Environmental tobacco smoke and male sex modify the influence of IL-13 genetic variants on cord blood IgE levels
To cite this article: Chen C‐H, Lee YL, Wu M‐H, Chen P‐J, Wei T‐S, Wu C‐T, Tung K‐Y, Chen WJ. Environmental tobacco smoke and male sex modify the influence of IL‐13 genetic variants on cord blood IgE levels. Pediatric Allergy Immunology 2012: 23: 456–463. Elevated cord blood IgE (cIgE) levels enhanc...
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| description | To cite this article: Chen C‐H, Lee YL, Wu M‐H, Chen P‐J, Wei T‐S, Wu C‐T, Tung K‐Y, Chen WJ. Environmental tobacco smoke and male sex modify the influence of IL‐13 genetic variants on cord blood IgE levels. Pediatric Allergy Immunology 2012: 23: 456–463.
Elevated cord blood IgE (cIgE) levels enhance the risk of childhood atopic diseases. However, genetic determinants of cIgE elevation and their potential modifiers remain inconclusive. We aimed to investigate the associations of single‐nucleotide polymorphisms (SNPs) in the IL‐13 gene (IL‐13) with cIgE elevation and their interactions with prenatal environmental tobacco smoke (ETS) and neonatal sex. A structured questionnaire regarding prenatal environmental exposures was completed during pregnancy. Birth information was extracted from the medical records. Cord blood from 794 term neonates was genotyped for three SNPs (rs1800925, rs20541, and rs848) of IL‐13 and measured for cIgE levels. SNP rs20541 and a 3‐SNP haplotype containing rs1800925, rs20541, and rs848 (denoted as h011) were significantly associated with cIgE elevation (p = 0.04 and 0.003, respectively). Two‐way interaction analysis revealed that the associations of IL‐13 rs20541 and h011 with cIgE elevation were synergistically enhanced by prenatal ETS (p for interaction = 0.03 and 0.03, respectively), but not by male sex. If the association analyses were stratified by prenatal ETS and neonatal sex simultaneously, IL‐13 rs20541 and h011 had the highest risks for cIgE elevation in male babies prenatally exposed to ETS, with adjusted odds ratios (95% confidence interval) being 3.03 (1.56–5.88) and 2.81 (1.54–5.15), respectively. When three‐way interactions were examined, both IL‐13 rs20541 and h011 exhibited significant interactions with male sex and ETS (p for interaction = 0.03 and 0.007, respectively). In conclusion, the influence of IL‐13 genetic variants on cIgE elevation was modified by male sex and prenatal ETS. |
| doi_str_mv | 10.1111/j.1399-3038.2012.01278.x |
| format | Article |
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Elevated cord blood IgE (cIgE) levels enhance the risk of childhood atopic diseases. However, genetic determinants of cIgE elevation and their potential modifiers remain inconclusive. We aimed to investigate the associations of single‐nucleotide polymorphisms (SNPs) in the IL‐13 gene (IL‐13) with cIgE elevation and their interactions with prenatal environmental tobacco smoke (ETS) and neonatal sex. A structured questionnaire regarding prenatal environmental exposures was completed during pregnancy. Birth information was extracted from the medical records. Cord blood from 794 term neonates was genotyped for three SNPs (rs1800925, rs20541, and rs848) of IL‐13 and measured for cIgE levels. SNP rs20541 and a 3‐SNP haplotype containing rs1800925, rs20541, and rs848 (denoted as h011) were significantly associated with cIgE elevation (p = 0.04 and 0.003, respectively). Two‐way interaction analysis revealed that the associations of IL‐13 rs20541 and h011 with cIgE elevation were synergistically enhanced by prenatal ETS (p for interaction = 0.03 and 0.03, respectively), but not by male sex. If the association analyses were stratified by prenatal ETS and neonatal sex simultaneously, IL‐13 rs20541 and h011 had the highest risks for cIgE elevation in male babies prenatally exposed to ETS, with adjusted odds ratios (95% confidence interval) being 3.03 (1.56–5.88) and 2.81 (1.54–5.15), respectively. When three‐way interactions were examined, both IL‐13 rs20541 and h011 exhibited significant interactions with male sex and ETS (p for interaction = 0.03 and 0.007, respectively). In conclusion, the influence of IL‐13 genetic variants on cIgE elevation was modified by male sex and prenatal ETS.