Population attributable risk for multimorbidity among adult women in India: Do smoking tobacco, chewing tobacco and consuming alcohol make a difference?

BACKGROUND: The present study aims to estimate the prevalence and correlates of multimorbidity among women aged 15-49 years in India. Additionally, the population attributable risk for multi-morbidity in reference to those women who smoke tobacco, chew tobacco, and consume alcohol is estimated. METHODS: The data was derived from the National Family Health Survey which was conducted in 2015-16. The effective sample size for the present paper 699,686 women aged 15-49 years in India. Descriptive statistics along with bivariate analysis were used to do the preliminary analysis. Additionally, binary logistic regression analysis was used to fulfil the objectives. RESULTS: About 1.6% of women had multimorbidity in India. The prevalence of multimorbidity was high among women from southern region of India. Women who smoke tobacco, chew tobacco and consume alcohol had 87% [AOR: 1.87CI: 1.65, 2.10], 18% [AOR: 1.18; CI: 1.10, 1.26] and 18% [AOR: 1.18; CI: 1.04, 1.33] significantly higher likelihood to suffer from multi-morbidity than their counterparts respectively. Population Attributable Risk for women who smoke tobacco was 1.2% (p<0.001), chew tobacco was 0.2% (p<0.001) and it was 0.2% (p<0.001) among women who consumed alcohol. CONCLUSION: The findings indicate the important role of lifestyle and behavioural factors such as smoking and chewing tobacco and consuming alcohol in the prevalence of multimorbidity among adult Indian women. The subgroups identified as at increased risk in the present study can be targeted while making policies and health decisions and appropriate comorbidity management can be implemented.

Joint effect of alcohol drinking and tobacco smoking on all-cause mortality and premature death in China: A cohort study.

BACKGROUND: Tobacco smoking and alcohol drinking are associated with several diseases, and studies on the joint effects of smoking and drinking are rare. OBJECTIVE: This study investigates the joint effects of tobacco smoking and alcohol drinking on all-cause and premature mortality in a contemporary cohort. METHODS: The China Health and Retirement Longitudinal Study (CHARLS) is an ongoing nationally representative survey of subjects aged over 45 years in China that was performed every two years for a total of three waves from 2011 to 2015 in China. We used weighted logistic regression models to estimate the joint effects of tobacco smoking and alcohol drinking on all-cause and premature mortality. RESULTS: After adjusting for prespecified confounders, the odds ratios (ORs) of all-cause mortality were 1.51 (95% CI: 1.09-2.10) and 1.47 (95% CI: 1.03-2.08) in smokers and smokers/drinkers, respectively. Compared with nonsmokers/nondrinkers, the OR of smokers/drinkers for premature death was 3.14 (95% CI: 1.56-6.34). In the female subgroup, there was an approximately 5-fold (OR = 4.95; 95% CI: 2.00-12.27) odds of premature mortality for smokers/drinkers compared to nonsmokers/nondrinkers. CONCLUSION: This study found a joint effect of tobacco smoking and alcohol drinking on all-cause and premature mortality among a contemporary and nationally representative cohort in China. Our results suggested that the joint effects were more pronounced in women, but further research is needed.

All-cause and cardiovascular disease mortality in underweight patients with diabetic nephropathy: BioBank Japan cohort.

We aimed to determine mortality risk in underweight patients with diabetic nephropathy for microalbuminuria or macroalbuminuria. We analyzed mortality and death-cause data from BioBank Japan, with baseline years 2003-2007. We analyzed mortality rates from all causes and ischemic heart disease, according to body mass index (<18.5, 18.5-21.9, 22-24.9 and ≥25 kg/m2 ). The mean (standard deviation) of patient age, body mass index, and glycated hemoglobin at enrollment was 61.6 years (11.7 years), 25.0 kg/m2 (4.4 kg/m2 ) and 7.7% (1.5%), respectively. Hazard ratios of all-cause and ischemic heart disease mortality were highest (1.79 [P = 0.0001] and 2.95 [P = 0.027], respectively) in patients with body mass index <18.5 kg/m2 , as compared with body mass index 22-24.9 kg/m2 . All-cause mortality risk for body mass index <18.5 kg/m2 was similar to that for current smokers (hazard ratio 1.70, P < 0.0001). Underweight could be a predictor of mortality risk in patients with diabetic nephropathy for microalbuminuria or macroalbuminuria.

