Maternal/fetal genetic constitution and environmental factors are vital to delivery of a healthy baby. In the United States (US), a low birth weight (LBW) baby is born every minute and a half. LBW, defined as weighing less than 5.5 lbs at birth, affects nearly 1 in 12 infants born in the US with resultant costs for the nation of more than 15 billion dollars annually. Infant
birth weight is the single most important factor affecting neonatal mortality. Various environmental and genetic risk factors for LBW have been identified. Several risks are preventable, such as cigarette smoking during pregnancy. Over one million babies are exposed prenatally to cigarette
smoke accounting for over 20% of the LBW incidence in the US. Cigarette
smoke exposure in utero results in a variety of adverse developmental outcomes with
intrauterine growth restriction and infant LBW being the most well documented. However, the mechanisms underlying the causes of LBW remain poorly understood. The purpose of this study was: (1) to establish an animal model of cigarette
smoke-induced in utero growth retardation and LBW using physiologically relevant inhalation exposure conditions which simulate "active" and "passive" tobacco
smoke exposures, and (2) to determine whether particular stages of development are more susceptible than others to the adverse effects of in utero
smoke exposure on embryo/fetal growth. Pregnant C57BL/6J mice were exposed to cigarette
smoke during three periods of gestation: pre-/peri-implantation (gestational days [gds] 1-5), post-implantation (gds 6-18), and throughout gestation (gds 1-17). Reproductive and fetal outcomes were assessed on gd 18.5. Exposure of dams to mainstream/sidestream cigarette
smoke, simulating "active" maternal smoking, resulted in decreases in
fetal weight and crown-rump length when exposed throughout gestation (gds 1-17). Similar results were seen when dams were exposed only during the first 5 days of gestation (pre-/peri-implantation period gds 1-5). Exposure of dams from the post-implantation period through gestation (gds 6-18) did not result in reduced
fetal weight, although a significant reduction in crown-rump length remained evident. Interestingly, maternal sidestream
smoke exposure, simulating exposure to environmental tobacco
smoke (ETS), during the pre-/peri-implantation period of development also produced significant decreases in
fetal weight and crown-rump length. Collectively, results from the present study confirm an association between prenatal exposure to either "active" or "passive" cigarette
smoke and in utero growth retardation. The data also identify a period of susceptibility to in utero cigarette
smoke exposure-induced growth retardation and LBW during pre-/peri-implantation embryonic development.