Biomonitoring Summary

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

Table of Phthalates and Urinary 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)
Aldrin (309-00-02)	Aldrin (309-00-02) Dieldrin (60-57-1)
Chlordane (12789-03-6)	Oxychlordane (27304-13-8) trans-Nonachlor (3734-49-4)
Dichlorodiphenyltrichloroethanes	p,p'-DDT (50-29-3) p,p'-DDE (72-55-9) o,p'-DDT (789-02-6)
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)	Pentachlorophenol (87-86-5) 2,4,6-Trichlorophenol (88-06-2) 2,4,5-Trichlorophenol (95-95-4)
Hexachlorocyclohexanes	beta-Hexachlorocyclohexane (319-85-7) gamma-Hexachlorocyclohexane (58-89-9)	Pentachlorophenol (87-86-5) 2,4,6-Trichlorophenol (88-06-2) 2,4,5-Trichlorophenol (95-95-4)
Mirex (2385-85-5)	Mirex (2385-85-5)
Chlorophenols, including 2,4,5-Trichlorophenol (95-95-4) 2,4,6-Trichlorophenol (88-06-2)		2,4,5-Trichlorophenol (95-95-4) 2,4,6-Trichlorophenol (88-06-2)

2,4,5-Trichlorophenol

CAS No. 95-95-4

2,4,6-Trichlorophenol

CAS No. 88-06-2
Metabolites of Organochlorine Pesticides and Other Environmental Chemicals

General Information

The chlorophenols, 2,4,5-trichlorophenol (2,4,5-TCP) and 2,4,6-trichlorophenol (2,4,6-TCP), are metabolites of several organochlorine chemicals, including hexachlorobenzene and hexachlorocyclohexanes. Historically, 2,4,5-TCP and 2,4,6-TCP were used as intermediates in the production of certain pesticides; 2,4,6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR, 1999). Trichlorophenols are no longer manufactured commercially, but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds. Formation of 2,3,7,8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2,4,5-trichlorophenol. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites. Both chemicals have been detected in air, surface water, soils, and sediments; however, recent sampling of U.S. public drinking water systems did not detect 2,4,6-TCP in any of the samples (U.S. EPA, 2006). Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR, 1999).

General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air. Exposure to trichlorophenols also may result from metabolism of lindane, hexachlorobenzene, other organochlorines, and polychlorinated benzenes (Kohil et al., 1976). Occupational exposures, usually at herbicide production or waste incineration facilities, may occur by inhalation or dermal routes. Such workers would probably be exposed to mixtures of chlorophenols, in addition to dioxins, furans, and other chlorinated compounds. However, recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al., 2003; Radon et al., 2004).

Human health effects from 2,4,5-TCP or 2,4,6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Laboratory animals chronically fed high doses of 2,4,6-TCP had increased rates of hepatic tumors, leukemias, and lymphomas. At lower doses, animals showed hepatocellular abnormalities. Neither 2,4,5-TCP nor 2,4,6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). IARC classifies combined exposures to polychlorophenols, which includes trichlorophenols, as being possibly carcinogenic to humans. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2,4,5-TCP and limited for 2,4,6-TCP. NTP classifies 2,4,6-TCP as reasonably anticipated to be a human carcinogen. More information about external exposure (i.e., environmental levels) and health effects is available from ATSDR at https://www.atsdr.cdc.gov/toxprofiles/index.asp.

