21st-Century Hazards of Smoking and Benefits of Cessation in the United States

Center for Global Health Research, Toronto, ON M5C 1N8, Canada.
New England Journal of Medicine (Impact Factor: 55.87). 01/2013; 368(4):341-50. DOI: 10.1056/NEJMsa1211128
Source: PubMed


Extrapolation from studies in the 1980s suggests that smoking causes 25% of deaths among women and men 35 to 69 years of age in the United States. Nationally representative measurements of the current risks of smoking and the benefits of cessation at various ages are unavailable.
We obtained smoking and smoking-cessation histories from 113,752 women and 88,496 men 25 years of age or older who were interviewed between 1997 and 2004 in the U.S. National Health Interview Survey and related these data to the causes of deaths that occurred by December 31, 2006 (8236 deaths in women and 7479 in men). Hazard ratios for death among current smokers, as compared with those who had never smoked, were adjusted for age, educational level, adiposity, and alcohol consumption.
For participants who were 25 to 79 years of age, the rate of death from any cause among current smokers was about three times that among those who had never smoked (hazard ratio for women, 3.0; 99% confidence interval [CI], 2.7 to 3.3; hazard ratio for men, 2.8; 99% CI, 2.4 to 3.1). Most of the excess mortality among smokers was due to neoplastic, vascular, respiratory, and other diseases that can be caused by smoking. The probability of surviving from 25 to 79 years of age was about twice as great in those who had never smoked as in current smokers (70% vs. 38% among women and 61% vs. 26% among men). Life expectancy was shortened by more than 10 years among the current smokers, as compared with those who had never smoked. Adults who had quit smoking at 25 to 34, 35 to 44, or 45 to 54 years of age gained about 10, 9, and 6 years of life, respectively, as compared with those who continued to smoke.
Smokers lose at least one decade of life expectancy, as compared with those who have never smoked. Cessation before the age of 40 years reduces the risk of death associated with continued smoking by about 90%.

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    • "Indeed, smoking alone may explain as much as 25% of the risk of mortality at midlife (Jha et al. 2013). It therefore follows that modifying health behaviors drastically reduces morbidity and mortality (Hyland, Barnoya and Corral 2012; Jha et al. 2013). Health behaviors are routinely modified in both individuals and throughout whole populations as a result of trends in political, economic, and technological change. "
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    ABSTRACT: Education is a fundamental cause of social inequalities in health because it influences the distribution of resources, including money, knowledge, power, prestige, and beneficial social connections, that can be used in situ to influence health. Recent studies have highlighted early-life cognition as commonly indicating the propensity for educational attainment and determining health and age of mortality. Health behaviors provide a plausible mechanism linking both education and cognition to later-life health and mortality. We examine the role of education and cognition in predicting smoking, heavy drinking, and physical inactivity at midlife using data from the Wisconsin Longitudinal Study (N = 10,317), National Survey of Health and Development (N = 5,362), and National Childhood Development Study (N = 16,782). Adolescent cognition was associated with education but was inconsistently associated with health behaviors. Education, however, was robustly associated with improved health behaviors after adjusting for cognition. Analyses highlight structural inequalities over individual capabilities when studying health behaviors. © American Sociological Association 2015.
    Journal of Health and Social Behavior 09/2015; 56(3):323-40. DOI:10.1177/0022146515594188 · 2.72 Impact Factor
    • "Smoking is a leading cause of preventable death and disability worldwide (Knopik et al., 2012; Schroeder, 2013; Thun et al., 2013; Whiteford and Baxter, 2013), and smoking cessation greatly diminishes the increased risk of mortality (Jha et al., 2013). Two pharmacotherapies have been shown to be more effective than others for smoking cessation: combination Nicotine Replacement Therapy (cNRT) and varenicline (Fiore and Baker, 2011; Fiore et al., 2008; Piper et al., 2009). "
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    ABSTRACT: Recent evidence suggests that the efficacy of smoking cessation pharmacotherapy can vary across patients based on their genotypes. This study tests whether the coding variant rs16969968 in the CHRNA5 nicotinic receptor gene predicts the effects of combination nicotine replacement therapy (cNRT) and varenicline on treatment outcomes. In two randomized smoking cessation trials comparing cNRT vs. placebo, and varenicline vs. placebo, we used logistic regression to model associations between CHRNA5 rs16969968 and abstinence at end of treatment. For abstinence at end of treatment, there was an interaction between cNRT and rs16969968 (X(2)=8.15, df=2, omnibus-p=0.017 for the interaction); individuals with the high-risk AA genotype were more likely to benefit from cNRT. In contrast, varenicline increased abstinence, but its effect did not vary with CHRNA5. However, the genetic effects differed between the placebo control groups across two trials (wald=3.94, df=1, p=0.047), this non-replication can alter the interpretation of pharmacogenetic findings. Results from two complementary smoking cessation trials demonstrate inconsistent genetic results in the placebo arms. This evidence highlights the need to compare the most effective pharmacotherapies with the same placebo control to establish pharmacogenetic evidence to aid decisions on medication choice for patients trying to quit smoking. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    Drug and alcohol dependence 06/2015; 154. DOI:10.1016/j.drugalcdep.2015.06.022 · 3.42 Impact Factor
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    • "Detailed smoking information was available for 50% of the participants with a history of smoking. Cigarette smoking in the US promotes at least a 10-year reduction in life expectancy (Jha et al., 2013), which may create a survivor bias due to premature death. In other words, the study of the effects of smoking in elders will be inescapably biased toward the healthiest smokers—those individuals who survived or did not experience significant smoking-related morbidity (Chang et al., 2012; Kukull, 2001). "
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    ABSTRACT: Background Cigarette smoking in adults is associated with abnormalities in brain neurobiology. Smoking-induced central nervous system oxidative stress (OxS) is a potential mechanism associated with these abnormalities. The goal of this study was to compare cognitively-normal elders on cerebrospinal fluid (CSF) levels of F2-isoprostane biomarkers of OxS. Methods Elders with a lifetime history of smoking (smokers; n = 50; 75 ± 5 years of age; 34 ± 28 pack-years; approximately 12% were actively smoking at the time of study) were compared to never-smokers (n = 61; 76 ± 6 years of age) on CSF iPF2α-III and 8,12, iso-iPF2α-VI F2-isoprostanes levels. F2-isoprostanes levels were quantitated with HPLC-atmospheric pressure chemical ionization-tandem mass spectrometry. Associations between F2-isoprostanes levels, hippocampal volumes, and cigarette exposure measures were also evaluated. Results Smokers showed higher iPF2α-III level than never-smokers. An age x smoking status interaction was observed for 8,12, iso-iPF2α-VI, where smokers demonstrate a significantly greater concentration with increasing age than non-smokers. In smokers only, higher 8,12, iso-iPF2α-VI concentration was associated with smaller hippocampal volume, and greater iPF2α-III level was related to greater pack years. Conclusions This is the first study to demonstrate that a history of cigarette smoking in cognitively-normal elders was associated with significantly elevated CSF F2-isoprostane levels and greater age-related increases in F2-isoprostane levels, and that higher F2-isoprostane levels in smokers were related to smaller hippocampal volume. These findings provide additional novel evidence that a history of chronic smoking during adulthood is associated with adverse effects on the human brain that are potentially persistent even with extended smoking cessation.
    Drug and Alcohol Dependence 09/2014; 142. DOI:10.1016/j.drugalcdep.2014.06.030 · 3.42 Impact Factor
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