Organochlorine Pesticides Overview
Organochlorine pesticides, an older class of pesticides, are effective against a variety of insects. These chemicals were introduced in the 1940s, and many of their uses have been cancelled or restricted by the U.S. EPA because of their environmental persistence and potential adverse effects on wildlife and human health. Many organochlorines are no longer used widely in the U.S., but other countries continue to use them. Hexachlorobenzene has been used primarily as a fungicide or biocide.
Organochlorine pesticides can enter the environment after pesticide applications, disposal of contaminated wastes into landfills, and releases from manufacturing plants that produce these chemicals. Some organochlorines are volatile, and some can adhere to soil or particles in the air. In aquatic systems, sediments adsorb organochlorines, which can then bioaccumulate in fish and other aquatic mammals. These chemicals are fat soluble, so they are found at higher concentrations in fatty foods. In the general population, diet is the main source of exposure, primarily through the ingestion of fatty foods such as dairy products and fish. Usage restrictions have been associated with a general decrease in serum organochlorine levels in the U.S. population and other developed countries (Hagmar et al, 2006; Kutz et al., 1991). Contaminated drinking water and air are usually minor exposure sources. Infants can be exposed through breast milk, and the fetus can be exposed in utero via the placenta. Workers can be exposed to organochlorines in the manufacture, formulation, or application of these chemicals. The FDA, U.S. EPA, and OSHA have developed standards for allowable levels of certain organochlorines in foods, the environment, and the workplace, respectively. Attributing human health effects to specific organochlorine chemicals is difficult because exposure to multiple organochlorine chemicals occurs often, and these chemicals may have similar actions.
The table shows selected parent organochlorines and their metabolites that can be measured in serum or urine. Measurements of these chemicals can reflect either recent or cumulative exposures, or both. Some of the metabolites can be produced from more than one pesticide. The level of a metabolite in a person's blood or urine may indicate exposure to the parent pesticide as well as to the metabolite itself.
|Organochlorine Pesticides and Metabolites Measured in the National Biomonitoring Program|
|Organochlorine pesticide (CAS number)||Serum pesticide or metabolite(s) (CAS number)||Urinary pesticide or metabolite(s) (CAS number)|
|Dieldrin (60-57-1)||Dieldrin (60-57-1)|
|Endrin (72-20-8)||Endrin (72-20-8)|
|Heptachlor (76-44-8)||Heptachlor epoxide (1024-57-3)|
|Hexachlorobenzene (118-74-1)||Hexachlorobenzene (118-74-1)||
|Mirex (2385-85-5)||Mirex (2385-85-5)|
CAS No. 2385-85-5
Mirex has not been produced or used in the U.S. since 1977. Formerly, its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.S., where it was applied directly to soil and by aerial spraying. Mirex binds strongly to soil, where it has a half-life of 12 years; it is a highly persistent chemical in the environment. Mirex has been detected in air, soil, sediments, water, aquatic organisms, animals, and foods. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR, 1995). The most likely sources of human exposure to mirex are eating fish from contaminated water or living in areas with soil contaminated by historic mirex manufacturing, disposal, or pesticide application. Some states and the U.S. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. Occupational exposure is limited to workers at sites where mirex contamination is present.
Mirex is absorbed through the skin and from the gastrointestinal tract, after which it is widely distributed in the body and stored in fat. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. Mirex is not metabolized in the body. In studies conducted in the 1970's and 1980's, mirex was detected in human adipose samples, especially those from persons living in the southeastern U.S. (Kutz et al., 1985, 1991). Mirex can cross the placenta and be excreted in breast milk, resulting in exposure to newborns and nursing infants.
Human health effects from mirex at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Laboratory animals fed high doses developed liver enlargement and liver tumors; reproductive toxicity included decreased fertility and testicular damage. In addition, developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR, 1995; Smith, 1991). The U.S. EPA has established environmental standards for mirex, and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue. IARC classifies mirex as possibly carcinogenic to humans, and NTP classifies mirex as reasonably anticipated to be a human carcinogen. More information about external exposure (i.e., environmental levels) and health effects is available from the ATSDR at http://www.atsdr.cdc.gov/toxprofiles/index.asp.
In the NHANES 1999-2000, 2001-2002, and 2003-2004 subsamples, as well as in a subsample of NHANES II (1976-1980) participants, serum mirex levels were generally below the limits of detection (CDC, 2009; Stehr-Green, 1989). Fishermen in New York who consumed Great Lakes sport fish had median levels of lipid-adjusted serum mirex that were lower than the 95th percentile value among males the NHANES 2001-2002 subsample (Bloom et al., 2005; CDC, 2009). In samples obtained between 1994 and 1997, Inuit mothers from three Arctic areas had geometric mean serum mirex levels that were threefold to sevenfold higher than non-Inuit mother from other Arctic regions. The geometric mean mirex levels of the Inuit mothers were 8, 7.8, and 4.7 ng/g of lipid, which is approximately twofold to threefold lower than the 90th percentile for females in the NHANES 2001-2002 subsample but similar to 95th percentile for females in the NHANES 2003-2004 subsample (CDC, 2009; Van Oostdam et al., 2004).
Finding a measurable amount of mirex in serum does not imply that the level of mirex causes an adverse health effect. Biomonitoring studies on levels of mirex provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of mirex than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.
Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for mirex and chlordecone [online]. August 1995. Available at URL: http://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=1190&tid=276. 12/28/12
Bloom MS, Vena JE, Swanson MK, Moysich KB, Olson JR. Profiles of ortho-polychlorinated biphenyl congeners, dichlorodiphenyldichloroethylene, hexachlorobenzene, and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Environ Res 2005;97(2):178-192.
Centers for Disease Control and Prevention (CDC). Fourth National Report on Human Exposure to Environmental Chemicals. 2009. [online] Available at URL: http://www.cdc.gov/exposurereport/. 12/28/12
Hagmar L, Wallin E, Vessby B, Jonsson BA, Bergman A, Rylander L. Intra-individual variations and time trends 1991-2001 in human serum levels of PCB, DDE and hexachlorobenzene. Chemosphere 2006;64(9):507-13.
Kutz FW, Strassman SC, Stroup CR, Carra JS, Leininger CC, Watts DL, et al. The human body burden of mirex in the southeastern United States. J Toxicol Environ Health 1985;15:385-394.
Kutz FW, Wood PH, Bottimore DP. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Rev Environ Contam Toxicol 1991;120:1-82.
Smith AG. Chlorinated Hydrocarbon Insecticides. In Hayes WJ, Jr and Laws ER, Jr, Eds. Handbook of Pesticide Toxicology, Vol. 2 Classes of Pesticides. New York, Academic Press, Inc. 1991 pp. 731-915.
Stehr-Green, PA. Demographic and seasonal influences on human serum pesticide residue levels. J Toxicol Environ Health 1989;27:405-421.
Van Oostdam JC, Dewailly E, Gilman A, Hansen JC, Odland JO, Chashchin V, et al. Circumpolar maternal blood contaminant survey, 1994-1997 organochlorine compounds. Sci Total Environ 2004;330:55-70.