Paper Health Physics. The Radiation Safety Journal. 94(3):228-241, March 2008.Thompson, Richard E. *; Nelson, Donald F. +; Popkin, Joel H. ++; Popkin, Zenaida ++
Abstract: mdash;: A study of lung cancer risk from residential radon exposure and its radioactive progeny was performed with 200 cases (58% male, 42% female) and 397 controls matched on age and sex, all from the same health maintenance organization. Emphasis was placed on accurate and extensive year-long dosimetry with etch-track detectors in conjunction with careful questioning about historic patterns of in-home mobility. Conditional logistic regression was used to model the outcome of cancer on radon exposure, while controlling for years of residency, smoking, education, income, and years of job exposure to known or potential carcinogens. Smoking was accounted for by nine categories: never smokers, four categories of current smokers, and four categories of former smokers. Radon exposure was divided into six categories (model 1) with break points at 25, 50, 75, 150, and 250 Bq m-3, the lowest being the reference. Surprisingly, the adjusted odds ratios (AORs) were, in order, 1.00, 0.53, 0.31, 0.47, 0.22, and 2.50 with the third category significantly below 1.0 (p < aor =" 0.30" p =" 0.005">
Monday, April 21, 2008
CASE-CONTROL STUDY OF LUNG CANCER RISK FROM RESIDENTIAL RADON EXPOSURE IN WORCESTER COUNTY, MASSACHUSETTS.
Long-Term Use of Supplemental Multivitamins, Vitamin C, Vitamin E, and Folate Does Not Reduce the Risk of Lung Cancer
Division of Pulmonary and Critical Care Medicine, and 2 Department of Epidemiology, University of Washington, Seattle, Washington; 3 Epidemiologic Research and Information Center, and 4 Health Services Research and Development, VA Puget Sound Health Care System, Seattle, Washington; 5 Departments of Epidemiology and Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; and 6 Cancer Prevention Program, Fred Hutchinson Cancer Research Center, Seattle, Washington
Correspondence and requests for reprints should be addressed to Christopher Slatore, M.D., University of Washington, Division of Pulmonary and Critical Care Medicine, 1959 NE Pacific Street, Box 356522, Seattle, WA 98195-6522. E-mail: cslatore@u.washington.edu
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Rationale: Lung cancer is the leading cause of cancer-related mortality in the United States. Although supplements are used by half the population, limited information is available about their specific effect on lung cancer risk.
Objectives: To explore the association of supplemental multivitamins, vitamin C, vitamin E, and folate with incident lung cancer.
Methods: Prospective cohort of 77,721 men and women aged 50–76 years from Washington State in the VITAL (VITamins And Lifestyle) study. Cases were identified through the Seattle–Puget Sound SEER (Surveillance, Epidemiology, and End Results) cancer registry.
Measurements and Main Results: Hazard ratios (HRs) for incident lung cancer according to 10-year average daily use of supplemental multivitamins, vitamin C, vitamin E, and folate. A total of 521 cases of lung cancer were identified. Adjusting for smoking, age, and sex, there was no inverse association with any supplement. Supplemental vitamin E was associated with a small increased risk of lung cancer (HR, 1.05 for every 100-mg/d increase in dose; 95% confidence interval [CI], 1.00–1.09; P = 0.033). This risk of supplemental vitamin E was largely confined to current smokers (HR, 1.11 for every 100-mg/d increase; 95% CI, 1.03–1.19; P < 0.01) and was greatest for non–small cell lung cancer (HR, 1.07 for every 100-mg/d increase; 95% CI, 1.02–1.12; P = 0.004).
Conclusions: Supplemental multivitamins, vitamin C, vitamin E, and folate were not associated with a decreased risk of lung cancer. Supplemental vitamin E was associated with a small increased risk. Patients should be counseled against using these supplements to prevent lung cancer.
Correspondence and requests for reprints should be addressed to Christopher Slatore, M.D., University of Washington, Division of Pulmonary and Critical Care Medicine, 1959 NE Pacific Street, Box 356522, Seattle, WA 98195-6522. E-mail: cslatore@u.washington.edu
'//-->
Rationale: Lung cancer is the leading cause of cancer-related mortality in the United States. Although supplements are used by half the population, limited information is available about their specific effect on lung cancer risk.
Objectives: To explore the association of supplemental multivitamins, vitamin C, vitamin E, and folate with incident lung cancer.
