Skin Absorption and Damage from PCBs Intro

Skin Absorption and Damage from PCBs

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Introduction

PCBs can be absorbed rapidly through the skin and cause internal injuries, such as liver damage. Numerous studies cite PCB skin contact as a significant health risk factor and several health and occupational safety agencies have recommended that workers wear protective gear to prevent such skin contact.
This is a concern in our community due to potential PCB skin absorption from contact with contaminated water, structures or soil along the Fox River and Green Bay. (See How Are Local People Exposed To PCBs? Also, see Reduce your own PCB exposure and protect your family.)

Serious skin damage and severe acne from PCB exposure was detected and discussed in the scientific literature as early as the 1930s (see History of PCBs.) Generally, these symptoms appear only at higher PCB doses, usually associated with occupational exposures or direct poisoning.

However, this does not mean a person is necessarily safe from other PCB health effects just because there is no clear evidence of skin damage.

Some scientists claim that PCBs do not cause Chloracne. Instead, they say that impurities in the PCBs are the true cause, from trace contamination with dioxins and furans. Other researchers seem to have demonstrated that pure PCBs alone cause Chloracne. Regardless of the truth in this matter, it makes little practical difference because we have all three chemicals (and more) present in Fox River and Green Bay sediments. (See PCBs, dioxins, furans and mercury – They Travel Together.)

What is Chloracne?

(from the EPA)

Chloracne and associated dermatologic changes are widely recognized responses to TCDD and other dioxin-like compounds [such as PCBs] in humans. Chloracne is a severe acne-like condition that develops within months of first exposure to high levels of dioxin. For many individuals, the condition disappears after discontinuation of exposure, despite serum levels of dioxin in the thousands of parts per trillion; for others, it may remain for many years. The duration of persistent chloracne is on the order of 25 years although cases of chloracne persisting over 40 years have been noted.

There are very little human data from which to determine definitively the doses at which chloracne is likely to occur. Data from occupational studies suggest that persistent chloracne is more often associated with exposures of high intensity, for long duration, and commencing at an early age. Acute exposures or chronic lower level exposures, if resulting in chloracne, have generally resulted in a condition that resolves itself in a matter of months to a few years.

Induction of chloracne in humans after exposure to dioxin and related compounds is supported by studies in laboratory animals. Rabbits, monkeys, and hairless mice have all proved useful in investigating this response. In addition, cellular systems provide a research tool in elucidating the chloracne response at the cellular level. Keratinocytes, the principal cell type in the epidermis, have been used as an in vitro model for studies of TCDD-induced hyperkeratosis, a feature of chloracne, in human- and animal-derived cell cultures. The response in these systems is analogous to the hyperkeratinization observed in vivo as a part of chloracne.

There is little doubt that chloracne is a human condition often attributable to exposure to dioxin and related compounds. The specific risk factors associated with this response are still obscure. Recognition of chloracne has been associated with high-level exposure to these compounds, and as such, may represent a biomarker of exposure. Because of the wide variability of the chloracnegenic response in humans and its varied persistence, however, the absence of chloracne is not a reliable indicator of low exposure to dioxin and related compounds.

(Source: The 1994 EPA Dioxin Reassessment Health Assessment, Volume III: Risk Characterization)

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