Biomonitoring Summary

Organochlorine Pesticides Overview


CAS No. 309-00-02


CAS No. 60-57-1
Also a Metabolite of Aldrin

General Information

Aldrin and dieldrin are no longer produced or used in the U.S. From the 1950s to 1970, both chemicals were applied mainly as a soil insecticide or seed dressing for food and commodity crops. Dieldrin was also used for mothproofing clothes and carpets. In tropical countries, dieldrin was used as a residual spray in residential dwellings to control vector-borne diseases such as malaria. The U.S. EPA cancelled agricultural uses of both pesticides in 1970; termiticide uses were cancelled in 1987. Aldrin is readily converted to dieldrin in the environment and in plants that take up the chemical. Aldrin volatilizes after agricultural soil applications or is converted to dieldrin, which volatilizes more slowly. These chemicals persist in the environment and bioaccumulate in foods (Jorgenson 2001; USGS, 2007). Aldrin is rarely detected in plants or animal tissues, but dieldrin has been detected in meats, dairy products, and in crops grown in soils that have been contaminated, usually by application, manufacturing, or disposal.

General population exposure to these chemicals occurs through the diet, and detection of dieldrin residue in foods has decreased over time (FDA, 2010). Inhalation exposure may occur among people living in residences where aldrin was applied historically as a pesticide. Aldrin and dieldrin are absorbed following ingestion, inhalation, and dermal application. After absorption, aldrin is metabolized to dieldrin so rapidly that aldrin is rarely detected. Dieldrin accumulates in fatty tissues, and its metabolites are excreted in bile and feces (ATSDR, 2002). It is also excreted in breast milk and can cross the placenta. The elimination half-life of dieldrin is approximately 1 year (IPCS, 1989; Jorgenson 2001).

Human health effects from aldrin and dieldrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. At high doses, aldrin and dieldrin block inhibitory neurotransmitters in the central nervous system (Narahashi et al., 1992). This blocking action can cause abnormal excitation of the brain, leading to symptoms such as headache, confusion, muscle twitching, nausea, vomiting, and seizures. When fed to experimental animals, both aldrin and dieldrin caused liver enlargement and liver tumors; dieldrin at higher doses caused irritability, tremors, and occasionally, seizures (Smith, 1991). When dieldrin was fed to pregnant rodents, the offspring had altered CNS neurotransmitter levels (Sanchez-Ramos et al., 1998) and behavioral changes (Carlson and Rosellini, 1987). Studies done in vitro showed that dieldrin binds to estrogen receptors (Soto et al., 1995), but no estrogenic effect was noted in a study that used cultured cells (Tully et al., 2000). Epidemiologic a
nd animal studies have not conclusively associated dieldrin exposure with risk for developing Parkinson’s disease (Corrigan et al., 2000; Kanthasamy et al., 2005; Li et al., 2005).

The U.S. EPA has established environmental standards for aldrin and dieldrin, and the FDA monitors foods for pesticide residues. OSHA has established workplace exposure standards for aldrin and dieldrin. IARC has determined that aldrin and dieldrin are not classifiable with regard to human carcinogenicity. Information about external exposure (i.e., environmental levels) and health effects is available from ATSDR at

Biomonitoring Information

In the NHANES 2001-2002 and 2003-2004 subsamples, serum aldrin levels were below the limit of detection, similar to results in a subsample of NHANES II (1976-1980) (Stehr-Green, 1989). Levels of aldrin also were not detectable in 1996-1997 pooled samples from New Zealand adults (Bates et al., 2004).

Serum dieldrin levels at the 95th percentile in NHANES 2001-2002 and 2003-2004 subsamples were approximately ten times lower than the corresponding percentile measured in NHANES II (1976-1980), in which only 10.6% of the subsample had dieldrin levels above the limit of detection (CDC, 2009; Stehr-Green 1989). The median level in pooled samples from New Zealand adults obtained in 1996-1997 was generally similar to the 90th percentile for adults in NHANES 2001-2004 (Bates et al., 2004; CDC, 2009). In samples obtained between 1973 and 1991 from Norwegian women, the median serum dieldrin level was generally similar to the 90th percentile for females in NHANES 2001-2004 (CDC, 2009; Ward et al., 2000). Danish women whose serum was collected in 1976 had a median dieldrin level near the 95th percentile for females in NHANES 2001-2004 (CDC, 2009; Hoyer et al., 1998). In a study of pesticide applicators with occupational exposure to aldrin, median levels of dieldrin were more than thirtyfold higher than the 95th perce
ntile in the NHANES 2001-2002 and 2003-2004 subsamples (CDC, 2009; Edwards and Priestly 1994).

Finding a measurable amount of aldrin or dieldrin in serum does not imply that the level of aldrin or dieldrin causes an adverse health effect. Biomonitoring studies on levels of aldrin and dieldrin provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of aldrin or dieldrin 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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