Polychlorinated biphenyls (PCBs) are a class of synthetic organic compounds with two phenyl rings as the basic structural unit. Chlorination of a biphenyl molecule can theoretically yield 209 chlorobiphenyls substituted with from one to 10 chlorine atoms, however, the practical number of useable compounds is ~102. They have a wide range of uses, are resistant to degradation in the environment and have extensively contaminated the food chain.

PCBs are soluble in fat or fat solvents, but highly insoluble in water (i.e. lipophilic & hydrophobic). Their solubility in water and in organic solvents affects their transport and persistence in the environment. PCBs are very stable compounds under pressure and extreme temperatures; they are non-flammable and withstand contact with strong acids and alkalis; electrically they are non-conducting.

PCBs tend to bind tightly to particulate matter such as dust, soil and fine sediments. PCBs adsorption onto and into lipid-rich organisms allows for biomagnification and bioaccumulation of these compounds within food chains. Long-lived organisms exposed to PCB-contaminated foods continue to accumulate these compounds through life, with reproductive females transferring some of their PCB residues onto their offspring via in utero development and through lactation.

Ecotoxicologist, Professor David Carpenter (University of Albany, New York) in a recent overview paper on the toxicity of Polychlorinated biphenyls (PCBs) detailed their known health effects:

“PCBs are:
alter immune system function;
cause adverse alterations of the nervous system, skin, thyroid, and sex steroid hormonal systems;
cause adverse alterations to the liver, kidney, pancreas, and the cardiovascular system.”

“As a result of these actions on multiple organ systems, humans who are exposed to PCBs are:
at increased risk of cancer,
at increased risk of infections,
at increased risk of reduced cognitive function accompanied by adverse behavioural effects,
at increased risk of hypothyroidism,
at increased risk of infertility,
at increased risk of ischemic heart disease, hypertension,
at increased risk of diabetes, 
at increased risk of liver disease,
at increased risk of asthma,
at increased risk of arthritis,
as well as giving birth to infants of lower than normal birth weight.”

“Some of these adverse effects, such as IQ deficits that result from perinatal exposure, are irreversible and cannot be treated but many other diseases, such as cancer, can be treated successfully if diagnosed early.”

Some of the dioxin-like PCB congeners are now banned but they are known to be persistent organic pollutants (POPs) that remain in the environment within plants, in food-chain animals, in soils, in wildlife, in fish, and of course in us for several decades.

For the reader what does this mean?

The slow process of international & national regulation through to banning of PCBs and other POPs is determined by scientific evidence of adverse public health & ecosystem health effects.

The majority of these toxicological risk assessments of PCBs are based on these synthetic poly-halogenated organic compounds binding to important cellular molecules that are responsible for cell growth, cell multiplication, endocrine & other important secretory functions within cells and tissues.

The synthetic PCBs that dominate the scientific literature are the so-called dioxin-like PCBs - these are coplanar PCBs for which the “toxic equivalents” [TEQ] has been determined. All the dioxin-like PCBs are compared against the most toxic dioxins - namely,  tetrachlorodibenzo-p-dioxin (TCDD) and the pentachlorodibenzo-p-dioxin (1,2,3,7,8 PeCDD).  These highest toxic equivalents ratings are principally based on the effect these molecules have on gene expression cell growth, cell appearance and function.  This is the reason they are considered carcinogenic or teratogenic.

Now many toxicologists and public health professionals are raising concerns about another range of serious adverse health effects caused by PCBs. These health effects are not triggered by the same cellular processes described above [those caused by the interaction of PCBs with aromatic hydrocarbon receptors (AhR) within cells].

Professor Isaac Pessah, (Centre for Children’s Environmental Health, Univ of California, Davis) has published research on the so-called non-coplanar PCBs (non-dioxin like PCBs) . These are the chemicals that, from a regulatory perspective, are currently considered of minor concern to public health safety and risk assessment.

His co-workers have demonstrated that perinatal exposure to non-coplanar PCBs (I.e. the PCBs not considered dioxin-like) can result in abnormal wiring of the brain region, the primary auditory cortex, that is essential in decoding and integrating sensory information generated by the cochlea (hearing centre). The mechanisms by which they produce their effects are not dependent on activation of the AhR cellular receptors. In fact the specific PCB tested has no measurable AhR activity.

From animal model research these adverse effects of exposure to non-dioxin PCBs has not been recognised by the regulatory measure of “toxicity” assigned to dioxin.

The improper wiring of the auditory cortex for example is unlikely to result in overt toxicological outcomes. Rather, if even a fraction of the abnormal pattern detected in our animal model was to take place in a developing child, the expected outcomes are expected to be language delays, diminished cognitive potential, and behavioural disorders. Although these outcomes are subtler than the overt toxicity ascribed to dioxin-like compounds, it is nevertheless as important to minimize the risks associated with exposure to specific synthetic molecules that have very high potency toward cellular molecules other than AhR receptors.

This is especially important because it is the non-coplanar PCBs that predominate in today’s environmental samples and in human tissues. [Read that sentence again]. Many in the regulatory arena have maintained that environmental PCB levels have been steadily declining and the need for tighter regulation is unwarranted. However because of this narrow “toxic equivalents” view, many non-coplanar persistent molecules have subsequently made it into global market, in large part based on their low AhR activities. These include the Polybrominated diphenyl ethers (PBDEs), triclosan, and other classes of chemicals that are very high use and likely to have additive actions with the non-coplanar PCBs.

The rationale that we do not regulate POPs on a basis other than their dioxin equivalency (TEQ) seems rather short sighted. Data that suggests potent non-AhR mechanisms could mediate more subtle negative developmental outcomes and impacts on human health should at least be considered in our risk assessment strategy.

David Obendorf

Some of the dioxin-like PCB congeners are now banned but they are known to be persistent organic pollutants (POPs) that remain in the environment within plants, in food-chain animals, in soils, in wildlife, in fish, and of course in us for several decades.

For the reader what does this mean?