2.50
Hdl Handle:
http://hdl.handle.net/10146/56174
Title:
Active and passive smoking and risk of ovarian cancer.
Authors:
Baker, J. A.; Odunuga, O. O.; Rodabaugh, K. J.; Reid, M. E.; Menezes, R. J.; Moysich, K. B.
Abstract:
It is unclear whether smoking is a risk factor for epithelial ovarian cancer, although some studies have suggested that it may be associated with an increased risk of mucinous tumors. This study investigated the effect of smoking and environmental tobacco smoke (ETS) on ovarian cancer risk among 434 women with primary epithelial ovarian, peritoneal, or fallopian cancers and 868 age- and region-matched hospital controls with nonneoplastic conditions. All participants completed a comprehensive epidemiologic questionnaire. Results indicate that decreased risk of ovarian cancer was associated with being a nonsmoker exposed to ETS (adjusted odds ratio [aOR] 0.68, 95% confidence interval [CI] 0.46-0.99), a former smoker (aOR 0.76, 95% CI 0.53-1.10), or a current smoker (aOR 0.53, 95% CI 0.32-0.88). A similar protective effect was noted for smokers with moderate or high exposure based on smoking intensity, duration, and cumulative exposure, as well as for never smokers exposed to ETS. Results did not differ substantially by histologic subtype. Although prevailing theories of ovarian cancer etiology implicate incessant ovulation, characteristics of the study population suggest that anovulation was not the protective mechanism in this study. Immunosuppression by nicotine or upregulation of enzymes that metabolize carcinogens may be responsible for the effects observed.
Citation:
Int. J. Gynecol. Cancer A16 Suppl 1:211-218
Journal:
International journal of gynecological cancer
Issue Date:
18-Mar-2009
URI:
http://hdl.handle.net/10146/56174
DOI:
10.1111/j.1525-1438.2006.00473.x
PubMed ID:
16515593
Additional Links:
http://www3.interscience.wiley.com/journal/118632388/abstract
Type:
Article
Language:
en
Description:
Cancer epidemiologyCancer type:ovarian cancerStudy design:case-controlStudy size:434 cases, 868 controlsDescription of cohort(s) studied:434 women with promary epithelial ovarian, peritoneal, fallopian tube cancer, 868 women randomly selectedExposure(s) evaluated:ETSConfounders controlled for:smoking habitsImpact on risk: nonsmokers with ETS EXPOSURE, OR 0.68, 95%CI 0.47-0.99Current smokers with ETS exposure, OR 0.5, 95% CI 0.34-0.9Never smokres with ETS exposure, OR 0.39, 95% CI 0.1-1.48, P=0.04Former smokers with ETS eposure OR 0.54, 95%CI 0.37-0.79, P=0.002Lifestyle modulation of cancer & cancer biomarkersLifestyle element evaluated:smokingOutcome studied (cancer or cancer biomarker):ovarian cancer riskMethod of biomarker analysis:questionnairesStudy type (in vitro, animals, humans): humansStudy design (if human):case-controlStudy size (if human):434 cases, 868 controlsDescription of cohort(s) studied (if human):434 women with promary epithelial ovarian, peritoneal, fallopian tube cancer, 868 women randomly selected. KEYWORDS CLASSIFICATION: adverse effects;Adult;Aged;cancer epidemiology;Case-Control Studies;etiology;Epidemiology;Female;Humans;Immunosuppression;Middle Aged;Neoplasms,Glandular and Epithelial;New York;Ovarian Neoplasms;Risk Factors;Smoke;Smoking;Tobacco;Tobacco Smoke Pollution;analysis.
ISSN:
1048-891X
Appears in Collections:
Articles with annotation

