Associations between oral hygiene habits,diet, tobacco and alcohol and risk of oral cancer: A case–control study from India

ObjectiveThis study examines the association between the incidence of oral cancer in India and oral hygiene habits, diet, chewing and smoking tobacco, and drinking alcohol. We also assessed the effects of oral hygiene habits with oral cancer risk among chewers versus never chewers.MethodsA hospital-based case–control study was conducted in Pune, India, based on face-to-face interviews, anthropometry, and intra-oral examinations conducted for 187 oral cancer cases and 240 controls.ResultsPoor oral hygiene score was associated with a significant risk of oral cancer (adjusted OR = 6.98; 95%CI 3.72–13.05). When stratified by tobacco-chewing habit, the poor oral hygiene score was a significant risk factor only among ever tobacco chewers (adjusted OR = 14.74; 95%CI 6.49–33.46) compared with never chewers (adjusted OR = 0.71; 95%CI 0.14–3.63). Dental check-ups only at the time of pain by ever-chewers with poor oral hygiene was associated with an elevated risk (adjusted OR = 4.22; 95%CI 2.44–7.29), while consumption of green, yellow, and cruciferous vegetables and citrus fruits was protective. A linear dose–response association was observed between oral cancer and chewing tobacco in terms of age at initiation, duration, and frequency of chewing per day (P < 0.001). Smoking more than 10 bidis/cigarettes per day (adjusted OR = 2.74; 95%CI 1.28–5.89) and for a duration >25 years (adjusted OR = 2.31; 95%CI 1.14–4.71) elevated the risk of oral cancer.ConclusionGood oral hygiene habits – as characterized by healthy gums, brushing more than once daily, use of toothpaste, annual dental check-ups, and a minimal number of missing teeth – can reduce the risk of oral cancer significantly. In addition to refraining from chewing/smoking tobacco, a diet adequate in fruits and vegetables may protect against the disease.     

Patterns and associations of smoking and electronic cigarette use among survivors of tobacco related and non-tobacco related cancers: A nationally representative cross-sectional analysis

BackgroundTobacco-use among cancer survivors leads to preventable morbidity, mortality, and increased healthcare costs. We sought to explore the prevalence of smoking and e-cigarette use among survivors of tobacco and non-tobacco related cancers.MethodsA cross-sectional analysis was conducted using the 2015–2018 National Health Interview Survey. Our primary outcome was the prevalence of current cigarette smoking or e-cigarette use among adults with self-reported history of tobacco related or non-tobacco related cancer. Logistic regression analysis was to assess the association of reported cancer type with cigarette smoking or e-cigarette use. Secondary outcomes included yearly trends and dual use.ResultsA total of 12,984 respondents reported a history of cancer, representing a weighted estimate of 5,060,059 individuals with a history of tobacco-related malignancy and 17,583,788 with a history of a tobacco and non-tobacco related cancer, respectively. Survivors of tobacco-related cancers had a significantly higher prevalence of current cigarette use (18.2 % vs 9.7 %, P < 0.0001), e-cigarette use (2.7 % vs 1.6 %, P < 0.0001) and similar rates of dual use. The prevalence of cigarette smoking among all survivors increased as time increased from the year of diagnosis up to 2 years post-diagnosis (P = 0.047). Odds of reporting current cigarette smoking use was higher for survivors of tobacco-related cancers, adjusted for sociodemographic factors (OR1.69, 95 % CI 1.44−1.99).ConclusionsSurvivors of tobacco-related cancers have a higher prevalence of current cigarette smoking and e-cigarette use compared to survivors of non-tobacco related cancers. There was a sequential increase in the prevalence of cigarette use during each subsequent year from the time of a new cancer diagnosis, underscoring the need for long term tobacco cessation support among newly diagnosed adults with cancer.     

