Encyclopaedia from P to Q

from A to C
from D to O
from R to Z

PBBs (polybrominated biphenyls), compounds that are in continuous use as flame retardants and fire extinguishers. They may have some of the same effects as PCBs. They also bioaccumulate as lipid soluble and persistent chemicals.

PBDEs (polybrominated diphenylethers), compounds that are in wide use as flame retardants. They may have some of the same effects as PCBs, but they are generally less potent. They also bioaccumulate as lipid soluble and persistent chemicals.

PCB, polychlorinated biphenyl (see that). See also PCB - specific items.

ΣPCB, the sum (total weight) of all PCB congeners.

Σ7PCB, the sum (total weight) of the seven marker PCBs (see this).

PCB - acute toxicity, toxicity occurring after a single dose within a few weeks. It is generally low, but it depends on the mixture of congeners, because dioxin-like (non-ortho, see ortho-PCBs) PCBs are much more toxic than other congeners. Their toxicity resembles that of dioxins (see PCDD/F - acute toxicity).

PCB - analysis, measurement of concentration of a compound in a sample. PCBs can be analysed by gas chromatography by using electron capture detector. This is a fairly widely available method, but if absolute accuracy and congener-specific analysis is needed, gas chromatography-mass spectrometry (see this) may be needed. This is a very expensive method not available in many laboratories in Europe.

PCB - biomagnification, property of PCB compounds to concentrate from one trophic level to the next (see also biomagnification). Many PCBs are extremely persistent in the environment. Increase in chlorination (see PCB - physicochemical properties) increases both stability and lipophilicity. Therefore they concentrate along the food chain, and species at the "top" of the food chain (such as seals or eagles) are in special danger.

PCB - carcinogenicity, capacity of PCBs to cause cancer. A number of long-term carcinogenicity studies have been carried out in mice and rats. Interpretation is complicated by the lack of information of minor impurities, especially PCDFs. Some tested mixtures were free of PCDFs. In many of these studies hepatocellular adenomas and/or carcinomas (tumours of the liver) were found although the increase was not always significant. PCB mixtures are considered non-genotoxic, PCBs do not cause mutations or chromosomal damage. Therefore rodent tumourigenicity is considered to be of epigenetic nature (promoting rather than initiating effect, see mutagenicity, promoters). IARC classifies PCBs as probable human carcinogens on the basis of animal data. Remarkable caution is needed in extrapolating the available animal data to humans. None of the available epidemiological studies provide conclusive evidence of an association between PCB exposure and increased cancer mortality. (For more information, see International Programme on Chemical Safety, Environmental Health Criteria 140, WHO, Geneva, 1993).

PCB - chemical structure, see chemical structures.

PCB - contaminants, by-products found unintentionally in PCB products. Technical PCBs contain a number of various chlorinated byproducts, e.g. about 40% chlorobenzenes, a few percent chloronaftalenes, and also small amounts of PCDDs and PCDFs (93% PCDFs and 7% PCDDs of the total PCDD/F content in the PCB product which caused the Yusho Rice Oil accident, pentaPCBs, tetraPCBs and hexaPCBs dominating). PCDFs have been detected up to 40 mg/kg (ΣPCDF) in PCBs. Because commercial products were not sold according to composition but according to their physical properties, there may be large variations both between preparations and between lots of a preparation.

PCB - disposal of. PCB oils cannot be burned in usual conditions, because they burn poorly and evaporate to the environment along with their PCDD/F impurities. PCDFs may also be formed during PCB burning. Therefore PCBs are considered problem waste, which must be incinerated by a well-controlled process in a high-quality waste incinerator at the temperature of 1000 - 1200 °C, and with an effective fly-ash filtering system (see also incineration).

PCB - elimination, process of discharging PCB out of the body. Elimination of chemicals out of the body is usually based on two mechanisms, excretion (such as in urine or faeces) or metabolism (chemical breakdown, often in the liver). Only water soluble materials can be excreted in the kidneys to urine, and PCBs as lipid soluble and poorly water soluble chemicals cannot be excreted practically at all as such. Metabolism tries to make them more water soluble, but especially higher chlorinated PCBs (see PCB - physicochemical properties) are metabolised very poorly, and therefore cannot be effectively excreted even with the help of metabolism. Therefore they accumulate in body fats, and their half-life (see this) may be even several years.