Full metadata record

DC FieldValue Language
dc.contributor.authorBaker, J. A.-
dc.contributor.authorOdunuga, O. O.-
dc.contributor.authorRodabaugh, K. J.-
dc.contributor.authorReid, M. E.-
dc.contributor.authorMenezes, R. J.-
dc.contributor.authorMoysich, K. B.-
dc.date.accessioned2009-03-18T10:54:26Z-
dc.date.available2009-03-18T10:54:26Z-
dc.date.issued2009-03-18T10:54:26Z-
dc.identifier.citationInt. J. Gynecol. Cancer A16 Suppl 1:211-218en
dc.identifier.issn1048-891X-
dc.identifier.pmid16515593-
dc.identifier.doi10.1111/j.1525-1438.2006.00473.x-
dc.identifier.urihttp://hdl.handle.net/10146/56174-
dc.descriptionCancer epidemiologyCancer type:ovarian cancerStudy design:case-controlStudy size:434 cases, 868 controlsDescription of cohort(s) studied:434 women with promary epithelial ovarian, peritoneal, fallopian tube cancer, 868 women randomly selectedExposure(s) evaluated:ETSConfounders controlled for:smoking habitsImpact on risk: nonsmokers with ETS EXPOSURE, OR 0.68, 95%CI 0.47-0.99Current smokers with ETS exposure, OR 0.5, 95% CI 0.34-0.9Never smokres with ETS exposure, OR 0.39, 95% CI 0.1-1.48, P=0.04Former smokers with ETS eposure OR 0.54, 95%CI 0.37-0.79, P=0.002Lifestyle modulation of cancer & cancer biomarkersLifestyle element evaluated:smokingOutcome studied (cancer or cancer biomarker):ovarian cancer riskMethod of biomarker analysis:questionnairesStudy type (in vitro, animals, humans): humansStudy design (if human):case-controlStudy size (if human):434 cases, 868 controlsDescription of cohort(s) studied (if human):434 women with promary epithelial ovarian, peritoneal, fallopian tube cancer, 868 women randomly selected. KEYWORDS CLASSIFICATION: adverse effects;Adult;Aged;cancer epidemiology;Case-Control Studies;etiology;Epidemiology;Female;Humans;Immunosuppression;Middle Aged;Neoplasms,Glandular and Epithelial;New York;Ovarian Neoplasms;Risk Factors;Smoke;Smoking;Tobacco;Tobacco Smoke Pollution;analysis.en
dc.description.abstractIt is unclear whether smoking is a risk factor for epithelial ovarian cancer, although some studies have suggested that it may be associated with an increased risk of mucinous tumors. This study investigated the effect of smoking and environmental tobacco smoke (ETS) on ovarian cancer risk among 434 women with primary epithelial ovarian, peritoneal, or fallopian cancers and 868 age- and region-matched hospital controls with nonneoplastic conditions. All participants completed a comprehensive epidemiologic questionnaire. Results indicate that decreased risk of ovarian cancer was associated with being a nonsmoker exposed to ETS (adjusted odds ratio [aOR] 0.68, 95% confidence interval [CI] 0.46-0.99), a former smoker (aOR 0.76, 95% CI 0.53-1.10), or a current smoker (aOR 0.53, 95% CI 0.32-0.88). A similar protective effect was noted for smokers with moderate or high exposure based on smoking intensity, duration, and cumulative exposure, as well as for never smokers exposed to ETS. Results did not differ substantially by histologic subtype. Although prevailing theories of ovarian cancer etiology implicate incessant ovulation, characteristics of the study population suggest that anovulation was not the protective mechanism in this study. Immunosuppression by nicotine or upregulation of enzymes that metabolize carcinogens may be responsible for the effects observed.en
dc.language.isoenen
dc.relation.urlhttp://www3.interscience.wiley.com/journal/118632388/abstracten
dc.subjectNicotineen
dc.subjectOvarian neoplasmen
dc.subjectSmokingen
dc.subjectTobaccoen
dc.subjectTobacco smoke pollutionen
dc.subject.meshAdult-
dc.subject.meshAged-
dc.subject.meshCase-Control Studies-
dc.subject.meshFemale-
dc.subject.meshHumans-
dc.subject.meshMiddle Aged-
dc.subject.meshNeoplasms, Glandular and Epithelial-
dc.subject.meshOvarian Neoplasms-
dc.subject.meshRisk Factors-
dc.subject.meshSmoking-
dc.subject.meshTobacco Smoke Pollution-
dc.titleActive and passive smoking and risk of ovarian cancer.en
dc.typeArticleen
dc.identifier.journalInternational journal of gynecological canceren

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