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An animal model of cigarette smoke-induced in utero growth retardation
Emily R Esposito1, Kristin H Horn, Robert M Greene
1University of Louisville Birth Defects Center, Department of Molecular, Cellular and Craniofacial Biology, University of Louisville, ULSD, 501 South Preston Street, Suite 301, Louisville, KY 40292, USA.
Insights
Prenatal exposure to cigarette smoke, both active and passive, is linked to low birth weight (LBW) and intrauterine growth restriction. The pre-/peri-implantation period is a critical window for susceptibility to these adverse effects.
Area of Science:
- Reproductive Biology
- Developmental Toxicology
- Perinatal Medicine
Background:
- Low birth weight (LBW) affects nearly 1 in 12 infants in the US, incurring significant national costs and impacting neonatal mortality.
- Cigarette smoking during pregnancy is a preventable risk factor, contributing to over 20% of LBW incidence.
- Mechanisms underlying LBW due to in utero smoke exposure remain poorly understood.
Purpose of the Study:
- To develop an animal model for cigarette smoke-induced intrauterine growth retardation and LBW.
- To simulate "active" and "passive" tobacco smoke exposures using physiologically relevant conditions.
- To identify developmental stages most susceptible to in utero smoke exposure effects on embryo/fetal growth.
Main Methods:
- Pregnant C57BL/6J mice were exposed to cigarette smoke during specific gestational periods: pre-/peri-implantation (days 1-5), post-implantation (days 6-18), and throughout gestation (days 1-17).
- Exposure conditions simulated "active" (mainstream/sidestream smoke) and "passive" (environmental tobacco smoke - ETS) maternal smoking.
- Reproductive and fetal outcomes, including fetal weight and crown-rump length, were assessed on gestational day 18.5.
Main Results:
- Exposure to "active" cigarette smoke throughout gestation or during the pre-/peri-implantation period significantly decreased fetal weight and crown-rump length.
- Exposure during the post-implantation period (days 6-18) did not reduce fetal weight but did reduce crown-rump length.
- Maternal ETS exposure during the pre-/peri-implantation period also significantly decreased fetal weight and crown-rump length.
Conclusions:
- Prenatal exposure to "active" or "passive" cigarette smoke is associated with in utero growth retardation and LBW.
- Embryonic development during the pre-/peri-implantation stage is particularly susceptible to cigarette smoke exposure-induced growth retardation and LBW.
Abstract:
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.