PCB - environmental persistence, ability of PCBs to continue existence in the environment. The stability of PCBs is a technical advantage, but it also means that they are extremely persistent in the environment. Increase in chlorination (see PCB - physicochemical properties) increases both stability and lipophilicity. Neither soil microbes nor animals are able to break down effectively the highly chlorinated PCBs (see also ortho-PCBs). This causes very slow elimination (see PCB - elimination). Because some PCBs are more persistent than others are, the spectrum of congeners in the environment, animals and humans is never quite identical to that in the original commercial product. In water, PCBs are adsorbed on sediments and organic matter. This decreases the rate of volatilisation, but also slows down the degradation.

PCB - half-life, time needed to decrease the amount of PCBs to one-half. There is no systematic information on the half-life of all PCB congeners in humans. The half-lives of the most toxic non-ortho PCBs have been estimated to vary from 0.1 to 13 years. Somewhat fragmentary information suggests that the half-lives of PCBs are on the average around one year (with much variation to each direction). See also half-life.

PCB - physicochemical properties. All PCBs are lipophilic (soluble in fats and oils) and practically insoluble in water, but lipophilicity increases by increasing rate of chlorination (see PCB - chemical structure). Technical mixtures are mobile to viscous oils depending on the rate of chlorination, and their boiling point varies from 300 to 400 °C. They resist high temperatures and oxidising conditions without breaking down. Their electrical conductivity is very low which made them suitable cooling liquids for electrical equipment.

PCB - sources. Emissions. PCBs were manufactured from 1930 to 1970s or 1980s (varying in different countries), and the total production was in excess of a million tonnes. PCBs are still manufactured e.g. in Russia. They have spread to the environment in accidents (such as transformer fires or leaks), from volatilisation of waste landfills and incineration of mixed municipal waste (e.g. plastic materials). The virtually universal distribution of PCBs suggests transport in air.
Human exposure. Food is the major source for human exposure to PCBs and dioxins, especially fatty foods: dairy products (butter, cheese, fatty milk), meat, egg, and fish. Some subgroups within the society (e.g., nursing babies and people consuming plenty of fish) may be highly exposed to these compounds and are thus at greater risk. Daily intake of PCBs is a few µg per person. PCB concentrations have been screened in two WHO international studies, and in Central Europe the concentrations have decreased in breast milk from 400-800 µg/kg (sum of six marker PCBs [see this] in milk fat) to 200-400 µg/kg from 1987 to 1993. The decrease in environmental concentrations is partly due to prohibition of the use of PCBs in Europe, partly due to improved incineration technology (see also PCDD/F - sources).

PCB - toxicity in humans. This is difficult to evaluate, because the exposure has usually been to a mixture of different congeners and also impurities such as PCDFs. Occupational exposure may be to different congeners than exposure of general public through food, because some congeners are more easily degraded in the environment than others. In occupational conditions skin rashes, itching, irritation of the conjunctivae, pigmentation of fingers and nails, chloracne, liver problems and neurological and unspecific psychological symptoms have been seen. In Yusho and Yu-Cheng incidents (see these) also various skin and nail problems were seen, as well as liver enlargement and immunological problems. In children of Yusho and Yu-Cheng patients skin problems, oedematous eyes, dentition at birth and lowered birth weight were seen, among others. Total exposures in these cases have been estimated at 600 to 1,800 mg per person (ΣPCB). The daily intake of PCBs in general population in most industrialised countries is of the order of some micrograms per person (ΣPCB). Such levels have not been associated with disease. (For a review, see Safe, Crit. Rev. Toxicol. 1994:24:87-149; for detailed evaluation, see International Programme on Chemical Safety, Environmental Health Criteria 140, WHO, Geneva, 1993).

