Polychlorinated biphenyls (PCB 153)

Polychlorinated biphenyls (PCBs) are a class of organic compounds with 1 to 10 chlorine atoms attached to biphenyl and a general chemical formula of C₁₂H_10XCl_X. The 209 possible compounds are called congeners, from three monochlorinated isomers to the fully chlorinated decachlorobiphenyl isomer. PCBs are mixtures of chlorinated hydrocarbons that have been used extensively since 1930 in a variety of industrial uses, including as dielectrics in transformers and large capacitors, as heat exchange fluids, as paint additives, in carbonless copy paper and in plastics, as caulking materials, elastic sealants and heat insulation. The value of PCBs for industrial applications is related to their chemical inertness, resistance to heat, nonflammability, low vapour pressure and high dielectric constant. PCBs are generally inert, they are resistant toalkalies, acids and they have high thermal stability. PCBs are produced by the chlorination of biphenyl by anhydrous chloride, under heated reaction conditions and in the presence of suitablecatalysts. The degree of chlorination varies depending on the reaction conditions. The result is a mixture of different congeners, and contains many impurities. Commercial PCB mixtures were sold based on the percentage of chlorine by weight, with each manufacturer utilizing their own system for identifying their products.

Polychlorinated biphenyls (PCBs) are a mixture of individual chemicals which are no longer produced, but are still found in the environment. Health effects that have been associated with exposure to PCBs include acne-like skin conditions in adults and neurobehavioral and immunological changes in children. PCBs are known to cause cancer in animals. PCBs have been found in at least 500 of the 1,598 National Priorities List sites identified by the Environmental Protection Agency (EPA).

The commercial production of the PCBs began in 1930. They have been widely used in electrical equipment, and smaller volumes of PCBs are used as fire-resistant liquid in nominally closed systems. By the end of 1980, the total world production of PCBs was in excess of 1 million tonnes and, since then, production has continued in some countries. Despite increasing withdrawal of the use, and restrictions on the production, of PCBs, very large amounts of these compounds continue to be present in the environment, either in use or as waste. In recent years, many industrialized countries have taken steps to control and restrict the flow of PCBs into the environment. The most influential force leading to these restrictions has probably been a 1973 recommendation from the Organisation for Economic Co-operation and Development (OECD, WHO and SC). Since then, the 24 OECD member countries have restricted the manufacture, sales, importation, exportation, and use of PCBs, as well as establishing a labelling system for these compounds.

Current sources of PCB release include volatilization from landfills containing transformer, capacitor, and other PCB-wastes, sewage sludge, spills, and dredge spoils, and improper (or illegal) disposal to open areas. Pollution may occur during the incineration of industrial and municipal waste. Most municipal incinerators are not effective in destroying PCBs. Explosions or overheating of transformers and capacitors may release significant amounts of PCBs into the local environment.

PCBs can be converted to PCDFs under pyrolytic conditions. The highest yield of PCDFs under laboratory conditions was obtained at a temperature between 550 and 700 °C. Thus, the uncontrolled burning of PCBs can be an important source of hazardous PCDFs. It is therefore recommended that destruction of PCB-contaminated waste should be carefully controlled, especially with regard to the burning temperature (above 1000 °C), residence time, and turbulence. In the atmosphere, PCBs exist primarily in the vapour phase; the tendency to adsorb on particulates increases with the degree of chlorination. The virtually universal distribution of PCBs suggests transport in air.

At present, the major source of PCB exposure in the general environment appears to be the redistribution of PCBs, previously introduced into the environment. This redistribution involves volatilization from soil and water into the atmosphere with subsequent transport in air and removal from the atmosphere via wet/dry deposition (of PCBs bound to particulates) and then re-volatilization.

PCBs have been released to the environment solely by human activity. Because PCBs are no longer manufactured in developed countries, significant releases of newly manufactured or imported materials to the environment do not occur. Rather, PCBs predominantly are redistributed from one environmental compartment to another (e.g., soil to water, water to air, air to water, sediments to water). Thus, for example, the majority of PCBs in air result from volatilization of PCBs from soil and water. Some PCBs may be released to the atmosphere from uncontrolled landfills and hazardous waste sites, incineration of PCB containing wastes, leakage from older electrical equipment in use, and improper disposal or spills.

PCBs may be released to water from accidental spillage of PCB containing hydraulic fluids, improper disposal, combined sewer overflows (CSOs) orstorm water runoff, and from runoff and leachate from PCB contaminated sewage sludge applied to farmland. PCBs may be released to soil from accidental leaks and spills, releases from contaminated soils in landfills and hazardous waste sites, deposition of vehicular emissions near roadway soil, and land application of sewage sludges containing PCBs. PCBs are globally circulated and are present in all environmental media. Atmospheric transport is the most important mechanism for global dispersion of PCBs. Biphenyls with 01 chlorine atom remain in the atmosphere, those with 14 chlorines gradually migrate toward polar latitudes in a series of volatilization/deposition cycles, those with 48 chlorinesremain in midlatitudes, and those with 89 chlorines remain close to the source of contamination. PCBs enter the atmosphere from volatilization from both soil and water surfaces. Once in the atmosphere, PCBs are present both in the vapour phase and sorbed to particles. Wet and dry deposition remove PCBs from the atmosphere. The dominant source of PCBs to surface waters is atmospheric deposition. However, redissolution of sediment bound PCBs also accounts for water concentrations. PCBs in water are transported by diffusion and currents. PCBs are removed from thewater column by sorption to suspended solids and sediments as well as by volatilization from water surfaces. Higher chlorinated congeners are more likely to sorb, while lower chlorinated congeners are more likely to volatilize. PCBs also leave the water column by concentrating in biota. PCBs accumulate most in higher trophic levels through the consumption of contaminated food. PCBs in soil are unlikely to migrate to groundwater because of strong binding to soil.

