On 20 December 2013, a report made by NIPSECT about the health risks of exposure to PCB in indoor air was published by the Danish Health and Medicines Authority.
In general, the main source of human PCB exposure is food intake, because especially fatty animal foodstuffs are always to a certain degree contaminated by PCB originated from the environmental background pollution. The average daily intake of PCB through food in the EU has been estimated to be 10-45 ng/kg body weight (bw). The most recent Danish intake estimate is a mean daily intake of PCB from food of 9 ng/kg bw and a maximum of 82 ng/kg bw. For an adult person weighing 60-70 kg, the order of magnitude for average daily intake via food would be about 0.6 µg PCB/day. The World Health Organization (WHO) has recommended a tolerable daily intake (TDI) of 20 ng PCB/kg bw; thus this intake is exceeded by a small proportion of the Danish population.
In case of exposure to indoor air concentrations of 300-3 000 ng PCB/m3, and if a person inhales 20 m3 polluted air daily during presence in the room, then the intake with indoor air will be 6 000-60 000 ng PCB6 or 10-100 fold the food intake. However, in praxis most people will stay indoors in the building shorter time, and intakes from food and indoor air cannot directly be compared, because of the different congeners present with lower chlorinated PCBs in the air but the indoor exposure is always on the top of the food exposure.
Studies in Sweden and Germany have shown that people exposed to PCB in indoor air 20-30 times more low-chlorinated PCB in the blood than not exposed. In the Danish “Farum Midtpunkt” study, exposed dwellers had about 4-folds higher total blood-PCB concentrations than the non-exposed: The longer the residence time, the higher the blood concentration of low-chlorinated PCBs.
The toxicities of PCB have been studied in animal bioassays. Most animal toxicity data refer to commercial PCB mixtures, and fewer data exist for the single congeners. In general, PCBs are readily absorbed orally, dermally and by inhalation. PCBs are resistant to metabolism and accumulate in the body, but some may be metabolized into hydroxy-PCBs, which may contribute independent toxic effects. The most toxic PCBs have a “co-planar” conformation similar to that of dioxin and are thus called non-ortho dioxin-like PCBs (DL-PCBs). They only constitute a small fraction of exposures from food and indoor air, but due to the higher toxicity, they should not be ignored. PCBs can elicit toxic effects from a variety of organs, and substantial species differences in sensitivity have been identified, and monkeys and human seem to be more susceptible than rodents.
The immune system is among the most sensitive of all organ systems to PCBs. PCBs cause atrophy of the thymus gland and immunosuppression in laboratory animals. Increasing evidence suggests that PCBs in humans also can cause dysregulation of the immune system through immunosuppression and immune stimulation/inflammation. PCB exposure is associated with an increased incidence of respiratory infections, ear infections, influenza, and chicken pox in children at preschool age. Increased blood-PCB concentrations are also associated with lower antibody responses to routine childhood vaccinations. In Slovakia, mothers with an increased blood-PCB concentration gave birth to children with a reduced thymus volume.
The endocrine system is also an important target for PCBs or their hydroxy metabolites. Some lower-chlorinated PCB congeners and metabolites exhibit weak estrogenic effects, while higher-chlorinated PCBs are primarily anti-estrogenic. PCB mixtures and congeners effectively reduce circulating concentrations of the thyroid hormone. Some PCB metabolites bind to the protein that transports this hormone in the blood. Endocrine disruption in humans is suggested by reduced sex hormone concentrations in serum.
PCBs may also trigger the development of obesity and of obesity-induced insulin resistance and hyperinsulinemia, thus suggesting possible induction of type-2 diabetes both in animals and humans. Many of studies have linked PCB exposure to the metabolic syndrome, insulin insensitivity and changes in insulin secretion. One study reported that the women with the highest 20% of the blood-PCB concentrations had a 3-fold increased risk of type-2 diabetes. The risk may be greater in overweight subjects, e.g., in obese subjects in Spain, the group with the highest PCB concentrations had a 9-fold increased risk of diabetes. A recent expert workshop organized by the US Institutes of Health concluded that PCBs are associated with an increased risk of type-2 diabetes, although the data were not sufficient to establish causality.
Reproductive toxicity in animals encompasses a range of adverse effects, such as decreased sperm counts, altered estrous/menstrual cycles, and greater incidence of malformations, fewer offspring per litter, lower birth weight, and less postnatal survival, weight gain, and functional levels of offspring. PCB may also interfere with the development and function of the reproductive system in humans. Reported effects include decreased sperm motility, impaired fetal growth, and increased risk of pregnancy loss.
The developing fetus and young infants are particularly vulnerable to PCB toxicity, and PCB may affect neurodevelopment and neuropsychological functions in children. Developmental neurotoxicity has emerged as a particularly vulnerable endpoint in chronic low-level PCB toxicity studies, and different NDL-PCBs seem to affect different targets in the brain. PCB28 seem to have a special affinity for brain effects. PCB may also be a risk factor for the development of Parkinson’s disease.
Among other likely or possible adverse effects in humans, blood-PCB concentrations have been linked to elevated blood pressure, elevated serum-cholesterol, formation of atherosclerotic plaques, and self-reported cardiovascular disease. Some of these effects may be associated with obesity.
Although PCB mixtures appear not to be genotoxic, PCBs may cause metabolic interference by converting non-genotoxic xenobiotics into genotoxic metabolites. Four commercial PCB mixtures have been tested in long-term studies in rats, and all caused liver tumors in females, Aroclor 1260 also in males. The DL-PCBs 126 and 118 cause cancer in rodents at several sites. NDL-PCBs 52 and 153 are promoters of liver tumors in mice.
In various groups of PCB-exposed workers, increased mortality from melanoma, brain cancer and intestinal cancer have been reported. Mortality of uterine cancer, prostate cancer, stomach cancer and multiple myeloma increased with estimated cumulative PCB exposure. In the most recent evaluation, in February 2013 the IARC working group concluded that there was sufficient evidence of carcinogenicity in humans, and PCBs were classified as carcinogenic to humans (Group 1).