PCB - trade names. Many companies in several countries have manufactured PCBs. The trade names include Apirolio, Aroclor, Clophen, Fenchlor, Kanechlor, Phenoclor, Pyralene, Pyranol, Pyroclor, Santotherm FR, and Sovol. Sometimes the trade name indicates the degree of chlorination, e.g. Aroclor 1254 contains 54 % of chlorine, 12 indicates the number of carbon atoms.

PCB - use. PCBs have been used since 1930 because of their stability and low flammability (see PCB - physicochemical properties) as insulating materials in electrical equipment (electrical capacitors, transformers), as plasticizers (softening materials) in plastic products, and for a variety of other industrial purposes (in gas-transmission turbines, vacuum pumps, hydraulic fluids, adhesives, fire retardants, wax extenders, lubricants, cutting oils, oils in heat exchangers etc.). The total production was in excess of a million tonnes. Common trademarks included Aroclor, Clophen, and Kanechlor (see PCB - trade names).

PCDD, polychlorinated dibenzo-p-dioxin. See this and PCDD - specific items.

PCDD - carcinogenicity, capacity of dioxins to cause cancer. TCDD has been shown to be carcinogenic (causing cancer) in several species of experimental animals. TCDD is not mutagenic, i.e. it does not cause mutations which may initiate a cancer cell by changing the genetic information of the cell. Rather TCDD is a promoting agent: it promotes the growth and transformation of already initiated cancer cells. It has also been proposed that TCDD will induce active oxygen radicals, which may secondarily cause genetic damage. These mechanisms may mean that there is a practical threshold level or dose, below which TCDD will not cause cancer.
In human beings cancer assessment has proved difficult, because, with the possible exception of Seveso accident (see this), the groups investigated have always been exposed to many chemicals simultaneously. Some of these (such as chlorophenols and several solvents) may be carcinogenic in their own right, and it is hard to know which chemical is responsible for the effect. In short, human carcinogenicity is likely, but very high exposures to TCDD and other dioxins are needed to cause a modest increase in cancer incidence. The maximum TCDD concentrations in Seveso were 56,000 ng/kg (TCDD in fat), in occupational studies max. 32,000 ng/kg (TEq in fat) and average 2,000 ng/kg (while the average concentrations in the population are 30 to 50 ng/kg, as I-TEq in fat). Regardless of the high concentrations, the increases in cancer rates were barely detectable (e.g. in the latest occupational study 13 % increase in total cancer). This means that dioxins are relatively weak carcinogens in humans (More information on this topic in IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 69, Lyon, 1997; Bertazzi et al., Epidemiology 1997:8:646-652; Steenland et al., J. Natl. Cancer Inst. 1999:91:779-786).

PCDD - chemical structure. See chemical structures.

PCDD/F, an abbreviation for PCDDs and PCDFs.

ΣPCDD/F, the sum (total weight) of the 17 PCDDs and PCDFs with a TEF value >0.

PCDD/F - acute toxicity. This is quite variable in different animal species (Table 1). Lethal dose of TCDD to guinea pigs is about 0.001 mg/kg b.w., and to Rhesus monkeys 0.07 mg/kg b.w., but hamsters can tolerate over 1 mg/kg b.w. Even strains within the same species can show a similarly wide difference: the LD50 values for rats vary from 0.010 to >10 mg/kg. Human lethal dose is not known, but human beings are not assumed to be one of the most sensitive species. In Seveso accident, the highest human TCDD concentrations were 56000 ng/kg (in fat), and it can be estimated that the acute dose had been around 0.005 mg/kg b.w. No humans died in the accident, but lots of small animals such as rabbits were found dead at the accident area.
No dose will kill the animal immediately, but a high dose causes the so called "wasting syndrome", the animal is anorectic and eats less than a quarter of the normal food intake, and dies after two to three weeks when the body weight has decreased by about 30-40 %. In some animals there may be liver damage including porphyria (disturbance of the synthesis of heme, the pigment of haemoglobin). Other typical features are atrophy of the thymus, disturbances in the levels of some amino acids and lipids, and induction of many oxidative enzymes. Other PCDD/Fs induce similar toxic effects, but they are less potent in line with their TEF (For detailed information, see Pohjanvirta & Tuomisto, Pharmacol. Rev. 1994:46:483-549). See also PCDD/F - toxicity in animals.

