Lung cancer is a leading cause of cancer-related deaths worldwide, with rising incidence in resource-limited settings. Research suggests an increased risk of lung cancer in individuals with a history of pulmonary tuberculosis (TB), but the association needs further clarification. This systematic review aims to provide a more comprehensive understanding of this relationship.

We systematically searched the PubMed/Medline, EMBASE, and Scopus databases for relevant studies up to March 15, 2024. The quality of the included studies was assessed using the Joanna Briggs Institute (JBI) critical appraisal checklist. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using either random-effects or fixed-effects models, depending on the level of heterogeneity. All statistical analyses were performed using Comprehensive Meta-Analysis Software, version 3.0.

A total of 37 studies were included (9 cohort and 28 case-control). A significant association between prior pulmonary TB and lung cancer was found in both cohort (OR: 2.3; 95% CI, 1.4-3.8) and case-control (OR: 1.9; 95% CI, 1.4-2.5) studies. Subgroup analyses revealed a stronger association in East Asia (OR: 2.4; 95% CI, 1.3-4.1).

Our study provides strong evidence of an increased risk of lung cancer following pulmonary TB. The findings emphasize the need for comprehensive public health strategies, including targeted screening, early detection, and smoking cessation. Future studies should investigate the mechanisms linking TB and lung cancer, as well as the effectiveness of integrated prevention programs, particularly in high-burden regions.

The possible association between history of pulmonary tuberculosis (TB) and lung cancer (LC) has attracted researchers' attention for several decades. This systematic review and meta-analysis aim to assess the association between previous pulmonary TB infection and LC risk.

A Systematic and comprehensive search was performed in the following databases: PubMed, Embase, clinical key, Web of Science and Google Scholar, in articles and abstracts published from 1987 to 2021. Thirty-two articles (involving 50,290 cases and 846,666 controls) met the inconclusive criteria. The Comprehensive Meta-Analysis version 2.2 software was used for this meta-analysis.

The result of this meta-analysis demonstrates that pre-existing active pulmonary TB increases the risk of LC (RR = 2.170, 95% confidence interval [CI] 1.833-2.569, p < .001, I² = 91.234%). The results showed that the risk of the history of active pulmonary TB infection in adenocarcinoma was 2.605 (95% CI 1.706-3.979, p < .001, I² = 55.583%), in small-cell carcinoma was 2.118 (95% CI 1.544-2.905, p < .001, I² = 0.0%), in squamous-cell carcinoma, was 3.570 (95% CI 2.661 - 4.791, p < .001, I² = 42.695%) and 2.746 (95% CI 2.300-3.279, p < .001, I² = 41.686%) for other histological types of LCs. According to these results, a history of active pulmonary TB increases the risk of LC.

This study emphasizes the importance of LC screening in pulmonary TB patients even after the infection is treated. With the increased chances of LC in a patient who had a history of active pulmonary TB, there could be a need for a further follow-up period after pulmonary TB recovery.

Tobacco use disorder (TUD), previously known as nicotine dependence, was associated with increased risk of lung cancer. However, little is known about the prevalence of TUD and symptom manifestation in smokers with lung cancer.

The aim of the present study was to investigate the prevalence of TUD using DSM-5 diagnostic criteria in patients diagnosed with lung cancer and analyze their tobacco use characteristics.

A total of 200 histologically confirmed lung cancer patients who used tobacco within the prior 12-month period at the time of diagnosis were recruited for this study. Participants were assessed using interviewer-administered questionnaires to determine TUD symptoms and smoking-related behaviors, and self-administered Fagerstrom Test for Nicotine Dependence (FTND) was also administered.

The prevalence of DSM-5 TUD was 92.0% (n = 184). Of a total of 200 subjects, 23 (11.5%), 35 (17.5%), and 126 (63.0%) were classified into mild, moderate, and severe TUD categories, respectively. A total of 19 (81.3%) moderate TUD and 98 (77.8%) severe TUD patients had attempted smoking cessation. Of these subjects, 21 (21.4%) severe TUD and 12 (63.2%) moderate TUD patients tried more than three times. The number of satisfied criteria under DSM-5 TUD was positively correlated with FTND score, cumulative lifetime smoking amount, and daily smoking levels.

Smokers diagnosed with lung cancer showed a high prevalence of DSM-5 TUD. Their heavy and consistent tobacco use suggests reduced motivation to abstain from smoking.

