P2-279 10-year mortality follow-up of maternal and paternal grandparents shows different patterns of association with their grandchildren's birth weights: the Lifeways Cross Generation Cohort Study (original) (raw)
American Journal of Epidemiology, 2002
Alcohol drinking increases the risk of several types of cancer, but studies of the relation between alcohol and lung cancer risk are complicated by smoking. The authors carried out meta-analyses for four study designs and conducted sensitivity analyses to assess the results. Pooled smoking-unadjusted relative risks (RRs) for brewery workers and alcoholics were 1.17 (95% confidence interval (CI): 0.99, 1.39) and 1.99 (95% CI: 1.66, 2.39), respectively, relative to population rates. For cohort and case-control studies, the authors conducted dosespecific meta-analyses for ethanol consumption of 1-499, 500-999, 1,000-1,999, and ≥2,000 g/month, relative to nondrinking. Smoking-adjusted RRs for ascending dose groups in cohort studies were 0.98 (95% CI: 0.79, 1.21), 0.92 (95% CI: 0.81, 1.04), 1.04 (95% CI: 0.88, 1.22), and 1.53 (95% CI: 1.04, 2.25), respectively. Smokingadjusted odds ratios for ascending groups in case-control studies were 0.63 (95% CI: 0.51, 0.78), 1.30 (95% CI: 0.98, 1.70), 1.13 (95% CI: 0.46, 2.75), and 1.86 (95% CI: 1.39, 2.49), respectively. Elevated odds ratios were seen for hospital-based case-control studies but not for population-based case-control studies. Sensitivity analyses indicated that smoking explained the elevated RRs in studies of alcoholics and that strong misclassification of smoking status could produce an elevated smoking-adjusted RR in cohort and case-control studies. Overall, evidence for a smoking-adjusted association between alcohol and lung cancer risk is limited to very high consumption groups in cohort and hospital-based case-control studies. At lower levels, any associations observed appear to be explained by confounding. Am J Epidemiol 2002;155:496-506. alcohol drinking; lung neoplasms; meta-analysis; smoking ).
Japanese Journal of Clinical Oncology, 2008
Background: The relationship between alcohol consumption and risk of lung cancer is controversial. Based on a systematic review of epidemiologic evidence, we evaluated this association among the Japanese population, who may be more susceptible to alcohol-related diseases than Western populations. Methods: Original data were obtained from MEDLINE searches using PubMed or from searches of the Ichushi database, complemented with manual searches. The evaluation of associations was based on the strength of evidence and the magnitude of association, together with biological plausibility as previously evaluated by the International Agency for Research on Cancer. Results: We identified seven cohort studies and two case-control studies. One cohort study demonstrated a strong positive association between alcohol drinking and the risk of female lung cancer, but the association almost disappeared after adjustment for smoking. The other eight studies showed a weak positive or no association. Although smoking is the bestestablished risk factor for lung cancer, only five cohort studies presented smoking-adjusted risks out of all nine identified. Furthermore, only two studies explicitly reported the risk estimate for ex-drinkers who may have quit alcohol drinking after the development or diagnosis of the disease and have an apparently higher risk. Conclusion: We conclude that the epidemiologic evidence on the association between alcohol drinking and lung cancer risk remains insufficient in terms of both the number and methodological quality of studies among the Japanese population.
