General introduction to dioxins and PCBs

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General introduction

Polychlorinated biphenyls (PCB-compounds) are a group of oily stable chemicals, which have been used because of their stability and low flammability as insulating materials in electrical equipment (transformers and capacitors), as plasticizers (softening materials) in plastic products, and for a variety of other industrial purposes. Their stability is a technical advantage, but it also means that they are extremely persistent in the environment. They also contain small amounts of dioxin impurities especially PCDFs, some of which are much more toxic than the main chemicals.

The production and use of PCBs have been discontinued in most countries, but large amounts remain in electrical equipment, plastic products, buildings (e.g. plastic carpeting, sealing materials), and in the environment. Because PCBs are considered problem waste, their disposal is expensive, and may sometimes lead to attempts to dispose of them by mixing them to other waste products. Two well-established environmental accidents have occurred, called Yusho (Japan) and Yu-Cheng (Taiwan). In both cases rice oil was contaminated and caused a number of health effects.

Polychlorinated dibenzo-p-dioxins (PCDDs) and related halogenated aromatic hydrocarbons (e.g., PCDFs), often called "dioxins" as a group, are ubiquitously present environmental contaminants. Some of them, notably TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) belong to the most toxic synthetic compounds known. They are very stable against chemical and microbiological degradation and therefore persistent in the environment. They are fat-soluble and thus tend to bioaccumulate in tissue lipid and in the food chain. These factors increase their potential hazards to humans and animals.

Burning produces dioxins.

The main new (de novo) sources of PCDD/Fs are combustion processes, such as waste incineration and metal smelting and refining. In Europe, the Baltic Sea is an important sink of PCBs and dioxins. However, recent studies have revealed a major problem at localised spots, due to the production and use of chlorophenols for impregnation of timber. In the most contaminated regions the concentration of PCDDs and PCDFs in soil and sediments appears to be incredibly high. An unpredictable source is old transformers and capacitors, each of which may contain several kilograms of PCBs and hundreds of milligrams of PCDD/Fs.

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. The current average body burden of dioxins is about 30-60 ng/kg (as I-TEq in fat; pg/g = ng/kg) or 300-600 ng (I-TEq) per person which is close to the lowest concentrations possibly causing health effects. 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 close to 40 ng/kg (as TEq in milk fat) to about 20 ng/kg from 1987 to 1993. The decrease in environmental concentrations is due to cessation of PCB use and improved incineration technology.

Dioxins and some PCBs cause multiple toxic effects.

Dioxins bring about a wide spectrum of biochemical and toxic effects in experimental animals. These effects depend on species, strain, gender, age and tissue. Various dioxin congeners (derivatives with the same basic structure) 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), 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 of PCBs 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. 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 1 to 5 mg/kg. Even strains within the same species can show a similarly wide difference: the LD50 values for rats vary from 0.01 to >10 mg/kg. The reasons for these intra- and interspecies differences are unclear. A peculiar wasting syndrome follows high single doses: the animals are anorectic and lose weight, followed by toxic effects in many organs. Some low-dose effects do not vary between species to the same extent as lethality and wasting. One of the most sensitive targets for TCDD appears to be the reproductive organ system in the developing foetus.

Dioxins and PCBs accumulate in the human body.

The fate of these chlorinated compounds in the body is unusual. Because they are fat-soluble and practically not at all water-soluble, they cannot be excreted in urine. Moreover, our body is not able to metabolise them. The excretion is so slow that their so called half-life is many years, which means that it takes years of our body to get rid of 50 % of the compound. Because dioxins are mixtures, every compound has a different half-life, but as a thumb rule one can say that an average half-life is ten years. This long half-life makes them highly cumulative compounds, i.e., they accumulate in the body over the decades even at a low exposure. Therefore it is important that the levels of these compounds in our food are minimised. Continuous exposures from contaminated food might lead in the long run to extremely high body burdens. On the other hand, the accumulation is so slow that it would take 40 to 50 years to reach a balance. During this ultimate steady state, the body burden (total amount of chemical in the body) is about 5000 daily doses. Therefore a short period of exposures exceeding the accepted limit values ten or even hundred times, would not remarkably change our body burden accumulated during the previous decades.

In humans, a wide variety of 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. Presently the effects have been proven only in the case of chloracne. The effect that has caused the greatest public concern is cancer, and IARC recently classified TCDD as a human carcinogen. Another concern in the society is the possible developmental effects. There is some data that dioxin exposure from breast milk is associated with abnormal development and mineralization of teeth.

Risk assessment is tricky.

A problem in dioxin risk assessment is to evaluate the actual effect of the very low concentrations in the environment of these very toxic compounds. There is wealth of information on environmental concentrations, levels in humans, epidemiological studies with indirect exposure information, effects after different exposures in animals, and on certain aspects of biochemical pathways. However, there are very few studies that are fully relevant for human risk assessment. Therefore the scientific community remains divided in the issue of the true risk of the present environmental concentrations of dioxins, and recommendations for tolerable daily intake values have varied even thousandfold between countries. There is, however, a fair agreement that the risk of cancer, while probably true at very high industrial or accidental exposures, is not very high. It may be that the most important risk is that of developmental effects.

Common sources of errors and practical difficulties.

Dioxin literature may be confusing, and some factors may cause difficulties unless the reader is aware of them. Firstly, different measures are used for different purposes. The amounts of PCBs may be given as a sum of all PCB-derivatives (called congeners, see this and ΣPCB) in the sample, or as a sum of the six or seven marker PCBs (see this), which are the easiest to measure. The amounts of PCDD/Fs are usually given as a sum of the 17 most relevant congeners (see ΣPCDD/F), or as TEqs (see this), normalised to the equivalents of TCDD. Confusing between these may cause a hundredfold error. The transforming factors, TEFs, are based on convention, so they may change from time to time, and TEqs should not be used without giving information on the absolute amounts at the same time.

Secondly, different units are used for different purposes (see units). The amounts of dioxins in the body are sometimes given as ng/kg b.w. (nanograms per kilogram body weight), but more often as pg/g fat (picograms per gram fat). Because human body contains 10-15 % of fat tissue, the difference may be tenfold. Both absolute weights and TEqs may be given per body weight or per unit of fat, preferably per kilogram, but often per gram. Especially Americans also use non-standard units ppm (parts per million, µg/g or mg/kg), ppb (parts per [American] billion, µg/kg), and ppt (parts per [American] trillion, ng/kg). So please be careful, thousandfold errors are easy to make.

Thirdly, different measures are used for different matrices. In fish and other food items dioxins and PCBs are often expressed per wet weight (fresh weight), because it is then easy to calculate human intake via food. However, in contaminated soil or sediment samples they are usually expressed per dry weight. The difference between these two measures may also be formidable. A minimum requirement for accurate expression is weight of substance, weight of matrix, and quality, e.g. ng/kg (WHO-TEq in fat).

Fourthly, single acute dose and average daily dose mean very different things for the exposed person. Approximately similar body burden of dioxins could be achieved either by a single dose of 5,000 pg, or by a lifelong intake of 1 pg/day. Therefore one should be very careful in comparing the amounts in the body and the amounts in the food. This booklet will hopefully also clarify some of these pitfalls.