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. 72-20-8
Endrin, a stereoisomer of dieldrin, is no longer manufactured in the U.S. All uses of the pesticide in the U.S. have been cancelled by the U.S. EPA. Endrin was used as an insecticide, rodenticide and avicide. Endrin was not widely used as a termiticide, unlike aldrin and dieldrin. Depending on soil conditions, endrin can persist for years. Ketoendrin is a major photodegradation product (IPCS, 1992). Endrin has been detected in soils, and occasionally at low levels in sediment and surface waters, largely the result of historical agricultural application or run off from contaminated soils (ATSDR, 1996; IPCS, 1992).
General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used, or from contact with contaminated soils and sediments in areas where endrin was applied, manufactured, or discarded. Over time, endrin has been detected with declining frequency in U.S. total diet surveys (FDA, 2010). Endrin is absorbed rapidly after ingestion, inhalation or dermal exposure routes. In the body, endrin is converted rapidly to its major metabolite, anti-12-hydroxyendrin. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. Because it is metabolized so rapidly, endrin usually is not detected in serum of exposed individuals, unless the dose is high and the exposure is very recent. Endrin does not accumulate in body tissues. (IPCS, 1992; Smith, 1991)
Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. At high doses, endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al., 1992). An epidemic of acute endrin poisoning, characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al., 1987). High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. Hepatic effects of endrin exposure have included necrosis, fatty infiltration, and inflammation (Smith, 1991). Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al., 1979; Kavlock et al., 1981).
The U.S. EPA has established environmental standards for endrin, and the FDA monitors foods for pesticide residues. Workplace exposure standards for endrin have been established by OSHA. IARC has determined that endrin is not classifiable with regard to human carcinogenicity. Information about external exposure (i.e., environmental levels) and health effects of endrin is available from ATSDR at http://www.atsdr.cdc.gov/toxprofiles/index.asp.
In the NHANES 2001-2002 and 2003-2004 subsamples, serum levels of endrin were below the limit of detection (CDC, 2009). This finding is consistent with other general population studies (Bates et al., 2004; Ward et al., 2000). In a small study of Spanish women hospitalized for elective surgery, endrin was detected in 9% of serum samples, with the highest value 6.24 ng/mL (about 6.24 ng/g of serum) (Botella et al., 2004).
Finding a measurable amount of endrin in serum does not imply that the level of endrin causes an adverse health effect. Biomonitoring studies on levels of endrin provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of endrin 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 endrin [online]. August 1996. Available at URL: http://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=617&tid=114. 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.
Botella B, Crespo J, Rivas A, Cerrillo I, Olea-Serrano MF, Olea N. Exposure of women to organochlorine pesticides in Southern Spain. Environ Res 2004;96:34-40.
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
Chernoff N, Kavlock RJ, Hanisch RC, Whitehouse DA, Gray JA, Gray LE, et al. Perinatal toxicity of endrin in rodents. I. Fetotoxic effects of prenatal exposure in hamsters. Toxicology 1979;13:155-65.
Food and Drug Administration (FDA). FDA Pesticide Program Residue Monitoring: 1993-2008. [online]. Updated 10/27/2010. Available at URL: http://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.
International Programme on Chemical Safety (IPCS). Environmental Health Criteria 130. Endrin [online]. 1992. Available at URL: http://www.inchem.org/documents/ehc/ehc/ehc130.htm. 12/28/12
Kavlock RJ, Chernoff H, Hanisch RC, Gray J, Rogers E, Gray LE. Perinatal toxicity of endrin in rodents. II. Fetotoxic effects of prenatal exposure in rats and mice. Toxicology 1981;21:141-50.
Kutz FW, Wood PH, Bottimore DP. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Rev Environ Contam Toxicol 1991;120:1-82.
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.
Rowley DL, Rab MA, Hardjotanojo W, Liddle J, Burse VW, Saleem M, Sokal D, et al. Convulsions caused by endrin poisoning in Pakistan. Pediatrics 1987;79(6):928-34.
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.
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.