OBJECTIVES: Active smoking has a well-documented role in the etiology of inflammatory bowel disease (IBD), but the role of passive smoking has been unclear. This meta-analysis examined the relationship between prenatal smoke exposure and childhood passive smoke exposure and the development of IBD. METHODS: We searched the MEDLINE and EMBASE databases to identify observational studies regarding the relationship between prenatal and/or childhood passive smoke exposure and the development of Crohn's disease (CD) and/or ulcerative colitis (UC). Pooled odds ratios (OR) were calculated for each relationship. RESULTS: A total of 534 and 699 potential studies were identified from the MEDLINE and EMBASE databases, respectively, of which 13 met all of our inclusion criteria. Overall, we did not observe a positive relationship between childhood passive smoke exposure and CD (OR 1.10, 95% confidence interval [CI] 0.92-1.30) or UC (OR 1.01, 95% CI 0.85-1.20). Likewise, we did not observe an association between prenatal smoke exposure and CD (OR 1.10, 95% CI 0.67-1.80), or prenatal smoke exposure and UC (OR 1.11, 95% CI 0.63-1.97). CONCLUSIONS: Our meta-analysis suggests that there is not a strong association between childhood passive smoke exposure and the development of CD. We found no evidence that childhood passive smoke exposure exerts a protective effect against UC, as is the case in active smoke exposure. The heterogeneity among the small number of studies limited the ability to draw conclusions about prenatal smoke exposure.
OBJECTIVES: Active smoking has a well-documented role in the etiology of inflammatory bowel disease (IBD), but the role of passive smoking has been unclear. This meta-analysis examined the relationship between prenatal smoke exposure and childhood passive smoke exposure and the development of IBD. METHODS: We searched the MEDLINE and EMBASE databases to identify observational studies regarding the relationship between prenatal and/or childhood passive smoke exposure and the development of Crohn's disease (CD) and/or ulcerative colitis (UC). Pooled odds ratios (OR) were calculated for each relationship. RESULTS: A total of 534 and 699 potential studies were identified from the MEDLINE and EMBASE databases, respectively, of which 13 met all of our inclusion criteria. Overall, we did not observe a positive relationship between childhood passive smoke exposure and CD (OR 1.10, 95% confidence interval [CI] 0.92-1.30) or UC (OR 1.01, 95% CI 0.85-1.20). Likewise, we did not observe an association between prenatal smoke exposure and CD (OR 1.10, 95% CI 0.67-1.80), or prenatal smoke exposure and UC (OR 1.11, 95% CI 0.63-1.97). CONCLUSIONS: Our meta-analysis suggests that there is not a strong association between childhood passive smoke exposure and the development of CD. We found no evidence that childhood passive smoke exposure exerts a protective effect against UC, as is the case in active smoke exposure. The heterogeneity among the small number of studies limited the ability to draw conclusions about prenatal smoke exposure.
Authors: S Baron; D Turck; C Leplat; V Merle; C Gower-Rousseau; R Marti; T Yzet; E Lerebours; J-L Dupas; S Debeugny; J-L Salomez; A Cortot; J-F Colombel Journal: Gut Date: 2005-03 Impact factor: 23.059
Authors: Devendra K Amre; Philippe Lambrette; Liliane Law; Alfreda Krupoves; Virginie Chotard; Florin Costea; Guy Grimard; David Israel; David Mack; Ernest G Seidman Journal: Am J Gastroenterol Date: 2006-05 Impact factor: 10.864
Authors: Fritz Horak; Tamas Fazekas; Angela Zacharasiewicz; Ernst Eber; Herbert Kiss; Alfred Lichtenschopf; Manfred Neuberger; Rudolf Schmitzberger; Burkhard Simma; Andree Wilhelm-Mitteräcker; Josef Riedler Journal: Wien Klin Wochenschr Date: 2011-12-22 Impact factor: 1.704