Cutaneous malignant melanoma and fluorescent lighting.

A population-based case-control study of cutaneous malignant melanoma occurring during 1980-81 was conducted in Perth, Western Australia. Three hundred and thirty-seven cases and 349 matched controls were reinterviewed in 1983 with regard to their fluorescent light exposure. The incidence rate of all melanomas was not associated with rate of exposure or cumulative exposure to all fluorescent lights or just those without diffusers. Separate analyses by histogenetic type and, where possible, body site of melanoma showed, in most instances, no consistent association between incidence rate of melanoma and exposure to fluorescent lights without diffusers. Incidence of melanomas of unclassifiable histogenetic type, however, increased with increasing duration of exposure (P-value for trend .02). This association was weaker and the P-value higher (.11) when exposure was considered only in residential rooms and offices, where light fittings are closest to the subject. Adjustment for the effects of total and intermittent sun exposure on melanoma rates did not alter the above trends appreciably.

Fluorescent light-induced chromosome damage in human IMR-90 fibroblasts. Role of hydrogen peroxide and related free radicals.

Exposure of human fibroblasts (IMR-90) to cool-white fluorescent light causes chromatid breaks and exchanges. This chromatid damage is caused largely by the production of hydrogen peroxide (H2O2) since it can be prevented almost completely by the addition of catalase. In support of this conclusion, exogenous H2O2 is shown to induce chromatid breaks. The clastogenic amounts of H2O2 generated during light exposure are formed within the cell since cells illuminated in saline showed the same extent of damage as cells in culture medium. Addition of selenite to the cultures during light exposure significantly decreases the chromatid damage in a dose-related manner and may be necessary to maintain sufficient activity of glutathione peroxidase. The free hydroxyl radical, . OH, appears to be partially responsible for the light-induced chromatid damage. Of the free-radical scavengers tested, i.e., mannitol, vitamin E, and dimethyl sulfoxide, only mannitol, which scavenges . OH, significantly decreases the light-induced chromatid damage. Thus, both . OH and H2O2 formed within the cell during light exposure are agents that directly or indirectly cause chromatid damage.