In March 1995, the California Environmental Protection Agency released a draft document entitled """"""""Developmental and reproductive effects of exposure to environmental tobacco smoke"""""""" (Cal EPA, 1995). Their conclusion, based on an analysis of some 17 human epidemiological studies was that by now there is sufficient evidence that ETS adversely affects fetal growth. In a large population, this could translate into a significant public health risk. We have developed an animal model of intrauterine growth retardation (IUGR). When pregnant rats are exposed through gestation under carefully controlled conditions to sidestream cigarette smoke (SS), a surrogate for environmental tobacco smoke (ETS), the average litter weight of the pups is reduced by a small (6%), but statistically significant amount. It is planned to establish dose-response and time-response relationships for the effects of SS on birthweight in rats and to define whether adverse effects are caused by full smoke or can be produced by the gaseous phase alone. Particularly, we will test the hypothesis that there are critical intervals during gestation where intrauterine development might be adversely affected influenced by exposure to SS. The observations will be correlated with measurements of biomarkers of exposure to SS in pregnant dams such as levels of blood nicotine, cotinine and carboxyhemoglobin as a function of ambient SS concentration. In mechanistic studies, we plan to test the hypothesis that specific fetal organs and tissues will show a reduced rate of cell proliferation after exposure of pregnant rats to SS. An alternative hypothesis will be to examine whether the IUGR produced in rats by exposure to cigarette SS is caused by a disturbance of energy metabolism within the fetus. The results should contribute important information to defining a proper risk assessment for the effects of ETS on the developing fetus.
