CAS No. 87-86-5
Also a Metabolite of Several Organochlorine Insecticides
Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide, bactericide, herbicide, mollusicide, algaecide and insecticide. Since 1984, PCP use in the U.S. has been restricted, and it is used primarily as a preservative for wood to be used outdoors (e.g., utility poles and fence posts). PCP cannot be used on wood in residential or agricultural buildings. PCP has been detected in soils, air, water and sediments because of the large amounts that were produced and used historically. In the environment, PCP is degraded by sunlight and metabolized rapidly by microorganisms, plants, and animals, so it is relatively non-persistent. General population exposure to PCP may occur by inhalation of contaminated air, ingestion of contaminated food or water, and dermal contact with PCP-treated products. Human exposure to PCP has become less common. Workers who manufacture or apply PCP may inhale it or absorb it through exposed skin.
PCP is absorbed rapidly and well by all exposure routes. After absorption, PCP is distributed to most tissues and is not extensively metabolized. The parent compound and conjugates, along with small amounts of tetrachlorohydroquinone and conjugates, are eliminated in the urine. After a single dose, PCP is eliminated over a few days (Braun et al., 1979); with repeated or chronic exposure, the elimination half-life may be a week or more (Uhl et al., 1986). PCP also may be eliminated in urine as a metabolite of hexachlorobenzene, other polychlorinated benzenes, and possibly of lindane (IPCS, 2002; Kohli et al., 1976; To-Figueras et al., 1997).
Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Acute, high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation. Effects including hyperthermia, hypertension, and metabolic acidosis were observed in adults and children severely exposed to PCP through ingestion, inhalation, or skin absorption. Death can result from seizures and cardiovascular collapse. In animals, chronically administered high doses of PCP were hepatotoxic, carcinogenic, and adversely affected thyroid function (U.S.EPA, 2004; van Raaij et al., 1991). Pentachlorophenol is not mutagenic or teratogenic. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.
The U.S. EPA has developed standards for PCP in drinking water and the environment, and the FDA has established a standard for bottled water. OSHA has established an occupational standard. More information about external exposure (i.e., environmental levels) and health effects is available from the U.S. EPA at https://www.epa.gov/pesticides/external icon and from ATSDR at https://www.atsdr.cdc.gov/toxprofiles/index.asp.
In NHANES 2003-2004, the 95th percentile urinary PCP levels among children aged 6-11 and 12-19 years were as much as 2.5 times lower than the corresponding percentile in a sample of German children aged 6-14 years in 1990-1992 (5.67 and 3.80, versus 14.9 µg/L, respectively) (CDC, 2012; Seifert et al., 2000). Among adults in the NHANES 2003-2004 subsample, the 95th percentile urinary PCP levels were generally similar to the comparable percentile in German adults (3.40 and 5.0 µg/L, respectively) (Becker et al., 2003). In a nonrandom subsample from NHANES III (1988-1994), urinary PCP levels at the 95th percentile appeared somewhat higher than 95th percentile values in adults in the NHANES 2003-2004 subsample (CDC, 2012; Hill et al., 1995). A small study of Michigan sportfish consumers reported mean urinary PCP levels of 1.3 µg/L, similar to the 75th percentile value in adults in the 2003-2004 NHANES subsample (Anderson et al., 1998; CDC, 2012). In a small sample of U.S. children in the 1980’s, the 95th percentile urinary PCP level of 110 µg/L was about 20 times higher than that for 6-11 year olds in NHANES 2003-2004 (CDC, 2012; Hill et al., 1989). Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al., 1989).
Finding a measurable amount of PCP in urine does not imply that the level of PCP causes an adverse health effect. Biomonitoring studies on levels of PCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of PCP than are found in the general population. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects.
Anderson HA, Falk, C, Hanrahan L, Olson J, Burse VW, Needham L, et al. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Environ Health Perspect 1998;106(5):279-89.
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.
Braun WH, Blau GE, Chenoweth MB. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Dev Toxicol Environ Sci 1979;4:289-96.
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
Cline RE, Hill RH, Phillips DL, Needham LL. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Arch Environ Contam Toxicol 1989;18:475-81.
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):469-74.
International Programme on Chemical Safety (IPCS). Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Lindane. 2002. available at URL: http://www.inchem.org/documents/jmpr/jmpmono/2002pr08.htmexternal icon. 1/10/13
Kohli J, Jones D, Safe A. The metabolism of higher chlorinated benzene isomers. Can J Biochem 1976;54(3):203-8.
Seifert B, Becker K, Helm D, Krause C, Schulz C, Seiwert M. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood, urine, hair, house dust, drinking water and indoor air. J Expo Anal Environ Epidemiol 2000;10:552-65.
To-Figueras J, Sala M, Otero R, Barrot C, Santiago-Silva M, Rodamilans M, et al. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Environ Health Perspect 1997;105(1):78-83.
Uhl S, Schmid P, Schlatter C. Pharmacokinetics of pentachlorophenol in man. Arch Toxicol 1986;58:182-6.
U.S. Environmental Protection Agency (U.S. EPA). PCP: Human Risk Characterization [online]. 11/30/2004. Available at URL: https://www.regulations.gov/fdmspublic/component/main?main=DocketDetail&d=EPA-HQ-OPP-2004-0402external icon. 1/10/13
van Raaij JA, van den Berg KJ, Engel R, Bragt PC, Notten WR. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Toxicology 1991: 67(1):107-16.