Prenatal exposures to alcohol, cigarettes, and other drugs of abuse are associated with numerous adverse consequences for affected offspring, including increased risk for substance use and abuse (Baer et al., 2003, Ernst et al., 2001, Glantz and Chambers, 2006, Streissguth et al., 2004). Animal studies have demonstrated physiological effects of prenatal exposures that could plausibly contribute to offspring substance use disorders (SUD), including abnormalities of neural reward systems (Malanga and Kosofsky, 2003). However, the causal effect of prenatal exposures on human offspring is less clear as maternal substance use during pregnancy frequently co-occurs with other environmental and genetic risk factors (Wendell, 2013). Epidemiological studies indicate that prenatal drug and alcohol exposure are modest direct contributors to increased substance abuse vulnerability (Glantz and Chambers, 2006), though some studies suggest that these associations are accounted for by correlated risks such as socioeconomic status or familial history of substance use disorders (D’Onofrio et al., 2012, Ellingson et al., 2012).
