conducted a study of 626 married couples in Michigan. After monkeys incur long-term oral exposure to commercial PCB mixtures, related dermal effects are well characterized and generally are similar to those observed in humans.
Ī skin lesion exactly like chloracne in humans has been observed in several species of animals experimentally exposed to PCBs. However, whether this outcome was systematically studied in these cohorts is unknown. No adverse dermal effects have been reported in persons who consume large amounts of Great Lakes fish contaminated with PCBs and other environmentally persistent chemicals, or in other cohorts from the general population. This co-contamination created controversy about the extent to which the health effects observed in the Yusho and Yu-Cheng populations can be attributed to PCBs legitimately, as opposed to the dibenzofuran co-contaminants. Unlike usual PCB mixtures, the Yusho and Yu-Cheng mixtures were heated in thermal heat exchangers during the cooking process, resulting in contamination of the oil by chlorinated dibenzofurans as well as PCBs.
Exposure to PCBs occurred by consuming rice oil that had become contaminated by heat-degraded PCBs during processing. In these episodes, persons were exposed to PCBs and their heat-degradation products, mainly polychlorinated dibenzofurans (PCDFs). Skin effects were reported widely among victims of the Yusho (Japan) and Yu-Cheng (Taiwan) poisoning episodes in 1968 and in 1978, respectively. In addition to chloracne, other dermal effects noted in some PCB-exposed workers include pigmentation disturbances of skin and nails, erythema and thickening of the skin, and burning sensations. The lesions are often refractory to treatment and can last for years or decades. Chloracne typically develops weeks or months after exposure. No reliable dose-response model exists for chloracne in exposed populations, and the dose-response relationship might be dependent on individual predisposition. However, the absence of chloracne does not rule out exposure. Ĭhloracne generally indicates systemic toxicity and can be caused by not only dermal contact but also ingestion of PCBs. The cysts and comedones can become inflamed and secondarily infected, and papules and cysts can be surrounded by edema and erythema. The most distinctive lesions are cystic and measure 1-10 mm, although comedonal lesions can also be present. The chin, periorbital, and malar areas are most often involved, although lesions might also appear in areas not usually affected by acne vulgaris (e.g., the chest, arms, thighs, genitalia, and buttocks). The resulting inflammatory folliculitis stimulates keratinization of the sebaceous gland ducts and outer root sheath of the hair, leading to the formation of keratin cysts. Chloracne usually begins with the formation of keratin plugs in the pilosebaceous orifices. In a person with PCB-induced chloracne, the acne-like lesions arise as a result of inflammatory responses to irritants in the sebaceous glands. Their blood PCB concentrations ranged from 41 to 1319 µg/kg. All of the workers with chloracne were employed in high exposure jobs. Among 80 workers who manufactured capacitors in Italy, 10 cases of acne or folliculitis, or both, and 5 cases of dermatitis were reported. Mild to moderate chloracne was observed in 7 of 14 workers exposed to 0.1 mg/m 3 Aroclors for an average duration of 14.3 months. This adverse health effects section addresses PCBs as a whole.Ĭhloracne and related dermal lesions have been reported in workers occupationally exposed to PCBs.