Lung cancer (LC) is often diagnosed late when curative intervention is no longer viable. However, current referral guidelines (e.g. UK National Institute for Health and Care Excellence guidelines) for suspected LC are based on a weak evidence base. Aim. The purpose of this systematic review is to identify symptoms that are independently associated with LC and to identify the key methodological issues relating to symptomatic diagnosis research in LC.

Medline, Ovid and Cumulative Index to Nursing and Allied Health Literature were searched for the period between 1946 and 2012 using the MeSH terms 'lung cancer' and 'symptom*'. Quality of each paper was assessed using Scottish Intercollegiate Guidelines Network and Consolidated Criteria for Reporting Qualitative Research Checklists and checked by a second and third reviewer.

Evidence regarding the diagnostic values of most symptoms was inconclusive; haemoptysis was the only symptom consistently indicated as a predictor of LC. Generally, evidence was weakened by methodological issues such as the lack of standardized data collection (recording bias) and the lack of comparability of findings across the different studies that extend beyond the spectrum of disease. Qualitative studies indicated that patients with LC experienced symptoms months before diagnosis but did not interpret them as serious enough to seek health care. Therefore, early LC symptoms might be under-represented in primary care clinical notes.

Current evidence is insufficient to suggest a symptom profile for LC across the disease stages, nor can it be concluded that classical LC symptoms are predictors of LC apart from, perhaps, haemoptysis. Prospective studies are now needed that systematically record symptoms and explore their predictive values for LC diagnosis.

The association between body mass index (BMI) and lung cancer is still disputed because of possible residual confounding by smoking and preclinical weight loss in case-control studies. We examined this association using data from the multicenter ICARE study in France, a large, population-based case-control study.

A total of 2,625 incident lung cancer cases and 3,381 controls were included. Weight was collected at interview, 2 years before the interview, and at age 30. Lifetime smoking exposure was calculated using the comprehensive smoking index (CSI). Adjusted odds ratios (aORs) and 95 % confidence intervals were estimated by unconditional logistic regression and controlled for age, area, education, CSI, occupational exposure, previous chronic bronchitis, and parental history of lung cancer. We also examined the role of weight change. Analyses were stratified by smoking status and sex.

When compared with that of men with normal BMI 2 years before the interview, lung cancer aORs (95 % CI) among men with BMIs of <18.5, 25-29.9, 30-32.4, and ≥32.5 kg/m(2) were 2.7 (95 % CI 1.2-6.2), 0.9 (95 % CI 0.7-1.1), 0.8 (95 % CI 0.6-1.1), and 0.8 (95 % CI 0.6-1.0), respectively (p(trend) = 0.02). Results were more pronounced among current smokers and were similar in men and women. Weight gain over time was associated with a significant decreased risk of lung cancer.

We found an inverse dose-dependent association between lung cancer risk and BMI 2 years prior to interview in current smokers. IMPACT STATEMENT: BMI might be an individual factor impacting the risk of lung cancer related to smoking's carcinogen-induced DNA damage.

A behavioral phenotype that characterizes nicotine dependence, the time to first cigarette after waking, is hypothesized to increase the risk of lung cancer.

A case-control study of histologically confirmed lung cancer was conducted. The current analysis included 4775 lung cancer cases and 2835 controls who were regular cigarette smokers.

Compared with subjects who smoked their first cigarette > 60 minutes after waking, the pack-years-adjusted odds ratio was 1.31 (95% confidence interval [95% CI], 1.11-1.54) for subjects who smoked 31 minutes to 60 minutes after waking and 1.79 (95% CI, 1.56-2.07) for subjects who smoked within 30 minutes of waking. The risk estimates were similar when smoking was modeled as total years, smoking status (current vs former), number of cigarettes smoked per day, years since quitting, and excess odds ratio. The findings were consistent for all histologic types of lung cancer.

The findings of the current study indicate that a specific nicotine dependence phenotype that is associated with the amount of smoke uptake per cigarette is independently associated with lung cancer risk. These findings may help to identify high-risk individuals who would benefit from targeted interventions.

A behavioral phenotype that characterizes nicotine dependence, the time to first cigarette after waking, is hypothesized to increase the risk of head and neck cancer.

A case-control study of histologically confirmed head and neck cancer was conducted that included 1055 cases and 795 controls with a history of cigarette smoking.

