Lung Cancer and Lifestyle Factors: Umbrella Review.

This review explores the effect of common everyday factors, such as alcohol, tea and coffee consumption, on the risk for lung cancer. We performed an umbrella review of current systematic reviews. The risk for lung cancer was increased with alcohol or coffee intake and decreased with tea intake. While evidence for alcohol is of low quality, the effect of coffee may be confounded by the smoking effect. The protective effect of tea intake is present, but the evidence is also of low quality.

Evaluating interactions of polygenic risk scores and NAT2 genotypes with tobacco smoking in bladder cancer risk.

Tobacco smoking is the most important risk factor for bladder cancer. Previous studies have identified the N-acetyltransferase (NAT2) gene in association with bladder cancer risk. The NAT2 gene encodes an enzyme that metabolizes aromatic amines, carcinogens commonly found in tobacco smoke. In our study, we evaluated potential interactions of tobacco smoking with NAT2 genotypes and polygenic risk score (PRS) for bladder cancer, using data from the UK Biobank, a large prospective cohort study. We used Cox proportional hazards models to measure the strength of the association. The PRS was derived using genetic risk variants identified by genome-wide association studies for bladder cancer. With an average of 10.1 years of follow-up of 390 678 eligible participants of European descent, 769 incident bladder cancer cases were identified. Current smokers with a PRS in the highest tertile had a higher risk of developing bladder cancer (HR: 6.45, 95% CI: 4.51-9.24) than current smokers with a PRS in the lowest tertile (HR: 2.41, 95% CI: 1.52-3.84; P for additive interaction = <.001). A similar interaction was found for genetically predicted metabolizing NAT2 phenotype and tobacco smoking where current smokers with the slow NAT2 phenotype had an increased risk of developing bladder cancer (HR: 5.70, 95% CI: 2.64-12.30) than current smokers with the fast NAT2 phenotype (HR: 3.61, 95% CI: 1.14-11.37; P for additive interaction = .100). Our study provides support for considering both genetic and lifestyle risk factors in developing prevention measures for bladder cancer.

Association between a family history of cancer and multiple primary lung cancer risks: a population-based analysis from China.

OBJECTIVES: The incidence of multiple primary lung cancer (MPLC) has increased in recent years. The risk factors of MPLC are not well studied, especially in the Asian population. This case-control study investigated the association between a family history of cancer and MPLC risk. METHODS: We used data from people who surgically confirmed MPLC with at least 2 nodes of Fujian Medical University Union Hospital and matched 1:2 normal individuals as controls between 2016 and 2017. Information on age, sex, lifestyle, personal history, and family history of cancer was collected using a self-administered questionnaire, and odds ratios (OR) were estimated using unconditional logistic regression. RESULTS: We included 2 104 patients. In total, 321 patients with histologically confirmed MPLC and 642 healthy controls were studied. The significantly higher ratio of current smokers was observed for the cases than the controls (54.1% vs. 30.0%). A family history of LC in first-degree relatives of the cases reported a significantly higher proportion than in the controls (15.3% vs. 8.6%). Family history of all cancers and LC significantly increased the risk of MPLC (OR = 1.64, P = 0.009 and OR = 2.59, P = 0.000, respectively). The multivariate analysis identified a significantly increased risk of MPLC (OR = 2.45, P = 0.000) associated with parents and siblings influenced by LC history. The younger age (aged < 55 years) of LC cases at diagnosis exhibited a significantly increased risk of MPLC (OR = 2.39, P = 0.000). A significant association with a family history of LC was found for male squamous carcinoma and male adenocarcinoma (OR = 1.59, p = 0.037 and OR = 1.64, p = 0.032, respectively). A positive association with LC history was only observed for female adenocarcinoma (OR = 2.23, p = 0.028). The risk of MPLC was not significantly associated with A family history of cancers in non-smokers (OR = 0.91, P = 0.236). Ever-smokers with a positive family history of cancer or LC had a significantly elevated risk of MPLC (OR = 4.01, P = 0.000 and OR = 6.49, P = 0.000, respectively). We also observed a very elevated risk for smokers with no family history (OR = 3.49, P = 0.000). Such a positive association was also observed in ever-smokers with no family history of LC (OR = 3.55, P = 0.000). Adenocarcinoma in females was prevalent and significantly associated with a family history of LC in risk of MPLC compared with other histologic subtypes. CONCLUSIONS: Our findings suggest an association between a family history of LC and MPLC risk among an Asian population. Smoking status and family history of LC have a synergistic effect on MPLC. These findings indicate that MPLC exhibits familiar aggregation and that inherited genetic susceptibility may contribute to the development of MPLC.

