The following abstract presents results of a study conducted by a contract laboratory for the National Toxicology Program. The findings may not have been peer reviewed and were not evaluated in accordance with the levels of evidence criteria established by NTP in March 2009. For more information, see the Explanation of Levels of Evidence for Developmental Toxicity. The findings and conclusions for this study should not be construed to represent the views of NTP or the U.S. Government.
Arsine gas is a potent hemolytic agent which causes rapid red blood cell destruction and renal failure (Fowler and Weissberg, 1974). It is used extensively in the semiconductor industry. 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 by inhalation to arsine at concentrations of 0, 0.025, 0.5, or 2.5 ppm on Gestation Days (gd) 6 through 15. There were 23-27 rats per group, and 24-25 pregnant mice/group. 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 assessed on gd 20, the arsenic content of maternal blood and fetal livers increased with increasing atmospheric arsine concentrations. There were significant adverse effects on all measured maternal hematologic indices after arsine exposure of 5 ppm from gd 4 through gd 15.
In mice, maternal spleen size was significantly increased in the 2.5 ppm group. However, 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 measurable levels of arsenic in maternal blood and fetal livers (2.5 ppm) did not adversely affect endpoints of developmental toxicity, therefore the no observed adverse effect level for maternal toxicity was 0.5 ppm while the NOAEL for developmental toxicity was 2.5 ppm.
This results of these studies appear in a published manuscript rather than a report: Morrissey RE, Fowler BA, Harris MW, Moorman MP, Jameson CW, Schwetz BA. Arsine: Absence of Developmental Toxicity in Rats and Mice. FAAT. 15(2):350-356. (1990)