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RECORD NUMBER: 12 OF 48

OLS Field Name OLS Field Data
Main Title Effect of Methyl Oleate Ozonide, a Possible Ozone Intermediate, on Normal and G-6-PD Deficient Erythrocytes.
Author Calabrese, E. J. ; Moore, G. S. ; Williams, P. ;
CORP Author Massachusetts Univ., Amherst. Dept. of Public Health.;Health Effects Research Lab., Research Triangle Park, NC.
Year Published 1982
Report Number EPA-R-805797; EPA/600/J-82/442;
Stock Number PB85-195758
Additional Subjects Erythrocytes ; Toxicity ; Ozone ; Blood analysis ; Public health ; Respiratory systems ; Air pollution ; Exposure ; Statistical analysis ; Dosage ; Risk ; Reprints ; Oleic acid/methyl-ozonyl ; Dehydrogenase/glucose-phosphate ; Air pollution effects(Humans) ; Chemical reaction mechanisms
Holdings
Library Call Number Additional Info Location Last
Modified
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Status
NTIS  PB85-195758 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 06/21/1988
Collation 8p
Abstract
While ozone (O3) has long been recognized as a respiratory tract irritant (STOKINGER 1957, 1965; YOUNG & SHAW 1964; MENZEL 1976), it has also been unequivocally established that it causes a wide variety of systemic effects including chromosomal aberrations in circulating lymphocytes (ZELAC et al. 1971, 1971a; MERZ et al. 1975), alters liver metabolism (GARDNER 1979; GRAHAM et al. 1982), and changes in erythrocyte metabolism indicative of oxidant stress (LARKIN et al. 1978; BUCKLEY et al. 1975). The mechanism by which O3 affects such systemic changes is unknown. However, it has been hypothesized that O3 exerts its toxicity via intermediates (MENZEL et al. 1975). While the nature of such intermediate(s) is not known, theoretical support exists that toxicity may be mediated by O3 induced formation of systemic oxonides and/or hydroperoxides (MENZEL 1979). The present study was designed to evaluate the effects of a possible ozone intermediate (i.e. methyloleate ozonide (MOO) on the red blood cells of normal and glucose-6-phosphate dehydrogenase (G-6-PD) deficient humans. G-6-PD deficient human erythrocytes have been previously hypothesized as being at greater risk to O3 (CALABRESEet al. 1977) but as yet no direct testing of that hypothesis has been published. (Copyright (c) 1982 Springer-Verlag New York Inc.)