Maternal Smoking and Oral Clefts: The Role of Detoxification Pathway Genes

Background: 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. Methods: We performed a combined case-control and family-triad study of babies born with oral clefts in No...

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Veröffentlicht in:Epidemiology (Cambridge, Mass.) Mass.), 2008-07, Vol.19 (4), p.606-615
Hauptverfasser: Lie, Rolv T., Wilcox, Allen J., Taylor, Jack, Gjessing, Håkon K., Saugstad, Ola Didrik, Aabyholm, Frank, Vindenes, Halvard
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container_issue 4
container_start_page 606
container_title Epidemiology (Cambridge, Mass.)
container_volume 19
creator Lie, Rolv T.
Wilcox, Allen J.
Taylor, Jack
Gjessing, Håkon K.
Saugstad, Ola Didrik
Aabyholm, Frank
Vindenes, Halvard
description Background: 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. Methods: 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). Results: 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. Conclusion: 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.
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There are also hypothetical pathways for a biologic effect involving toxic chemicals in cigarette smoke. Methods: 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). Results: 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. Conclusion: 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.</description><identifier>ISSN: 1044-3983</identifier><identifier>EISSN: 1531-5487</identifier><identifier>DOI: 10.1097/EDE.0b013e3181690731</identifier><identifier>PMID: 18449058</identifier><language>eng</language><publisher>Philadelphia, PA: Lippincott Williams &amp; Wilkins</publisher><subject>Adult ; Arylamine N-Acetyltransferase - genetics ; Biological and medical sciences ; BIRTH DEFECTS ; Case-Control Studies ; Children ; Cigarette smoking ; Cigarettes ; Cleft lip ; Cleft Lip - epidemiology ; Cleft Lip - etiology ; Cleft Lip - genetics ; Cleft palate ; Cleft Palate - epidemiology ; Cleft Palate - genetics ; Congenital Abnormalities - epidemiology ; Facial bones, jaws, teeth, parodontium: diseases, semeiology ; Female ; Haplotypes ; Humans ; Infant, Newborn ; Medical sciences ; Middle Aged ; Miscellaneous ; Mothers ; Nicotiana - adverse effects ; Non tumoral diseases ; Norway - epidemiology ; Otorhinolaryngology. Stomatology ; Polymorphism, Single Nucleotide - genetics ; Pregnancy ; Pregnancy Trimester, First ; Public health. Hygiene ; Public health. Hygiene-occupational medicine ; Questionnaires ; Risk Assessment ; Secondhand smoke ; Smoke - adverse effects ; Smoke - analysis ; Smoking - adverse effects ; Smoking - epidemiology ; Smoking - genetics ; Surveys and Questionnaires ; Tobacco smoking ; Tobacco, tobacco smoking ; Toxicology</subject><ispartof>Epidemiology (Cambridge, Mass.), 2008-07, Vol.19 (4), p.606-615</ispartof><rights>Copyright ©2008 Lippincott Williams &amp; Wilkins</rights><rights>2008 Lippincott Williams &amp; Wilkins, Inc.</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4377-1f65046dde12dc764f5923c956a586393c421cbd368d089492a01eef7b5accfd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/25662594$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/25662594$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,780,784,803,885,27924,27925,58017,58250</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=20458324$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18449058$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lie, Rolv T.</creatorcontrib><creatorcontrib>Wilcox, Allen J.</creatorcontrib><creatorcontrib>Taylor, Jack</creatorcontrib><creatorcontrib>Gjessing, Håkon K.</creatorcontrib><creatorcontrib>Saugstad, Ola Didrik</creatorcontrib><creatorcontrib>Aabyholm, Frank</creatorcontrib><creatorcontrib>Vindenes, Halvard</creatorcontrib><title>Maternal Smoking and Oral Clefts: The Role of Detoxification Pathway Genes</title><title>Epidemiology (Cambridge, Mass.)</title><addtitle>Epidemiology</addtitle><description>Background: 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. Methods: 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). Results: 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. Conclusion: 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.</description><subject>Adult</subject><subject>Arylamine N-Acetyltransferase - genetics</subject><subject>Biological and medical sciences</subject><subject>BIRTH DEFECTS</subject><subject>Case-Control Studies</subject><subject>Children</subject><subject>Cigarette smoking</subject><subject>Cigarettes</subject><subject>Cleft lip</subject><subject>Cleft Lip - epidemiology</subject><subject>Cleft Lip - etiology</subject><subject>Cleft Lip - genetics</subject><subject>Cleft palate</subject><subject>Cleft Palate - epidemiology</subject><subject>Cleft Palate - genetics</subject><subject>Congenital Abnormalities - epidemiology</subject><subject>Facial bones, jaws, teeth, parodontium: diseases, semeiology</subject><subject>Female</subject><subject>Haplotypes</subject><subject>Humans</subject><subject>Infant, Newborn</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Miscellaneous</subject><subject>Mothers</subject><subject>Nicotiana - adverse effects</subject><subject>Non tumoral diseases</subject><subject>Norway - epidemiology</subject><subject>Otorhinolaryngology. Stomatology</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Pregnancy</subject><subject>Pregnancy Trimester, First</subject><subject>Public health. Hygiene</subject><subject>Public health. Hygiene-occupational medicine</subject><subject>Questionnaires</subject><subject>Risk Assessment</subject><subject>Secondhand smoke</subject><subject>Smoke - adverse effects</subject><subject>Smoke - analysis</subject><subject>Smoking - adverse effects</subject><subject>Smoking - epidemiology</subject><subject>Smoking - genetics</subject><subject>Surveys and Questionnaires</subject><subject>Tobacco smoking</subject><subject>Tobacco, tobacco smoking</subject><subject>Toxicology</subject><issn>1044-3983</issn><issn>1531-5487</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU9vEzEQxS0Eom3gGwDaC71tGa__rM0BCaWhgIqKoJwtxzvubuusi70h9NtjSNQAvthj_96bkR8hzyicUNDtq8Xp4gSWQBkyqqjU0DL6gBxSwWgtuGofljNwXjOt2AE5yvkagBZGPCYHVHGuQahD8vGTnTCNNlRfV_FmGK8qO3bVRSoX84B-yq-ryx6rLzFgFX11ilP8OfjB2WmIY_XZTv3G3lVnOGJ-Qh55GzI-3e0z8u3d4nL-vj6_OPswf3teO87atqZeCuCy65A2nWsl90I3zGkhrVCSaeZ4Q92yY1J1oDTXjQWK6NulsM75js3Im63v7Xq5ws7hOJVxzW0aVjbdmWgH8-_LOPTmKv4wQkgAJorB8c4gxe9rzJNZDdlhCHbEuM6moZyCbHQB-RZ0Keac0N83oWB-h2BKCOb_EIrsxd8D7kW7Xy_Ayx1gs7PBJzu6Id9zDfACNXzffxNDSSnfhPUGk-nRhqk3UBaVXNUNgIK2VDX8iXhGnm9l13mKaW8rpGyE5uwX4QypDA</recordid><startdate>200807</startdate><enddate>200807</enddate><creator>Lie, Rolv T.</creator><creator>Wilcox, Allen J.</creator><creator>Taylor, Jack</creator><creator>Gjessing, Håkon K.</creator><creator>Saugstad, Ola Didrik</creator><creator>Aabyholm, Frank</creator><creator>Vindenes, Halvard</creator><general>Lippincott Williams &amp; Wilkins</general><general>Lippincott Williams &amp; Wilkins, Inc</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T2</scope><scope>7U1</scope><scope>7U2</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>200807</creationdate><title>Maternal Smoking and Oral Clefts: The Role of Detoxification Pathway Genes</title><author>Lie, Rolv T. ; Wilcox, Allen J. ; Taylor, Jack ; Gjessing, Håkon K. ; Saugstad, Ola Didrik ; Aabyholm, Frank ; Vindenes, Halvard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4377-1f65046dde12dc764f5923c956a586393c421cbd368d089492a01eef7b5accfd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult</topic><topic>Arylamine N-Acetyltransferase - genetics</topic><topic>Biological and medical sciences</topic><topic>BIRTH DEFECTS</topic><topic>Case-Control Studies</topic><topic>Children</topic><topic>Cigarette smoking</topic><topic>Cigarettes</topic><topic>Cleft lip</topic><topic>Cleft Lip - epidemiology</topic><topic>Cleft Lip - etiology</topic><topic>Cleft Lip - genetics</topic><topic>Cleft palate</topic><topic>Cleft Palate - epidemiology</topic><topic>Cleft Palate - genetics</topic><topic>Congenital Abnormalities - epidemiology</topic><topic>Facial bones, jaws, teeth, parodontium: diseases, semeiology</topic><topic>Female</topic><topic>Haplotypes</topic><topic>Humans</topic><topic>Infant, Newborn</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Miscellaneous</topic><topic>Mothers</topic><topic>Nicotiana - adverse effects</topic><topic>Non tumoral diseases</topic><topic>Norway - epidemiology</topic><topic>Otorhinolaryngology. Stomatology</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Pregnancy</topic><topic>Pregnancy Trimester, First</topic><topic>Public health. Hygiene</topic><topic>Public health. 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There are also hypothetical pathways for a biologic effect involving toxic chemicals in cigarette smoke. Methods: 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). Results: 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. Conclusion: 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.</abstract><cop>Philadelphia, PA</cop><pub>Lippincott Williams &amp; Wilkins</pub><pmid>18449058</pmid><doi>10.1097/EDE.0b013e3181690731</doi><tpages>10</tpages></addata></record>
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subjects Adult
Arylamine N-Acetyltransferase - genetics
Biological and medical sciences
BIRTH DEFECTS
Case-Control Studies
Children
Cigarette smoking
Cigarettes
Cleft lip
Cleft Lip - epidemiology
Cleft Lip - etiology
Cleft Lip - genetics
Cleft palate
Cleft Palate - epidemiology
Cleft Palate - genetics
Congenital Abnormalities - epidemiology
Facial bones, jaws, teeth, parodontium: diseases, semeiology
Female
Haplotypes
Humans
Infant, Newborn
Medical sciences
Middle Aged
Miscellaneous
Mothers
Nicotiana - adverse effects
Non tumoral diseases
Norway - epidemiology
Otorhinolaryngology. Stomatology
Polymorphism, Single Nucleotide - genetics
Pregnancy
Pregnancy Trimester, First
Public health. Hygiene
Public health. Hygiene-occupational medicine
Questionnaires
Risk Assessment
Secondhand smoke
Smoke - adverse effects
Smoke - analysis
Smoking - adverse effects
Smoking - epidemiology
Smoking - genetics
Surveys and Questionnaires
Tobacco smoking
Tobacco, tobacco smoking
Toxicology
title Maternal Smoking and Oral Clefts: The Role of Detoxification Pathway Genes
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