Effects of cigarette smoking on semen quality, reproductive hormone levels, metabolic profile, zinc and sperm DNA fragmentation in men: results from a population-based study.

Background: Cigarette smoking seems to have a negative impact on men's reproductive health, but our knowledge of its effects on the reproductive function of Russian men is still very limited. The purpose of this study was to evaluate the effect of cigarette smoking on semen quality, including sperm DNA fragmentation, hormonal, zinc and metabolic status in young men from the general multi-ethnic Russian population (n=1,222, median age 23 years) and to find out the ethno-specific effects of smoking by comparing male groups of different ethnicity. Methods: Each participant filled out a standardized questionnaire, provided one blood and semen sample. Semen parameters, serum reproductive hormones, lipids, glucose, uric acid and seminal zinc were analyzed. Participants were classified as smokers (n=450) and non-smokers (n=772), and smokers were stratified into moderate (≤10 cigarettes/day) and heavy (>10 cigarettes/day) smokers. Results: In the entire study population, heavy smokers were characterized by a decrease in semen volume, total sperm count, sperm concentration and motility, and an increase in sperm DNA fragmentation and teratozoospermia compared with non-smokers (p<0.05). There was also a reduction in the serum and seminal zinc level as well as an impairment in metabolic health in smokers compared with non-smokers (p<0.05). No significant differences between smokers and non-smokers were found for serum levels of LH, FSH, inhibin B, testosterone and estradiol. In the second part of our study, the most numerous ethnic groups of Slavs (n=654), Buryats (n=191), and Yakuts (n=125) were selected from the entire study population. Among three ethnic groups, the smoking intensity was higher in Slavs than in Buryats or Yakuts suggesting a greater tobacco addiction in Slavs than in Asians. A decrease in semen parameters and seminal zinc levels, and an increase in sperm DNA fragmentation and teratozoospermia was observed only in smoking Slavs (p<0.05); moderate decrease in testosterone and increase in triglyceride levels were revealed in smoking Yakuts (p<0.05), but no significant changes were detected in smoking Buryats. Conclusion: We concluded that cigarette smoking has an ethno-specific effect on male reproductive function, probably due to the different activity of the seminal antioxidant system, which is yet to be elucidated.

Smoking Cessation and Pancreatic Cancer Risk in Individuals With Prediabetes and Diabetes: A Nationwide Cohort Study.

BACKGROUND: Individuals with diabetes and prediabetes are at increased risk of pancreatic cancer. However, little is known about the effects of smoking or smoking cessation on pancreatic cancer risk in individuals with diabetes and prediabetes. We investigated the association between smoking status (particularly smoking cessation) and pancreatic cancer risk according to glycemic status. PATIENTS AND METHODS: This nationwide cohort study included 9,520,629 adults without cancer who underwent the Korean National Health Screening in 2009 and were followed until 2018. Hazard ratios and 95% confidence intervals for pancreatic cancer were estimated after adjusting for potential confounders. RESULTS: During the 78.4 million person-years of follow-up, 15,245 patients were newly diagnosed with pancreatic cancer. Among individuals with diabetes and prediabetes, current smoking synergistically increased pancreatic cancer risk (all P<.01). However, quitters with diabetes and prediabetes had a pancreatic cancer risk comparable to that of never-smokers (all P>.05). For pancreatic cancer in current smokers, quitters, and never-smokers, respectively, the hazard ratios were 1.48 (95% CI, 1.40-1.58), 1.11 (95% CI, 1.03-1.19), and 1.00 (reference) among individuals with normoglycemia; 1.83 (95% CI, 1.70-1.97), 1.28 (95% CI, 1.18-1.39), and 1.20 (95% CI, 1.14-1.26) among individuals with prediabetes; and 2.72 (95% CI, 2.52-2.94), 1.78 (95% CI, 1.63-1.95), and 1.63 (95% CI, 1.54-1.72) among individuals with diabetes. There were no differences in risk between quitters with a <20 pack-year smoking history and never-smokers in all glycemic status groups. CONCLUSIONS: Pancreatic cancer risk synergistically increased in current smokers with diabetes and prediabetes. However, smoking cessation reduced the synergistically increased risk of pancreatic cancer to the level of never-smokers, especially when smoking history was <20 pack-years. More individualized and intensive cancer prevention education should be underscored for individuals at an increased risk of pancreatic cancer beyond the one-size-fits-all approach.

