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© 1990 Oxford University Press

research-article

Arsine: Absence of Developmental Toxicity in Rats and Mice

RICHARD E. MORRISSEY1, BRUCE A. FOWLER2, MARTHA W. HARRIS, MICHAEL P. MOORMAN, C. W. JAMESON and BERNARD A. SCHWETZ

Division of Toxicology Research and Testing, National Toxicology Program N1EHS, Research Triangle Park, North Carolina 27711

Received December 21, 1989; accepted April 17, 1990

Arsine: Absence of Developmental Toxicity in Rats and Mice. MORRISSEY, R. E., FOWLER, B. A., HARRIS, M. W., MOORMAN, M. P., JAMESON, C. W., AND SCHWETZ, B. A. (1990). Fun-dam. Appl. Toxicol. 15, 350–356. Arsine gas is a potent hemolytic agent but the effects of exposure to tolerated concentrations on pregnancy and prenatal development have not been reported. In the present evaluation, groups of bred mice and rats were exposed to arsine at concentrations of 0.025, 0.5, or 2.5 ppm on Gestation Days (gd) 6 through 15. Animals were killed on gd 17 (mice) or on gd 20 (rats) and endpoints of maternal and developmental toxicity were evaluated. In rats, maternal spleens were enlarged in the 2.5 ppm group and there was a decrease in packed red cell volume in pregnant rats. Fetuses weighed more than in the control group but other endpoints of developmental toxicity were not affected by arsine exposure. In another experiment involving separate groups of rats, the arsenic content of maternal blood and fetal livers increased with increasing atmospheric arsine concentrations, as assessed on gd 20. In mice, maternal spleen size was significantly increased in the 2.5 ppm group. The number of live fetuses, mean fetal body weight, and percentages of resorptions or malformations per litter were not affected by arsine exposure. In conclusion, arsine at atmospheric concentrations that caused increases in maternal spleen size and measureable levels of arsenic in maternal blood and fetal livers did not adversely affect endpoints of developmental toxicity


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