Vitamin D receptor polymorphism and colorectal cancer-specific and all-cause mortality

BackgroundThe vitamin D receptor (VDR) gene is present in colorectal cancer (CRC) cells and its genetic variants have been associated with an increased risk of CRC. The association with colorectal cancer prognosis remains widely unexplored.Methods1397 colorectal cancer patients participating in two cancer cohorts (ESTHER II and VERDI) and in a population-based case–control study (DACHS) were followed for 5 years. Unadjusted and adjusted hazard ratios for all-cause mortality (469 events) and CRC-specific mortality (336 events) were estimated for VDR variants rs731236 (TaqI), rs2228570 (FokI), rs11568820 (Cdx2), and rs1989969 (VDR-5132).ResultsNo association was found between VDR polymorphism and CRC specific and all-cause mortality. Adjusted hazard ratios ranged from 0.79 (95% CI 0.57–1.12) to 1.14 (95% CI 0.89–1.46) for CRC-specific mortality and from 0.89 (95% CI 0.67–1.18) to 1.22 (95% CI 0.99–1.50) for all-cause mortality. All 95% confidence intervals included the null value.ConclusionsOur findings do not support the hypothesis that the common VDR gene variants investigated in this study are of clinical relevance with respect to CRC prognosis.     

Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98

Objective To measure the relation between environmental tobacco smoke, as estimated by smoking in spouses, and long term mortality from tobacco related disease.Design Prospective cohort study covering 39 years.Setting Adult population of California, United States.Participants 118 094 adults enrolled in late 1959 in the American Cancer Society cancer prevention study (CPS I), who were followed until 1998. Particular focus is on the 35 561 never smokers who had a spouse in the study with known smoking habits.Main outcome measures Relative risks and 95% confidence intervals for deaths from coronary heart disease, lung cancer, and chronic obstructive pulmonary disease related to smoking in spouses and active cigarette smoking.Results For participants followed from 1960 until 1998 the age adjusted relative risk (95% confidence interval) for never smokers married to ever smokers compared with never smokers married to never smokers was 0.94 (0.85 to 1.05) for coronary heart disease, 0.75 (0.42 to 1.35) for lung cancer, and 1.27 (0.78 to 2.08) for chronic obstructive pulmonary disease among 9619 men, and 1.01 (0.94 to 1.08), 0.99 (0.72 to 1.37), and 1.13 (0.80 to 1.58), respectively, among 25 942 women. No significant associations were found for current or former exposure to environmental tobacco smoke before or after adjusting for seven confounders and before or after excluding participants with pre-existing disease. No significant associations were found during the shorter follow up periods of 1960-5, 1966-72, 1973-85, and 1973-98.Conclusions The results do not support a causal relation between environmental tobacco smoke and tobacco related mortality, although they do not rule out a small effect. The association between exposure to environmental tobacco smoke and coronary heart disease and lung cancer may be considerably weaker than generally believed.     

Association between Body Mass Index and Prognosis of Colorectal Cancer: A Meta-Analysis of Prospective Cohort Studies

Studies have reported conflicting results on the association between body mass index (BMI) and prognosis of colorectal cancer. Therefore, we have conducted a meta-analysis of prospective studies, which examined the association of pre- and post-diagnostic BMI with colorectal cancer-specific mortality and all-cause mortality in patients with colorectal cancer. We searched Medline and EMBASE database published between 1970 and September 2014. A total of 508 articles were identified, of which 16 prospective cohort studies were included for the current meta-analysis. The analysis included 58,917 patients who were followed up over a period ranging from 4.9 to 20 years (median: 9.9 years). We found that being underweight before cancer diagnosis was associated with increased all-cause mortality (Relative risk [RR]: 1.63, 95% CI: 1.18–2.23, p < 0.01) and being obese (BMI ≥ 30 kg/m²) before cancer diagnosis was associated with increased colorectal cancer-specific mortality (RR: 1.22, 95% CI: 1.003–1.35, p < 0.01) and all-cause mortality (RR: 1.25, 95% CI: 1.14–1.36, p < 0.01). On the other hand, being underweight (RR: 1.33, 95% CI: 1.20–1.47, p < 0.01), obese (RR: 1.08, 95% CI: 1.03–1.3, p < 0.01), and class II/III obese (BMI ≥ 35 kg/m²; RR: 1.13, 95% CI: 1.04–1.23, p < 0.01) after diagnosis were associated with significantly increased all-cause mortality. Being obese prior to diagnosis of colorectal cancer was associated with increased colorectal cancer-specific mortality and all-cause mortality, whereas being obese after diagnosis was associated with increased all-cause mortality. The associations with being underweight may reflect reverse causation. Maintaining a healthy body weight should be discussed with colorectal cancer survivors.     