Relationship between smoking and tuberculosis recurrence: A systematic review and meta-analysis.

INTRODUCTION: Of the problems in tuberculosis (TB) control program is the recurrence of this disease. In some studies, smoking has been reported as the most important risk factor. Therefore, the present study aimed at examining the association between smoking and tuberculosis recurrence using meta-analysis. METHODS: To report the findings of this meta-analysis, we used PRISMA. The protocol of this study has been recorded in PROSPERO. The research question has been formulated based on PICO, and the search was performed using both MeSH and non-MeSH keywords. After screening and selecting the articles and evaluating their quality using the NOS checklist, the overall estimate of the odds ratio of tuberculosis recurrence in smokers was assessed with a 95% confidence interval. RESULTS: Fourteen studies met the inclusion criteria. The total number of samples in the group of patients with tuberculosis recurrence was 1988 with 855 (43%) smokers, and in the group of patients affected by tuberculosis without recurrence, it was 27,226 with 7503 (27.56%) smokers. In 13 studies, the odds ratio of tuberculosis recurrence was higher in smokers; this difference was statistically significant in 12 of them. Combining the results of these 14 studies, the odds ratio of tuberculosis recurrence in smokers was 2.10 times higher, using the random effects model (95% CI:1.69, 2.61). CONCLUSION: Based on the results of study present, smoking increases the risk of tuberculosis recurrence. Therefore, to eradicate tuberculosis by 2030, more serious interventions should be taken to quit smoking, which in turn reduces the incidence of tuberculosis.

Nicotine Use During Pregnancy: Cessation and Treatment Strategies.

Abstract: The use of tobacco and nicotine products during pregnancy is known to increase the risk of adverse effects on the fetus. Increased education and research have resulted in greater rates of smoking cessation during pregnancy, with a decline from 13.2% of pregnant individuals smoking in 2006 to 7.2% in 2016. However, smoking while pregnant still proves to be a prevalent issue that is associated with numerous adverse outcomes, including low birth weight, preterm birth, and developmental delays. Smoking cessation before or during pregnancy can help mitigate these effects, but the appropriate treatment can be challenging to ascertain. Accordingly, clinicians should look to provide individualized care composed of behavioral counseling in conjunction with pharmacotherapies when indicated, combined with ongoing support and education.

Smoking and the risk of atopic dermatitis: A two-sample mendelian randomization study.

Atopic dermatitis (AD) is considered to be one of the most common chronic diseases. It has been shown that smoking is associated with atopic dermatitis, but previous studies were mainly observational, which may be biased. The present study conducted a 2-sample mendelian randomization (MR) study to investigate the causal relationship. The present study obtained data on "ever smoked" and "atopic dermatitis" from published large-scale genome-wide association studies. The data were obtained from the UK Biobank and BioBank Japan. Three methods were used to perform a 2-sample MR analysis and also performed sensitivity analysis. The odds ratio and 95% confidence interval (CI) between smoking and AD calculated by MR-Egger regression, weighted median, and random-effects inverse variance weighting method were 1.096 (95% CI.756-1.587) and 1.159 (95% CI 1.040-1.292), respectively, 1.137 (95% CI .975-1.325). The inverse variance weighting method showed statistical significance between the 2 and a causal relationship between smoking and AD. In conclusion, the results of our MR analysis suggest that smoking is likely to affect the incidence of AD.

Development of an Electronic Health Record-Based Algorithm for Predicting Lung Cancer Screening Eligibility in the Population-Based Research to Optimize the Screening Process Lung Research Consortium.

