Abstract

OBJECTIVE--Erythemagenic (295-305 nm) ultraviolet-B (UVB) radiation is toxic to patients with systemic lupus erythematosus (SLE). Cool white fluorescent lamp emissions produce a similar toxicity even though the UVB radiation emitted is primarily at the relatively non-erythemagenic wavelength of 313 nm. The purpose of this study was to determine if fluorescent light, presumably acting predominantly along the 313 nm wavelength, exhibits photochemical activity sufficient to account for toxicity. METHODS--The photochemical activity of fluorescent light was assessed by testing its capacity to activate urocanic acid, a plentiful and potent epidermal immunological mediator normally activated by polychromatic UVB radiation but activated maximally at 313 nm. Irradiation-induced isomerisation of trans-urocanic to cis-urocanic acid was quantitated by UV spectroscopy after separation of the isomers by high performance liquid chromatography. RESULTS--Fluorescent light irradiation of solutions containing the photoreceptor trans-urocanic acid produced a cumulative conversion of trans-to-cis-urocanic acid. This photochemical activity was compared with that of erythemagenic sunlamps, high in polychromatic UVB emissions. When normalised for UVB irradiance, the accumulation of cis-urocanic acid produced by both light sources was essentially equivalent. Conventional acrylic diffusers that absorb UVB emissions eliminated the fluorescent light-induced reaction. CONCLUSION--The results indicate that radiation from fluorescent lamps possesses substantial photoimmunological capability, sufficient to activate a potent, potentially dangerous, disease-modifying, immunomodulatory pathway and that poorly erythemagenic, primarily monochromatic UVB photons are responsible.