The pack-years-adjusted odds ratio was 1.42 (95% confidence interval [95% CI], 1.02-1.99) for an interval of 31 minutes to 60 minutes to first cigarette after waking and 1.59 (95% CI, 1.19-2.11) for an interval of 1 minute to 30 minutes. The risk estimates were similar when smoking was modeled as total years, smoking status (current vs former), number of cigarettes smoked per day, years since quitting, and excess odds ratio. Findings were consistent for cancers of the floor of the mouth, palate, and pharynx.

Time to first cigarette is an indicator of increased nicotine dependence, smoke uptake, and risk of head and neck cancer. This high-risk group of individuals would benefit from targeted smoking interventions.

There has been conflicting evidence concerning the possible association between tuberculosis (TB) and subsequent risk of lung cancer. To investigate whether currently published epidemiological studies can clarify this association, we performed a systematic review of 37 case-control and 4 cohort studies (published between January 1966 and January 2009) and a meta-analysis of risk estimates, with particular attention to the role of smoking, passive smoking and the timing of diagnosis of TB on this relationship. Data for the review show a significantly increased lung cancer risk associated with preexisting TB. Importantly, the association was not due to confounding by the effects of tobacco use (RR=1.8, 95% confidence interval (CI)=1.4-2.2, among never smoking individuals), lifetime environmental tobacco smoke exposure (RR=2.9, 95%CI=1.6-5.3, after controlling) or the timing of diagnosis of TB (the increased lung cancer risk remained 2-fold elevated for more than 20 years after TB diagnosis). Interestingly, the association was significant with adenocarcinoma (RR=1.6, 95%CI=1.2-2.1), but no significant associations with squamous and small cell type of lung cancer were observed. Although no causal mechanism has been demonstrated for such an association, present study supports a direct relation between TB and lung cancer, especially adenocarcinomas.

Previous studies have suggested that physical activity may lower lung cancer risk. The association of physical activity with reduced chronic inflammation provides a potential mechanism, yet few studies have directly related inflammatory markers to cancer incidence. The relation among physical activity, inflammation, and lung cancer risk was evaluated in a prospective cohort of 4,831 subjects, 43 to 86 years of age, in Beaver Dam, Wisconsin. A total physical activity index was created by summing up kilocalories per week from sweat-inducing physical activities, city blocks walked, and flights of stairs climbed. Two inflammatory markers, WBC count and serum albumin, were measured at the baseline examination. During an average of 12.8 years of follow-up, 134 incident cases of lung cancer were diagnosed. After multivariable adjustment, participants in the highest tertile of total physical activity index had a 45% reduction in lung cancer risk compared with those in the lowest tertile (hazard ratio, 0.55; 95% confidence interval, 0.35-0.86). Participants with WBC counts in the upper tertile (>or=8 x 10(3)/microL) were 2.81 (95% confidence interval, 1.58-5.01) times as likely to develop lung cancer as those with counts in the lowest tertile (<6.4 x 10(3)/microL). Serum albumin was not related to lung cancer risk. There was no evidence that inflammation mediated the association between physical activity and lung cancer risk, as the physical activity risk estimates were essentially unchanged after adjustment for WBC count. Although the potential for residual confounding by smoking could not be eliminated, these data suggest that physical activity and WBC count are independent risk factors for lung cancer.

Molecular epidemiological approaches are being used to study how physical activity may protect against cancer. Prior epidemiological data suggest that physical activity protects against lung cancer; however, interpretation of these data is complicated by potential confounding by smoking. Glutathione (GSH) detoxifies cigarette smoke carcinogens and the paper tests whether physical activity levels are associated with blood GSH levels. Study subjects were enrolled in a chemoprevention trial testing whether antioxidant micronutrient supplementation reduces genetic damage from cigarette smoking. Physical activity data were collected by questionnaire from 178 subjects at 12 months of follow-up in the trial. Total GSH (tGSH), which is the sum of free and protein-bound GSH and glutathione disulfide levels, was measured using the 5,5'-dithiobis-(2-nitrobenzenoic acid) colormetric assay with red blood cell samples collected at the 12-month time point. In multivariate linear regression analyses that controlled for gender and cigarettes smoked per day, tGSH was positively associated with hours per week of moderate intensity activity (beta=0.005, p=0.02). Hours per week of vigorous intensity activity were unassociated with tGSH and the effect of moderate activity remained after control for vigorous activity. The results are consistent with prior research showing differential effects of moderate and vigorous activity and suggest a mechanism through which physical activity may influence lung cancer risk.