PURPOSE: Lung cancer screening (LCS) guidelines in the United States recommend LCS for those age 50-80 years with at least 20 pack-years smoking history who currently smoke or quit within the last 15 years. We tested the performance of simple smoking-related criteria derived from electronic health record (EHR) data and developed and tested the performance of a multivariable model in predicting LCS eligibility. METHODS: Analyses were completed within the Population-based Research to Optimize the Screening Process Lung Consortium (PROSPR-Lung). In our primary validity analyses, the reference standard LCS eligibility was based on self-reported smoking data collected via survey. Within one PROSPR-Lung health system, we used a training data set and penalized multivariable logistic regression using the Least Absolute Shrinkage and Selection Operator to select EHR-based variables into the prediction model including demographics, smoking history, diagnoses, and prescription medications. A separate test data set assessed model performance. We also conducted external validation analysis in a separate health system and reported AUC, sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and accuracy metrics associated with the Youden Index. RESULTS: There were 14,214 individuals with survey data to assess LCS eligibility in primary analyses. The overall performance for assigning LCS eligibility status as measured by the AUC values at the two health systems was 0.940 and 0.938. At the Youden Index cutoff value, performance metrics were as follows: accuracy, 0.855 and 0.895; sensitivity, 0.886 and 0.920; specificity, 0.896 and 0.850; PPV, 0.357 and 0.444; and NPV, 0.988 and 0.992. CONCLUSION: Our results suggest that health systems can use an EHR-derived multivariable prediction model to aid in the identification of those who may be eligible for LCS.

Contribution of smoking, disease history, and survival to lung cancer disparities in Black individuals.

BACKGROUND: Lung cancer is the leading cause of cancer deaths and disproportionately affects self-identified Black or African American ("Black") people, especially considering their relatively low self-reported smoking intensity rates. This study aimed to determine the relative impact of smoking history and lung cancer incidence risk, histology, stage, and survival on these disparities. METHODS: We used 2 lung cancer models (MichiganLung-All Races and MichiganLung-Black) to understand why Black people have higher rates of lung cancer deaths. We studied how different factors, such as smoking behaviors, cancer development, histology, stage at diagnosis, and lung cancer survival, contribute to these differences. RESULTS: Adjusted for smoking history, approximately 90% of the difference in lung cancer deaths between the overall and Black populations (born in 1960) was the result of differences in the risk of getting lung cancer. Differences in the histology and stage of lung cancer and survival had a small impact (4% to 6% for each). Similar results were observed for the 1950 and 1970 birth cohorts, regardless of their differences in smoking patterns from the 1960 cohort. CONCLUSIONS: After taking smoking into account, the higher rate of lung cancer deaths in Black people can mostly be explained by differences in the risk of developing lung cancer. As lung cancer treatments and detection improve, however, other factors may become more important in determining differences in lung cancer mortality between the Black and overall populations. To prevent current disparities from becoming worse, it is important to make sure that these improvements are available to everyone in an equitable way.

Association between smoking and incident back pain: A prospective cohort study with 438 510 participants.

Background: Although smoking is a known potential contributor to back pain, there is still a lack of quantitative studies on the effects of different doses on back pain (BP) occurrence, including a lack of a longitudinal cohorts. To address this gap, we aimed to investigate the association between various smoking-related exposures and back pain incidence to advance global efforts toward smoking cessation and guide primary prevention of BP. Methods: In this prospective cohort study, we retrieved data on 438 510 patients from the UK Biobank who were free of back pain and who were recruited in 2006-2010, and followed them up from baseline through 1 April 2022. We extracted data on smoking-related exposures, including smoking status (SS), number of cigarettes smoked daily (CPD), and pack-years of own smoking (PY) and examined back pain incidence as an outcome. We used a Cox proportional hazard model adjusted for several covariates, multiple imputation methods, and population attribution fraction. Results: During the median follow-up of 12.98 years, 31 467 participants developed BP, with incidence rates in former and current smokers of 1.13 (95% confidence interval (CI) = 1.10-1.16, P < 0.000) and 1.50 (95% CI = 1.45-1.56, P < 0.000), respectively. The hazard ratios (HRs) of participants who smoked more than 30 CPD and those with more than 30 PY were 1.45 (95% CI = 1.36-1.55, P < 0.000) and 1.45 (95% CI = 1.40-1.50, P < 0.000), respectively. Relative to male, female smokers were at more risk of developing BP. Not smoking, quitting smoking, and reducing CPD and PY could lower the BP risk by 7.8%, 5.4%, 9.8%, and 18.0%, respectively. Conclusions: Ever smoking, higher cigarette consumption daily, and increased smoking intensity were associated with an increased BP risk. This association was stronger in female smokers. Not smoking, smoking cessation, and reducing smoking volume and intensity were effective measures to prevent BP occurrence.

