One in 5 Americans — roughly 45 million adults — smoke,1
and close to 40% are women. Estimates indicate that 1 in 10 pregnant mothers smoke cigarettes, which is a rate far higher than the 1% goal proposed by Healthy People 2010.2
Smoking during pregnancy has been identified as the single most preventable cause of illness and death among mothers and infants.3
This behaviour has been linked to many deleterious effects that put the newborn at increased risk for adverse health outcomes. For example, maternal smoking during pregnancy is dose-dependently associated with low birth weight and reduced growth of the fetal head,4
the harbingers of impaired cognition that could help explain the observed associations between prenatal cigarette smoke exposure (PCSE) and increased risks for attention-deficit hyperactivity disorder, antisocial behaviours and neurocognitive deficits in the offspring (see Neuman and colleagues5
for a list of references). However, the mechanisms underlying such long-term effects in the offspring have been difficult to establish, likely because of the confounding effects of many genetic, epigenetic, developmental and environmental factors, whose combined actions help train these associations. Our goal is not to present a comprehensive review of these factors and associations but to focus on the type of disruptive behaviours categorized as conduct disorders.
Conduct disorders encompass a group of aggressive and nonaggressive behavioural and emotional syndromes in children and adolescents who have difficulty following rules and behaving in socially acceptable ways. These disorders affect between 3% and 8% of preadolescent and adolescent boys and are more common in boys than in girls.6
According to some estimates, smoking during early pregnancy may account for up to 25% of externalizing (aggressive) behaviours, which include conduct disorders.6
In the past 15 years, numerous epidemiologic surveys have documented robust links between PCSE and externalizing conduct disorders.7–17
An association with aggressive behaviours was also suggested by a large longitudinal Danish study that found that maternal smoking predicted persistent criminal outcome in male offspring even after correcting for parental characteristics or perinatal complications.18
Collectively, the specificity of these effects and their timing strongly suggest that maternal smoking may contribute to the development of conduct disorders including aggressive behaviours, a hypothesis that is supported by preclinical studies.19
Disturbingly, the association could be self-perpetuating because PCSE appears to be a risk factor for nicotine dependence later in life,20
and a childhood history of conduct disorder may be a risk factor for maternal smoking during pregnancy.21
Indeed, it is possible that a significant overlap exists between the genes that confer vulnerability to conduct disorders and those that modulate smoking behaviours.
The challenging issue is to determine whether exposure to tobacco smoke while in utero can cause antisocial behaviours or whether it merely indicates the presence of other risk factors (e.g., common genetic vulnerabilities, postnatal exposure to cigarette smoke) that modulate or lead to this class of psychiatric disorders in the offspring. Included among these factors are a mother's subsequent smoking habits,22
a mother's history of antisocial behaviour17,23
and depression symptoms17
and the family's socioeconomic status10,17
or loading for alcohol dependence.24
Moreover, in one study correcting for parental depression and antisocial behaviour, general heritable influences and social deprivation virtually obliterated the association between PCSE and conduct disorders.17
Nonetheless, such negative findings do not rule out the contribution of an interaction between a specific gene(s) (not properly represented in the study's cohort), environment (smoke exposures) and development. Indeed, just as cannabis use in adolescence appears to modulate the risk for the later development of schizophreniform symptoms only in those with a specific genetic vulnerability (i.e., carriers of Val allele at the catechol-O
-methyltransferase [COMT] locus),25
it is conceivable, according to the cumulative data, that PCSE may add significantly to the risk of later developing conduct disorders only in carriers of a specific genetic vulnerability, such as the low monoamine oxidase A (MAOA) expressing allele.