Alcohol Consumption and Risk of Lung Cancer: The Framingham Study
JNCI Journal of the National Cancer Institute, 2002
Background: Reports on the association between alcohol consumption and the risk of lung cancer have been inconsistent. The purpose of this study was to assess this association in a cohort study. Methods: This study included 4265 participants in the original population-based Framingham Study cohort and 4973 subjects in the offspring cohort. Alcohol consumption data were collected periodically for both cohorts. We used the risk sets method to match control subjects to each case patient based on age, sex, smoking variables, and year of birth. We used a conditional logistic regression model to estimate the relative risk of lung cancer according to alcohol consumption. Results: Alcohol consumption was generally light to moderate (i.e., <12 g/day) in both cohorts. During mean follow-ups of 32.8 years in the original and 16.2 years in the offspring cohorts, 269 cases of lung cancer occurred. In categories of total alcohol consumption of 0, 0.1-12, 12.1-24, and greater than 24 g/day, the crude incidence rates of lung cancer were 7.4, 13.6, 16.4, and 25.2 cases per 10 000 person-years, respectively, in the original cohort and 6.6, 4.3, 7.9, and 12.3 cases per 10 000 personyears, respectively, in the offspring cohort. However, after adjustment for age, sex, pack-years of smoking, smoking status, and year of birth in a multivariable conditional logistic regression model, relative risks for lung cancer from the lowest to the highest category of alcohol consumption were 1.0 (referent), 1.0 (95% confidence interval [CI] = 0.5 to 2.1), 1.0 (95% CI = 0.5 to 2.3), and 1.1 (95% CI = 0.5 to 2.3), respectively, in the original cohort and 1.0, 1.4 (95% CI = 0.5 to 3.6), 1.1 (95% CI = 0.3 to 3.6), and 2.0 (95% CI = 0.7 to 5.7), respectively, in the offspring cohort. Conclusion: Alcohol consumption among subjects in the Framingham Study, most of whom were light to moderate drinkers, was not statistically significantly associated with the risk of lung cancer.
Alcohol consumption and risk of lung cancer: a pooled analysis of cohort studies
The American journal of clinical nutrition, 2005
Although smoking is the primary cause of lung cancer, much is unknown about lung cancer etiology, including risk determinants for nonsmokers and modifying factors for smokers. We hypothesized that alcohol consumption contributes to lung cancer risk. We conducted a pooled analysis using standardized exposure and covariate data from 7 prospective studies with 399,767 participants and 3137 lung cancer cases. Study-specific relative risks (RRs) and CIs were estimated and then combined to calculate pooled multivariate RRs by using a random-effects model. We found a slightly greater risk for the consumption of > or = 30 g alcohol/d than for that of 0 g alcohol/d in men (RR: 1.21; 95% CI: 0.91, 1.61; P for trend = 0.03) and in women (RR: 1.16; 95% CI: 0.94, 1.43; P for trend = 0.03). In male never smokers, the RR for consumption of > or = 15 g alcohol/d rather than 0 g alcohol/d was 6.38 (95% CI: 2.74, 14.9; P for trend < 0.001). In women, there were few never-smoking cases and no...
Does binge drinking increase the risk of lung cancer: results from the Findrink study
The European Journal of Public Health, 2009
Background: There are controversies on the role of alcohol in lung cancer but no studies have examined the role of alcohol consumption patterns. We examined the association between binge drinking and lung cancer. Methods: Prospective population based study of 2267 middle aged men from Finland without a history of lung cancer at baseline. Results: There were 65 cases of lung cancer during an average follow-up of 16.7 years. The relative risk (RR) of lung cancer for binge drinkers was 1.89 (95% CI 1.10-3.20) after adjusting for age, examination year, family history of cancer, smoking, socioeconomic status (SES), leisure-time physical activity and body mass index (BMI). No increased risk was observed among non-smoking binge drinkers, RR 1.48 (95% CI 0.89-2.47). Binge drinking smokers had increased risks of lung cancer in all categories of daily smoking compared with non-binge drinking smokers. The RR were 2.70 (95% CI 1.61-4.53), 2.35 (95% CI 1.38-3.96) and 2.24 (95% CI 1.29-3.80) for those who smoked 1-19, 20-29 and 30/day, respectively. Conclusion: Binge drinking is not associated with an increased risk of lung cancer among non-smokers but among smokers, it is associated with an increased risk irrespective of the number of cigarettes smoked daily. Even though the number of lung cancer cases among non-smokers was relatively small, the fact that the increased risk was limited to only smokers means that residual confounding by smoking may play a role. Larger studies are needed to clarify this association.
