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. 309-00-02
CAS No. 60-57-1
Also a Metabolite of Aldrin
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 and 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 https://www.atsdr.cdc.gov/toxprofiles/index.asp.
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 percentile 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.
Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for aldrin/dieldrin [online]. September 2002. Available at URL: https://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=317&tid=56. 12/28/12
Bates MN, Buckland SJ, Garrett N, Ellis H, Needham LL, Patterson DG Jr, et al. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Chemosphere 2004;54:1431-43.
Carlson JN, Rosellini RA. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Psychopharmacology (Berl) 1987;91(1):122-6.
Centers for Disease Control and Prevention (CDC). Fourth National Report on Human Exposure to Environmental Chemicals. 2009. [online] Available at URL: https://www.cdc.gov/exposurereport/. 12/28/12
Corrigan FM, Wienburg CL, Shore RF, Daniel SE, Mann D. Organochlorine insecticides in substantia nigra in Parkinson's disease. J Toxicol Environ Health, Part A 2000;59:229-34.
Edwards JW, Priestly BG. Effect of occupational exposure to aldrin on urinary D-glucaric acid, plasma dieldrin, and lymphocyte sister chromatid exchange. Int Arch Occup Environ Health 1994;66(4):229-34.
Food and Drug Administration (FDA). FDA Pesticide Program Residue Monitoring: 1993-2008. [online]. Updated 10/27/2010. Available at URL: https://www.fda.gov/Food/FoodSafety/FoodContaminantsAdulteration/Pesticides/ResidueMonitoringReports/default.htm. 12/18/12
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.
Hoyer AP, Grandjean P, Jorgensen T, Brock JW, Hartvig HB. Organochlorine exposure and risk of breast cancer. Lancet 1998;352:1816-20.
International Programme on Chemical Safety (IPCS). Environmental Health Criteria 91. Aldrin and Dieldrin [online]. 1989. Available at URL: http://www.inchem.org/documents/ehc/ehc/ehc91.htm. 12/28/12
Jorgenson JL. Aldrin and dieldrin: A review of research on their production environmental deposition and fate, bioaccumulation, toxicology, and epidemiology in the United States. Environ Health Perspect 2001;109(Supp1):113-39.
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Li AA, Mink PJ, McIntosh LJ, Teta MJ, Finley B. Evaluation of epidemiologic and animal data associating pesticides with Parkinson's disease. J Occup Environ Med 2005;47:1059-87.
Narahashi T, Frey JM, Ginsburg KS, Roy ML. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Toxicol Lett 1992;64-65 Spec. No:429-36.
Sanchez-Ramos J, Facca A, Basit A, Song S. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Exp Neurol 1998;150:263-21.
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.
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Stehr-Green, PA. Demographic and seasonal influences on human serum pesticide residue levels. J Toxicol Environ Health 1989;27:405-21.
Tully DB, Cox, VT, Mumtaz MM, David VL, Chapin RE. Six high-priority organochlorine pesticides, either singly or in combination, are nonestrogenic in transfected HeLa cells. Reprod Toxicol 2000;14:95-102.
United States Geological Survey (USGS). Pesticides in the Nation's Stream and Ground Water, 1992-2001. Revised Feb. 15, 2007 [online]. Available at URL: https://pubs.usgs.gov/circ/2005/1291/. 12/28/12
Ward EM, Schulte P, Grajewski B, Andersen A, Patterson DG Jr, Turner W, et al. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Cancer Epidemiol Biomarkers Prev 2000;9:1357-67.