Mortalidad atribuida al consumo de tabaco en Brasil, 2016 / Mortality attributed to tobacco consumption in Brazil, 2016

RESUMEN: Objetivo: Actualizar la estimación de la mortalidad atribuida al consumo de tabaco en Brasil en población de 35 y más años. Métodos: Se aplicó un método dependiente de prevalencia, basado en la fracción atribuida poblacional. Este método estima la mortalidad atribuida a partir de la mortalidad observada en Brasil (fuente: Sistema de Información de Mortalidad del Sistema Único de Salud de Brasil-2016); de las prevalencias de fumadores, exfumadores y nunca fumadores (Encuesta Nacional de Salud de Brasil-2013) y del exceso de riesgo de morir (riesgo relativo) que tienen los fumadores y exfumadores en comparación con los nunca fumadores (5 estudios de cohortes norteamericanos). Se presentan estimaciones de mortalidad atribuida globales, por sexo, grupo de edad (35-54; 55-64; 65-74 y 75 años en adelante) y 3 grupos de enfermedades: tumores malignos, enfermedades cardiometabólicas y respiratorias. Resultados: En 2016, el consumo de tabaco causó con 163.831 muertes en Brasil, el 67% (109.369) fue en hombres y cuatro de cada diez (62.791) sucedieron antes de los 65 años. El 42% de la mortalidad atribuida se asocia a enfermedades cardiometabólicas, seguidas de respiratorias (34%) y tumorales (24%), sin diferencias por sexo. Conclusión: El 14% de las muertes que sucedieron en Brasil durante 2016 en población de 35 y más años se atribuye al consumo de tabaco. Realizar de forma periódica estimaciones de MA es necesario para valorar y fortalecer las leyes de control de tabaquismo implantadas.

ABSTRACT: Objective: To update the estimation of tobacco attributable mortality (AM) in the Brazilian population aged 35 years old and older. Methods: A prevalence-dependent analysis was applied based on the population attributed fraction. This method estimates the tobacco AM taking into account the mortality observed in Brazil (source: Brazilian Mortality Information System - 2016); the prevalence of smokers, former smokers, and never smokers (National Health Survey Brazil - 2013) and the excess of risk of death (relative risk) of smokers and former smokers in comparison to never smokers (derived from 5 North American cohorts). Estimates of overall AM are shown by gender, age group (35-54; 55-64; 65-74; and 75 years old and older) and 3 groups: malignant tumors, cardiometabolic diseases, and respiratory diseases. Results: In 2016, tobacco consumption caused 163,831 deaths in Brazil, 67% (109,369) were in men and four out of ten (62,791) occurred before the age of 65. Without differences by gender, 42% of the AM is associated with cardiometabolic diseases, followed by respiratory diseases (34%) and malignant tumors (24%). Conclusion: During 2016, 14% of the deaths occurred in the Brazilian population aged 35 years old and older were attributed to tobacco consumption. Periodic tobacco AM estimations are mandatory to assess and strengthen smoking control strategies and policies.

Mortality attributed to tobacco consumption in Brazil, 2016. / Mortalidad atribuida al consumo de tabaco en Brasil, 2016.

OBJECTIVE: To update the estimation of tobacco attributable mortality (AM) in the Brazilian population aged 35 years old and older. METHODS: A prevalence-dependent analysis was applied based on the population attributed fraction. This method estimates the tobacco AM taking into account the mortality observed in Brazil (source: Brazilian Mortality Information System - 2016); the prevalence of smokers, former smokers, and never smokers (National Health Survey Brazil - 2013) and the excess of risk of death (relative risk) of smokers and former smokers in comparison to never smokers (derived from 5 North American cohorts). Estimates of overall AM are shown by gender, age group (35-54; 55-64; 65-74; and 75 years old and older) and 3 groups: malignant tumors, cardiometabolic diseases, and respiratory diseases. RESULTS: In 2016, tobacco consumption caused 163,831 deaths in Brazil, 67% (109,369) were in men and four out of ten (62,791) occurred before the age of 65. Without differences by gender, 42% of the AM is associated with cardiometabolic diseases, followed by respiratory diseases (34%) and malignant tumors (24%). CONCLUSION: During 2016, 14% of the deaths occurred in the Brazilian population aged 35 years old and older were attributed to tobacco consumption. Periodic tobacco AM estimations are mandatory to assess and strengthen smoking control strategies and policies.