Methods: Prospective cohort of 77,721 men and women aged 50–76 years from Washington State in the VITAL (VITamins And Lifestyle) study. Cases were identified through the Seattle–Puget Sound SEER (Surveillance, Epidemiology, and End Results) cancer registry.
Measurements and Main Results: Hazard ratios (HRs) for incident lung cancer according to 10-year average daily use of supplemental multivitamins, vitamin C, vitamin E, and folate. A total of 521 cases of lung cancer were identified. Adjusting for smoking, age, and sex, there was no inverse association with any supplement. Supplemental vitamin E was associated with a small increased risk of lung cancer (HR, 1.05 for every 100-mg/d increase in dose; 95% confidence interval [CI], 1.00–1.09; P = 0.033). This risk of supplemental vitamin E was largely confined to current smokers (HR, 1.11 for every 100-mg/d increase; 95% CI, 1.03–1.19; P < 0.01) and was greatest for non–small cell lung cancer (HR, 1.07 for every 100-mg/d increase; 95% CI, 1.02–1.12; P = 0.004).
Conclusions: Supplemental multivitamins, vitamin C, vitamin E, and folate were not associated with a decreased risk of lung cancer. Supplemental vitamin E was associated with a small increased risk. Patients should be counseled against using these supplements to prevent lung cancer.
Cigarette Smoking and Risk of Fatal Breast Cancer
From the Department of Epidemiology and Statistics, American Cancer Society Atlanta, GA
Reprint requests to Dr. Eugenia E. Calle, American Cancer Society, 1599 Clifton Road, NE, Atlanta, GA 30329
The authors examined the association of fatal breast cancer and cigarette smoking in a large, prospective mortality study of US adults. After 6 years of follow-up, 880 cases of fatal breast cancer were observed in a cohort of 604,412 women who were cancer-free at interview in 1982. Cox proportional hazards modeling, adjusted for other risk factors, found that current smoking was significantly related to fatal breast cancer risk (adjusted rate ratio (RR) = 1.26, 95% confidence interval (Cl) 1.05–1.50). A negative association was observed for former smokers, but this was not statistically significant (RR = 0.85, 95% Cl 0.70–1.03). The association of current smoking with fatal breast cancer risk increased with increasing numbers of cigarettes per day and with total number of years smoked. For smokers of 40 or more cigarettes per day, the rate ratio was 1.74 (95% Cl 1.15–2.62). The authors hypothesize that these results may be due to either a poorer prognosis among breast cancer cases who smoke or a delayed diagnosis among current smokers who do not receive mammograms as often as never or former smokers. Women who smoke should be targeted for breast cancer screening services.
breast neoplasms; cohort studies; risk; smoking; women
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Reprint requests to Dr. Eugenia E. Calle, American Cancer Society, 1599 Clifton Road, NE, Atlanta, GA 30329
The authors examined the association of fatal breast cancer and cigarette smoking in a large, prospective mortality study of US adults. After 6 years of follow-up, 880 cases of fatal breast cancer were observed in a cohort of 604,412 women who were cancer-free at interview in 1982. Cox proportional hazards modeling, adjusted for other risk factors, found that current smoking was significantly related to fatal breast cancer risk (adjusted rate ratio (RR) = 1.26, 95% confidence interval (Cl) 1.05–1.50). A negative association was observed for former smokers, but this was not statistically significant (RR = 0.85, 95% Cl 0.70–1.03). The association of current smoking with fatal breast cancer risk increased with increasing numbers of cigarettes per day and with total number of years smoked. For smokers of 40 or more cigarettes per day, the rate ratio was 1.74 (95% Cl 1.15–2.62). The authors hypothesize that these results may be due to either a poorer prognosis among breast cancer cases who smoke or a delayed diagnosis among current smokers who do not receive mammograms as often as never or former smokers. Women who smoke should be targeted for breast cancer screening services.
breast neoplasms; cohort studies; risk; smoking; women
CiteULike Connotea Del.icio.us What's this?
