Maternal cigarette smoking and oral clefts: a population-based study.

Khoury, Muin J.; Weinstein, Alyse; Panny, Susan R.; Holtzman, Neil A.; Lindsay, P K; Farrel, K; Eisenberg, M.

doi:10.2105/ajph.77.5.623

Cited by 92 publications

(38 citation statements)

References 25 publications

(10 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…An OR of 1.50 (95% CI: 1.05-2.14) for CL/P was reported in a Danish study (Bille et al, 2007). Despite the positive association identified between maternal smoking and clefting in Denmark, the decrease in smoking prevalence among pregnant women in the last 20 years in Denmark did not seem to reduce the rate of cleft prevalence as suggested by the similar occurrence of clefts in 1988-2001 to the occurrence in 1962-1987(Bille et al, 2005. As hypothesized by the authors, this might be due to the weak causal association between smoking and oral clefting.…”

Section: Cigarette Smoking and Oral Cleftsmentioning

confidence: 89%

“…Cigarette smoke exposure, along with alcohol (Romitti et al, 2007) and nutrition (Yazdy et al, 2007) are the most studied environmental factors in the causes of oral clefts. Positive association between maternal cigarette smoking and CL/P or CPO in their offspring have been reported in several studies (Khoury et al, 1987(Khoury et al, , 1989Beaty et al, 1997;Kallen, 1997a;Wyszynski et al, 1997;Chung et al, 2000;Wyszynski and Wu, 2002); nevertheless, this association failed to be confirmed in some other studies (Werler et al, 1990;Christensen et al, 1999;Lieff, 1999;Mitchell et al, 2001). Little et al (2004) performed a meta-analysis of the association between maternal smoking during pregnancy and oral clefts using data from 24 case-control and cohort studies.…”

Section: Cigarette Smoking and Oral Cleftsmentioning

confidence: 99%

See 1 more Smart Citation

Review on genetic variants and maternal smoking in the etiology of oral clefts and other birth defects

Shi

Wehby

Murray

2008

Birth Defects Research Pt C

152

124

View full text Add to dashboard Cite

A spectrum of adverse pregnancy outcomes, including preterm birth, low birth weight, and birth defects has been linked with maternal smoking during pregnancy. This article includes a review of studies investigating interactions between genetic variants and maternal smoking in contributing to birth defects using oral clefting as a model birth defect. The primary gene-smoking studies for other major birth defects are also summarized. Gene-environment interaction studies for birth defects are still at an early stage with several mixed results, but evolving research findings have begun to document clinically and developmentally important interactions. As samples and data become increasingly available, more effort is needed in designing innovative analytical methods to study gene-environment interactions.

show abstract

Section: Cigarette Smoking and Oral Cleftsmentioning

confidence: 89%

Section: Cigarette Smoking and Oral Cleftsmentioning

confidence: 99%

Review on genetic variants and maternal smoking in the etiology of oral clefts and other birth defects

Shi

Wehby

Murray

2008

Birth Defects Research Pt C

152

124

View full text Add to dashboard Cite

show abstract

“…Smoking is practised by about a third of the world's population aged 15 years or older, including some 12% of women [109]. Cigarette smoking during pregnancy was associated with cleft defects [6,99,110]. In contrast, some studies found no association with maternal smoking for any form oral clefts [111,112].…”

Section: Environmental Factors Causing Cleftmentioning

confidence: 99%

Molecular Genetics of Non-Syndromic Clefts Revisited

Rajasekhar¹,

Lakkakula²,

KS³

2011

Int J Genet

View full text Add to dashboard Cite

Cleft of the lip and palate (CL/P) are generally divided in to two groups, isolated cleft palate and cleft with or without cleft palate representing a heterogeneous group of disorders affecting the upper lip and the roof the mouth. Non-syndromic cleft lip and palate incidence is 1 in 700 to 1000 live babies with ethnic and geographic variations. Various independent association and linkage studies using different populations have identified several loci. Numerous genes have been reported in studies demonstration associations and/or linkage of the cleft lip and palate phenotypes to alleles of microsatellite markers and single nucleotide polymorphisms within specific genes that regulate transcription factor, growth factor, cell signalling and detoxification metabolisms. Currently, efforts are focussed to identify the genes and genetic variations within the numerous candidate genes that have been found to associate with the expression of the orofacial cleft phenotype. In conclusion, the genetic basis of CL/P is still contentious because of genetic complexity of clefting.

show abstract

“…Recently, it has been proposed that chemical carcinogens may also be involved in the development of various forms of cardiovascular disease (2,3). In addition, smoking tobacco products during pregnancy is associated with an increased risk to the unborn child, resulting in preterm delivery, decreased birth weight, stillbirth, and a number of serious congenital malformations (4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Detection of Carcinogen-DNA Adducts in Human Fetal Tissues by the 32 P-Postlabeling Procedure

Hansen¹,

Asmussen²,

Autrup³

1993

Environmental Health Perspectives

View full text Add to dashboard Cite

Tobacco smoke contains a number of genotoxic compounds that are metabolized to their biologically active forms that subsequently react with cellular DNA to form covalently boundcarcinogen-DNA adducts. Several analytical procedures have been developed to detect these adducts in human tissues. Using the nuclease P1-enhanced 32P-postlabeling procedure for bulky adducts, we have detected at least 24 adducts in DNA isolated from placenta and umbilical cord DNA. Adducts were detected in both smokers and nonsmokers, but the relative adduct level (RAL) was significantly higher in smokers (42. 8, 8 cases) than in nonsmokers (19.7, 11 cases). The origin of the adducts in nonsmokers remains unknown. The adduct levels in artery DNA were significantly lower than in the vein and the placenta, and a paired nonparametric analysis showed a significant association between the adduct levels in the three tissues. Our results show a maternal transfer of carcinogens present in cigarette smoke to fetal tissues and show that the tissues can metabolize the carcinogens to their DNA binding metabolites. The presence of adducts in fetal tissues may be indicative of genomic damage and may predispose the individual for the development of a serious disease iter in life.

show abstract

Maternal cigarette smoking and oral clefts: a population-based study.

Cited by 92 publications

References 25 publications

Review on genetic variants and maternal smoking in the etiology of oral clefts and other birth defects

Review on genetic variants and maternal smoking in the etiology of oral clefts and other birth defects

Molecular Genetics of Non-Syndromic Clefts Revisited

Detection of Carcinogen-DNA Adducts in Human Fetal Tissues by the 32 P-Postlabeling Procedure

Contact Info

Product

Resources

About