OBJETIVO: Actualizar la estimación de la mortalidad atribuida al consumo de tabaco en Brasil en población de 35 y más años. MÉTODOS: Se aplicó un método dependiente de prevalencia, basado en la fracción atribuida poblacional. Este método estima la mortalidad atribuida a partir de la mortalidad observada en Brasil (fuente: Sistema de Información de Mortalidad del Sistema Único de Salud de Brasil-2016); de las prevalencias de fumadores, exfumadores y nunca fumadores (Encuesta Nacional de Salud de Brasil-2013) y del exceso de riesgo de morir (riesgo relativo) que tienen los fumadores y exfumadores en comparación con los nunca fumadores (5 estudios de cohortes norteamericanos). Se presentan estimaciones de mortalidad atribuida globales, por sexo, grupo de edad (35-54; 55-64; 65-74 y 75 años en adelante) y 3 grupos de enfermedades: tumores malignos, enfermedades cardiometabólicas y respiratorias. RESULTADOS: En 2016, el consumo de tabaco causó con 163.831 muertes en Brasil, el 67% (109.369) fue en hombres y cuatro de cada diez (62.791) sucedieron antes de los 65 años. El 42% de la mortalidad atribuida se asocia a enfermedades cardiometabólicas, seguidas de respiratorias (34%) y tumorales (24%), sin diferencias por sexo. CONCLUSIÓN: El 14% de las muertes que sucedieron en Brasil durante 2016 en población de 35 y más años se atribuye al consumo de tabaco. Realizar de forma periódica estimaciones de MA es necesario para valorar y fortalecer las leyes de control de tabaquismo implantadas.

Tobacco smoking in patients with heart failure and coronary artery disease: A 20-year experience at Duke University Medical Center.

Smoking is associated with incident heart failure (HF), yet limited data are available exploring the association between smoking status and long-term outcomes in HF with reduced vs. preserved ejection fraction (i.e., HFrEF vs. HFpEF). METHODS: We performed a retrospective analysis of HF patients undergoing coronary angiography from 1990-2010. Patients with coronary artery disease (CAD) and HF were stratified by EF (< 50% vs. ≥50%), smoking status (prior/current vs. never smoker), and level of smoking (light/moderate vs. heavy). Time-from-catheterization-to-event was examined using Cox proportional hazard modeling for all-cause mortality (ACM), ACM/myocardial infarction/stroke (MACE), and ACM/HF hospitalization with testing for interaction by HF-type (HFrEF vs. HFpEF). RESULTS: Of 14,406 patients with CAD and HF, 85% (n = 12,326) had HFrEF and 15% (n = 2080) had HFpEF. At catheterization, 61% of HFrEF and 57% of HFpEF patients had a smoking history. After adjustment, there was a significant interaction between HF-type and the association between smoking status and MACE (interaction P = .009). Smoking history was associated with increased risk for MACE in patients with HFrEF (adjusted hazard ratio [HR] 1.18 [1.12-1.24]), but not HFpEF (HR 1.01 [0.90-1.12]). Active smokers had increased mortality following adjustment compared to former smokers regardless of HF-type (HFrEF HR 1.19 [1.06-1.32], HFpEF HR 1.30 [1.02-1.64], interaction P = .50). Heavy smokers trended towards increased risk of adverse outcomes versus light/moderate smokers; these findings were consistent across HF-type (interaction P > .12). CONCLUSION: Smoking history was independently associated with worse outcomes in HFrEF but not HFpEF. Regardless of HF-type, current smokers had higher risk than former smokers.

The effect of ß-carotene on the mortality of male smokers is modified by smoking and by vitamins C and E: evidence against a uniform effect of nutrient.

A previous analysis of the Alpha-Tocopherol Beta-Carotene (ATBC) Study on male smokers found that ß-carotene supplementation increased the risk of pneumonia 4-fold in those who started smoking at the age of ≥21 years and smoked ≥21 cigarettes/d (a subgroup of 7 % of the study population). The present study hypothesised that ß-carotene increases mortality in the same subgroup. The ATBC Study (1985-1993) recruited 29 133 Finnish male smokers (≥5 cigarettes/d) aged 50-69 years. Cox regression models were constructed to estimate the effect of ß-carotene supplementation in subgroups. ß-Carotene increased mortality (risk ratio 1·56; 95 % CI 1·06, 2·3) in those who started to smoke at ≥21 years and smoked ≥21 cigarettes/d. Within this subgroup, there was strong evidence of further heterogeneity. The effect of ß-carotene supplementation was further modified by dietary vitamin C intake, fruit and vegetable intake (P = 0·0004), and by vitamin E supplementation (P = 0·011). Thus, harm from ß-carotene was not uniform within the study population. Interactions between ß-carotene and vitamins C and E were seen only within a subgroup of 7 % of the ATBC participants, and therefore should not be extrapolated to the general population. Heterogeneity of the ß-carotene effect on mortality challenges the validity of previous meta-analyses that have pooled many diverse antioxidants for one single estimate of effect using the assumption that a single estimate equally applies to all antioxidants and all people. Trial registration: ClinicalTrials.gov NCT00342992.