This article has been cited by other articles:
C. Nagata, T. Mizoue, K. Tanaka, I. Tsuji, K. Wakai, M. Inoue, S. Tsugane, and Research Group for the Development and EvaluationTobacco Smoking and Breast Cancer Risk: An Evaluation Based on a Systematic Review of Epidemiological Evidence among the Japanese PopulationJpn. J. Clin. Oncol., June 1, 2006; 36(6): 387 - 394. [Abstract] [Full Text] [PDF]
S. Colilla, P. W. Kantoff, S. L. Neuhausen, A. K. Godwin, M. B. Daly, S. A. Narod, J. E. Garber, H. T. Lynch, M. Brown, B. L. Weber, et al.The joint effect of smoking and AIB1 on breast cancer risk in BRCA1 mutation carriersCarcinogenesis, March 1, 2006; 27(3): 599 - 605. [Abstract] [Full Text] [PDF]
S. Murin, K. E. Pinkerton, N. E. Hubbard, and K. EricksonThe Effect of Cigarette Smoke Exposure on Pulmonary Metastatic Disease in a Murine Model of Metastatic Breast CancerChest, April 1, 2004; 125(4): 1467 - 1471. [Abstract] [Full Text] [PDF]
W. K. Al-Delaimy, E. Cho, W. Y. Chen, G. Colditz, and W. C. WilletA Prospective Study of Smoking and Risk of Breast Cancer in Young Adult WomenCancer Epidemiol. Biomarkers Prev., March 1, 2004; 13(3): 398 - 404. [Abstract] [Full Text]
P. Reynolds, S. Hurley, D. E. Goldberg, H. Anton-Culver, L. Bernstein, D. Deapen, P. L. Horn-Ross, D. Peel, R. Pinder, R. K. Ross, et al.Active Smoking, Household Passive Smoking, and Breast Cancer: Evidence From the California Teachers StudyJ Natl Cancer Inst, January 7, 2004; 96(1): 29 - 37. [Abstract] [Full Text] [PDF]
P. D. Terry and T. E. RohanCigarette Smoking and the Risk of Breast Cancer in Women: A Review of the LiteratureCancer Epidemiol. Biomarkers Prev., October 1, 2002; 11(10): 953 - 971. [Abstract] [Full Text] [PDF]
K. Conway, S. N. Edmiston, L. Cui, S. S. Drouin, J. Pang, M. He, C.-K. Tse, J. Geradts, L. Dressler, E. T. Liu, et al.Prevalence and Spectrum of p53 Mutations Associated with Smoking in Breast CancerCancer Res., April 1, 2002; 62(7): 1987 - 1995. [Abstract] [Full Text] [PDF]
S. Murin and J. InciardiCigarette Smoking and the Risk of Pulmonary Metastasis From Breast CancerChest, June 1, 2001; 119(6): 1635 - 1640. [Abstract] [Full Text] [PDF]
D. Wartenberg, E. E. Calle, M. J. Thun, C. W. Heath Jr., C. Lally, and T. WoodruffPassive Smoking Exposure and Female Breast Cancer MortalityJ Natl Cancer Inst, October 18, 2000; 92(20): 1666 - 1673. [Abstract] [Full Text] [PDF]
M. D. Gammon, H. Hibshoosh, M. B. Terry, S. Bose, J. B. Schoenberg, L. A. Brinton, J. L. Bernstein, and W. D. ThompsonCigarette Smoking and Other Risk Factors in Relation to p53 Expression in Breast Cancer among Young WomenCancer Epidemiol. Biomarkers Prev., March 1, 1999; 8(3): 255 - 263. [Abstract] [Full Text] [PDF]
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R.S. Richardson, C. Coggins, J. E. Haddow, G. E. Palomaki, B. A. Chilmonczyk, and P. BoyleThe Hazards of Active and Passive SmokingN. Engl. J. Med., November 18, 1993; 329(21): 1580 - 1581. [Full Text]
P. BoyleThe Hazards of Passive -- And Active -- SmokingN. Engl. J. Med., June 10, 1993; 328(23): 1708 - 1709. [Full Text]
L. Stayner, J. Bena, A. J. Sasco, R. Smith, K. Steenland, M. Kreuzer, and K. StraifLung Cancer Risk and Workplace Exposure to Environmental Tobacco SmokeAm J Public Health, March 1, 2007; 97(3): 545 - 551. [Abstract] [Full Text] [PDF]
J. Subramanian and R. GovindanLung Cancer in Never Smokers: A ReviewJ. Clin. Oncol., February 10, 2007; 25(5): 561 - 570. [Abstract] [Full Text] [PDF]
I. Stepanov, S. S. Hecht, G. Duca, and I. MardariUptake of the Tobacco-Specific Lung Carcinogen 4-(Methylnitrosamino)-1-(3-pyridyl)-1-Butanone by Moldovan ChildrenCancer Epidemiol. Biomarkers Prev., January 1, 2006; 15(1): 7 - 11. [Abstract] [Full Text] [PDF]
L. Thomas, L. A. Doyle, and M. J. EdelmanLung Cancer in Women: Emerging Differences in Epidemiology, Biology, and TherapyChest, July 1, 2005; 128(1): 370 - 381. [Abstract] [Full Text] [PDF]
P. Vineis, M. Alavanja, P. Buffler, E. Fontham, S. Franceschi, Y. T. Gao, P. C. Gupta, A. Hackshaw, E. Matos, J. Samet, et al.Tobacco and Cancer: Recent Epidemiological EvidenceJ Natl Cancer Inst, January 21, 2004; 96(2): 99 - 106. [Full Text] [PDF]