Table 1. Acute toxicity (measured as median lethal dose) of TCDD in animal species and strains. The LD50 values (see this) are based on the administered dose in mammals and birds and measured concentrations in fish.

PCDD/F - analysis. At the concentrations present in the environment or in living tissues, PCDD/Fs can be reliably analysed only by using gas chromatography-mass spectrometry (see this) with high resolution. This is an expensive method and because of extensive sample purification steps, the procedure will take several weeks. There are few laboratories in Europe to assay PCDD/Fs reliably from animal or human tissues.

PCDD/F - biomagnification, property of PCDD/F compounds to concentrate from one trophic level to the next (see also biomagnification). Many PCDD/Fs are extremely persistent in the environment. Increase in chlorination (see PCDD/F - physicochemical properties) increases both stability and lipophilicity. Therefore they concentrate along the food chain, and species at the "top" of the food chain (such as seals or eagles) are in special danger.

PCDD/F - concentration in humans. Dioxins in the body are almost exclusively in fat because of their lipid solubility and poor water solubility. In some tissues dioxins may also be bound to specific proteins. The most reliable method to measure dioxin levels is to measure their concentrations in fat. Dioxin levels are the same on fat basis in most organs of the body, so there is plenty in very fatty tissues and little in lean tissues. Importantly there is the same concentration of dioxins in milk fat as in the fat of serum or of adipose tissue. This gives a possibility to measure dioxin levels without invasive methodology. WHO has organised two rounds of international intercalibrations whereupon milk dioxin levels in many countries were measured by strictly similar methods to make them comparable. The levels of seventeen PCDD/Fs in milk fat of primiparae mothers in central Europe were in 1994 about 20 ng/kg (as WHO TEqs in fat), and in less industrialised areas often around 10 ng/kg. However, since the cumulation (see this) of dioxins is very slow, the concentrations will increase during most of the lifetime. In Finland, the level in 20 year old population is 5-20 ng/kg (TEq in fat), but in 60 year old population it is 20-100 ng/kg. In chemical industries concentrations of up to several thousand ng/kg have been measured, and the highest measured concentrations in Seveso accident (see this) were 56,000 ng/kg (TCDD in fat). Dioxin concentrations have decreased during 1980s and 1990s (see also body burden and PCDD/F - sources).

PCDD/F - elimination, process of discharging PCDD/Fs out of the body. This is very slow in all mammals, because these compounds are lipophilic, and cannot be excreted in urine, and also poorly degradable by the enzymatic machinery of the body (see also PCB - elimination). Generally, PCDFs are eliminated a little faster than PCDDs. Half lives of the 17 most important PCDD/Fs are shown in Table 2. (modified from Liem & Theelen, Dioxins: Chemical analysis, exposure and risk assessment, University of Utrecht, 1997).

Table 2. Elimination half-lives of the most important PCDD/Fs.

PCDD/F - environmental persistence, ability of PCDD/Fs to continue existence in the environment. Many PCDD/Fs are extremely persistent in the environment. Increase in chlorination (see PCDD/F - physicochemical properties) increases both stability and lipophilicity. Neither soil microbes nor animals are able to break down effectively those PCDDs with "lateral" chlorines, i.e. chlorines in positions 2,3,7, and 8. This causes especially slow elimination (see PCDD/F - elimination), and due to biomagnification (see bioaccumulation, biomagnification) those particular compounds are present in the organisms of higher trophic levels (such as birds and mammals). Since the same group of PCDDs with chlorines in 2,3,7,8-positions are also more toxic than others, they are toxicologically the most important congeners.

PCDD/F - half-life, time needed to decrease the amount of chemical to one-half (see PCDD/F - elimination).