Environmental Causes of Idiopathic Pulmonary Fibrosis.

Idiopathic pulmonary fibrosis (IPF), the most common and severe of the idiopathic interstitial pneumonias, is a chronic and relentlessly progressive disease, which occurs mostly in middle-aged and elderly males. Although IPF is by definition "idiopathic", multiple factors have been reported to increase disease risk, aging being the most prominent one. Several occupational and environmental exposures, including metal dust, wood dust and air pollution, as well as various lifestyle variables, including smoking and diet, have also been associated with an increased risk of IPF, probably through interaction with genetic factors. Many of the predisposing factors appear to act also as trigger for acute exacerbations of the disease, which herald a poor prognosis. The more recent literature on inhalation injuries has focused on the first responders in the World Trade Center attacks and military exposure. In this review, we present an overview of the environmental and occupational causes of IPF and its pathogenesis. While our list is not comprehensive, we have selected specific exposures to highlight based on their overall disease burden.

The effect of a smoking cessation program for patients in cancer treatment: a quasi-experimental intervention study.

BACKGROUND: Compared to non-smokers, smokers have reduced effects of cancer treatment, and increased risk of treatment-related toxicity. Quitting smoking can improve treatment effects and reduce side effects. This study reports on the potential impact of a smoking cessation program on smoking cessation rates among patients in cancer treatment. MATERIAL AND METHODS: Cancer patients 18 years and older who smoked, with survival prognosis ≥12 months, not suffering dementia or other mental illness, and who were referred to cancer treatment at six Norwegian hospitals were invited to participate. The study took place from 2017 to 2020 and used a pre-test-posttest non-equivalent control group design. The intervention group received structured smoking cessation guidance based on Motivational Interviewing combined with cost-free nicotine replacement products, while the control group received standard smoking cessation treatment. Self-reported smoking status were registered at baseline and at 6 months' follow up. RESULTS: 76% of patients smoked at baseline and 44% at follow-up in the intervention group, correspondingly 72% and 49% in the control group. In an analysis of differences in within-person change, the reduction in the intervention group was 13 percentage points larger (95% CI = (0.25, -0.005), p = 0.041). Adjusting for gender, age, education, labour market participation and partnership status did not attenuate the estimated effect (18 percentage point difference, 95% CI = (-0.346, -0.016), p = 0.032). Demographic factors and dropout rate differed somewhat between the groups with a higher dropout rate in the intervention group, 54% vs. 51%, respectively). CONCLUSION: Offering a structured smoking cessation program based on Motivational Interviewing and cost-free nicotine replacement products to cancer patients can increase cessation rates in comparison to standard smoking cessation care.

Effect of Smoking Cessation on the Risk of Subarachnoid Hemorrhage: A Nested Case-Control Study in Korean Men.

BACKGROUND: Smoking is a well-established risk factor for subarachnoid hemorrhage (SAH), and current smokers have an increased risk of SAH. However, there are insufficient data on whether smoking cessation in current smokers reduces the risk of SAH. METHODS: A nested case-control study was conducted based on the National Health Insurance Service-National Health Screening Cohort, which comprises nationwide health claims data and a national health screening program in Korea (2002-2019). We constructed a cohort of current male smokers without a history of stroke at the baseline health screening (2002-2003). From this cohort, cases were defined as individuals who experienced a nontraumatic SAH during the follow-up period up to 2019. Five controls were matched to each case using incidence density sampling. Smoking status (continuation or cessation) before the occurrence of SAH was evaluated using the repeated national health screening program. We conducted a multivariable conditional logistic regression analysis, adjusting for alcohol consumption, physical activity, body mass index, systolic blood pressure, and fasting blood glucose levels, to evaluate the association between SAH risk and smoking cessation. RESULTS: At baseline, there were 112 142 current male smokers. After excluding individuals with prior stroke or insufficient data, the cohort consisted of 105 223 eligible participants (mean age, 50.3±8.5 years). Among them, we identified 318 cases of SAH and 1590 matched controls. Those who quit smoking had a significantly lower risk of SAH compared with current smokers (adjusted odds ratio, 0.55 [95% CI, 0.41-0.73]). The risk of SAH decreased with a longer period of smoking cessation. The risk reduction with smoking cessation was consistent even among prior heavy smokers. CONCLUSIONS: Smoking cessation in current male smokers reduced the risk of SAH, and the risk reduction was greater as the cessation period increased. These findings warrant intensive efforts to encourage smokers, even heavy smokers, to quit.