</description><identifier>ISSN: 0905-6157</identifier><identifier>EISSN: 1399-3038</identifier><identifier>DOI: 10.1111/j.1399-3038.2012.01278.x</identifier><identifier>PMID: 22432974</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Biological and medical sciences ; Blood ; Cohort Studies ; cord blood ; environmental tobacco smoke ; Female ; Fetal Blood - immunology ; Fetal Blood - metabolism ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; General aspects ; Genetic diversity ; Humans ; Hypersensitivity - immunology ; IgE ; IL-13 polymorphism ; Immunoglobulin E - blood ; Immunoglobulin E - immunology ; Infant, Newborn ; Interleukin-13 - genetics ; Male ; Medical sciences ; Polymorphism ; Polymorphism, Single Nucleotide ; Pregnancy ; Prenatal Exposure Delayed Effects - immunology ; Risk ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; sex ; Sex Factors ; Smoking ; Tobacco smoke ; Tobacco Smoke Pollution - adverse effects</subject><ispartof>Pediatric allergy and immunology, 2012-08, Vol.23 (5), p.456-463</ispartof><rights>2012 John Wiley & Sons A/S</rights><rights>2015 INIST-CNRS</rights><rights>2012 John Wiley & Sons A/S.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5158-d158e6d5adde80775cbfbc31d9e07737849c3c2af75e1825b94a24585484c8c53</citedby><cites>FETCH-LOGICAL-c5158-d158e6d5adde80775cbfbc31d9e07737849c3c2af75e1825b94a24585484c8c53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1399-3038.2012.01278.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1399-3038.2012.01278.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26151528$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22432974$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Chien-Han</creatorcontrib><creatorcontrib>Lee, Yungling Leo</creatorcontrib><creatorcontrib>Wu, Ming-Hsun</creatorcontrib><creatorcontrib>Chen, Pao-Jen</creatorcontrib><creatorcontrib>Wei, Tien-Shan</creatorcontrib><creatorcontrib>Wu, Che-Tsung</creatorcontrib><creatorcontrib>Tung, Kuan-Yen</creatorcontrib><creatorcontrib>Chen, Wei J.</creatorcontrib><title>Environmental tobacco smoke and male sex modify the influence of IL-13 genetic variants on cord blood IgE levels</title><title>Pediatric allergy and immunology</title><addtitle>Pediatr Allergy Immunol</addtitle><description>To cite this article: Chen C‐H, Lee YL, Wu M‐H, Chen P‐J, Wei T‐S, Wu C‐T, Tung K‐Y, Chen WJ. Environmental tobacco smoke and male sex modify the influence of IL‐13 genetic variants on cord blood IgE levels. Pediatric Allergy Immunology 2012: 23: 456–463.
Elevated cord blood IgE (cIgE) levels enhance the risk of childhood atopic diseases. However, genetic determinants of cIgE elevation and their potential modifiers remain inconclusive. We aimed to investigate the associations of single‐nucleotide polymorphisms (SNPs) in the IL‐13 gene (IL‐13) with cIgE elevation and their interactions with prenatal environmental tobacco smoke (ETS) and neonatal sex. A structured questionnaire regarding prenatal environmental exposures was completed during pregnancy. Birth information was extracted from the medical records. Cord blood from 794 term neonates was genotyped for three SNPs (rs1800925, rs20541, and rs848) of IL‐13 and measured for cIgE levels. SNP rs20541 and a 3‐SNP haplotype containing rs1800925, rs20541, and rs848 (denoted as h011) were significantly associated with cIgE elevation (p = 0.04 and 0.003, respectively). Two‐way interaction analysis revealed that the associations of IL‐13 rs20541 and h011 with cIgE elevation were synergistically enhanced by prenatal ETS (p for interaction = 0.03 and 0.03, respectively), but not by male sex. If the association analyses were stratified by prenatal ETS and neonatal sex simultaneously, IL‐13 rs20541 and h011 had the highest risks for cIgE elevation in male babies prenatally exposed to ETS, with adjusted odds ratios (95% confidence interval) being 3.03 (1.56–5.88) and 2.81 (1.54–5.15), respectively. When three‐way interactions were examined, both IL‐13 rs20541 and h011 exhibited significant interactions with male sex and ETS (p for interaction = 0.03 and 0.007, respectively). In conclusion, the influence of IL‐13 genetic variants on cIgE elevation was modified by male sex and prenatal ETS.