There is evidence for an effect of cigarette smoking on risk of oral clefts. There are also hypothetical pathways for a biologic effect involving toxic chemicals in cigarette smoke.
We performed a combined case-control and family-triad study of babies born with oral clefts in Norway in the period 1996 to 2001, with 88% participation among cases (n = 573) and 76% participation among controls (n = 763). Mothers completed a questionnaire 4 months after birth of the baby. DNA was collected from parents and children, and assayed for genes related to detoxification of compounds of cigarette smoke (NAT1, NAT2, CYP1A1, GSTP1, GSTT1, and GSTM1).
For isolated cleft lip (with or without cleft palate) there was a dose-response effect of smoking in the first trimester. The odds ratio rose from 1.6 (95% confidence interval = 1.0-2.5) for passive smoking to 1.9 (0.9-4.0) for mothers who smoked more than 10 cigarettes per day. There was little evidence of an association with cleft palate. Genetic analyses used both case-control and family-triad data. In case-triads we found an association between a NAT2 haplotype and isolated cleft lip (relative risk of 1.6 with 1 copy of the allele and 2.5 with 2 copies), but with little evidence of interaction with smoking. Other genes did not show associations, and previously described interactions with smoking were not confirmed.
First-trimester smoking was clearly associated with risk of cleft lip. This effect was not modified by variants of genes related to detoxification of compounds of cigarette smoke.
"Smokeless tobacco increases the risk for pharyngeal and esophageal cancers (Silverman, 2001). There is emerging evidence relating maternal smoking with the development of cleft lip in the child (Mirbod and Ahing, 2000; Little et al., 2004; Lie et al., 2008). Also some studies relate maternal smoking to development of primary caries in children (Aligne et al., 2003; Shenkin et al., 2004). "
[Show abstract][Hide abstract] ABSTRACT: Background:
The objective of the study was to determine the knowledge, attitude and behaviors of the practicing dentists regarding tobacco cessation counseling (TCC) in Chhattisgarh state and also the barriers that prevent them from doing so.
Materials and methods:
The study was conducted among dental practitioners of Raipur district, Chhattisgarh state (India). The sampling frame was registration with the State Dental Council and practicing in Raipur district. A questionnaire was personally administered and the practitioners were given explanations regarding how to complete it. Only descriptive statistics were calculated (SPSS version 16 for Windows).
Based on the responding dentists' self reports, 76% were not confident in TCC, 48% did not assume TCC to be their responsibility, 17% considered that it might have a negative impact on their clinical practice, whereas 24% considered it might take away precious time from their practice, 25% considered TCC by dentists to be effective to a considerable extent and 80% considered TCC activities are not effective due to lack of formal training, 69% considered dental clinics as an appropriate place for TCC but 82% thought there must be separate TCC centre and 100% of the dentists wanted TCC training to be a part of practice and that it should be included in dental curriculum. Some 95% of them were of the view that tobacco products should be banned in India and 86% responded that health professionals must refrain from tobacco habits so to act as role models for society.
Dental professionals must expand their armamentarium to include TCC strategies in their clinical practice. The dental institutions should include TCC in the curriculum and the dental professionals at the primary and the community health care level should also be trained in TCC to treat tobacco dependence.
Asian Pacific journal of cancer prevention: APJCP 10/2013; 14(10):6141-5. DOI:10.7314/APJCP.2013.14.10.6141 · 2.51 Impact Factor
"Several studies suggest that maternal smoking moderately increases OFC risk, with some variation across studies in the magnitude of the effects and the affected cleft type (Bille et al. 2007; Chung et al. 2000; Honein et al. 2007; Khoury, Gomez-Farias, and Mulinare 1989; Lie et al. 2008; Lieff et al. 1999; Little et al. 2004a; MacLehose et al. 2009; Shaw et al. 2009; Werler et al. 1990). Two meta-analyses of earlier studies estimated 1.3 times increased odds for OFC (Little, Cardy, and Munger 2004b; Wyszynski, Duffy, and Beaty 1997). "
[Show abstract][Hide abstract] ABSTRACT: This study uses instrumental variable (IV) models with genetic instruments to assess the effects of maternal smoking on the child's risk of orofacial clefts (OFC), a common birth defect. The study uses genotypic variants in neurotransmitter and detoxification genes relateded to smoking as instruments for cigarette smoking before and during pregnancy. Conditional maximum likelihood and two-stage IV probit models are used to estimate the IV model. The data are from a population-level sample of affected and unaffected children in Norway. The selected genetic instruments generally fit the IV assumptions but may be considered "weak" in predicting cigarette smoking. We find that smoking before and during pregnancy increases OFC risk substantially under the IV model (by about 4-5 times at the sample average smoking rate). This effect is greater than that found with classical analytic models. This may be because the usual models are not able to consider self-selection into smoking based on unobserved confounders, or it may to some degree reflect limitations of the instruments. Inference based on weak-instrument robust confidence bounds is consistent with standard inference. Genetic instruments may provide a valuable approach to estimate the "causal" effects of risk behaviors with genetic-predisposing factors (such as smoking) on health and socioeconomic outcomes.
Health Services and Outcomes Research Methodology 07/2011; 11(1-2):54-78. DOI:10.1007/s10742-011-0071-9
"Although a large number of maternal exposures have been reported to influence the risk of orofacial clefts at critical stages of development, only a handful have survived scrutiny after being tested in large, well-characterized populations. Maternal smoking (Zeiger and Beaty, 2002; Little et al., 2004; Lie et al., 2008 "
[Show abstract][Hide abstract] ABSTRACT: With an average worldwide prevalence of approximately 1.2/1000 live births, orofacial clefts are the most common craniofacial birth defects in humans. Like other complex disorders, these birth defects are thought to result from the complex interplay of multiple genes and environmental factors. Significant progress in the identification of underlying genes and pathways has benefited from large populations available for study, increased international collaboration, rapid advances in genotyping technology, and major improvements in analytic approaches. Here we review recent advances in genetic epidemiological approaches to complex traits and their applications to studies of nonsyndromic orofacial clefts. Our main aim is to bring together a discussion of new and previously identified candidate genes to create a more cohesive picture of interacting pathways that shape the human craniofacial region. In future directions, we highlight the need to search for copy number variants that affect gene dosage and rare variants that are possibly associated with a higher disease penetrance. In addition, sequencing of protein-coding regions in candidate genes and screening for genetic variation in noncoding regulatory elements will help advance this important area of research.
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