Lung Hypoplasia in Developing Mice and Rats Induced by Maternal Exposure to Nitrofen

Abstract: The effects of maternal exposure to 2, 4‐dichlorophenyl‐p‐nitrophenyl ether (nitrofen) on prenatal lung growth were examined by dietary administration (2,000 ppm in ICR mice and 500 ppm in CD rats). Embryos and/or fetuses (conceptuses) were removed from dams on days 12 to 18 of gestation in mice and on days 14 to 20 of gestation in rats. Body and lung weights of the conceptuses were measured. General growth retardation was noted especially in the later period of intrauterine life in both mice and rats. Bilateral retardation of lung development of the nitrofen exposed conceptuses was noticed throughout intrauterine life including the periods before the closure of pleuroperitoneal canals in both species indicating that nitrofen induced primary lung hypoplasia. In mice, the left lung was more hypoplastic than the right one, while it was opposite in rats. The species specificity in side prevalence of the developmental retardation of the lung was observed even before completion of the embryonic diaphragm and it was well in accord with the side on which posterolateral diaphragmatic hernia (Bochdalek's diaphragmatic hernia, BDH) took place later. We conclude that nitrofen induces primary lung hypoplasia regardless of the presence or absence of BDH.