PCDD/F - limit values, concentrations that are not to be exceeded in a matrix. There are no limit values in EU concerning human food. As to animal feed, there is a limit value for citrus pulp pellets: 500 pg/kg or 0.5 ng/kg (WHO-TEq in d.w.); for exhaust gases, there is a limit value of 1 ng/Nm³ (I-TEq in normalised cubic meter). Generally applied proposed values for PCDD/F in milk are as follows: target value <0.9 ng/kg (TEq in milk fat), limit value of distribution to consumers 3.0 ng/kg; ban for marketing 5.0 ng/kg.

PCDD/F - physicochemical properties. All PCDD/Fs are non-volatile, lipophilic (soluble in fats and oils) and poorly water soluble, but lipophilicity increases by increasing rate of chlorination (see PCDD - chemical structure, PCDF - chemical structure). Their octanol/water distribution (indicating relative lipid to water solubility, see lipophilicity) is of the order of a million to hundred million (log P_ow 6.5 to 8.8) explaining the high tendency to move toward lipids from water.

PCDD/F - risk assessment. This has been very difficult for several reasons. Mechanisms of toxicity are not yet understood. Large variations of acute toxicity between laboratory species have added to uncertainties in species extrapolation. Also variations in elimination rate are remarkable between species, half-life in rats is three weeks, in humans 7-8 years. Therefore long-term effects are more difficult to evaluate than short-term effects (see tolerable daily intake). Until recently cancer risk was considered the most important risk, and there was uncertainty and disagreement of the dose extrapolation. Recent epidemiological studies after high occupational and accidental exposures have, however, shown the cancer risk to be rather small, and in the general population it is probably not the most relevant risk. If there is any risk at the present background levels, it is likely to be developmental effects. One of the most sensitive effects seems to be the mineralization defect in teeth of children with the highest exposure via breast milk.
WHO scientific panel reassessed dioxin risks in 1998, and the new recommendation for tolerable daily intake level is 1 to 4 pg/kg/day (in TEq per b.w.) during lifetime exposure. Two points are important here. One is that some of the most important sources are beneficial for health for other reasons, e.g. breast milk and fish. It is not rational to limit their use on the basis of theoretical risks. The second is that PCDD/Fs accumulate very slowly (see cumulation). Therefore only exposures over years are important, unless the exposure is very high (such as an accident).

PCDD/F - sources. Formation. PCDD/Fs will form in small amounts, if there are carbon, oxygen and chlorine available in the presence of metal catalysts at suitable temperatures, which optimally means 400 to 700 °C. The most important sources of PCDD/Fs are incineration of mixed waste in too low temperatures, metal smelting and refining, chlorine bleaching of pulp (Figure 6). Another source is occurrence as impurities of many chlorinated chemicals such as PCBs, chlorophenols, phenoxy acid herbicides, and hexachlorophene.
Human exposure. Food is the major source for human exposure to PCBs and dioxins, especially fatty foods: dairy products (butter, cheese, fatty milk), meat, egg, and fish (Figure 7). The current average body burden of dioxins is about 30-60 ng/kg (I-TEq in fat) or 300-600 ng (I-TEq per person) (see body burden) which is close to the lowest concentrations possibly causing health effects. Average daily intake in many countries is 1 to 2 pg/kg (TEq per b.w.) or about 100 pg per person. Some subgroups within the society (e.g., nursing babies and people consuming plenty of fish) may be highly exposed to these compounds and are thus at greater risk. Dioxin concentrations have been screened in two WHO international studies, and in Central Europe the concentrations have decreased in breast milk from 30-40 ng/kg (TEq in milk fat) to 15-20 ng/kg from 1987 to 1993. The decrease in environmental concentrations is mostly due to improved incineration technology.

 
 

Figure 6. Emission sources of PCDD/Fs in United Kingdom in 1995 (I-TEq). The total emissions are 630 – 3400 g/year (I-TEq).

 

Figure 7. Different food items as sources of PCDD/Fs in some European countries. A time series from 1982 to 1992 is presented from United Kingdom. King & Fiedler, AEA Technology (1999) DRAFT Compilation of EU Dioxin Exposure and Health Data, Section 4 Human Exposure.