P. N. Lee, J. S. Fry, and B. ForeyRevisiting the Association between Environmental Tobacco Smoke Exposure and Lung Cancer Risk: V. Overall ConclusionsIndoor and Built Environment, March 1, 2002; 11(2): 59 - 82. [Abstract] [PDF]
K. T. Bogen and H. WitschiLung tumors in A/J mice exposed to environmental tobacco smoke: estimated potency and implied human riskCarcinogenesis, March 1, 2002; 23(3): 511 - 519. [Abstract] [Full Text] [PDF]
M.S. JaakkolaEnvironmental tobacco smoke and health in the elderlyEur. Respir. J., January 1, 2002; 19(1): 172 - 181. [Abstract] [Full Text] [PDF]
P. N Lee, B. Forey, and J. S. FryRevisiting the Association between Environmental Tobacco Smoke Exposure and Lung Cancer Risk: IV. Investigating Heterogeneity between StudiesIndoor and Built Environment, January 1, 2002; 11(1): 4 - 17. [Abstract] [PDF]
G. Liu, D. P. Miller, W. Zhou, S. W. Thurston, R. Fan, L.-L. Xu, T. J. Lynch, J. C. Wain, L. Su, and D. C. ChristianiDifferential Association of the Codon 72 p53 and GSTM1 Polymorphisms on Histological Subtype of Non-Small Cell Lung CarcinomaCancer Res., December 1, 2001; 61(24): 8718 - 8722. [Abstract] [Full Text] [PDF]
P. N. Lee, B. Forey, and J. S. FryRevisiting the Association between Environmental Tobacco Smoke Exposure and Lung Cancer Risk: III. Adjustment for the Biasing Effect of Misclassification of Smoking HabitsIndoor and Built Environment, November 1, 2001; 10(6): 384 - 398. [Abstract] [PDF]
J. S. Fry and P. N. LeeRevisiting the Association between Environmental Tobacco Smoke Exposure and Lung Cancer Risk: II. Adjustment for the Potential Confounding Effects of Fruit, Vegetables, Dietary Fat and EducationIndoor and Built Environment, January 1, 2001; 10(1): 20 - 39. [Abstract] [PDF]
J. S. Fry and P. N. LeeRevisiting the Association between Environmental Tobacco Smoke Exposure and Lung Cancer Risk: I. The Dose-Response Relationship with Amount and Duration of Smoking by the HusbandIndoor and Built Environment, November 1, 2000; 9(6): 303 - 316. [Abstract] [PDF]
C.-H. Lee, Y.-C. Ko, W. Goggins, J.-J. Huang, M.-S. Huang, E.-L. Kao, and H.-Z. WangLifetime environmental exposure to tobacco smoke and primary lung cancer of non-smoking Taiwanese womenInt. J. Epidemiol., April 1, 2000; 29(2): 224 - 231. [Abstract] [Full Text] [PDF]
R. A. Hiatt and B. K. RimerA New Strategy for Cancer Control ResearchCancer Epidemiol. Biomarkers Prev., November 1, 1999; 8(11): 957 - 964. [Full Text]
P.N. Lee and A.J. ThorntonReview : A Critical Commentary on Views Expressed by IARC in Relation to Environmental Tobacco Smoke and Lung CancerIndoor and Built Environment, May 1, 1998; 7(3): 129 - 145. [Abstract] [PDF]
A K HackshawLung cancer and passive smokingStatistical Methods in Medical Research, April 1, 1998; 7(2): 119 - 136. [Abstract] [PDF]
P. N LeeDifficulties in assessing the relationship between passive smoking and lung cancerStatistical Methods in Medical Research, April 1, 1998; 7(2): 137 - 163. [Abstract] [PDF]
M. Sugita, T. Izuno, and M. KanamoriRecalculation of Summarised Odds Ratios for the Relationship between Passive Smoking and Lung Cancer Based on Data in the EPA ReportIndoor and Built Environment, May 1, 1995; 4(3-4): 177 - 181. [Abstract] [PDF]
R.S. Richardson, C. Coggins, J. E. Haddow, G. E. Palomaki, B. A. Chilmonczyk, and P. BoyleThe Hazards of Active and Passive SmokingN. Engl. J. Med., November 18, 1993; 329(21): 1580 - 1581. [Full Text]
P. BoyleThe Hazards of Passive -- And Active -- SmokingN. Engl. J. Med., June 10, 1993; 328(23): 1708 - 1709. [Full Text]
Enviromental Tobacco Smoke and Lung Cancer Risk in Nonsmoking Women
Heather G. Stockwell*, Allan L. Goldman, Gary H. Lyman, Charles I. Noss, Adam W. Armstrong, Patricia A. Pinkham, Elizabeth C. Candelora, Marcia R. Brusa
Department of Epideminology and Biostatistics, University of South Florida Tampa, FlaDepartment of Internal Medcine, University of South Florida Tampa, FlaDepartment of Environmental and Occupational Health, College of Public Health University of South Florida Tampa, Fla
*Correspondence to: Heather G. Stockwell, Sc.D., Department of Epidemiolgy and Biostatistics, College of Public Health Unversity of south Florida, Tampa, FL 33612–3805.