The relation between resting heart rate and cancer incidence,cancer mortality and all-cause mortality in patients with manifest vascular disease

BackgroundPrevious studies suggest that elevated resting heart rate (RHR) is related to an increased risk of cancer mortality. The aim of this study was to evaluate the relation between RHR and cancer incidence and mortality in patients with vascular disease.MethodsPatients with manifest vascular disease (n = 6007) were prospectively followed-up for cancer incidence and mortality. At baseline, RHR was obtained from an electrocardiogram. The relation between RHR and cancer incidence, cancer mortality and total mortality was assessed using competing risks models.ResultsDuring a median follow-up of 6.0 years (interquartile range: 3.1–9.3) 491 patients (8%) were diagnosed with cancer and 907 (15%) patients died, 248 (27%) died from cancer. After adjustment for potential confounders, the hazard ratio (HR) for incident cancer per 10 beats/min increase in RHR was 1.00 (95% confidence interval [CI]: 0.93–1.07). There was a trend toward an increased risk of colorectal cancer in patients with higher RHR (HR 1.15, 95% CI 0.97–1.36). The risk of all-cause mortality was increased in patients in the highest quartile of RHR compared to the lowest quartile (HR 1.86, 95% CI 1.53–2.27), but no effect of RHR on cancer mortality was observed (HR 1.01, 95% CI 0.70–1.46).ConclusionsIn patients with manifest vascular disease, elevated RHR was related to a higher risk of premature all-cause mortality, but this was not due to increased cancer mortality. RHR was not related to risk of overall cancer incidence, although a relation between elevated RHR and incident colorectal cancer risk could not be ruled out.     

Epigenetic,Genetic and Environmental Interactions in Esophageal Squamous Cell Carcinoma from Northeast India

Background

Esophageal squamous cell carcinoma (ESCC) develops as a result of complex epigenetic, genetic and environmental interactions. Epigenetic changes like, promoter hypermethylation of multiple tumour suppressor genes are frequent events in cancer, and certain habit-related carcinogens are thought to be capable of inducing aberrant methylation. However, the effects of environmental carcinogens depend upon the level of metabolism by carcinogen metabolizing enzymes. As such key interactions between habits related factors and carcinogen metabolizing gene polymorphisms towards modulating promoter methylation of genes are likely. However, this remains largely unexplored in ESCC. Here, we studied the interaction of various habits related factors and polymorphism of GSTM1/GSTT1 genes towards inducing promoter hypermethylation of multiple tumour suppressor genes.

Methodology/Principal Findings

The study included 112 ESCC cases and 130 age and gender matched controls. Conditional logistic regression was used to calculate odds ratios (OR) and multifactor dimensionality reduction (MDR) was used to explore high order interactions. Tobacco chewing and smoking were the major individual risk factors of ESCC after adjusting for all potential confounding factors. With regards to methylation status, significantly higher methylation frequencies were observed in tobacco chewers than non chewers for all the four genes under study (p<0.01). In logistic regression analysis, betel quid chewing, alcohol consumption and null GSTT1 genotypes imparted maximum risk for ESCC without promoter hypermethylation. Whereas, tobacco chewing, smoking and GSTT1 null variants were the most important risk factors for ESCC with promoter hypermethylation. MDR analysis revealed two predictor models for ESCC with promoter hypermethylation (Tobacco chewing/Smoking/Betel quid chewing/GSTT1 null) and ESCC without promoter hypermethylation (Betel quid chewing/Alcohol/GSTT1) with TBA of 0.69 and 0.75 respectively and CVC of 10/10 in both models.