Loss of life expectancy from air pollution compared to other risk factors: a worldwide perspective.

AIMS: Long-term exposure of humans to air pollution enhances the risk of cardiovascular and respiratory diseases. A novel Global Exposure Mortality Model (GEMM) has been derived from many cohort studies, providing much-improved coverage of the exposure to fine particulate matter (PM2.5). We applied the GEMM to assess excess mortality attributable to ambient air pollution on a global scale and compare to other risk factors. METHODS AND RESULTS: We used a data-informed atmospheric model to calculate worldwide exposure to PM2.5 and ozone pollution, which was combined with the GEMM to estimate disease-specific excess mortality and loss of life expectancy (LLE) in 2015. Using this model, we investigated the effects of different pollution sources, distinguishing between natural (wildfires, aeolian dust) and anthropogenic emissions, including fossil fuel use. Global excess mortality from all ambient air pollution is estimated at 8.8 (7.11-10.41) million/year, with an LLE of 2.9 (2.3-3.5) years, being a factor of two higher than earlier estimates, and exceeding that of tobacco smoking. The global mean mortality rate of about 120 per 100 000 people/year is much exceeded in East Asia (196 per 100 000/year) and Europe (133 per 100 000/year). Without fossil fuel emissions, the global mean life expectancy would increase by 1.1 (0.9-1.2) years and 1.7 (1.4-2.0) years by removing all potentially controllable anthropogenic emissions. Because aeolian dust and wildfire emission control is impracticable, significant LLE is unavoidable. CONCLUSION: Ambient air pollution is one of the main global health risks, causing significant excess mortality and LLE, especially through cardiovascular diseases. It causes an LLE that rivals that of tobacco smoking. The global mean LLE from air pollution strongly exceeds that by violence (all forms together), i.e. by an order of magnitude (LLE being 2.9 and 0.3 years, respectively).

Similarities and Differences Between Sexes and Countries in the Mortality Imprint of the Smoking Epidemic in 34 Low-Mortality Countries, 1950-2014.

INTRODUCTION: The smoking epidemic greatly affected mortality levels and trends, especially among men in low-mortality countries. The objective of this article was to examine similarities and differences between sexes and low-mortality countries in the mortality imprint of the smoking epidemic. This will provide important additions to the smoking epidemic model, but also improve our understanding of the differential impact of the smoking epidemic, and provide insights into its future impact. METHODS: Using lung-cancer mortality data for 30 European and four North American or Australasian countries, smoking-attributable mortality fractions (SAMF) by sex, age (35-99), and year (1950-2014) were indirectly estimated. The timing and level of the peak in SAMF35-99, estimated using weighting and smoothing, were compared. RESULTS: Among men in all countries except Bulgaria, a clear wave pattern was observed, with SAMF35-99 peaking, on average, at 33.4% in 1986. Eastern European men experienced the highest (40%) and Swedish men the lowest (16%) peak. Among women, SAMF35-99 peaked, on average, at 18.1% in 2007 in the North American/Australasian countries and five Northwestern European countries, and increased, on average, to 7.5% in 2014 in the remaining countries (4% in Southern and Eastern Europe). The average sex difference in the peak is at least 25.6 years in its timing and at most 22.9 percentage points in its level. CONCLUSIONS: Although the progression of smoking-attributable mortality in low-mortality countries was similar, there are important unexpected sex and country differences in the maximum mortality impact of the smoking epidemic driven by cross-country differences in economic, political, and emancipatory progress. IMPLICATIONS: The formal, systematic, and comprehensive analysis of similarities and differences between sexes and 34 low-mortality countries in long-term time trends (1950-2014) in smoking-attributable mortality provided important additions to the Global Burden of Disease study and the descriptive smoking epidemic model (Lopez et al.). Despite a general increase followed by a decline, the timing of the maximum mortality impact differs more between sexes than previously anticipated, but less between regions. The maximum mortality impact among men differs considerably between countries. The observed substantial diversity warrants country-specific tobacco control interventions and increased attention to the current or expected higher smoking-attributable mortality shares among women compared to men.

Impact of nations meeting the MPOWER targets between 2014 and 2016: an update.