Global disease burden and its attributable risk factors of peripheral arterial disease.

Peripheral arterial disease (PAD) is a prevalent subtype of atherosclerotic cardiovascular diseases. It is crucial to assess the PAD-related burden and its attributable risk factors. We use the Global Burden of Disease study 2019 database to calculate the incidence, prevalence, mortality, disability-adjusted life years (DALY), attributable risk factors and estimated annual percentage change. The disease burden of PAD grows significantly with age accompanied by prominent heterogeneity between male and female. Despite the increase in the absolute numbers of disease burden from 1990 to 2019, the global PAD-related age-standardized death rate (ASDR) and age-standardized disability-adjusted life years rate (ASDALYR) have a mild downward trend from 1990 to 2019, which negatively correlated with sociodemographic index (SDI). Smoking and high systolic blood pressure (SBP) were the primary attributable risk factors for males (ASDR: 33.4%; ASDALYR: 43.4%) and females (ASDR: 25.3%; ASDALYR: 27.6%), respectively. High fasting plasma glucose (FPG) had become the second risk factor for ASDR (males: 28.5%; females: 25.2%) and ASDALYR (males: 29.3%; females: 26.3%) with an upward tendency. Low-middle SDI regions were predicted to have the most remarkable upward trend of PAD-related burden caused by high FPG. Smoking caused more disease burden in males before 85-90 years old and females before 65-70 years old, while high FPG and high SBP caused more burden after that. The patterns of PAD-related burden and its attributable risk factors are heterogeneous across ages, genders, and SDI regions. To reduce disease burden, tailored strategies should be implemented.

Cancer-prone Phenotypes and Gene Expression Heterogeneity at Single-cell Resolution in Cigarette-smoking Lungs.

Single-cell RNA sequencing (scRNA-seq) technologies have been broadly utilized to reveal molecular mechanisms of respiratory pathology and physiology at single-cell resolution. Here, we established single-cell meta-analysis (scMeta-analysis) by integrating data from eight public datasets, including 104 lung scRNA-seq samples with clinicopathologic information and designated a cigarette-smoking lung atlas. The atlas revealed early carcinogenesis events and defined the alterations of single-cell transcriptomics, cell population, and fundamental properties of biological pathways induced by smoking. In addition, we developed two novel scMeta-analysis methods: VARIED (Visualized Algorithms of Relationships In Expressional Diversity) and AGED (Aging-related Gene Expressional Differences). VARIED analysis revealed expressional diversity associated with smoking carcinogenesis. AGED analysis revealed differences in gene expression related to both aging and smoking status. The scMeta-analysis paves the way to utilize publicly-available scRNA-seq data and provide new insights into the effects of smoking and into cellular diversity in human lungs, at single-cell resolution. SIGNIFICANCE: The atlas revealed early carcinogenesis events and defined the alterations of single-cell transcriptomics, cell population, and fundamental properties of biological pathways induced by smoking.

Longstanding smoking associated with frontal brain lobe atrophy: a 32-year follow-up study in women.