Conclusion

Our study identified a possible interaction between tobacco consumption and carcinogen metabolizing gene polymorphisms towards modulating promoter methylation of tumour suppressor genes in ESCC.     

Smoking,Menthol Cigarettes and All-Cause,Cancer and Cardiovascular Mortality: Evidence from the National Health and Nutrition Examination Survey (NHANES) and a Meta-Analysis

Background

The U.S. Food and Drug Administration has the authority to regulate tobacco product constituents, including menthol, if the scientific evidence indicates harm. Few studies, however, have evaluated the health effects of menthol cigarette use.

Objective

To investigate associations of cigarette smoking and menthol cigarette use with all-cause, cancer and cardiovascular risk in U.S. adults.

Methods

We studied 10,289 adults ≥ 20 years of age who participated in the National Health and Nutrition Examination Survey from 1999-2004 and were followed through December 2006. We also identified studies comparing risk of all-cause mortality, cardiovascular disease and cancer for menthol and nonmenthol cigarette smokers and estimates were pooled using random-effects models.

Results

Fifty-five percent of participants were never smokers compared to 23%, 17% and 5% of former, current nonmenthol and current menthol cigarette smokers, respectively. The adjusted hazard ratios (95% CI) for former, current nonmenthol and current menthol cigarette smokers compared to never smokers were 1.24 (0.96, 1.62), 2.40 (1.56, 3.71) and 2.07 (1.20, 3.58), respectively, for all-cause mortality; 0.92 (0.62, 1.37), 2.10 (1.02, 4.31) and 3.48 (1.52, 7.99) for cardiovascular mortality; and 1.91 (1.21, 3.00), 3.82 (2.19, 6.68) and 2.03 (1.00, 4.13) for cancer mortality. Using data from 3 studies of all-cause mortality, 5 of cardiovascular disease and 13 of cancer, the pooled relative risks (95% CI) comparing menthol cigarette smokers to nonmenthol cigarette smokers was 0.94 (0.85, 1.05) for all-cause mortality, 1.28 (0.91, 1.80) for cardiovascular disease and 0.84 (0.76, 0.92) for any cancer.

Conclusions

In a representative sample of U.S. adults, menthol cigarette smoking was associated with increased all-cause, cardiovascular and cancer mortality with no differences compared to nonmenthol cigarettes. In the systematic review, menthol cigarette use was associated with inverse risk of cancer compared to nonmenthol cigarette use with some evidence of an increased risk for cardiovascular disease.     

Pre-diagnostic smoking behaviour and poorer prognosis in a German breast cancer patient cohort – Differential effects by tumour subtype,NAT2 status,BMI and alcohol intake

