Biomonitoring Summary

Organochlorine Pesticides Overview

Dichlorodiphenyltrichloroethane (DDT)

CAS No. 50-29-3

General Information

Dichlorodiphenyltrichloroethane (DDT) has been used widely as a broad spectrum insecticide in agriculture and for control of vector-borne diseases. It was produced and used in the U.S. after World War II until 1972, when virtually all use of it was banned. It is still used in some countries, particularly for endemic vector and malaria control. DDT was used at one time as a treatment for head and body lice. DDT usually refers to the technical product, which is a mixture containing p,p’-DDT (65%-80%), o,p’-DDT (15%-21%), p,p’-DDD (4% or less), and trace amounts of several related compounds. DDT is converted in the environment to other more stable chemical forms, including 1,1′-(2,2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1,1′-dichloro-(2,2-bis(p-chlorophenyl) ethane (DDD). These chemicals are highly persistent in soil, sediments, air, and water, as well as in plant and animal tissues. The biodegradation half-life of DDT in soil varies from 2 to 15 years, depending on conditions.

In the general U.S. population, food, particularly meat, fish, and dairy products, continues to be the primary source of DDT exposure, although DDT and DDE intakes have decreased over time (FDA, 2010; Gunderson, 1988). Food imported from countries that still use DDT may contain the chemical or its residues. DDT can be absorbed after ingestion, inhalation, or dermal exposure. In the body, DDT is converted to DDE and several other metabolites. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR, 2002; Smith, 1991). Only a small proportion of DDT is metabolized and excreted (Smith, 1991). DDT and DDE can cross the placenta, resulting in fetal exposure. Both chemicals are excreted in breast milk, resulting in exposure to nursing infants (Rogan, 1996).

Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown. In high dose, accidental exposures, overt signs of acute human toxicity include vomiting, tremor, and seizures. Experimental human dosing studies conducted over an 18 month period and during which doses well above environmental levels were given did not demonstrate overt clinical abnormalities (ATSDR, 2002; Hayes et al., 1956). In laboratory animals, both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al., 1998). DDT may bind to estrogen receptors (Chen et al., 1997); and o,p’-DDD and p,p’-DDE can produce anti-androgenic effects (Gray et al., 2001). Animal studies reported reduced fertility, premature delivery, reproductive organ abnormalities, and altered behavior after neonatal exposure (Eriksson and Talts, 2000; Gray et al., 2001). Reproductive effects in humans affecting birth weight, fertility, and duration of lactation, have not been consistently demonstrated (Beard, 2006; Gladen and Rogan, 1995; Jusko et al., 2006), although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al., 2001). Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al., 2004; Jusko et al., 2006; Longnecker et al., 2002; Mariussen and Fonnum, 2006). Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard, 2006; Calle et al., 2002; Snedeker, 2001). Studies of DDT exposure and pancreatic cancer, lung cancer, and leukemia have also been inconclusive (ADSDR. 2002; Beard, 2006). It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.g., polychlorinated biphenyls, other organochlorines, dioxins and furans).

A workplace standard for DDT has been established by OSHA and a guidance established by ACGIH. IARC classifies DDT (p,p’-DDT) as a possible human carcinogen. NTP considers DDT as being reasonably anticipated to be a human carcinogen. More information about external exposure (i.e., environmental levels) and health effects is available from the U.S. EPA at icon and from ATSDR at

Biomonitoring Information

DDE persists in the body longer than DDT, so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. In general, levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR, 2002; Smith, 1991). Since the 1970’s, mean serum levels of DDT and DDE in the U.S. population declined by about fivefold to tenfold (Anderson et al., 1998; Stehr-Green, 1989). Declining DDE levels over time have also been observed in the German population, and the most recent median levels for German adults and children are similar to comparable levels in NHANES (Becker et al., 2002; CDC, 2009; Heudorf et al., 2003; Link et al., 2005). Median DDE levels among a population-based sample of Swedish women in 1996-1997 were similar to females in the NHANES 1999-2000 subsample (CDC, 2009; Glynn et al., 2003). A study of New Zealand adults sampled in 1996-1997 reported median DDE levels that were about threefold higher than the median for adults in the NHANES 1999-2000 subsample (Bates et al., 2004; CDC, 2009). In a population-based sample of men and women from eastern Slovakia, the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels, respectively, for males and females in the NHANES 1999-2000 subsample (CDC, 2009; Pavuk et al., 2004).

Compared to females in the NHANES 1999-2000 subsample, mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of nearby agriculture (Botella et al., 2004; CDC, 2009). A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among U.S. males in NHANES (Bhatnagar et al., 2004; CDC, 2009). Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers, 309 versus 268 ng/g lipid, which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al., 2005; CDC, 2009). High mean levels of whole blood DDT (about 3,860 ng/L) and DDE (about 14,490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al., 1971). Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300g/L, considerably higher than levels in NHANES (Smith, 1991).

In the NHANES 1999-2000, 2001-2002 and 2003-2004 subsamples, serum levels of o,p’-DDT were below the limits of detection (CDC, 2009). In a subsample of NHANES II (1976-1980) participants, less than one percent had detectable serum levels of o,p’-DDT (Stehr-Green, 1989).

Finding a measurable amount of p,p’-DDT, o,p’-DDT, or p,p’-DDE in serum does not imply that the level of the chemical causes an adverse health effect. Biomonitoring studies on levels of DDT and DDE provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DDT or DDE 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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Page last reviewed: April 7, 2017