Kandel, Wu, and Davies selleck chemicals Dorsomorphin (1994) reported a fourfold increase in tobacco use among girls aged 9�C17 years with PCSE. Griesler, Kandel, and Davies (1998) showed that this association was a mediated relationship: PCSE was significantly associated with higher levels of child behavior problems that, in turn, increased the likelihood of lifetime smoking among daughters. In the Maternal Health Practices and Child Development (MHPCD) Project, 10-year-old PCSE offspring had a 5.5-fold increased risk for early tobacco experimentation (Cornelius, Leech, Goldschmidt, & Day, 2000). In the Ottawa Prenatal Prospective Study (OPPS; Porath & Fried, 2005), PCSE significantly predicted offspring cigarette smoking initiation. Thus, PCSE is associated with early initiation of tobacco use among offspring.

PCSE also predicts greater quantity and frequency of offspring cigarette use. At 14 years, offspring with PCSE in the MHPCD study smoked significantly more cigarettes than those without PCSE (Cornelius, Leech, Goldschmidt, & Day, 2005). Findings from a birth cohort of over 7,000 offspring demonstrated that maternal smoking during pregnancy had an independent effect on the quantity of cigarettes smoked among 14-year-olds (O��Callaghan et al., 2006). In a retrospective study of children in treatment for smoking cessation, PCSE predicted accelerated progression from experimentation to daily use among girls and earlier experimentation among the boys (Oncken, McKee, Krishnan-Sarin, O��Malley, & Mazure, 2004). PCSE has been also shown to be significantly related to lifetime tobacco dependence (Buka, Shenassa, & Niaura, 2003; Lieb, Schreier, Hildegard, & Wittchen, 2003).

While the association between PCSE and offspring tobacco use is well documented, there are few reports about the effects of PCSE on initiation and use of marijuana, alcohol, and other illicit drugs. In the MHPCD study, a significant bivariate relation between PCSE and offspring marijuana use at age 14 was not significant after controlling for home environment (Day, Goldschmidt, & Thomas, 2006). The OPPS also did not find a significant relation between PCSE and marijuana use at ages 16�C21 (Porath & Fried, 2005). There are no reports of an association between PCSE and offspring alcohol use. There is a biological basis for a relation between PCSE and offspring substance use.

Prenatal nicotine exposure has been shown to increase plasma testosterone in mice offspring, and this alteration increases nicotine seeking in the offspring (Smith, Cloak, Poland, Torday, & Ross, 2003). In a study by Slotkin (2008), there was an upregulation of nicotinic acetylcholine Dacomitinib receptors (nAChR) among adult rats exposed to nicotine in the immediate neonatal period, a time comparable to the third trimester in humans. Subsequently, the modification of the neurotransmitters affects the reward system and increases susceptibility to drug use.