PCDD/F - tooth effects. These were clearly shown in Yusho incident (see this). At lower concentrations in Finland, defective mineralization of the first permanent molar teeth, which are formed during the two first years of life, correlated with PCDD/F exposure during breast-feeding. This may be the most sensitive effect of PCDD/Fs ever seen in humans.

PCDD/F - toxicity in animals. Dioxins bring about a wide spectrum of biochemical and toxic effects in experimental animals. These effects depend on dose, species, strain, gender, age and tissue. Various dioxin congeners (see this) tend to elicit a similar battery of alterations, although the congeners are differently potent. TCDD serves as a surrogate for the whole group of chemicals. For the most part, the mechanisms of these impacts are still obscure. This hampers rational risk assessment. A common denominator appears to be the so called AH receptor (AHR) (see this), which mediates the biological effects of TCDD in cells. Some of the most toxic PCBs have dioxin-like toxicity based on AH receptor, but e.g. some effects on the nervous system are believed to have a different mechanism.
A characteristic feature of the acute toxicity is an exceptionally large variation in sensitivity among species (see PCDD/F - acute toxicity). To the guinea pig, TCDD is the most toxic synthetic compound known with an LD50 value (dose lethal to 50% of animals) of only ca. 0.001 mg/kg, but the hamster tolerates a thousandfold higher dose. The reasons for these intra- and interspecies differences are unclear, but some are due to differences in the AH receptors. One of the most sensitive targets for TCDD appears to be the reproductive organ system in the developing foetus (Table 3). (For detailed information, see Pohjanvirta & Tuomisto, Pharmacol. Rev. 1994:46:483-549).

Table 3. Some toxic and biochemical effects after TCDD, and body burdens related to the effects. Some of the data are based on the results of a single study.

PCDD/F - toxicity in humans. Acute toxicity after large doses was best seen after the Seveso accident (see this). The most remarkable effect was chloracne, especially in children exposed to high doses appearing between two weeks and two months, and sometimes continuing for years. Chloracne has regularly been described even after heavy occupational exposures to PCDDs and other chlorinated chemicals. Also elevations of liver enzymes in blood were seen in Seveso victims indicating liver damage. There were signs of disturbed porphyrin metabolism (synthesis of heme, the pigment of haemoglobin) and increases in serum lipids (both triglycerides and cholesterol). A number of other health effects have been linked to high exposure to dioxins, including mood alterations, reduced cognitive performance, diabetes, changes in white blood cells, dental defects, endometriosis, decreased male/female ratio of births and decreased testosterone and (in neonates) elevated thyroxin levels. As yet such effects have not been proven as caused by PCDD/Fs. The effect that has caused the greatest public concern is cancer, and IARC recently classified TCDD as a human carcinogen (see PCDD - carcinogenicity). Another concern in the society are the possible developmental effects. There is recent data that dioxin exposure from breast milk is associated with abnormal development and mineralization of teeth.

PCDD/F - use. PCDD/Fs have never been synthesised for any other purpose than research, but they are formed as unintentional by-products in chemical syntheses of 2,4,5-trichlorophenol (an intermediate of antiseptic hexachlorophene and herbicide 2,4,5-T) and in many burning processes (see PCDD - sources).

PCDF, polychlorinated dibenzofuran. See that and PCDF - specific items; since the properties are usually very close, a treatise is usually given under PCDD/F.

PCDF - chemical structure. See chemical structures.

PCDF - carcinogenicity, capacity of PCDFs to cause cancer. There are no long-term carcinogenicity studies on PCDFs in animals. Some short-term studies may suggest tumourigenic effects, and animal studies on technical PCBs containing PCDFs as impurities cause liver tumours (see PCB - carcinogenicity). In Japan (Yusho incident, 22 year follow-up) there is some indication on increased liver cancer in men, but in Taiwan (Yu-Cheng incident) after 12 year follow-up there is no increase (see these). Therefore evidence is inadequate to deem PCDFs carcinogenic, but due to the fact that they bind to the AH receptor and the assumption that the carcinogenicity of dioxins is mediated by this receptor, and in addition due to the "precautionary principle", PCDFs are usually considered carcinogens in decision-making (see also PCDD - carcinogenicity).

penta-, five. E.g., pentachloro- five chlorine atoms in a molecule.

pentachlorophenol. See chlorophenols.

