Elsevier

Comprehensive Psychiatry

Volume 51, Issue 2, March–April 2010, Pages 106-109
Comprehensive Psychiatry

Prenatal exposure to tobacco and risk for schizophrenia: a retrospective epidemiological study

https://doi.org/10.1016/j.comppsych.2009.03.012Get rights and content

Abstract

Introduction

In animal studies, long-term prenatal nicotinic exposure alters the development of dopaminergic neurons. To determine whether prenatal smoking exposure was associated with schizophrenia, using a retrospective design study, we compared the prevalence of tobacco use during pregnancy in mothers of subjects with and without schizophrenia.

Methods

One hundred patients with schizophrenia, 100 nonschizophrenic-matched subjects, and their respective mothers were interviewed. The prevalence of smoking was measured in these individuals as well as in their respective mothers during the pregnancy.

Results

Patients with schizophrenia smoked more often compared with controls (73% vs 57%). In contrast, the prevalence of smoking during pregnancy did not differ between the groups of mothers. Indeed, the amount of tobacco used was significantly lower in mothers of patients with schizophrenia vs mothers of nonpsychotic subjects.

Conclusion

This study did not show any association between prenatal tobacco exposure and further development of schizophrenia.

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.

References (25)

  • SextonM. et al.

    A clinical trial of change in maternal smoking and its effect on birth weight

    JAMA

    (1984)
  • FrankD.A. et al.

    Growth, development, and behaviour in early childhood following prenatal cocaine exposure: a systematic review

    J Am Med Assoc

    (2001)
  • Cited by (14)

    • Prenatal and perinatal risk and protective factors for psychosis: a systematic review and meta-analysis

      2020, The Lancet Psychiatry
      Citation Excerpt :

      Umbrella reviews show that paternal age older than 35 years is a significant risk factor for psychosis27 and anxiety disorders,32 and higher paternal ages are associated with autism spectrum disorder.30 Conversely, only one primary study showed a significant association between maternal ages 30–34 and psychosis,47 but most studies did have ORs slightly higher than 1. Maternal age 30–34 has also been associated with autism spectrum disorder in an umbrella review.30

    • Increased risk of developing schizophrenia in animals exposed to cigarette smoke during the gestational period

      2017, Progress in Neuro-Psychopharmacology and Biological Psychiatry
      Citation Excerpt :

      A novel hypothesis ranks schizophrenia as a neurodevelopmental disorder that affects 0.5–1.0% of the world's population (Rapoport et al., 2005). Maternal smoking comprises an environmental event investigated as a risk factor for the onset of schizophrenia in adulthood, which affects cognitive and behavioural disorders (Baguelin-Pinaud et al., 2010). Preclinical studies have demonstrated that exposure to nicotine induces changes in the developmental neurochemical markers of dopamine (DA) and may cause hyperactivity in offspring (Azam et al., 2007).

    • Prenatal tobacco smoke exposure, risk of schizophrenia, and severity of positive/negative symptoms

      2013, Schizophrenia Research
      Citation Excerpt :

      This is reflected on the very low frequency of schizophrenia that ranged from 0.14% to 0.18%. The study of Baguelin-Pinaud et al. (2010) that failed to show an association between maternal smoking and schizophrenia has certain methodological limitations. The lack of an age-limit for the patients studied allows for a long recall-period of the smoking status during pregnancy.

    • Chronic exposure to cigarette smoke during gestation results in altered cholinesterase enzyme activity and behavioral deficits in adult rat offspring: Potential relevance to schizophrenia

      2013, Journal of Psychiatric Research
      Citation Excerpt :

      It has been suggested that prenatal CS exposure (PCSE) induces long-term behavioral and neurochemical abnormalities that occur in schizophrenia (Boutwell and Beaver, 2010; Schneider et al., 2011). However, a recent study showed no association between prenatal tobacco exposure and schizophrenia symptoms in adulthood, although this study presented some limitations (e.g., small sample size) (Baguelin-Pinaud et al., 2010). In fact, studies identified the need to examine if the effects of PCSE persist into adulthood, and contribute to behavioral and neurochemical changes similar to symptoms of schizophrenia (Heath et al., 2010; Jacobsen et al., 2006).

    View all citing articles on Scopus
    View full text