Urinary levels of volatile organic carcinogen and toxicant biomarkers in relation to lung cancer development in smokers
Identifieur interne : 008705 ( Main/Merge ); précédent : 008704; suivant : 008706Urinary levels of volatile organic carcinogen and toxicant biomarkers in relation to lung cancer development in smokers
Auteurs : Jian-Min Yuan [États-Unis] ; Yu-Tang Gao [République populaire de Chine] ; RENWEI WANG [États-Unis] ; MENGLAN CHEN [États-Unis] ; Steven G. Carmella [États-Unis] ; Stephen S. Hecht [États-Unis]Source :
- Carcinogenesis : (New York. Print) [ 0143-3334 ] ; 2012.
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Abstract
Besides polycyclic aromatic hydrocarbons (PAH) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which are established lung carcinogens, tobacco smoke also contains relatively large quantities of volatile organic carcinogens and toxicants, including 1,3-butadiene, ethylene oxide, benzene, acrolein and crotonaldehyde. Although animal experiments showed that some of these compounds can induce tumors in multiple organs including the lung, epidemiological studies of their relationship with lung cancer in smokers have not been reported. Therefore, in this study, we quantified urinary mercapturic acid metabolites of 1,3-butadiene, ethylene oxide, benzene, acrolein and crotonaldehyde in addition to urinary biomarkers for PAH, NNK and nicotine in 343 lung cancer cases and 392 matched controls among a cohort of 18 244 Chinese men in Shanghai, China, followed from 1986 to 2006. Compared with the lowest quartiles, highest quartiles of all measured mercapturic acids were associated with statistically significantly ˜2-fold increased risk for lung cancer (all P's for trend <0.01) after adjustment for smoking intensity and duration. The positive associations between biomarkers of ethylene oxide, benzene or acrolein and lung cancer risk remained statistically significant after adjustment for biomarkers of PAH and NNK, whereas urinary total cotinine completely explained the mercapturic acid metabolites and lung cancer associations (all P's for trend ≥0.39). We conclude that mercapturic acid metabolites of 1,3-butadiene, ethylene oxide, benzene, acrolein and crotonaldehyde may not be independent risk predictors of lung cancer among Shanghai smokers, in contrast to biomarkers of PAH, NNK and nicotine exposure.
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Carmella</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Masonic Cancer Center, University of Minnesota</s1><s2>Minneapolis, MN</s2><s3>USA</s3><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Minneapolis, MN</wicri:noRegion></affiliation></author><author><name sortKey="Hecht, Stephen S" sort="Hecht, Stephen S" uniqKey="Hecht S" first="Stephen S." last="Hecht">Stephen S. Hecht</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Masonic Cancer Center, University of Minnesota</s1><s2>Minneapolis, MN</s2><s3>USA</s3><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Minneapolis, MN</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Carcinogenesis : (New York. Print)</title><title level="j" type="abbreviated">Carcinogenesis : (N. Y., Print)</title><idno type="ISSN">0143-3334</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Carcinogenesis : (New York. Print)</title><title level="j" type="abbreviated">Carcinogenesis : (N. Y., Print)</title><idno type="ISSN">0143-3334</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Biological marker</term><term>Bronchopulmonary</term><term>Carcinogen</term><term>Carcinogenesis</term><term>Human</term><term>Lung cancer</term><term>Poison</term><term>Smoker</term><term>Tobacco smoking</term><term>Toxicity</term><term>Urine</term><term>Volatiles</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Urine</term><term>Matière volatile</term><term>Carcinogène</term><term>Toxicité</term><term>Toxique</term><term>Marqueur biologique</term><term>Bronchopulmonaire</term><term>Cancer du poumon</term><term>Carcinogenèse</term><term>Fumeur</term><term>Homme</term><term>Tabagisme</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term><term>Tabagisme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Besides polycyclic aromatic hydrocarbons (PAH) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which are established lung carcinogens, tobacco smoke also contains relatively large quantities of volatile organic carcinogens and toxicants, including 1,3-butadiene, ethylene oxide, benzene, acrolein and crotonaldehyde. Although animal experiments showed that some of these compounds can induce tumors in multiple organs including the lung, epidemiological studies of their relationship with lung cancer in smokers have not been reported. Therefore, in this study, we quantified urinary mercapturic acid metabolites of 1,3-butadiene, ethylene oxide, benzene, acrolein and crotonaldehyde in addition to urinary biomarkers for PAH, NNK and nicotine in 343 lung cancer cases and 392 matched controls among a cohort of 18 244 Chinese men in Shanghai, China, followed from 1986 to 2006. Compared with the lowest quartiles, highest quartiles of all measured mercapturic acids were associated with statistically significantly ˜2-fold increased risk for lung cancer (all P's for trend <0.01) after adjustment for smoking intensity and duration. The positive associations between biomarkers of ethylene oxide, benzene or acrolein and lung cancer risk remained statistically significant after adjustment for biomarkers of PAH and NNK, whereas urinary total cotinine completely explained the mercapturic acid metabolites and lung cancer associations (all P's for trend ≥0.39). We conclude that mercapturic acid metabolites of 1,3-butadiene, ethylene oxide, benzene, acrolein and crotonaldehyde may not be independent risk predictors of lung cancer among Shanghai smokers, in contrast to biomarkers of PAH, NNK and nicotine exposure.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li><li>États-Unis</li></country><region><li>Pennsylvanie</li></region><settlement><li>Pittsburgh</li></settlement><orgName><li>Université de Pittsburgh</li></orgName></list><tree><country name="États-Unis"><noRegion><name sortKey="Yuan, Jian Min" sort="Yuan, Jian Min" uniqKey="Yuan J" first="Jian-Min" last="Yuan">Jian-Min Yuan</name></noRegion><name sortKey="Carmella, Steven G" sort="Carmella, Steven G" uniqKey="Carmella S" first="Steven G." last="Carmella">Steven G. Carmella</name><name sortKey="Hecht, Stephen S" sort="Hecht, Stephen S" uniqKey="Hecht S" first="Stephen S." last="Hecht">Stephen S. Hecht</name><name sortKey="Menglan Chen" sort="Menglan Chen" uniqKey="Menglan Chen" last="Menglan Chen">MENGLAN CHEN</name><name sortKey="Renwei Wang" sort="Renwei Wang" uniqKey="Renwei Wang" last="Renwei Wang">RENWEI WANG</name><name sortKey="Yuan, Jian Min" sort="Yuan, Jian Min" uniqKey="Yuan J" first="Jian-Min" last="Yuan">Jian-Min Yuan</name></country><country name="République populaire de Chine"><noRegion><name sortKey="Gao, Yu Tang" sort="Gao, Yu Tang" uniqKey="Gao Y" first="Yu-Tang" last="Gao">Yu-Tang Gao</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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