Volatilization from soil appears to be an important loss mechanism, it is more important for the lower chlorinated congeners than for the higher chlorinated congeners. Vapour phase PCBs accumulate in the aerial parts of terrestrial vegetation and food crops by vapour to plant transfer. The ability of PCBs to be degraded or transformed in the environment depends on the degree of chlorination of the biphenyl molecule as well ason the isomeric substitution pattern. The vapour phase reaction of PCBs with hydroxyl radicals is the dominant transformation process in the atmosphere, while photolysis appears to be the only viable chemical degradation process in water. Biodegradation has been demonstrated under both aerobic and an aerobic conditions and is the major degradation process for PCBs in soil and sediment.

Monitoring studies conducted over the years have shown that atmospheric concentrations of PCBs have decreased since the late 1970s. Water monitoring studies indicate that PCB concentrations are generally higher near sites of anthropogenic input and in inshore waters.The detection of PCBs in blood, adipose tissue, breast milk, and other tissue samples from the general population indicates widespread exposureto PCBs from environmental sources.

The hepatotoxicity of PCBs in rats is reasonably well characterized for acuteduration oral exposure, but it is unclear if the liver is the most sensitive target organ for acute exposure. Other targets appear to include the kidneys, stomach, and thyroid, but insufficient information exists to determine if effects in these or other tissues occur at lower doses or are more critical than effects in the liver.

PCBs are well absorbed after exposure by all routes, and distribution to and retention by adipose tissue has been observed in humans after inhalation, oral, and/or dermal exposure. Mobilization of PCBs from adipose tissue to target organs is likely to be similar regardless of theroute of exposure.

The preponderance of toxicity data for PCBs is available from animals exposed to PCBs in the diet in intermediateduration studies. Studies have been performed with various species, but the rat, monkey, and mink have been tested most extensively. The liver, skin, and stomach are unequivocal targets, but existing studies do not identify NOAELs for effects in these organs in monkeys and minks. Anaemia consistently occursin monkeys at doses similar to those producing other effects, but a NOAEL and the relative importance of this effect is not known. There is evidence suggesting that effects occur in the thyroid and adrenal glands of rats at doses lower than those producing effects in other tissues in monkeys and minks, but these doses are in proximity to those producing developmental toxicity in monkeys. A series of intermediateduration studies in infant monkeys found neurodevelopmental effects of a low dose of a congener mixture that simulated the congener composition of human breast milk. The single dose level tested was a LOAEL that was used as the basis for the intermediate MRL.

Some information is available on effects of PCBs in animals by inhalation or dermal exposure for intermediate durations. Although limited by various study inadequacies including insufficient numbers of animals, dose levels, end points and NOAEL data, this information is essentially consistent with the oral data in indicating that the liver, kidneys, thyroid and skin are main targets of toxicity.

Some epidemiological studies of PCB exposed workers, which involve inhalation and dermal exposure, have provided evidences that PCBs were associated with adverse health effects, including hepatic and dermal changes. Reported effects on the respiratory system and gastrointestinal tract in these workers are suggestive.

There is growing evidence that immunologic, reproductive, and thyroid effects are effects of concern in PCB exposed populations. Relatively fewtoxicity studies of animals with chronic oral exposure to PCBs have been performed, and chronic inhalation and dermal toxicity studies with animals, which could support or refute the findings of occupational studies, are lacking. Although limited in quantity, the available chronic animal oral toxicity data essentially corroborate the results of intermediateduration studies with respect to effects in the liver, skin, stomach, blood, and thyroid, but provide no information on renal effects.

Limited information is available on reproductive effects of PCBs in humans. In women, there was no apparent effect of occupational exposure tovarious Aroclor mixtures on mean number of pregnancies. Due to study limitations and lack of information on gravidity in other studies, theeffect of PCBs on human conception is unclear.