BackgroundInconsistent associations of smoking and breast cancer-specific mortality might be explained by subgroups of patients with different susceptibility to harmful effects of smoking.MethodsWe used a prospective cohort of 3340 postmenopausal breast cancer patients aged 50–74 and diagnosed with invasive tumours 2001–2005 in Germany, with a median follow-up time of 6 years. The effect of pre-diagnostic smoking behaviour on mortality outcomes and risk of recurrence was investigated using delayed entry Cox regression analysis. Differential effects according to N-acetyltransferase (NAT2) status, BMI, alcohol consumption, and tumour subtypes were assessed.ResultsOverall, smoking at time of breast cancer diagnosis versus never/former smoking was non-significantly associated with increased breast cancer-specific mortality and risk of recurrence (HR 1.23, 95% CI 0.93–1.64, and HR 1.29, 95% CI 0.95–1.75, respectively). Associations were consistently stronger in NAT2 slow than in fast acetylators for all mortality outcomes. Breast cancer-specific mortality was significantly increased in smokers with NAT2 slow acetylating status (HR 1.77, 95% CI 1.13–2.79) but not in those with fast acetylating status (HR 1.09, 95% CI 0.60–1.98; P_{heterogeneity} = 0.19). Smoking was associated with significantly poorer outcomes for triple negative and luminal A-like tumours (e.g. all-cause mortality: HR 1.93, 95% CI 1.02–3.65, and HR 2.08, 95% CI 1.40–3.10, respectively). Risk of recurrence was significantly increased for women with HER2 positive tumours (HR 3.64, 95% CI 1.22–10.8). There was significant heterogeneity by BMI for non-breast cancer-specific mortality (<25 kg/m²: HR 2.52, 95% CI 1.52–4.15 vs. ≥25 kg/m²: HR 0.94, 95% CI 0.38–2.36; P_{heterogeneity} = 0.04).ConclusionThe harmful effects of smoking may be particularly relevant for certain subgroups of breast cancer patients. This may include patients with NAT2 slow acetylation status or with tumour subtypes other than luminal B, such as luminal A tumours who usually have a rather good prognosis. Emphasis on smoking cessation programmes for all cancer patients should be strengthened.     

CYP2C9 genotype does not affect risk of tobacco-related cancer in the general population

Background: CYP2C9 enzymes are important in the metabolism of procarcinogenic chemicals such as polycyclic aromatic hydrocarbons (PAHs) found in tobacco smoke. Two functional variants in the CYP2C9 gene (CYP2C9*2 and CYP2C9*3) are known to be associated with decreased enzyme activity towards tolbutamide and warfarin, while this has not been investigated for PAHs. We hypothesised that these two variants in the CYP2C9 gene influence risk of tobacco-related cancer. Methods: In a prospective study of the general population (n = 10 392) with 60 years of follow-up, the Copenhagen City Heart Study, we associated two variants of CYP2C9 (CYP2C9*2 and CYP2C9*3) with risk of tobacco-related cancer and all cancer. All results were re-tested in a cross-sectional study of the general population (n = 36 856), the Copenhagen General Population Study. Results: We found no association between any of the CYP2C9 genotypes and risk of tobacco-related cancer, individual tobacco-related cancers, or all cancer. For the combined carriers (any CYP2C9*2 or CYP2C9*3 heterozygotes or homozygotes) vs. non-carriers we had 90% statistical power to exclude measures of relative risks below/above 0.8/1.2 and 0.9/1.1 in the Copenhagen City Heart Study and below/above 0.8/1.3 and 0.9/1.1 in the Copenhagen General Population Study for tobacco-related cancer and all cancer, respectively. Conclusion: Genetic variations in CYP2C9 do not affect risk of tobacco-related cancers.     

Association between exercise habits and stroke,heart failure,and mortality in Korean patients with incident atrial fibrillation: A nationwide population-based cohort study