Background: Exposure to envionmental tobacco smoke (passive smoking )has been suggested to be a cause of lung cancer, although early epidemiologic studies have produced in-consistent result. Purpose: We conducted an epidemilogic case-control study to assess the relation-ship between exposure to envirmental tobacco smoke and lungcancer risk among women who have never smoked (i.e., having smoked for a total of <6 n ="210)" n =" 301)" or =" 2.4;" ci =" 1.1–5.4).">
Department of Epideminology and Biostatistics, University of South Florida Tampa, FlaDepartment of Internal Medcine, University of South Florida Tampa, FlaDepartment of Environmental and Occupational Health, College of Public Health University of South Florida Tampa, Fla
*Correspondence to: Heather G. Stockwell, Sc.D., Department of Epidemiolgy and Biostatistics, College of Public Health Unversity of south Florida, Tampa, FL 33612–3805.
Background: Exposure to envionmental tobacco smoke (passive smoking )has been suggested to be a cause of lung cancer, although early epidemiologic studies have produced in-consistent result. Purpose: We conducted an epidemilogic case-control study to assess the relation-ship between exposure to envirmental tobacco smoke and lungcancer risk among women who have never smoked (i.e., having smoked for a total of <6 n ="210)" n =" 301)" or =" 2.4;" ci =" 1.1–5.4).">
Skin Cancer in a Subtropical Australian Population: Incidence and Lack of Association with Occupation
Queensiand Institute of Medical Research Queensiand, Australia2Sunshine Coast sQueensiand, Australia3Sullivan and Nicolaldes Gold Coast, Queensiand, Australia
Reprint requests to Dr. Adele Green, Epidemiology Unit, Queensiand Institute of Medical Research, P.O. Royal Brisbane Hospital, Queensland 4029, Australia.
Because it is not possible to monitor skin cancer accurately using routine methods, special surveys have been undertaken in Nambour, a typical subtropical community in Queensland, Australia. Estimates of incidence reported here are based on skin cancers medically treated between 1985 and 1992 and new cases diagnosed by dermatologists in two examination clinics in 1986 and 1992. Among men and women aged 18–69 years in 1986, age-adjusted incidence rates of basal cell carcinoma were 2,074 and 1,579 per 100,000 per year, respectively—the highest incidence rates of a specific cancer ever reported. Squamous cell carcinoma occurred at half the rate of basal cell carcinoma among men and at about one third the rate among women. Although as expected, fair skin, a history of repeated sunburns, and nonmalignant solar skin damage diagnosed by dermatologists were strongly associated with both types of skin cancer, outdoor occupation was not. Significant self-selection was observed among outdoor workers, whereby people with fair or medium complexions and a tendency to sunburn were systematically underrepresented among those in long-term outdoor occupations although they accounted for more than 80 percent of the community study sample. The mitigating effect of this selection bias may partly explain the paradox of the lack of quantitative evidence of a causal link between sun exposure and skin cancer in humans. Am J Epidemiol 199
Reprint requests to Dr. Adele Green, Epidemiology Unit, Queensiand Institute of Medical Research, P.O. Royal Brisbane Hospital, Queensland 4029, Australia.