OBJECTIVE: To examine the association between midlife tobacco smoking and late-life brain atrophy and white matter lesions. METHODS: The study includes 369 women from the Prospective Population Study of Women in Gothenburg, Sweden. Cigarette smoking was reported at baseline 1968 (mean age=44 years) and at follow-up in 1974-1975 and 1980-1981. CT of the brain was conducted 32 years after baseline examination (mean age=76 years) to evaluate cortical atrophy and white matter lesions. Multiple logistic regressions estimated associations between midlife smoking and late-life brain lesions. The final analyses were adjusted for alcohol consumption and several other covariates. RESULTS: Smoking in 1968-1969 (adjusted OR 1.85; 95% CI 1.12 to 3.04), in 1974-1975 (OR 2.37; 95% CI 1.39 to 4.04) and in 1980-1981 (OR 2.47; 95% CI 1.41 to 4.33) were associated with late-life frontal lobe atrophy (2000-2001). The strongest association was observed in women who reported smoking at all three midlife examinations (OR 2.63; 95% CI 1.44 to 4.78) and in those with more frequent alcohol consumption (OR 6.02; 95% CI 1.74 to 20.84). Smoking in 1980-1981 was also associated with late-life parietal lobe atrophy (OR 1.99; 95% CI 1.10 to 3.58). There were no associations between smoking and atrophy in the temporal or occipital lobe, or with white matter lesions. CONCLUSION: Longstanding tobacco smoking was mainly associated with atrophy in the frontal lobe cortex. A long-term stimulation of nicotine receptors in the frontal neural pathway might be harmful for targeted brain cell.

Lung Cancer Risk Attributable to Active Smoking in China: A Systematic Review and Meta-Analysis.

Objective: No consensus exists on the relative risk ( RR) of lung cancer (LC) attributable to active smoking in China. This study aimed to evaluate the unified RR of LC attributable to active smoking among the Chinese population. Methods: A systematic literature search of seven databases was conducted to identify studies reporting active smoking among smokers versus nonsmokers in China. Primary articles on LC providing risk estimates with their 95% confidence intervals ( CIs) for "ever" "former" or "current" smokers from China were selected. Meta-analysis was used to estimate the pooled RR of active smoking. Results: Forty-four unique studies were included. Compared with that of nonsmokers, the pooled RR (95% CI) for "ever" "former" and "current" smokers were 3.26 (2.79-3.82), 2.95 (1.71-5.08), and 5.16 (2.58-10.34) among men, 3.18 (2.78-3.63), 2.70 (2.08-3.51), and 4.27 (3.61-5.06) among women, and 2.71 (2.12-3.46), 2.66 (2.45-2.88), and 4.21 (3.25-5.45) in both sexes combined, respectively. Conclusion: The RR of LC has remained relatively stable (range, 2-6) over the past four decades in China. Early quitting of smoking could reduce the RR to some extent; however, completely refraining from smoking is the best way to avoid its adverse effects.

Associations of smoking and alcohol consumption with the development of open angle glaucoma: a retrospective cohort study.

OBJECTIVES: To investigate the associations of alcohol consumption and smoking with the development of perimetric glaucoma in patients with suspected glaucoma. DESIGN: A retrospective cohort study of patients suspected to have glaucoma enrolled in the Diagnostic Innovations in Glaucoma Study (DIGS) and the African Descent and Glaucoma Evaluation Study (ADAGES). SETTING: Three tertiary glaucoma centres in the USA. PARTICIPANTS: 825 eyes of 610 patients with glaucoma suspect eyes with normal visual fields (VF) at baseline were followed over an average of 9 years from the DIGS and ADAGES studies. OUTCOME MEASURES: Development of glaucoma was defined as occurrence of three consecutive abnormal VF tests during follow-up. Univariable and multivariable Cox regression models were used to investigate lifestyle-related factors associated with development of VF loss over time. RESULTS: VF tests were abnormal three times in a row in 235 (28.5%) eyes. Alcohol consumption was associated with a higher risk of developing glaucoma (HR 1.57, 95% CI 1.03 to 2.38, p=0.037). In men, the risk of developing glaucoma in alcohol drinkers (HR 1.92, 95% CI 1.00 to 3.68, p=0.048) was greater than non-alcohol drinkers. In individuals of African descent, the risk of developing glaucoma in alcohol drinkers (HR 1.79, 95% CI 1.02 to 3.15, p=0.043) was greater than non-alcohol drinkers. Age was a modifier of the relationship between smoking and glaucomatous VF defects (p=0.048). The risk of developing glaucoma in smokers (HR 1.73, 95% CI 1.10 to 2.72, p=0.019) was greater than never smokers after adjustment for confounding factors in older patients (age >61 years). CONCLUSION: Alcohol consumption was associated with an increased risk of developing glaucoma, particularly in men and individuals of African descent. The risk of developing glaucoma among smokers suspected of having glaucoma was influenced by age, with older individuals having a higher risk than younger people. TRIAL REGISTRATION NUMBER: NCT00221897 and NCT00221923.