BackgroundThere is a paucity of information about cardiovascular outcomes related to exercise habit change after a new diagnosis of atrial fibrillation (AF). We investigated the association between exercise habits after a new AF diagnosis and ischemic stroke, heart failure (HF), and all-cause death.Methods and findingsThis is a nationwide population-based cohort study using data from the Korea National Health Insurance Service. A retrospective analysis was performed for 66,692 patients with newly diagnosed AF between 2010 and 2016 who underwent 2 serial health examinations within 2 years before and after their AF diagnosis. Individuals were divided into 4 categories according to performance of regular exercise, which was investigated by a self-reported questionnaire in each health examination, before and after their AF diagnosis: persistent non-exercisers (30.5%), new exercisers (17.8%), exercise dropouts (17.4%), and exercise maintainers (34.2%). The primary outcomes were incidence of ischemic stroke, HF, and all-cause death. Differences in baseline characteristics among groups were balanced considering demographics, comorbidities, medications, lifestyle behaviors, and income status. The risks of the outcomes were computed by weighted Cox proportional hazards models with inverse probability of treatment weighting (IPTW) during a mean follow-up of 3.4 ± 2.0 years. The new exerciser and exercise maintainer groups were associated with a lower risk of HF compared to the persistent non-exerciser group: the hazard ratios (HRs) (95% CIs) were 0.95 (0.90–0.99) and 0.92 (0.88–0.96), respectively (p < 0.001). Also, performing exercise any time before or after AF diagnosis was associated with a lower risk of mortality compared to persistent non-exercising: the HR (95% CI) was 0.82 (0.73–0.91) for new exercisers, 0.83 (0.74–0.93) for exercise dropouts, and 0.61 (0.55–0.67) for exercise maintainers (p < 0.001). For ischemic stroke, the estimates of HRs were 10%–14% lower in patients of the exercise groups, yet differences were statistically insignificant (p = 0.057). Energy expenditure of 1,000–1,499 MET-min/wk (regular moderate exercise 170–240 min/wk) was consistently associated with a lower risk of each outcome based on a subgroup analysis of the new exerciser group. Study limitations include recall bias introduced due to the nature of the self-reported questionnaire and restricted external generalizability to other ethnic groups.ConclusionsInitiating or continuing regular exercise after AF diagnosis was associated with lower risks of HF and mortality. The promotion of exercise might reduce the future risk of adverse outcomes in patients with AF.

Using a population-based cohort study, Dr. Choi and colleagues studied patients with atrial fibrillation to determine whether their exercise habits were associated with occurrence of ischemic stroke, heart failure, and all-cause mortality.     

Differences in risk factors for head and neck cancer among men and women in Nepal: A case-control study

BackgroundHead and neck cancer (HNC) is a major cause of cancer morbidity and mortality in Nepal. The study aims to investigate differences in risk factors for head and neck cancer by sex in Nepal.MethodsA hospital-based case-control study was conducted at the B.P. Koirala Memorial Cancer Hospital in Nepal from 2016 to 2018. A semi-structured questionnaire consisting of socio-demographic characteristics, dietary habits, reproductive factors, household air pollution, tobacco use (smoking and chewing), alcohol consumption, and second-hand smoking was used to collect the data. Odds ratios (OR) and 95 % confidence intervals (CI) were estimated using unconditional logistic regression adjusting for potential confounders.ResultsA total of 549 HNC cases (438 men and 111 women) and 601 age-matched healthy controls (479 men and 122 women) were recruited in this study. An increased risk of HNC for low education level and family income were observed among men (adjusted odds ratio (AOR) for 3rd grade and less= 1.58, 95 % CI= 1.14–2.18; AOR for family monthly income < 5000 Rupees = 1.64, 95 % CI 1.20–2.24). The AORs among women were higher than the men for known risk factors (AOR for smoking 1.34 (95 % CI 0.96–1.86) for men, 2.94 (95 % CI 1.31–6.69) for women; AOR for tobacco chewing 1.76 (95 % CI 1.27–2.46) for men, 10.22 (95 % CI 4.53–23.03) for women).ConclusionOur results point to an effect modification by sex for HNC risk factors with high AORs observed among women.     

A Prospective Study of Tobacco Smoking and Mortality in Bangladesh

Background

Limited data are available on smoking-related mortality in low-income countries, where both chronic disease burden and prevalence of smoking are increasing.

Methods

Using data on 20, 033 individuals in the Health Effects of Arsenic Longitudinal Study (HEALS) in Bangladesh, we prospectively evaluated the association between tobacco smoking and all-cause, cancer, and cardiovascular disease mortality during ∼7.6 years of follow-up.Cox proportional hazards models were used to estimate hazard ratios (HRs) and their 95% confidence intervals (CIs) for deaths from all-cause, cancer, CVD, ischemic heart disease (IHD), and stroke, in relation to status, duration, and intensity of cigarette/bidi and hookah smoking.