</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Blood</subject><subject>Cohort Studies</subject><subject>cord blood</subject><subject>environmental tobacco smoke</subject><subject>Female</subject><subject>Fetal Blood - immunology</subject><subject>Fetal Blood - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>General aspects</subject><subject>Genetic diversity</subject><subject>Humans</subject><subject>Hypersensitivity - immunology</subject><subject>IgE</subject><subject>IL-13 polymorphism</subject><subject>Immunoglobulin E - blood</subject><subject>Immunoglobulin E - immunology</subject><subject>Infant, Newborn</subject><subject>Interleukin-13 - genetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects - immunology</subject><subject>Risk</subject><subject>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><subject>sex</subject><subject>Sex Factors</subject><subject>Smoking</subject><subject>Tobacco smoke</subject><subject>Tobacco Smoke Pollution - adverse effects</subject><issn>0905-6157</issn><issn>1399-3038</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUuP0zAUhSMEYsrAX0CWEBKbBD8bZ8Fi6JShogIkQLO0HOdmSMexi52U9t_j0FIkVljyS_7O9dU5WYYILkgarzcFYVWVM8xkQTGhRZqlLPYPstn54WE2wxUW-ZyI8iJ7EuMGY1KyOXmcXVDKGa1KPsu2S7frgnc9uEFbNPhaG-NR7P09IO0a1GsLKMIe9b7p2gMavgPqXGtHcAaQb9FqnROG7sDB0Bm006HTbojIO2R8aFBtvW_Q6m6JLOzAxqfZo1bbCM9O-2X27d3y6-J9vv50s1pcrXMjiJB5kxaYN0I3DUhclsLUbW0YaSpIN1ZKXhlmqG5LAURSUVdcUy6k4JIbaQS7zF4d626D_zFCHFTfRQPWagd-jIrgeUVxyQVL6It_0I0fg0vdKcIZJ7zElCRKHikTfIwBWrUNXa_DIZVSUypqoybz1WS-mlJRv1NR-yR9fvpgrHtozsI_MSTg5QnQ0WjbBu1MF_9yKUMiqEzcmyP3s7Nw-O8G1Oer1XRK-vyo7-IA-7Neh3s1T6YKdfvxRt1-qBbX12-x-sJ-Abr5tZE</recordid><startdate>201208</startdate><enddate>201208</enddate><creator>Chen, Chien-Han</creator><creator>Lee, Yungling Leo</creator><creator>Wu, Ming-Hsun</creator><creator>Chen, Pao-Jen</creator><creator>Wei, Tien-Shan</creator><creator>Wu, Che-Tsung</creator><creator>Tung, Kuan-Yen</creator><creator>Chen, Wei J.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>201208</creationdate><title>Environmental tobacco smoke and male sex modify the influence of IL-13 genetic variants on cord blood IgE levels</title><author>Chen, Chien-Han ; Lee, Yungling Leo ; Wu, Ming-Hsun ; Chen, Pao-Jen ; Wei, Tien-Shan ; Wu, Che-Tsung ; Tung, Kuan-Yen ; Chen, Wei J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5158-d158e6d5adde80775cbfbc31d9e07737849c3c2af75e1825b94a24585484c8c53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Blood</topic><topic>Cohort Studies</topic><topic>cord blood</topic><topic>environmental tobacco smoke</topic><topic>Female</topic><topic>Fetal Blood - immunology</topic><topic>Fetal Blood - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>General aspects</topic><topic>Genetic diversity</topic><topic>Humans</topic><topic>Hypersensitivity - immunology</topic><topic>IgE</topic><topic>IL-13 polymorphism</topic><topic>Immunoglobulin E - blood</topic><topic>Immunoglobulin E - immunology</topic><topic>Infant, Newborn</topic><topic>Interleukin-13 - genetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects - immunology</topic><topic>Risk</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</topic><topic>sex</topic><topic>Sex Factors</topic><topic>Smoking</topic><topic>Tobacco smoke</topic><topic>Tobacco Smoke Pollution - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Chien-Han</creatorcontrib><creatorcontrib>Lee, Yungling Leo</creatorcontrib><creatorcontrib>Wu, Ming-Hsun</creatorcontrib><creatorcontrib>Chen, Pao-Jen</creatorcontrib><creatorcontrib>Wei, Tien-Shan</creatorcontrib><creatorcontrib>Wu, Che-Tsung</creatorcontrib><creatorcontrib>Tung, Kuan-Yen</creatorcontrib><creatorcontrib>Chen, Wei J.