OBJECTIVE: Since the WHO released the Monitoring tobacco use and tobacco control policies; Protecting from the dangers of tobacco smoke; Offering help to quit tobacco; Warning the public about the dangers; Enforcing bans on advertising, promotion and sponsorship; and Raising tobacco taxes (MPOWER) policy package to assist nations with implementing the Framework Convention on Tobacco Control (FCTC), 88 countries have adopted at least one MPOWER policy at the highest level as of 2014. Building on previous evaluations, we estimated the reduction in smoking-attributable deaths (SADs) from all policies newly adopted at the highest level between 2014 and 2016. METHODS: For each nation that implemented highest level policies, the difference in policy effect sizes from previously validated SimSmoke models for the policies in effect in 2014 and 2016 were multiplied by the number of smokers in that nation to derive the reduction in the number of smokers. Based on research that half of all smokers die from smoking, we derived SADs averted. FINDINGS: In total, 43 nations adopted at least one highest-level MPOWER policy between 2014 and 2016, resulting in 14.6 million fewer SADs. The largest number of SADs averted were due to stronger health warnings (13.3 million), followed by raising taxes (0.6 million), increased marketing bans (0.4 million), smoke-free air laws (0.3 million) and cessation interventions (2500). CONCLUSION: These findings demonstrate the continuing public health impact of tobacco control policies adopted globally since the FCTC, and highlight the importance of more countries adopting MPOWER policies at the highest level to reduce the global burden of tobacco use.

Gender Differences in Labour Losses Associated with Smoking-Related Mortality.

The aim of this paper was to estimate the number of premature deaths, years of potential productive life lost (YPPLL) and labour losses attributable to tobacco smoking due to premature death by gender for the Spanish population. The human capital approach was applied. Employment, gross wage and death data were obtained from the Spanish National Institute of Statistics. Relative risks of death due to cigarette smoking and former smoking were applied. The base case used an annual discount rate of 3% and an annual labour productivity growth rate of 1%. Univariate deterministic sensitivity analysis was performed on discount rates and labour productivity growth rates. Between 2002 and 2016, smoking was estimated to cause around 13,171-13,781 annual deaths in the population under 65 years of age (legal retirement age) in Spain. This increase was mostly due to female deaths. YPPLLs for females have increased over the years, while for males they have fallen markedly. Labour losses associated with smoking mortality ranged from €2269 million in 2002 to €1541 in 2016 (base year 2016). In fact, labour productivity losses have decreased over the years for men (-39.8%) but increased sharply for women (101.6%). The evolution of monetary value of lost productivity due to smoking mortality shows clearly differentiated trends by gender.

Active Tobacco Use in Patients with Claudication Does Not Affect Outcomes after Endovascular Interventions.

BACKGROUND: With the advent of endovascular procedures, the indications for intervention in claudicants have become less strict. Many interventionalists, however, will not intervene in patients with lifestyle-limiting claudication unless they have discontinued tobacco use. Many patients are unable to comply with this goal, and there is little published evidence to suggest that continued tobacco use results in poorer outcomes. We sought to determine if it is justified to deny this group of patients endovascular, potentially lifestyle-improving, procedures based on their outcomes. METHODS: A retrospective chart review was performed between 2007 and 2011 at a midsize community teaching hospital. Patients included had documented lifestyle-limiting claudication, underwent endovascular therapy, and had no previous vascular intervention. Patients were divided into 2 groups: active smokers (AS) and nonsmokers (NS) including former and never smokers. The primary outcome was the need for reintervention and the secondary outcomes were the need for surgical revascularization, limb loss, myocardial infarction (MI), stroke, and death. RESULTS: One hundred thirty-eight patients met inclusion criteria with 89 being male (64.5%). Forty-seven (34%) were active smokers versus 91 (66%) who were nonsmokers. Mean age at initial intervention for all 138 subjects was 66.34 years (standard deviation 10.7) and was not statistically different between the AS and NS groups. Mean follow-up was 3.6 years and was not significantly different between the two groups. Between the two groups (AS vs NS), there was no statistically significant difference between the rate of reintervention, surgical bypass, and limb loss. We also did not observe any significant difference in the rate of MI, stroke, or death during our follow-up period. CONCLUSIONS: Although tobacco use has been shown to negatively impact bypass patency, our data show that it does not appear to increase the need for reintervention, conversion to open surgical revascularization, limb loss, or other morbidities in patients undergoing endovascular interventions for claudication. We continue to strongly recommend all our patients who smoke to discontinue tobacco use. Our results, however, do not support the notion that those patients who are unable to quit should be denied the potential benefit of an endovascular intervention. The most important limitation of our study is the small numbers of patients available for review. Larger studies will be necessary to confirm our findings.