Results

Among men, cigarette/bidi smoking was positively associated with all-cause (HR 1.40, 95% CI 1.06 1.86) and cancer mortality (HR 2.91, 1.24 6.80), and there was a dose-response relationship between increasing intensity of cigarette/bidi consumption and increasing mortality. An elevated risk of death from ischemic heart disease (HR 1.87, 1.08 3.24) was associated with current cigarette/bidi smoking. Among women, the corresponding HRs were 1.65 (95% CI 1.16 2.36) for all-cause mortality and 2.69 (95% CI 1.20 6.01) for ischemic heart disease mortality. Similar associations were observed for hookah smoking. There was a trend towards reduced risk for the mortality outcomes with older age at onset of cigarette/bidi smoking and increasing years since quitting cigarette/bibi smoking among men. We estimated that cigarette/bidi smoking accounted for about 25.0% of deaths in men and 7.6% in women.

Conclusions

Tobacco smoking was responsible for substantial proportion of premature deaths in the Bangladeshi population, especially among men. Stringent measures of tobacco control and cessation are needed to reduce tobacco-related deaths in Bangladesh.     

Lifetime Smoking History and Cause-Specific Mortality in a Cohort Study with 43 Years of Follow-Up

BackgroundIn general, smoking increases the risk of mortality. However, it is less clear how the relative risk varies by cause of death. The exact impact of changes in smoking habits throughout life on different mortality risks is less studied.MethodsWe studied the impact of baseline and lifetime smoking habits, and duration of smoking on the risk of all-cause mortality, mortality of cardiovascular diseases (CVD), chronic obstructive pulmonary disease (COPD), any cancer and of the four most common types of cancer (lung, colorectal, prostate, and breast cancer) in a cohort study (Vlagtwedde-Vlaardingen 1965–1990, with a follow-up on mortality status until 2009, n = 8,645). We used Cox regression models adjusted for age, BMI, sex, and place of residence. Since previous studies suggested a potential effect modification of sex, we additionally stratified by sex and tested for interactions. In addition, to determine which cause of death carried the highest risk we performed competing-risk analyses on mortality due to CVD, cancer, COPD and other causes.ResultsCurrent smoking (light, moderate, and heavy cigarette smoking) and lifetime persistent smoking were associated with an increased risk of all-cause, CVD, COPD, any cancer, and lung cancer mortality. Higher numbers of pack years at baseline were associated with an increased risk of all-cause, CVD, COPD, any cancer, lung, colorectal, and prostate cancer mortality. Males who were lifetime persistent pipe/cigar smokers had a higher risk of lung cancer [HR (95% CI) = 7.72 (1.72–34.75)] as well as all-cause and any cancer mortality. A longer duration of smoking was associated with a higher risk of COPD, any and lung cancer [HR (95% CI) = 1.06 (1.00–1.12), 1.03 (1.00–1.06) and 1.10 (1.03–1.17) respectively], but not with other mortality causes. The competing risk analyses showed that ex- and current smokers had a higher risk of cancer, CVD, and COPD mortality compared to all other mortality causes. In addition, heavy smokers had a higher risk for COPD mortality compared to cancer, and CVD mortality.ConclusionOur study indicates that lifetime numbers of cigarettes smoked and the duration of smoking have different impacts for different causes of mortality. Moreover, our findings emphasize the importance of smoking-related competing risks when studying the smoking-related cancer mortality in a general population and that smoking cessation immediately effectively reduces the risk of all-cause and any cancer mortality.     

Beta-blocker usage and prostate cancer survival: A nested case–control study in the UK Clinical Practice Research Datalink cohort