To calculate a pooled estimate of relative risk (RR) of lung cancer associated with exposure to passive smoking in never smoking women exposed to smoking spouses. This study is an updated meta-analysis that also assesses the differences between estimated risks according to continent and study type using meta-regression.

From a total of 101 primary studies, 55 studies are included in this meta-analysis, of which, 7 are cohort studies, 25 population-based case-control and 23 non-population-based case-control studies. Twenty previously published meta-analyses are also reviewed. Fixed and random effect models and meta-regression are used to obtain pooled estimates of RR and P-value functions are used to demonstrate consistency of results.

The pooled RR for never-smoking women exposed to passive smoking from spouses is 1.27 (95% CI 1.17-1.37). The RR for North America is 1.15 (95% CI 1.03-1.28), Asia, 1.31 (95% CI 1.16-1.48) and Europe, 1.31 (1.24-1.52). Sequential cumulative meta-analysis shows no trend. There is no strong evidence of publication bias.

The abundance of evidence, consistency of finding across continent and study type, dose-response relationship and biological plausibility, overwhelmingly support the existence of a causal relationship between passive smoking and lung cancer.

We conducted a qualitative review to estimate for adults (1) the lifetime and current prevalence of DSM/ICD-defined nicotine dependence and (2) the prevalence of individual DSM/ICD dependence criteria. Systematic computer searches and other methods located eleven population-based surveys of adults (>or=18 year olds) and two of young adults (18-30 year olds). In the USA and Germany, about 25% of adults had been dependent on nicotine in their lifetime, including 15% who were currently dependent. Similar or higher rates were seen in Asian men but <5% of Asian women had been dependent. About a third of ever-smokers and half of current smokers either had been or were currently dependent on nicotine and this did not consistently differ by age, country or sex. Impaired control over tobacco use was the most commonly endorsed criteria and giving up activities to use and spending lots of time with nicotine were the least commonly endorsed. Nicotine dependence is one of the most common mental disorders; however, about half of current smokers do not meet DSM/ICD dependence criterion.

Research conducted predominantly in male populations on physical activity and lung cancer has yielded inconsistent results. We examined this relationship among 416,277 men and women from the European Prospective Investigation into Cancer and Nutrition (EPIC). Detailed information on recent recreational, household and occupational physical activity, smoking habits and diet was assessed at baseline between 1992 and 2000. Relative risks (RR) were estimated using Cox regression. During 6.3 years of follow-up we identified 607 men and 476 women with incident lung cancer. We did not observe an inverse association between recent occupational, recreational or household physical activity and lung cancer risk in either males or females. However, we found some reduction in lung cancer risk associated with sports in males (adjusted RR = 0.71; 95% confidence interval 0.50-0.98; highest tertile vs. inactive group), cycling (RR = 0.73; 0.54-0.99) in females and non-occupational vigorous physical activity. For occupational physical activity, lung cancer risk was increased for unemployed men (adjusted RR = 1.57; 1.20-2.05) and men with standing occupations (RR = 1.35; 1.02-1.79) compared with sitting professions. There was no evidence of heterogeneity of physical activity associations across countries, or across any of the considered cofactors. For some histologic subtypes suggestive sex-specific reductions, limited by subgroup sizes, were observed, especially with vigorous physical activity. In total, our study shows no consistent protective associations of physical activity with lung cancer risk. It can be assumed that the elevated risks found for occupational physical activity are not produced mechanistically by physical activity itself but rather reflect exposure to occupation-related lung cancer risk factors.

A case-control study was conducted to investigate the relationship between diet and the risk of lung cancer among women non-smokers and to compare with women smokers in the same population. Data collected by personal interviews from 435 microscopically confirmed cases and 1710 controls were analysed using unconditional logistic regression. In addition to results for all study subjects, associations between diet and lung cancer risk were compared between two highly contrasting groups: smokers (odds ratio (OR) 7.03) and non-smokers (OR 1.00). A protective effect of frequent (daily or several times per week) black tea drinking appeared among non-smoking women (OR 0.65, 95% confidence interval (CI) 0.43-0.99). Among smoking women, protective effects were observed for frequent intake of milk/dairy products (OR 0.56, 95% CI 0.32-0.96), coffee (OR 0.47, 95% CI 0.25-0.88), and wine consumption (daily or weekly OR 0.60, 95% CI 0.37-0.98; monthly OR 0.60, 95% CI 0.39-0.94). Inverse associations with the risk appeared for physical exercise for smokers only, and for the body mass index both among non-smoking and smoking women. Some items of diet may contribute to variation in risk among women in the Czech Republic; their importance seems to vary in relation to their status in smoking, the dominant factor in the aetiology of lung cancer.

