In schools and other buildings where there is concern about exposures to PCBs, inhalation of contaminated air is usually the exposure pathway of greatest concern. However, few, if any, laboratory studies have specifically considered whether the inhalation of PCBs results in the same or different health effects than those observed when PCBs are ingested.
In their risk assessment models, the USEPA assumes that exposure to PCBs by all routes of exposure are toxicologically equivalent. Since most or all of the animal toxicity studies used to assess PCBs have been feeding studies (using the ingestion pathway), this is the mode of exposure that we know the most about. However, there are some good reasons to suspect that inhalation exposures may be different from ingestion due to the way PCBs behave once they enter the body. This is particularly true because the liver is one of the principle target organs for PCBs.
When any toxic material is ingested (or a pharmaceutical product for that matter) absorption usually begins in the stomach and is generally completed in the small intestine. As chemicals are transferred into the circulatory system from the digestive organs, their first destination in the body is the liver. So if a chemical gives rise to liver toxicity, ingestion can be a particularly damaging route of administration because the toxic material proceeds directly to the liver from the digestive tract.
By contrast, when a toxic material is inhaled, it enters the lungs, transfers to the blood, goes to the heart and from there enters the general circulatory system. By the time an inhaled toxic material reaches the liver, its concentration has been reduced by dilution into the overall volume of blood in the body. What’s more, in the case of lipid (fat) soluble chemicals like PCBs, a high percentage of the dose entering the body by inhalation will become sequestered in other fatty tissues before the PCBs ever reach the liver. The overall effect would be to reduce the potential toxicity to the liver.
Interestingly there are pharmaceuticals that exhibit similar effects, testosterone is a good example. When used as a pharmaceutical, testosterone can not be given orally, that is by ingestion, because it can cause liver toxicity. This is despite the fact that it is a naturally occurring hormone. However, when given by routes of administration that reduce the concentration that the liver sees at any one time, testosterone does not harm the liver.
At this time I am not aware of good animal studies that test whether inhaled PCBs are in fact less toxic than ingested PCBs. However, there are a large number of well documented human studies where people were exposed to PCBs by inhalation in occupational settings. These studies consistently show less toxicity than has been predicted by EPA’s health effects models. It could be that this lower than expected toxicity is due to inhalation being the exposure pathway for these people rather than ingestion. If this is true, then it supports the idea that low concentrations of PCBs in air may be less hazardous than thought.