolites are phenol, catechol, hydroquinone, 1,2,4-benzenetriol, and to a lesser extent, trans, trans-muconic acid, which are eliminated in urine as glucuronide and sulfate conjugates (Ross, 2000). Urinary S-phenylmercapturic and t,t- muconic acids are used for monitoring workplace exposure. A very small amount of unchanged benzene is eliminated in the breath.

Accidental and intentional exposures to high concentrations of benzene vapor can lead rapidly to euphoria, central nervous system depression, cardiac arrhythmias, followed by unconsciousness and death (ATSDR, 2007). Workers have developed skin irritation following repeated dermal exposure and mucous membrane irritation following repeated vapor inhalation (ATSDR, 2007). Epidemiologic studies of workers in industries involving benzene have found that benzene exposure can cause bone marrow suppression and increases the risk of various leukemias (Savitz and Andrews, 1997). Supportive evidence for benzene carcinogenicity comes from animal studies and from in vitro studies demonstrating the clastogenic properties of benzene on blood forming cells (NTP, 1986; Ross, 2000). The background exposure levels for the general population have been estimated to be much lower than the estimated lowest effect level for benzene at which leukemia risk is increased (Duarte-Davidson, et al., 2001).

Workplace standards and guidelines for benzene have been established by OSHA and ACGIH, respectively. The U.S. EPA has established environmental and drinking water standards for benzene, and the FDA has established a bottled water standard. Benzene is classified as a known human carcinogen by IARC and by NTP. Information about external exposure (ie., environmental levels) and health effects is available from ATSDR at

Biomonitoring Information

Levels of blood benzene reflect recent exposure. The median levels of blood benzene observed in the NHANES 2001-2006 subsamples appear slightly lower than the median level in a nonrepresentative subsample of adults in NHANES III (1988-1994) (Ashley et al., 1994; CDC, 2012), as well for other previous studies of the U.S. general population (Bonanno et al., 2001; Buckley et al., 1997; Sexton et al., 2005 and 2006; Lin et al., 2008), and studies from other countries (Brugnone et al., 1994; Navasumrit et al., 2005).

Smoking, residing, or working in urban areas and exposure to gasoline and petroleum products can result in blood benzene levels that are higher than those in the nonsmoking general population (Ashley et al., 1995; Carrer et al., 2000; Backer et al., 1997). The amount and duration of cigarette smoking increases the likelihood of higher blood benzene levels (Bonanno et al., 2001; Churchill et al., 2001; Lin et al., 2008). Workers exposed to gasoline fumes, such as garage mechanics, drivers, and street vendors, and workers exposed to solvent fumes have been found to have blood benzene levels as much as tenfold higher than levels in the general population (Brugnone, et al., 1994 and 1999; Moolenaar et al., 1997; Perbellini et al., 2002; Romieu et al., 1999).

Finding a measurable amount of benzene in blood does not imply that the level of benzene causes an adverse health effect. Biomonitoring studies of blood benzene can provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of benzene than levels found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.


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Moolenaar RL, Brockton JH, Ashley DL, Middauth JP, Etzel RA. Blood benzene concentrations in workers exposed to oxygenated fuel in Fairbanks, Alaska. Int Arch Occup Environ Health 1997;69:139-143.

National Toxicology Program (NTP). Toxicology and carcinogenesis studies of benzene (CAS No. 71-43-2) in F344/N rats and B6C3F1 mice (gavage studies). National Toxicology Program Tech Rep Series No. 289. 1986 [online]. Available at URL: 10/16/12

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