Comprehensive reviews of lifestyle changes and dietary supplements that may prevent bladder cancer are needed in order to facilitate discussions between clinicians and patients.

Novel data exist that numerous lifestyle/diet and dietary supplements may lower the risk of this disease. For example, reducing arsenic exposure, incorporating dietary changes, and vitamin E supplements continue to accumulate research that supports their use with some patients at a higher risk for this disease. Regardless, smoking cessation seems to have the largest impact on reducing risk and incorporating these other changes after smoking cessation may reduce an individual's risk to an even greater extent.

However, a large percentage of cases of individuals diagnosed with this cancer apparently have no known etiology. Diets lower in calories or possibly specific sub-types of fat, and higher in fruits and especially vegetables, seem to provide some protection. Other dietary/supplement options may affect risk, but these benefits could be seriously attenuated by smoking. Dietary selenium, but currently not selenium supplements, may also affect risk, especially in non-smokers. Dietary vitamin E, and vitamin E supplements, may provide some protection. Non-selective (e.g. non-steroidal anti-inflammatory drugs) and selective cyclooxygenase-2 inhibitors are generating interest because bladder tumors seem to contain higher concentrations of this enzyme. Drinking-water quality, especially arsenic concentrations, may seriously affect risk. Providing recommendations for patients with regard to some of these lifestyle modifications is currently recommended because the majority of these alterations are also recommended currently for cardiovascular or general oncology disease reduction.

We examined the association between physical activity and lung cancer in a prospective cohort of 27,087 male smokers, ages 50-69 years, enrolled in the Alpha-Tocopherol, Beta Carotene Cancer Prevention (ATBC) Study. After an average of 10 years of follow-up, 1,442 lung cancer cases were diagnosed. Cox proportional hazards models were used to estimate the relative risk (RR) and 95% confidence intervals (CI) of lung cancer associated with self-reported occupational and leisure-time activity, adjusted for age, supplement group, body mass index, cigarettes smoked daily, years of smoking, education, energy intake and vegetable intake. There were no associations between occupational, leisure-time or combined categories of physical activity with lung cancer risk; however, age appeared to modify the effect of leisure-time activity (p = 0.02). Within increasing quartiles of age, the RRs (CI) for men active in leisure time compared to sedentary men were 0.77 (0.54-1.09), 0.74 (0.57-0.95), 1.09 (0.89-1.33) and 1.03 (0.88-1.21). These data suggest that among smokers, neither occupational nor leisure-time activity is associated with lung cancer risk. There may, however, be some modest risk reduction associated with leisure activity among younger smokers. Published 2002 Wiley-Liss, Inc.

Few data are available to explain the ongoing increase in lung cancer mortality among Czech women. The study is aimed at examining the role of smoking and known or suspected cofactors.

Data collected by in-person interviews from 269 female lung cancer cases and 1079 controls were analyzed using unconditional logistic regression and other methods.

Cigarette smoking was the most important factor associated with excess risk of lung cancer among women. Risk was increased both among current smokers (OR = 10.30), long-term ex-smokers (> or =10 years ago; OR = 3.79), and short-term ex-smokers (<10 years ago; OR = 14.63), all compared against never-smokers. In addition, significant associations with risk were found for chronic cough, chronic phlegm of less than 2-year duration, and shortness of breath. Inverse associations emerged for physical exercise and body mass index. Excess risk associated with consumption of red meat and poultry, and protective effects associated with intake of vegetables were restricted to squamous-, small-, and large-cell cancers combined, but were not apparent for adenocarcinoma.

While smoking has been verified to be the main determinant of lung cancer risk among Czech women, cofactors such as diet, history of lung disease, and lifestyle factors may have a contributory role.

Apart from smoking, certain occupational exposures, and schistosomiasis, little is known about other potential lifestyle risk factors for bladder cancer. Other investigations thus far have also been important because of the large number of individuals who are diagnosed with this cancer that apparently have no known risk factors. Preventing the recurrence of bladder cancer has generated some interest because several preliminary trials have found that a combination dietary supplement of vitamins and minerals or a probiotic agent (Lactobacillus casei) may impact this outcome favorably. Advising patients on some of these lifestyle modifications is currently recommended because the majority of them are also currently recommended for cardiovascular disease reduction.