Oral studies with animals provide conclusive evidence for reproductive toxicity of PCBs in females of various species and some evidence for effects in male rats. Effects that have been induced in female animals include estrus changes and reduced implantation rate in adult rats and/or their offspring, decreased conception in mice, partial or total reproductive inhibition in minks, and menstrual alterations and decreased fertility in monkeys. Monkeys (Rhesus) and minks are the most sensitive species tested, although reproductive effects were not induced at dosesquite as low as those inducing the critical neurobehavioral, immunological, and dermal/ocular effects used to derive the intermediate and chronic MRLs. In male animals, short term exposure to high oral doses of Aroclor 1254 induced no changes in the weight or histology of the testes or accessory glands in adult rats, although seminal vesicle weights and caudal epididymal weights and sperm counts were reduced in rats that were exposed for several months as weanlings. No studies in male mice or rats evaluated reproductive capability. There is limited evidence of hypoactivity of the seminiferous tubules in monkeys that were chronically exposed to a dose of Aroclor 1248 that also caused clinical signs of toxicity. In contrast to the limited evidence for reproductive effects in male adult animals, fertility was markedly reduced in male offspring of rats that were lactationally exposed to relatively high doses of Aroclor 1254, and results of oral and subcutaneous studies withsingle congeners have also shown that gestational and neonatal exposures can adversely affect morphology and production of sperm and fertilityin male rats and mice. Effects on male reproductive organs appear to involve postnatal developmentallyspecific vulnerable periods ofresponsiveness.

There is sufficient evidence that commercial PCB mixtures containing 60% chlorine by weight are carcinogenic in rats. Aroclor 1254 and other lower chlorinated commercial PCB mixtures have a lower carcinogenic potential than the 60% chlorine mixtures. Although the evidence that PCBsare carcinogenic in rats is conclusive.

Human studies provide suggestive evidence that PCBs are carcinogenic. The carcinogenicity of PCBs in humans has been investigated in retrospective cohort mortality studies, which investigated cancer in exposed workers, and in case control studies of environmental exposure that examined associations between serum or adipose tissue levels of PCBs and occurrence of cancer. Some of the mortality studies suggest tha toccupational exposures to PCBs were associated with cancer at several sites, particularly the liver, biliary tract, intestines, and skin(melanoma). There is no clear association between occupational exposures to PCBs and cancer in other tissues, including the brain, hematopoietic, and lymphatic. The hypothesis that environmental exposure to PCBs can cause breast cancer in humans is controversial and needs tobe further studied. A number of case control studies have investigated possible associations between breast cancer and concentrations of PCBs inbreast tissue or blood in the general population. Breast adipose levels of total PCBs or individual congeners were increased in women with breast cancer in some but not all studies. Other environmental exposure studies used serum PCB concentrations as the marker of exposure with blood samples taken after the diagnosis of breast cancer, or prospectively collected prior to diagnosis. None of the serum studies found significantly different mean blood levels of PCBs in breast cancer cases and controls. There also were no significant associations between riskof breast cancer and serum PCBs in most of these studies, although some data suggest that risk may be increased in some subgroups of postmenopausal women. Many of the better designed studies were prospective, and none of the prospective studies found that PCBs were associated with the occurrence of breast cancer.

Department of Health and Human Services (DHHS) has stated that PCBs may reasonably be anticipated to be carcinogens. Both US EPA and the International Agency for Research on Cancer (IARC) have determined that PCBs are probably carcinogenic to humans.

US EPA Method 8082: Polychlorinated Biphenyls (PCBs) by Gas Chromatography

• S EPA Method 9078: Screening Test Method for Polychlorinated Biphenyls in Soil
• UA EPA Method 9079: Screening Test Method for Polychlorinated Biphenyls in Transformer Oil
• US EPA Method 8270C: Semivolatile Organic Compounds by Gas Chromatography/Mass Spectrometry (GC/MS)
• ISO 6468 (1996) Water quality Determination of certain organochlorine insecticides, polychlorinated biphenyls and chlorobenzenes Gas chromatographic method after liquidliquid extraction
• ISO 10382 (2002): Soil quality Determination of organochlorine pesticides and polychlorinated biphenyls Gaschromatographic method with electron capture detection
• ISO 15318 (1999): Pulp, paper and board Determination of 7 specified polychlorinated biphenyls (PCB)
• ISO 17858 (2007): Water quality Determination of dioxinlike polychlorinated biphenyls Method using gas chromatography/mass spectrometry
• AOAC Official Method 990.07 Polychlorinated Biphenyls (as Aroclor 1254) in Serum. Gas Chromatographic Method. AOAC International
• AOAC Official Method 974.21 Polychlorinated Biphenyls in Paper and Paperboard. Gas Chromatographic Method. AOAC International

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[2] US EPA. [2009]. Estimation Programs Interface Suite™ for Microsoft® Windows, v 4.00]. United States Environmental Protection Agency, Washington, DC, USA

[3] Li, N., Wania, F., Lei, Y.D., Daly, G.L. (2003) A comprehensive and critical compilation, evaluation, and selection of physicalchemical property data for selected polychlorinated biphenyls. J. Phys. Chem. Ref. Data 32, 1545–1590.

[4] IPCS: Intox Databank, http://www.intox.org/databank/index.htm

[5] ATSDR: Agency for toxic substances and disease registery, http://www.atsdr.cdc.gov/

[6] TOXNET: TOXikology Data NETwork TOXNET - http://toxnet.nlm.nih.gov/

[7] IRZ: Integrovaný registr znečišťování životního prostředí (IRZ) : http://www.irz.cz/