Biomonitoring Information

In the NHANES 2003-2004, 2005-2006, 2007-2008, and 2009-2010 subsamples, adult urinary 2,4,6-TCP levels at the 95thpercentile (1.1-1.3 µg/L) were about half the value 3.3 µg/L in a nonrandom adult subsample from NHANES III (Hill et al., 1995) and similar to the 95thpercentile value of 1.3 µg/L reported in German adults aged 18-69 years (Becker et al., 2003; CDC, 2012). Among 6-11 year old children in NHANES 2003-2004, the 95th percentile urinary 2,4,6-TCP level was approximately one half the value in the corresponding percentile for a small group of2-6 year old children living near an herbicide manufacturing facility: 1.9 versus 4 µg/L, respectively (CDC, 2012; Hill et al., 1989). In the same 2-6 year old children, the 95th percentile urinary 2,4,5-TCP, 7.0 µg/L, was more than 20 times greater than the corresponding percentile for 6-11 year old children in NHANES 2003-2004 (0.30 µg/L) (CDC, 2012; Hill et al., 1989). The 95th percentiles for urinary 2,4,5-TCP among adults in NHANES 2003-2004 were slightly higher than values reported in German adults aged 18-69 years: 0.4 and 0.9 µg/L (Becker et al., 2003; CDC, 2012). A small study of adults who ate Great Lakes sport fish reported a mean urine 2,4,5-TCP level of 0.7 µg/L, which is about two times greater than the 95%tile in NHANES 2003-2004 (Anderson et al., 1998; CDC, 2012). Urinary 2,4,5-TCP and 2,4,6-TCP were monitored in a group of hazardous waste incinerator workers from 1999-2002. Mean values of2,4,5-TCP (0.2-0.6 g/g creatinine) and 2,4,6-TCP (0.7-3.5 g/g creatinine) were similar or slightly lower than the higher percentiles (75th -95th) for males in NHANES 2003-2004 (Agramunt et al., 2003; CDC, 2012). In harbor workers exposed to chlorophenol-contaminated river silt, the 75th percentile urinary 2,4,6-TCP level, 0.36 g/g creatinine, was similar to the corresponding percentile in adult males in NHANES 2003-2004 (CDC, 2012; Radon et al., 2004). Sawmill workers exposed to chlorophenol wood preservatives had mean urinary 2,4,6-TCP levels ranging from 278 to 992 µg/L, more than 750 times greater than the 95th percentile level for adult males in the NHANES 2003-2004 subsample (CDC, 2012; Pekari et al., 1991).

Finding a measurable amount of 2,4,5-TCP or 2,4,6-TCP in urine does not imply that the level of2,4,5-TCP or 2,4,6-TCP causes an adverse health effect. Biomonitoring studies on levels of2,4,5-TCP and 2,4,6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2,4,5-TCP or 2,4,6-TCP than are found in the general population. Biomonitoring data will also help scientists plan and conduct research about 2,4,5-TCP or 2,4,6-TCP exposure and health effects.

References

Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for chlorophenols [online]. July 1999. Available at URL: https://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=941&tid=195. 12/28/12

Agramunt MC, Domingo A, Domingo JL, Corbella J. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Toxicol Lett 2003;146:83-91.

Anderson HA, Falk C, Hanrahan L, Olson J, Burse VW, Needham LL, et al. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. The Great Lakes Consortium. Environ Health Perspect 1998;106(5):279-289.

Becker K, Schulz C, Kaus S, Seiwert M, Seifert B. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Int J Hyg Environ Health 2003; 206:15-24.

Centers for Disease Control and Prevention (CDC). Fourth National Report on Human Exposure to Environmental Chemicals. Updated Tables. September 2012. [online] Available at URL: https://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.

Hill RH Jr, Head SL, Baker S, Gregg M, Shealy DB, Bailey SL, et al. Pesticide residues in urine of adults living in the United States: reference range concentrations. Environ Res 1995;71:99-108.

Hill RH Jr, To T, Holler JS, Fast DM, Smith SJ, Needham LL, et al. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Arch Environ Contam Toxicol 1989;18(4):469-474.

Kohli J, Jones D, Safe A. The metabolism of higher chlorinated benzene isomers. Can J Biochem 1976;54(3):203-208.

Kutz FW, Wood PH, Bottimore DP. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Rev Environ Contam Toxicol 1991;120:1-82.

Pekari K, Luotamo M, Jarvisalo J, Lindroos L, Aitio A. Urinary excretion of chlorinated phenols in saw-mill workers. Int Arch Occup Environ Health 1991;63:57-62.

Radon K, Wegner R, Heinrich-Ramm R, Baur X, Poschadel B, Szadkowski D. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Am J Ind Med 2004;45:440-445.

U. S. Environmental Protection Agency (U.S.EPA). The analysis of occurrence data from the first unregulated contaminant monitoring regulation (UCMR 1) in support of regulatory determinations for the second drinking water contaminant candidate list (CCL2). Office of Drinking Water (4607M). EPA 815-R-08-013. June 2008. [online] Available at URL: https://www.epa.gov/safewater/ccl/pdfs/reg_determine2/report_ccl2-reg2_ucmr1_occurrencereport.pdfpdf iconexternal icon. 12/28/12

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Page last reviewed: April 7, 2017

Content source: Centers for Disease Control and Prevention