Robert P. Murray

Whether menthol cigarettes confer a higher risk of death than plain cigarettes is not known. The Lung Health Study (LHS) enrolled 5,887 adult smokers in a clinical trial of smoking cessation and ipratropium in the prevention of chronic obstructive pulmonary disease. LHS participants have been subjected to surveillance for mortality from all causes for 14 years. We examined these data for differences between self-reported smokers of menthol cigarettes versus plain cigarettes. Using proportional hazards regression methods, we found no differences in hazard ratios for coronary heart disease, cardiovascular disease, lung cancer, or death from any cause. Contrary to expectations about nicotine dependence, we found that users of menthol cigarettes had smoked fewer pack-years at baseline. We found no difference in success at smoking cessation with or without menthol. We conclude that our data contain no evidence that mentholation of cigarettes increases the hazards of smoking.

We describe the persistence of discrepancies between biochemical measures of smoking and self-reported smoking status in a cohort of clinical trial participants across 5 years. The Lung Health Study, a randomized trial in 10 clinical centers in North America, enrolled 3923 participants in smoking intervention and 1964 in usual care in 1987 and 1988. Smoking status was assessed at baseline and at five annual follow-up visits by selfreport, salivary cotinine and expired-air carbon monoxide. Compared to self-report, sensitivity and specificity of cotinine and carbon monoxide were similar across 5 years. Evidence of error in self-reports of quitting smoking persisted across 5 years, although it declined over time. Multivariate models confirmed that self-report bias was characteristic of the early years in the study. Significant covariates differed between cotinine and carbon monoxide models. When cotinine was used for verification, about half of the individuals in the smoking intervention group with self-report bias at the first year continued to exhibit bias for 5 years. In absolute terms, the errors associated with measurement were small, but they persisted over 5 years. Some differences appeared to be related to the distinction that carbon monoxide verification was immediate, while cotinine verification was deferred.

The health effects of a binge pattern of alcohol consumption have not been widely investigated. The objective of this study was to evaluate the cardiovascular consequences of binge drinking (consumption of eight or more drinks at one sitting) and usual (nonbinge) drinking in a longitudinal, population-based study. Data obtained from 1,154 men and women aged 18–64 years interviewed in Winnipeg, Manitoba, Canada, in 1990 and 1991 were linked to health care utilization and mortality records. Using an 8-year follow-up period, the authors performed separate Cox proportional hazards regression analyses for men and women on time to first event for physician visits, hospitalizations, and deaths due to coronary heart disease, hypertension, and other cardiovascular disease. Binge drinking increased the risk of coronary heart disease in both men (hazard ratio (HR) = 2.26, 95% confidence interval (CI): 1.22, 4.20) and women (HR = 1.10, 95% CI: 1.02, 1.18). It increased the risk of hypertension in men (HR = 1.57, 95% CI: 1.04, 2.35) but not in women. Binge drinking had no effect on the risk of other cardiovascular disease. In contrast, usual drinking had significant cardioprotective effects in both men and women. Thus, the harmful effects of binge drinking on cardiovascular disease morbidity and mortality can be disaggregated from the protective effects of usual drinking at various levels of consumption.

This paper evaluates the hypothesis that Black smokers will respond differently than Whites to a smoking cessation intervention program where no adjustments are made in recognition of cultural differences. The responses of Black smokers who were recruited into the Lung Health Study (LHS) to the smoking cessation intervention are described. Black quit rates are compared with those of Whites. The LHS enrolled 5887 men and women smokers, aged 35–60 years, of whom 3923 were randomized to a group cessation intervention and 1964 to usual care. Blacks and Whites from six clinics who had complete covariate data (200 Blacks and 2868 Whites) were compared on baseline smoking characteristics and subsequent smoking cessation outcomes. Logistic models were constructed to adjust for baseline smoking variables and demographic characteristics to evaluate the effect of treatment group on smoking cessation among Blacks and Whites. At baseline, Blacks reported smoking fewer cigarettes than Whites, but had higher mean levels of salivary cotinine. The adjusted odds ratio of quitting at 1 year for the smoking intervention group vs. the usual care group was 1.48 for Blacks and 5.99 for Whites. This difference between Blacks and Whites was highly significant (p = 0.002). Across 5 years, the adjusted odds ratios of quitting were 1.87 for Blacks and 3.34 for Whites (p = 0.06). Although the treatment effect was stronger for Whites than for Blacks, over the 5 years of the study there was a significant treatment effect for Blacks. Indicators of physical dependence on nicotine at baseline were inconsistent in indicating whether Blacks were more dependent. We conclude that Blacks and Whites differed significantly in their response to the LHS group smoking intervention program.

It has been proposed that social integration would act as a confounder in the relationship between alcohol consumption and all-cause mortality. This study tested the assumption that the J-shaped relationship between drinking and all-cause mortality may partly reflect a protective effect of social integration, to the extent that moderate drinkers are more socially integrated than either abstainers or heavy drinkers, and to the extent that social integration offers direct protection from mortality. This hypothesis was tested using data from 10,832 of the 12,866 men in the Multiple Risk Factor Intervention Trial (MRFIT). Indicators of social integration were derived from an exploratory factor analysis of 25 relevant items in the MRFIT data and from a scale of six items selected by the investigators. We failed to confirm a direct protective effect of social integration. Nondrinkers had the highest rates of all-cause mortality. Compared with heavy drinking, relative risks of all-cause mortality for abstinence, light and moderate drinking were unaffected by inclusion of social integration variables in the proportional hazards models. The MRFIT data fail to confirm a confounding effect of social integration.