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dc.contributor.authorMai, Xiao-Mei
dc.contributor.authorLanghammer, Arnulf
dc.contributor.authorCamargo, Carlos Arthuro
dc.contributor.authorChen, Yue
dc.date.accessioned2017-06-12T06:55:04Z
dc.date.available2017-06-12T06:55:04Z
dc.date.created2013-01-11T15:28:09Z
dc.date.issued2012
dc.identifier.citationAmerican Journal of Epidemiology. 2012, 176 (12), 1169-1176.nb_NO
dc.identifier.issn0002-9262
dc.identifier.urihttp://hdl.handle.net/11250/2445682
dc.description.abstractThe impact of low vitamin D status on asthma development is unclear. The authors investigated the relation between the baseline serum 25-hydroxyvitamin D (25(OH)D) level and incident asthma in adults, including possible effect modification by allergy status, using allergic rhinitis as a proxy measure. A cohort of 25,616 Norwegian adults aged 19–55 years participated in 2 surveys of the Nord-Trøndelag Health Study known as HUNT 2 (1995–1997) and HUNT 3 (2006–2008). Of this cohort, a nested case-control study included 584 new-onset asthma cases and 1,958 nonasthma controls whose baseline serum 25(OH)D levels were measured. After adjustment for potential asthma risk factors, the baseline serum level of 25(OH)D (<50 nmol/L) was not significantly associated with asthma in either women (adjusted odds ratio = 0.94, 95% confidence interval (CI): 0.67, 1.32) or men (adjusted odds ratio = 1.47, 95% CI: 0.93, 2.32). In men, allergic rhinitis modified the association with the adjusted odds ratio being 0.87 (95% CI: 0.36, 2.06) among men with allergic rhinitis and 2.32 (95% CI: 1.06, 5.10) among men without allergic rhinitis. The serum 25(OH)D level was not associated with incident asthma in women, regardless of allergy status. Low vitamin D status was not significantly associated with incident asthma in most adults, but it may have increased risk among men without allergy.nb_NO
dc.language.isoengnb_NO
dc.publisherOxford University Pressnb_NO
dc.titleSerum 25-Hydroxyvitamin D levels and incident asthma in adults; the HUNT studynb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.description.versionacceptedVersionnb_NO
dc.source.pagenumber1169-1176nb_NO
dc.source.volume176nb_NO
dc.source.journalAmerican Journal of Epidemiologynb_NO
dc.source.issue12nb_NO
dc.identifier.doi10.1093/aje/kws235
dc.identifier.cristin986449
dc.relation.projectNorges forskningsråd: 201895/V50nb_NO
dc.description.localcode© The Author 2012. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. This is the authors' accepted and refereed manuscript to the article.nb_NO
cristin.unitcode194,65,20,0
cristin.unitnameInstitutt for samfunnsmedisin
cristin.ispublishedtrue
cristin.fulltextpostprint
cristin.qualitycode2


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