Biomonitoring Summary

Organochlorine Pesticides Overview


CAS No. 118-74-1

General Information

Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.S. primarily as a fungicide and seed treatment until the U.S. EPA cancelled its use in 1984. Although it is not manufactured as an end-product in the U.S., HCB may be created as either a by-product or an impurity in the manufacturing process for certain chemicals and pesticides.

Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications, and has been detected in soil, air, water, and sediment (Barber et al., 2005). It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR, 2002). The general population may be exposed to HCB through diet, particularly by consuming fish, wildfowl, or game taken from areas with HCB contamination, and foods with a high fat content. The FDA dietary surveys have shown that over time, HCB has been detected in fewer foods since the 1980s (FDA, 2010; Gunderson, 1988). Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.

HCB is well absorbed after oral administration, distributes widely throughout the body, and accumulates in fatty tissues where it persists for years. HCB is slowly metabolized, and elimination occurs by renal and fecal routes; breast milk is an additional route of elimination in nursing women. Urinary metabolites include pentachlorophenol (PCP), 2,4,5-trichlorophenol (2,4,5-TCP) and 2,4,6-trichlorophenol (2,4,6-TCP) (To-Figueras et al., 1997); these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al., 1976). Therefore, measuring HCB in serum is a specific indicator of exposure to the parent chemical.

Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Chronic feeding studies in animals have demonstrated kidney injury, immunologic abnormalities, reproductive and developmental toxicities, and liver and thyroid cancers (ATSDR, 2002). In humans, very high, acute doses produce central nervous system depression and seizures. HCB interferes with normal heme synthesis, which is manifested by increased delta-aminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity. With chronic exposure, a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda. This condition, as well as hypertrichosis, arthritis, thyromegaly, anorexia, and weakness, were seen in an epidemic of poisoning in Turkey that occurred from 1955 to 1959 when HCB-treated seed grain was diverted for bread production. Infants were exposed transplacentally and through breast milk, and many died before 2 years of age (Peters et al., 1982; Schmid, 1960).

IARC classifies hexachlorobenzene as possibly carcinogenic to humans, and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen. ACGIH has developed workplace exposure limits for HCB. The U.S. EPA has established a drinking water standard, and the FDA has established a bottled water standard for HCB. More information about external exposure (i.e., environmental levels) and health effects is available from the U.S. EPA at from ATSDR at

Biomonitoring Information

Serum concentrations reflect the body burden of HCB. HCB levels were generally below the limits of detection in the NHANES 1999-2000 and 2001-2002 subsamples (CDC, 2009). As a result of the lower limit of detection in NHANES 2003-2004, more HCB levels were quantified. Age-related increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al., 2002; Bertram et al., 1986; Glynn et al., 2003). In a representative sample of the 1998 German adult population, HCB levels were directly related to age, and the geometric mean concentration of HCB in whole blood was 0.44 g/L, lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 2001-2002, but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al., 2002; CDC, 2009). In the 1976-1980 NHANES subsample, HCB detection in serum also was proportional to age, but overall, only 4.9% of participants had quantifiable levels (Stehr-Green, 1989). In Spain, factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher, respectively, than the limits of detection (on a whole weight basis) in NHANES 1999-2000 and 2001-2002 (CDC, 2009; Herrero et al., 1999). Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al., 2005; Bradman et al., 2006). Over the past two decades, however, declines in background HCB levels ranging from around 50%-90% have been documented in studies using cord blood (Dallaire et al., 2002; Lackman, 2002) and among children (Link et al., 2005); the more recent values in these studies were similar to the lipid adjusted limit of detection in NHANES 1999-2000 and 2001-2002 (CDC, 2009; Dallaire et al., 2002; Lackmann, 2002; Link et al., 2005).

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


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Available at URL: 12/28/12

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