The effect of smoking intensity on all-cause and cause-specific mortality-a Mendelian randomization analysis.

BACKGROUND: Smoking is an important cause of mortality and recent studies have suggested that even low-intensity smoking might be associated with increased mortality. Still, smoking is associated with lower socio-economic status as well as other potential risk factors, and disease onset might motivate smoking cessation, thus residual confounding and reverse causality might bias results. We aimed to assess the evidence of a causal relationship between smoking intensity and cause-specific as well as all-cause-mortality using Mendelian randomization analyses. METHODS: We included 56 019 participants from the Norwegian HUNT2 Study and 337 103 participants from UK Biobank, linked to national registry data on causes of death. We estimated associations of self-reported smoking as well as the genetic variant rs1051730 as an instrument for smoking intensity with all-cause and cause-specific mortality. We subsequently meta-analysed the results from the two cohorts. RESULTS: Each effect allele of the rs1051730 was associated with a 9% increased hazard of all-cause mortality [95% confidence interval (CI) 6-11] among ever smokers. Effect alleles were also associated with death by neoplasms [hazard ratio (HR) 1.11, 95% CI 1.06-1.15], circulatory diseases (HR 1.06, 95% CI 1.01-1.11) and respiratory diseases (HR 1.15, 95% CI 1.05-1.26) among ever smokers. The association was stronger among ever than never smokers for all-cause mortality (p < 0.001), neoplasms (p = 0.001) and respiratory diseases (p = 0.038). CONCLUSIONS: Our results indicate a causal effect of smoking intensity on all-cause mortality and death by neoplasms and respiratory diseases. There was weaker evidence of a causal effect of smoking intensity on death by circulatory diseases.

Tobacco Smoking and Dementia in a Kentucky Cohort: A Competing Risk Analysis.

Tobacco smoking was examined as a risk for dementia and neuropathological burden in 531 initially cognitively normal older adults followed longitudinally at the University of Kentucky's Alzheimer's Disease Center. The cohort was followed for an average of 11.5 years; 111 (20.9%) participants were diagnosed with dementia, while 242 (45.6%) died without dementia. At baseline, 49 (9.2%) participants reported current smoking (median pack-years = 47.3) and 231 (43.5%) former smoking (median pack-years = 24.5). The hazard ratio (HR) for dementia for former smokers versus never smokers based on the Cox model was 1.64 (95% CI: 1.09, 2.46), while the HR for current smokers versus never smokers was 1.20 (0.50, 2.87). However, the Fine-Gray model, which accounts for the competing risk of death without dementia, yielded a subdistribution hazard ratio (sHR) = 1.21 (0.81, 1.80) for former and 0.70 (0.30, 1.64) for current smokers. In contrast, current smoking increased incidence of death without dementia (sHR = 2.38; 1.52, 3.72). All analyses were adjusted for baseline age, education, sex, diabetes, head injury, hypertension, overweight, APOEɛ4, family history of dementia, and use of hormone replacement therapy. Once adjusted for the competing risk of death without dementia, smoking was not associated with incident dementia. This finding was supported by neuropathology on 302 of the participants.

Tobacco Smoking and Mortality in Asia: A Pooled Meta-analysis.

