H. Mcgrath et al., FLUORESCENT LIGHT ACTIVATES THE IMMUNOMODULATOR CIS-UROCANIC ACID IN-VITRO - IMPLICATIONS FOR PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS, Annals of the Rheumatic Diseases, 53(6), 1994, pp. 396-399
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 f
luorescent light, presumably acting predominantly along the 313 nm wav
elength, exhibits photochemical activity sufficient to account for tox
icity. Methods-The photochemical activity of fluorescent light was ass
essed by testing its capacity to activate urocanic acid, a plentiful a
nd potent epidermal immunological mediator normally activated by polyc
hromatic UVB radiation but activated maximally at 313 nm. Irradiation-
induced isomerisation of trans-urocanic to cis-urocanic acid was quant
itated by UV spectroscopy after separation of the isomers by high perf
ormance liquid chromatography. Results-Fluorescent light irradiation o
f solutions containing the photoreceptor trans-urocanic acid produced
a cumulative conversion of trans- to cis-urocanic acid. This photochem
ical activity was compared with that of erythemagenic sun-lamps, high
in polychromatic UVB emissions. When normalized for UVB irradiance, th
e accumulation of cis-urocanic acid produced by both light sources was
essentially equivalent. Conventional acrylic diffusers that absorb UV
B emissions eliminated the fluorescent light-induced reaction. Conclus
ion-The results indicate that radiation from fluorescent lamps possess
es substantial photoimmunological capability, sufficient to activate a
potent, potentially dangerous, disease-modifying, immunomodulatory pa
thway and that poorly erythemagenic, primarily monochromatic UVB photo
ns are responsible.