Phenoclor, a commercial PCB product. See PCB - trade names.

phenoxy acids. See chlorophenoxyacetic acid herbicides.

physicochemical properties. See PCB - physicochemical properties, PCDD/F - physicochemical properties.

picogram (pg), 0.000,000,000,001 g. See units.

polychlorinated biphenyls (PCB-compounds), a group of oily stable chemicals, which are mixtures of many congeners (see chemical structures). They are very poorly water soluble and lipophilic (see PCB - physicochemical properties), and therefore accumulate in lipids (fats) of living organisms (see PCB - environmental persistence), and bioaccumulate in trophic levels (see PCB - biomagnification). They contain small amounts (1 to 40 mg/kg) of PCDFs as impurities (see PCB - contaminants). (For detailed information, see International Programme on Chemical Safety, Environmental Health Criteria 140, WHO, Geneva, 1993; Safe, Crit. Rev. Toxicol. 1994:24:87-149).

polychlorinated dibenzofurans (PCDFs), a group of related chemicals that are usually present in mixtures and usually as minor impurities among other chemicals such as PCBs and chlorophenols. They are quite similar to PCDDs both chemically and biologically (see PCDF and PCDD - specific items; since the properties are usually very close, a treatise is mostly given under PCDD/F). (For detailed information, see IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 69, pp. 345-423, Lyon, 1997).

polychlorinated dibenzo-p-dioxins (PCDDs), a group of related chemicals which are usually present in mixtures and usually as minor impurities among other chemicals such as PCBs, chlorophenols, phenoxy acid herbicides, hexachlorophene antiseptic etc. They are poorly water soluble and lipophilic (see PCDD/F - physicochemical properties), and therefore accumulate in lipids (fats) of living organisms (see PCDD/F - environmental persistence), and bioaccumulate in trophic levels (see PCDD/F - biomagnification). (For detailed information, see IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 69, pp. 33-343, Lyon, 1997).

ppb, parts per billion (American). A non-standard concentration unit equal to ng/g or µg/kg or 10^-9 g/g.

ppt, parts per trillion (American). A non-standard concentration unit equal to pg/g or ng/kg or 10^-12 g/g.

precautionary principle, administrative principle to act in the state of uncertainty assuming that the worst prediction is true (see conservative risk assessment).

profile of congeners (spectrum of congeners, congener profile), the variety of different congeners of PCB or PCDD/F in a particular sample. The proportion of each congener in the total PCB or PCDD/F may change along the food chain, because different congeners are differently metabolised and taken up by organisms, and therefore the spectrum in human beings (see TEq, Figure 8) is very different from that of the original source, e.g. a commercial PCB mixture.

promoters, a class of chemicals that promote the development of cancer. Usually the development of cancer is divided to the stages of initiation and promotion. Some chemicals may cause an error in the genetic message of a cell (see mutagenicity), and the cell will be transformed to a cancer cell. A single cancer cell will usually not develop to a full-blown cancer, unless other factors promote its growth and development. Promoters are a large class of chemicals that cause promotion by several mechanisms, the simplest is just a tissue damage that makes the cells divide to replace destroyed cells. Dioxin-like chemicals are strong promoters of cancer development, but they are not mutagenic.

proteins, one of the most important macromolecules of our body and all living organisms. They are formed of amino acids (see this), and usually synthesised in ribosomes, small cell organelles, by the code transferred by messenger RNA (see RNA).

Pyralene, a commercial PCB product. See PCB - trade names.

Pyroclor, a commercial PCB product. See PCB - trade names.
 
 

Contents of the Synopsis

Information on the publication
General introduction

Burning produces dioxins
Dioxins and some PCBs cause multiple toxic effects.
Dioxins and PCBs accumulate in the human body.
Risk assessment is tricky.
Common sources of errors and practical difficulties.

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from D to O
from P to Q 
from R to Z