The study objective was to assess whether exposure to sunlamps and sunbeds represents a risk factor for cutaneous malignant melanoma (CMM). A 1-to-1 unmatched case-control study was conducted among subjects 20 years old or more with naturally non-pigmented skin in Germany, France and Belgium. A total of 420 consecutive patients with CMM diagnosed from 1 January 1991 onward were derived from hospital registers; 447 controls with no history of skin cancer were chosen at random in the same municipality as the cases. Exposure to sunlamps or sunbeds starting before 1980 is associated with a crude estimated risk of CMM of 2.71 (95% CI: 1.06-7.78) for at least 10 hr of accumulated exposure. This risk is of 2.12 (95% CI: 0.84-5.37) after adjustment for age, sex, hair colour and average number of holiday weeks each year in sunny resorts. Subjects who experienced skin-burn due to sunlamps or sunbeds, and who had accumulated at least 10 hr of exposure, displayed a crude estimated CMM risk of 4.47 (95% CI: 1.45-13.7), which rose to 8.97 (95% CI: 2.10-38.6) for those who exposed their skin for tanning purposes. The risk associated with skin-burn is only marginally modified after multiple adjustments for host characteristics and recreational exposure to sunlight. Apparently, sunlamps and sunbeds share the increased risk of CMM, which seems to concentrate in subjects exhibiting hazardous behaviour towards ultraviolet radiation sources. However, although it is reasonable to believe that high doses of pure ultraviolet A radiation can be dangerous, this is not firmly established by this study. Most exposures to ultraviolet A tanning devices began after 1980; therefore, epidemiologic studies have difficulty in revealing any increase in risk of CMM starting after 1980 because of the latent period between exposure and occurrence of melanoma. Public health authorities should have a cautious approach towards the rapidly developing fashion of tanning under sunlamps or sunbeds.
Use of sunscreens is widely advocated as a preventive measure against sun-induced skin cancers. However, to date, no epidemiologic study has reported a decreased melanoma risk associated with sunscreen use. We have conducted a case-control study aimed at evaluating the influence of sunscreen use on the occurrence of cutaneous malignant melanoma. In 1991 and 1992, 418 melanoma cases and 438 healthy controls were interviewed in Germany, France and Belgium. The questionnaire used differentiated between regular sunscreens, psoralen sunscreen (prepared with 5-methoxypsoralen, a tanning activator and photocarcinogen), and self-tanning cosmetics (which produce a tan without ultraviolet radiation). After adjusting for age, sex, hair colour and holiday weeks spent each year in sunny resorts, the melanoma risk was of 1.50 (95% Cl:1.09-2.06) for regular sunscreens, and of 2.28 (95% Cl: 1.28-4.04) for psoralen sunscreens. No melanoma risk was associated with use of self-tanning cosmetics. Among subjects with a poor ability to tan, psoralen sunscreen users displayed a melanoma risk of 4.45 (95% Cl: 1.25-15.8) when compared with regular sunscreen users. There was a significant negative interaction between regular sunscreen use and sunburns experienced in adulthood. Use of sunscreens, especially psoralen sunscreen, was associated with higher density of pigmented lesions of the skin. Although we cannot exclude the presence of an unknown confounding factor, our results support the hypothesis that sunscreens do not protect against melanoma, probably because of their ability to delay or avoid sunburn episodes, which may allow prolonged exposure to unfiltered ultraviolet radiation. Serious doubts are raised regarding the safety of sunscreens containing psoralens.
Monoclonal antibodies (mAb) derived from BALB/c mice immunized with human anti-HLA-A2 cloned cytotoxic T lymphocytes (CTL) were screened for their ability to block, in the absence of complement, the cytolytic activity of the immunizing CTL clone. Eight cytolysis-inhibiting mAb have been derived. One of these was directed against a monomorphic determinant expressed on HLA-class I molecules and thus probably inhibited cytolysis via a target cell antigen-masking effect. The 7 other mAb recognized "CTL function-associated structures" and did not have to interfere with target cell antigens in order to inhibit cytolysis. F(ab')2 and Fab fragments of these 7 mAb were also inhibitory. Competitive inhibition of binding and preliminary biochemical analysis suggested that these 7 mAb defined on cloned CTL various epitopes of a structure of 30 kDa disulfide-bonded into several multimeric forms when analyzed without reduction. The inhibitory effect of these 7 mAb has been investigated on a series of short-term (1 month) and long-term (greater than 10 months) expanded cloned CTL lines derived in vitro from an in vivo allosensitized individual exhibiting various specificities. Unexpectedly, only 10% of these CTL clones were inhibited. Flow cytofluorimetric analysis further revealed that noninhibited and inhibited CTL clones expressed similar amounts of the 30-kDa structure. Consequently, the inhibition of CTL was heterogeneous when analyzed at the clonal level and not simply related to the presence or absence of this structure. Furthermore, the ability of CTL clones to be inhibited appeared to be unrelated to their HLA-A, B or C specificity or to their lytic activity. The connections between this mAb-defined structure and CTL function are discussed.
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