Because it is not possible to monitor skin cancer accurately using routine methods, special surveys have been undertaken in Nambour, a typical subtropical community in Queensland, Australia. Estimates of incidence reported here are based on skin cancers medically treated between 1985 and 1992 and new cases diagnosed by dermatologists in two examination clinics in 1986 and 1992. Among men and women aged 18–69 years in 1986, age-adjusted incidence rates of basal cell carcinoma were 2,074 and 1,579 per 100,000 per year, respectively—the highest incidence rates of a specific cancer ever reported. Squamous cell carcinoma occurred at half the rate of basal cell carcinoma among men and at about one third the rate among women. Although as expected, fair skin, a history of repeated sunburns, and nonmalignant solar skin damage diagnosed by dermatologists were strongly associated with both types of skin cancer, outdoor occupation was not. Significant self-selection was observed among outdoor workers, whereby people with fair or medium complexions and a tendency to sunburn were systematically underrepresented among those in long-term outdoor occupations although they accounted for more than 80 percent of the community study sample. The mitigating effect of this selection bias may partly explain the paradox of the lack of quantitative evidence of a causal link between sun exposure and skin cancer in humans. Am J Epidemiol 199
cause of cancer
Alcohol Consumption and All-Cause and Cancer Mortality among Middle-aged Japanese Men: Seven-year Follow-up of the JPHC Study Cohort I.
Original Contributions American Journal of Epidemiology. 150(11):1201-1207, December 1, 1999.Tsugane, Shoichiro 1; Fahey, Michael T. 1; Sasaki, Satoshi 1; Baba, Shunroku 2; for the JPHC Study Group *
Abstract: To examine the association between alcohol consumption and mortality in Japan, where mortality and lifestyle differ substantially from Western countries, a population-based prospective study was conducted in four public health center areas as part of the Japan Public Health Center-based prospective study on cancer and cardiovascular disease (JPHC). After excluding subjects with self-reported serious diseases at baseline, 19,231 men aged 40-59 years who reported their alcohol intake were followed from 1990 through 1996, and 548 deaths were documented. The association between all-cause mortality and alcohol consumption was J-shaped. The lowest risk was observed for men who consumed 1-149 g/week (relative risk (RR) = 0.64, 95% confidence interval (CI) 0.46, 0.88), while the highest risk was seen for men who consumed >=450 g/week (RR = 1.32, 95% CI 1.00, 1.74), after adjustment for possible confounders. The association did not change after excluding deaths that occurred in the first 2 years of follow-up. However, the association was modified by smoking, and beneficial effects of moderate drinking were largely limited to nonsmokers. The risk of cancer death showed a similar trend, but increased more in heavy drinkers. The background characteristics of moderate drinkers were healthier than either nondrinkers or heavy drinkers. The authors conclude that moderate alcohol consumption was associated with the lowest risks of all-cause and cancer mortality, especially among nonsmokers.
Copyright 1999 by The Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland, USA. All rights reserved.
Original Contributions American Journal of Epidemiology. 150(11):1201-1207, December 1, 1999.Tsugane, Shoichiro 1; Fahey, Michael T. 1; Sasaki, Satoshi 1; Baba, Shunroku 2; for the JPHC Study Group *
Abstract: To examine the association between alcohol consumption and mortality in Japan, where mortality and lifestyle differ substantially from Western countries, a population-based prospective study was conducted in four public health center areas as part of the Japan Public Health Center-based prospective study on cancer and cardiovascular disease (JPHC). After excluding subjects with self-reported serious diseases at baseline, 19,231 men aged 40-59 years who reported their alcohol intake were followed from 1990 through 1996, and 548 deaths were documented. The association between all-cause mortality and alcohol consumption was J-shaped. The lowest risk was observed for men who consumed 1-149 g/week (relative risk (RR) = 0.64, 95% confidence interval (CI) 0.46, 0.88), while the highest risk was seen for men who consumed >=450 g/week (RR = 1.32, 95% CI 1.00, 1.74), after adjustment for possible confounders. The association did not change after excluding deaths that occurred in the first 2 years of follow-up. However, the association was modified by smoking, and beneficial effects of moderate drinking were largely limited to nonsmokers. The risk of cancer death showed a similar trend, but increased more in heavy drinkers. The background characteristics of moderate drinkers were healthier than either nondrinkers or heavy drinkers. The authors conclude that moderate alcohol consumption was associated with the lowest risks of all-cause and cancer mortality, especially among nonsmokers.
Copyright 1999 by The Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland, USA. All rights reserved.
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