Importance: Understanding birth cohort-specific tobacco smoking patterns and their association with total and cause-specific mortality is important for projecting future deaths due to tobacco smoking across Asian populations. Objectives: To assess secular trends of tobacco smoking by countries or regions and birth cohorts and evaluate the consequent mortality in Asian populations. Design, Setting, and Participants: This pooled meta-analysis was based on individual participant data from 20 prospective cohort studies participating in the Asia Cohort Consortium. Between September 1, 2017, and March 31, 2018, a total of 1 002 258 Asian individuals 35 years or older were analyzed using Cox proportional hazards regression analysis and random-effects meta-analysis. The pooled results were presented for mainland China; Japan; Korea, Singapore, and Taiwan; and India. Exposures: Tobacco use status, age at starting smoking, number of cigarettes smoked per day, and age at quitting smoking. Main Outcomes and Measures: Country or region and birth cohort-specific mortality and the population attributable risk for deaths from all causes and from lung cancer. Results: Of 1 002 258 participants (51.1% women and 48.9% men; mean [SD] age at baseline, 54.6 [10.4] years), 144 366 deaths (9158 deaths from lung cancer) were ascertained during a mean (SD) follow-up of 11.7 (5.3) years. Smoking prevalence for men steadily increased in China and India, whereas it plateaued in Japan and Korea, Singapore, and Taiwan. Among Asian male smokers, the mean age at starting smoking decreased in successive birth cohorts, while the mean number of cigarettes smoked per day increased. These changes were associated with an increasing relative risk of death in association with current smoking in successive birth cohorts of pre-1920, 1920s, and 1930 or later, with hazard ratios for all-cause mortality of 1.26 (95% CI, 1.17-1.37) for the pre-1920 birth cohort, 1.47 (95% CI, 1.35-1.61) for the 1920s birth cohort, and 1.70 (95% CI, 1.57-1.84) for the cohort born in 1930 or later. The hazard ratios for lung cancer mortality were 3.38 (95% CI, 2.25-5.07) for the pre-1920 birth cohort, 4.74 (95% CI, 3.56-6.32) for the 1920s birth cohort, and 4.80 (95% CI, 3.71-6.19) for the cohort born in 1930 or later. Tobacco smoking accounted for 12.5% (95% CI, 8.4%-16.3%) of all-cause mortality in the pre-1920 birth cohort, 21.1% (95% CI, 17.3%-24.9%) of all-cause mortality in the 1920s birth cohort, and 29.3% (95% CI, 26.0%-32.3%) of all-cause mortality for the cohort born in 1930 or later. Tobacco smoking among men accounted for 56.6% (95% CI, 44.7%-66.3%) of lung cancer mortality in the pre-1920 birth cohort, 66.6% (95% CI, 58.3%-73.5%) of lung cancer mortality in the 1920s birth cohort, and 68.4% (95% CI, 61.3%-74.4%) of lung cancer mortality for the cohort born in 1930 or later. For women, tobacco smoking patterns and lung cancer mortality varied substantially by countries and regions. Conclusions and Relevance: In this study, mortality associated with tobacco smoking continued to increase among Asian men in recent birth cohorts, indicating that tobacco smoking will remain a major public health problem in most Asian countries in the coming decades. Implementing comprehensive tobacco-control programs is warranted to end the tobacco epidemic.

Effects of smoking on outcomes of hematopoietic cell transplantation: a systemic review and future directions.

Hematopoietic cell transplantation (HCT) survivors are at risk of increased mortality compared to the general population. Smoking by HCT survivors has been reported to impact a variety of health outcomes, resulting in an increased risk for infections, cardio-pulmonary diseases, and cancer. The purpose of our study was to conduct a systematic literature search to determine the relationship between tobacco smoking pre-HCT and post-HCT outcomes. We conducted an electronic literature search from all languages from multiple peer-reviewed databases of studies that evaluated the effects of tobacco smoking prior to HCT on clinical outcomes. Data were extracted from the studies according to a strict selection criterion. Due to differences in primary endpoint and different populations evaluated in different studies, a meta-analysis was not possible, and a descriptive quantitative analysis is provided. Out of the 447 publications fulfilling the selection criteria for the electronic search, 17 articles were included in the final sample. The studies varied in terms of study design, patient characteristics, and HCT type. Considerable variability in definition of smoking was observed. We found that smoking pre-HCT was associated with a higher incidence of cardiovascular diseases, new infections, pulmonary complications, and cancers in comparison to non-smokers. Moreover, smoking pre-HCT was significantly associated with increased risks of both relapse and non-relapse mortality, and inversely related to median overall survival. Smoking adversely affects mortality in all HCT survivors by increasing the risks of both malignant and non-malignant complications. Thus, guidelines are urgently needed to formulate lifestyle factor modifications for HCT survivors focusing on smoking cessation strategies and abstinence maintenance in former smokers. Given the strength of these findings, guidelines should include systematic definitions of smoking for use in clinical trials as well as in standardized data reporting.

Longitudinal study to assess impact of smoking at diagnosis and quitting on 1-year survival for people with non-small cell lung cancer.

