Prenatal exposure to tobacco and risk for schizophrenia: a retrospective epidemiological study
Introduction
In addition to genetic factors, environmental factors may also play a significant role in the etiology of schizophrenia [1].
Maternal smoking during pregnancy is associated with obstetric abnormalities and low birth weight [2], [3] that may lead to developmental disorders in childhood [4], [5], [6] and might also constitute risk factors for further development of schizophrenia. Prenatal smoking exposure has also been associated with further cognitive or behavioral disorders [7], [8], [9] such as specific subtypes of attention-deficit/hyperactivity disorder in genetically at risk children [10]. Although the underlying neurobiological mechanism responsible for these disorders remains controversial, alterations in development of central dopamine systems have been implicated [11].
In animal studies, maternal nicotine exposure produces alterations in the development of dopamine neurochemical markers and induces hyperactivity in the offspring that is believed to result from alterations in mesolimbic and nigrostriatal dopaminergic systems (for review, see Azam et al [12]). In the same way, disturbances in the mesolimbic dopaminergic system have been hypothesized in schizophrenia (for review, see Meisenzahl et al [13]), but to date, there are few reported epidemiological data regarding prenatal tobacco exposure in schizophrenia. Because long-term prenatal nicotinic exposure alters the development of dopaminergic neurons [11], [12], it has been suggested that one potential site of action for nicotine in producing these changes may be through direct action of nicotinic acetylcholine receptors (nAChRs) on immature developing dopamine neurons. Moreover, nAChRs may play critical functional roles throughout dopamine neuronal maturation and, via this mechanism, might increase the risk of subsequent schizophrenia in subjects who have been exposed prenatally to tobacco.
The aim of our study was to search for a potential association between prenatal tobacco exposure and subsequent development of schizophrenia. Moreover, we carried out a retrospective epidemiologically matched case-control study to compare the history of tobacco use during pregnancy between the mothers of 2 groups of subjects (schizophrenic patients and nonpsychotic matched subjects).
Section snippets
Study subjects
Inpatients or outpatients with schizophrenia or schizoaffective disorders (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria), consecutively admitted to Dieppe and Le Rouvray Hospitals between June 1 and December 31, 2006, were eligible for the study (group A). Subjects admitted to the emergency ward of our university hospital for nonpsychiatric reasons during the same period were also considered eligible for the study (group B). This latter group was matched with
Sample description
Two-hundred sixteen patients with schizophrenia and 9 patients with schizoaffective disorders were included. Among these patients, in 65 cases, the mother had died; in 17 cases, the interview of the mother was not possible; 24 patients were lost to follow-up; 2 patients were siblings (one was excluded from the study); 3 patients died during the recruitment period; 2 had no information about their biological parents; 2 had a mother living abroad; and in 10 cases, the patients or the mothers
Discussion
In accordance with previous data [15], in our study, the prevalence of tobacco use was higher in patients with schizophrenia (73%) as compared with controls (57%) with a higher percentage among men than women in both groups. In contrast, in the general population, Beck et al [16] reported a lower prevalence of smokers of 40% and 30% among men and women, respectively, aged between 25 and 34 years. In our sample of nonpsychotic subjects, the level of education was low, which may have contributed
Acknowledgment
The authors are grateful to Richard Medeiros, Rouen University Hospital Medical Editor, for editing the manuscript.
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