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Pediatric allergy and immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Chien-Han</au><au>Lee, Yungling Leo</au><au>Wu, Ming-Hsun</au><au>Chen, Pao-Jen</au><au>Wei, Tien-Shan</au><au>Wu, Che-Tsung</au><au>Tung, Kuan-Yen</au><au>Chen, Wei J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Environmental tobacco smoke and male sex modify the influence of IL-13 genetic variants on cord blood IgE levels</atitle><jtitle>Pediatric allergy and immunology</jtitle><addtitle>Pediatr Allergy Immunol</addtitle><date>2012-08</date><risdate>2012</risdate><volume>23</volume><issue>5</issue><spage>456</spage><epage>463</epage><pages>456-463</pages><issn>0905-6157</issn><eissn>1399-3038</eissn><abstract>To cite this article: Chen C‐H, Lee YL, Wu M‐H, Chen P‐J, Wei T‐S, Wu C‐T, Tung K‐Y, Chen WJ. Environmental tobacco smoke and male sex modify the influence of IL‐13 genetic variants on cord blood IgE levels. Pediatric Allergy Immunology 2012: 23: 456–463.
Elevated cord blood IgE (cIgE) levels enhance the risk of childhood atopic diseases. However, genetic determinants of cIgE elevation and their potential modifiers remain inconclusive. We aimed to investigate the associations of single‐nucleotide polymorphisms (SNPs) in the IL‐13 gene (IL‐13) with cIgE elevation and their interactions with prenatal environmental tobacco smoke (ETS) and neonatal sex. A structured questionnaire regarding prenatal environmental exposures was completed during pregnancy. Birth information was extracted from the medical records. Cord blood from 794 term neonates was genotyped for three SNPs (rs1800925, rs20541, and rs848) of IL‐13 and measured for cIgE levels. SNP rs20541 and a 3‐SNP haplotype containing rs1800925, rs20541, and rs848 (denoted as h011) were significantly associated with cIgE elevation (p = 0.04 and 0.003, respectively). Two‐way interaction analysis revealed that the associations of IL‐13 rs20541 and h011 with cIgE elevation were synergistically enhanced by prenatal ETS (p for interaction = 0.03 and 0.03, respectively), but not by male sex. If the association analyses were stratified by prenatal ETS and neonatal sex simultaneously, IL‐13 rs20541 and h011 had the highest risks for cIgE elevation in male babies prenatally exposed to ETS, with adjusted odds ratios (95% confidence interval) being 3.03 (1.56–5.88) and 2.81 (1.54–5.15), respectively. When three‐way interactions were examined, both IL‐13 rs20541 and h011 exhibited significant interactions with male sex and ETS (p for interaction = 0.03 and 0.007, respectively). In conclusion, the influence of IL‐13 genetic variants on cIgE elevation was modified by male sex and prenatal ETS.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>22432974</pmid><doi>10.1111/j.1399-3038.2012.01278.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Biological and medical sciences Blood Cohort Studies cord blood environmental tobacco smoke Female Fetal Blood - immunology Fetal Blood - metabolism Fundamental and applied biological sciences. Psychology Fundamental immunology General aspects Genetic diversity Humans Hypersensitivity - immunology IgE IL-13 polymorphism Immunoglobulin E - blood Immunoglobulin E - immunology Infant, Newborn Interleukin-13 - genetics Male Medical sciences Polymorphism Polymorphism, Single Nucleotide Pregnancy Prenatal Exposure Delayed Effects - immunology Risk Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis sex Sex Factors Smoking Tobacco smoke Tobacco Smoke Pollution - adverse effects |
| title | Environmental tobacco smoke and male sex modify the influence of IL-13 genetic variants on cord blood IgE levels |
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