OBJECTIVES: To update the prevalence of smoking in people as they were diagnosed with non-small cell lung cancer (NSCLC) and to see whether smoking status at baseline and quitting are independently associated with 1-year survival. DESIGN: A real-world cohort study following patients from diagnosis for up to 1 year or until death. SETTING: UK multi-centre study (28 sites) based in secondary and primary care. PARTICIPANTS: 1124 patients with newly diagnosed NSCLC between 2010-2016. MAIN OUTCOME MEASURES: Smoking status was validated at diagnosis and at every routine and emergency hospital visit. Cancer treatments were offered according to local multi-disciplinary team decisions following UK guidelines and smoking cessation treatments offered according to local practice /availability. Survival analysis and Cox Proportional Hazards Modelling examined the associations of a) smoking at baseline and b) quitting smoking, on survival at 1 year. RESULTS: 77% of never smokers, 60% of ex-smokers and 57% of current smokers, were alive at 1 year (p = 0.01). After adjusting for age, stage, EGOG, surgery and gender, ex smokers (adjusted HR 1.96, 95% CI 1.16-2.31) and current smokers (aHR 2.04, 1.19-3.48) were both more likely to die within one year. 23% of smokers with NSCLC quit within 3 months of diagnosis. At 1 year, 69% of those who quit were alive versus 53% of those who continued to smoke (p < 0.01). After adjusting the risk of dying was lower (aHR 0.75), in those who quit smoking, although this was not statistically significant (p = 0.23). CONCLUSIONS: This is the largest prospective study that validates smoking in NSCLC; it shows a third of people are smoking at the time of diagnosis. Smokers have lower 12-month survival than never and ex -smokers. Quitting smoking was associated with 25% reduction in mortality which may be clinically important although not statistically significant, after adjusting for other factors.

Smoking Status and Survival Among a National Cohort of Lung and Colorectal Cancer Patients.

INTRODUCTION: The purpose of this study was to explore the association of smoking status and clinically relevant duration of smoking cessation with long-term survival after lung cancer (LC) or colorectal cancer (CRC) diagnosis. We compared survival of patients with LC and CRC who were never-smokers, long-term, medium-term, and short-term quitters, and current smokers around diagnosis. METHODS: We studied 5575 patients in Cancer Care Outcomes Research and Surveillance (CanCORS), a national, prospective observational cohort study, who provided smoking status information approximately 5 months after LC or CRC diagnosis. Smoking status was categorized as: never-smoker, quit >5 years prior to diagnosis, quit between 1-5 years prior to diagnosis, quit less than 1 year before diagnosis, and current smoker. We examined the relationship between smoking status around diagnosis with mortality using Cox regression models. RESULTS: Among participants with LC, never-smokers had lower mortality risk compared with current smokers (HR 0.71, 95% CI 0.57 to 0.89). Among participants with CRC, never-smokers had a lower mortality risk as compared to current smokers (HR 0.79, 95% CI 0.64 to 0.99). CONCLUSIONS: Among both LC and CRC patients, current smokers at diagnosis have higher mortality than never-smokers. This effect should be further studied in the context of tumor biology. However, smoking cessation around the time of diagnosis did not affect survival in this sample. IMPLICATIONS: The results from our analysis of patients in the CanCORS consortium, a large, geographically diverse cohort, show that both LC and CRC patients who were actively smoking at diagnosis have worse survival as compared to never-smokers. While current smoking is detrimental to survival, cessation upon diagnosis may not mitigate this risk.

A dynamic, modifiable model for estimating cost-effectiveness of smoking cessation interventions in pregnancy: application to an RCT of self-help delivered by text message.

BACKGROUND AND AIMS: Previous evaluations of smoking cessation interventions in pregnancy have several limitations. Our solution to these limitations is the Economics of Smoking in Pregnancy (ESIP) model, which estimates the life-time cost-effectiveness of smoking cessation interventions in pregnancy from a National Health Service (NHS) and personal social services perspective. We aim to (1) describe how ESIP has been constructed and (2) illustrate its use with trial data. METHODS: ESIP links mothers' and offspring pregnancy outcomes to estimate the burdens of smoking-related disease they experience with different rates of smoking in pregnancy, both in pregnancy and throughout their life-times. Smoking rates are inputted by model users. ESIP then estimates the costs of treating disease burdens and also mothers' and offspring life-years and quality-adjusted life years (QALYs). By comparing costs incurred and healthy life following different smoking rates, ESIP estimates incremental cost-effectiveness and benefit-cost ratios for mothers or offspring or both combined. We illustrate ESIP use using data from a pragmatic randomized controlled trial that tested a smoking cessation intervention in pregnancy. RESULTS: Throughout women's and offspring life-times, the intervention proved cheaper than usual care, having a negative incremental cost of £38.37 (interquartile range = £21.46-56.96) and it improved health, demonstrating a 0.04 increase in incremental QALYs for mothers and offspring, implying that it is 'dominant' over usual care. Benefit-cost ratios suggested that every £1 spent would generate a median of £14 (interquartile range = £8-20) in health-care savings. CONCLUSIONS: Economics of Smoking in Pregnancy is the first economic model to link mothers' and infants' costs and benefits while reporting cost-effectiveness in readily-comparable units. Using ESIP with data from a trial which reported only short-term economic analysis showed that the intervention was very likely to be cost-effective in the longer term and to generate health-care savings.