Cigarette smoking, alcohol consumption and primary liver cancer: A case-control study in the USA
International Journal of Cancer, 1988
Cigarette smoking and alcohol consumption were examined as potential risk factors in a case-control study of primary liver cancer (PLC). A total of 165 PLC cases and 465 matched controls from several US hospitals were studied. A weak but statistically significant (p <0.05) dose-response relationship was observed between alcohol consumption and PLC in elderly females independent of other major risk factors (adjusted OR = 1.87 and 3.48 for 1–2 and >3 drinks per day, respectively) and a similar trend was evident in elderly males. The risk for PLC was also elevated in elderly females who were current cigarette smokers (adjusted OR = 3.30). Our results suggest that alcohol consumption and cigarette smoking may have minor age- and sex-specific effects on the development of PLC, and underscore the need for further investigations to elucidate major PLC risk factors in US populations.
British journal of …, 1997
Numerous epidemiological studies have shown that alcohol and tobacco consumption are the main risk factors for oesophageal cancer in Western countries. In these studies, the consumption of both alcohol and tobacco has almost always been measured as current mean intake. The present case-control study investigates the association between alcohol and tobacco consumption and the risk of oesophageal cancer by assessing exposure as total lifetime intake, mean weekly intake, duration of consumption and former and current consumption. Between 1991 and 1994, 208 cases and 399 control subjects were selected from three French university hospitals (Caen, Dijon and Toulouse). Eligible cases were men aged less than 85 years admitted to one of these hospitals with histologically proven squamous cell carcinoma of the oesophagus. During the interview, complete tobacco and alcohol consumption histories were recorded. Our findings suggest that alcohol consumption and tobacco consumption influence the risk of oesophageal cancer in different ways. In the case of alcohol, the relationship between the odds ratio and mean weekly intake was linear, the risk depending solely on mean weekly intake, with former and current consumption having similar effects. With regard to tobacco, the relationship between the odds ratio and mean weekly intake was loglinear; the risk depended mainly on the duration of consumption and former consumption had a lesser effect than current consumption. Our study suggests that total lifetime intake is not a correct measure of exposure for either alcohol or tobacco: for a given lifetime consumption of tobacco, a moderate intake during a long period carries a higher risk than a high intake during a shorter period and, conversely, for a given lifetime consumption of alcohol, a high intake during a shorter period carries a higher risk than a moderate intake during a longer period. Our results confirm the very low risk associated with a low alcohol intake, even over long periods. In contrast, there is a steep increase in the risk associated with smoking at even low mean intakes if these are continued over long periods. Our findings also suggest that even heavy smokers may benefit from quitting.
American Journal of Epidemiology, 2010
The authors investigated the relation between alcohol consumption and lung cancer risk in the Environment and Genetics in Lung Cancer Etiology (EAGLE) Study, a population-based case-control study. Between 2002 and 2005, 2,100 patients with primary lung cancer were recruited from 13 hospitals within the Lombardy region of Italy and were frequency-matched on sex, area of residence, and age to 2,120 randomly selected controls. Alcohol consumption during adulthood was assessed in 1,855 cases and 2,065 controls. Data on lifetime tobacco smoking, diet, education, and anthropometric measures were collected. Adjusted odds ratios and 95% confidence intervals for categories of mean daily ethanol intake were calculated using unconditional logistic regression. Overall, both nondrinkers (odds ratio ¼ 1.42, 95% confidence interval: 1.03, 2.01) and very heavy drinkers (60 g/day; odds ratio ¼ 1.44, 95% confidence interval: 1.01, 2.07) were at significantly greater risk than very light drinkers (0.1-4.9 g/day). The alcohol effect was modified by smoking behavior, with no excess risk being observed in never smokers. In summary, heavy alcohol consumption was a risk factor for lung cancer among smokers in this study. Although residual confounding by tobacco smoking cannot be ruled out, this finding may reflect interplay between alcohol and smoking, emphasizing the need for preventive measures.