All representative types of microbial insecticides ( i.e. bacteria, fungi, protozoans, viruses ) are inactivated by exposure to the ultraviolet-A ( UV-A ), ultra violet-B UV-B) spectrum (280-400nm) of sunlight lgnoffo et al. 1977). Solar inactivation of Bacillus thuringiensis Berliner and other entomopathogens is a a widely recognized phenomenon. Exposure for short periods (<24h) to wavelenghts below 500 nm inactivates spores, degrades protein structures of virial inclusion bodies, and may inactivate B.thuringiensis crystalline toxins. The half-life for B.thuringiensis has been estimated at 3.8h. when exposed to an ultraviolet (UV) source representative of the UV radiation in natural sunlight ( Ignoffo et al. 4977 ). Numerons attempts have been made to develope protective measures against damaging UV radiation under field conditions, but success has been limited, suggesting that effects of solar radiation on entomopathogens are not sufficiently understood Raun & Jackson 1966, Ahmed et al 1973, Morris 1983). Two general hyposeses have been formulated to explain the sunlight inactivation of the microbial insecticides. Sunlight may have a direct effect on microbial DNA by including de/eterions cross-1inkings, strand breaks or development of labile sites or both (Tyrrell 1973, Tyrrell et al 1974 ). Although his hypothesis could explain sunlight inactivation of living micro organisms, it would not explain inactivation of the nonliving, crystalline endotoxin of Bacillus thuringiensis. Another hyposthesis that might explain the sunlight inactivation of both types of microbial insecticides is sunlight generation of highly reactive radicals ( e.g. peroxides, sigletoxygen, hydroxyls ) that would, in turn, degrade the insecticidally active active entity ( Yoakum & Eisenstark 1972, Ananthaswamy & Eisenstark 1976, McCormick etal 1976, Ignoffo & Garcia 1992, Pozsgay et al 1987, Ignoffo et al 1989).