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The large case control study of patients with inflammatory bowel disease (IBD) in the French paediatric population by Baron et al has clarified the role of well established genetic and environmental risk factors, as well as suggesting novel environmental risk factors (Gut 2005;54:357–63).
However, we caution the authors on dismissal of the role of passive smoking in the risk of IBD development in childhood. Our own data would suggest that analysing smoking data during pregnancy and at birth is more important in the development of childhood IBD, rather than assessing smoking during childhood and at disease onset, as performed in this current study.
We have performed a case control study in South East Scotland of children with early onset IBD, matching cases of IBD diagnosed at less than 16 years of age with same sex and age (±1) year controls attending the same general practice.1 In total, we matched 62 pairs of cases and controls, with a median age of disease onset in cases of 10.6 years. We demonstrated that parental smoking during pregnancy and around the time of birth was more common in parents of IBD cases, at 54% compared with control parents at 29% (p = 0.01; odds ratio (OR) 2.87 (95% confidence interval (CI) 1.23–6.66)). Maternal smoking during pregnancy and at birth was also more common in IBD cases than in controls, at 23% versus 6.2% (p = 0.04; OR 4.46 (95% CI 1.16–17.1), and in mothers of patients with Crohn’s disease, at 27.8% versus control mothers at 8.3% (p = 0.03; OR 4.23 (95% CI 1.05–16.97)). There was no significant effect seen when paternal smoking in pregnancy and at birth was analysed in IBD cases versus controls (p = 0.27). These data replicate the publication by Lashner and colleagues2 who studied 72 IBD cases and controls and found a similar relationship to smoking at birth—this was increased in children who later developed IBD in childhood (OR 3.02) and CD in childhood (OR 5.32).3 The authors of this study also demonstrated that maternal smoking at birth was important in the development of IBD and CD.2
We agree with the findings of Baron et al that parental/passive smoke exposure outside of the perinatal period, including at the time of IBD diagnosis, is not associated with the risk of developing IBD in children (p = 0.18). This lack of association between passive smoke exposure in childhood and development of childhood IBD has also been replicated by Lashner and colleagues.2 It is important to note that the other studies quoted by Baron et al in relation to the risk of passive smoking in IBD patients relate to the risk of adult onset IBD after passive smoke exposure during childhood, not the risk of developing IBD as a child.3,4 The mechanism by which smoke exposure during pregnancy and at birth leads to an increased risk of childhood IBD can only be a subject for speculation, but it is interesting to note a recent study has demonstrated chromosomal abnormalities in fetal epithelial cells in women who smoke during pregnancy.5
In conclusion, our study agrees with previously published data to suggest a role between passive smoke exposure during pregnancy and at birth with the risk of childhood development of IBD. When assessing passive smoking in relation to childhood onset IBD, investigators should survey smoke exposure in the perinatal period and during childhood.
We thank Russell et al for their interest in our study, concerning the link between passive smoking and the risk of IBD in children.
We agree that it is important to take into account the role of passive smoking not only during childhood and at disease onset but also during the perinatal period. We also looked at this point in our study but came to different conclusions: 9.6% of mothers of IBD patients smoked during pregnancy versus 9.25% of control mothers (odds ratio (OR) 0.95 (95% confidence interval (CI) 0.53–1.72); p = 0.88). When considering only mothers of Crohn’s disease patients and control mothers, values were 9.9% and 9.5%, respectively (OR 0.95 (95% CI 0.50–1.81); p = 0.87). Moreover, concerning passive smoking during childhood, the findings were 14.2% and 12.8% for IBD patients and controls, respectively (OR 0.87 (95% CI 0.52–1.46); p = 0.60) and 15.3% for Crohn’s disease patients versus 14.4% for controls (OR 0.92 (95% CI 0.53–1.61); p = 0.77).
Due to the high number of questions and findings in our case control study, we only reported positive findings and what we considered as being the most important negative results. In conclusion, we confirm that in our study there was no link between IBD and passive smoking, including exposure during pregnancy and at birth.
Conflict of interest: None declared.
Conflict of interest: None declared.
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