BackgroundRecent laboratory and epidemiological evidence suggests that beta-blockers could inhibit prostate cancer progression. Methods: We investigated the effect of beta-blockers on prostate cancer-specific mortality in a cohort of prostate cancer patients. Prostate cancer patients diagnosed between 1998 and 2006 were identified from the UK Clinical Practice Research Database and confirmed by cancer registries. Patients were followed up to 2011 with deaths identified by the Office of National Statistics. A nested case–control analysis compared patients dying from prostate cancer (cases) with up to three controls alive at the time of their death, matched by age and year of diagnosis. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using conditional logistic regression. Results: Post-diagnostic beta-blocker use was identified in 25% of 1184 prostate cancer-specific deaths and 26% of 3531 matched controls. There was little evidence (P = 0.40) of a reduction in the risk of cancer-specific death in beta-blocker users compared with non-users (OR = 0.94 95% CI 0.81, 1.09). Similar results were observed after adjustments for confounders, in analyses by beta-blocker frequency, duration, type and for all-cause mortality. Conclusions: Beta-blocker usage after diagnosis was not associated with cancer-specific or all-cause mortality in prostate cancer patients in this large UK study.     

Weight loss and mortality: A gender-specific analysis of the Tromsø study

Background: Weight loss has been associated with increased mortality, but findings have been inconsistent.Objective: The aim of this study was to examine the association between weight loss and mortality, with a focus on gender differences.Methods: This was a population-based cohort study in northern Norway of adults, aged 20 to 54 years in 1979, who participated in 2 or 3 consecutive health surveys in 1979–80, 1986–87, and 1994–95. Weight and height were measured at each survey. The Cox proportional hazards regression model was used to estimate hazard ratios for mortality between levels of body mass index (BMI) change during 11 years of follow-up. Participants with prior cardiovascular disease or cancer, or incident cancer within the first 2 years of follow-up, were excluded, as were participants who were pregnant, had missing data, or did not give written consent.Results: A total of 4881 men and 5051 women participated in the present study. The mean age at start of follow-up was 50.8 years (range, 35–70 years) in men and 49.2 years (range, 35–65 years) in women. In men, weight loss was associated with increased all-cause, cardiovascular, and noncardiovascular mortality. The hazard ratio for men for all-cause mortality with a 10-year BMI decrease of 2 kg/m² versus a BMI increase of 1 kg/m² was 2.09 (95% CI, 1.56–2.81). The association was not significantly modified by initial BMI, age, smoking status, or self-reported attempts of weight loss, or by exclusion of subjects with self-reported poor health, diabetes mellitus, high blood pressure, or high alcohol intake. In women, no association between BMI change and mortality was observed. However, in the subgroup of women who reported no weight-loss attempts, BMI change was significantly associated with mortality risk (P = 0.022).Conclusions: In this study of a Norwegian population, weight loss was associated with excess mortality in men in all subgroups of weight-loss attempts, daily smoking, and overweight. In women, the only significant effect of BMI change on mortality was observed in those who reported no weight-loss attempts. The observed findings could not be explained by preexisting disease.     

Relationship between serum levels of insulin-like growth factors and subsequent risk of cancer mortality: Findings from a nested case–control study within the Japan Collaborative Cohort Study

Background: We investigated the association between serum levels of IGF-I, IGF-II, and IGFBP-3 and the subsequent risk of cancer mortality. Methods: Our case–control study examined samples from 914 cancer deaths and their 2739 matched controls within the Japan Collaborative Cohort Study. Blood samples were obtained at the baseline and stored at ?80 °C until analysis for IGF-I, IGF-II, and IGFBP-3 levels. The conditional logistic model was used to estimate odds ratios (ORs) for cancer mortality associated with these serum levels. Results: The adjusted ORs for IGF-I quartiles ranged from 0.81 to 0.96 but were not significant. The adjusted ORs and 95% confidence interval (CI) for the second, third, and fourth IGF-II quartiles were 0.64 (95% CI: 0.52–0.79), 0.71 (95% CI: 0.58–0.88), and 0.73 (95% CI: 0.59–0.91), respectively, while those for the respective IGFBP-3 quartiles were 0.77 (95% CI: 0.63–0.96), 0.75 (95% CI: 0.60–0.94), and 0.71 (95% CI: 0.56–0.90). In the model of IGF-I, and IGF-II additionally adjusted for IGFBP-3, the associations of high IGFs levels were similar as observed in the above models, while the association of IGFBP-3 shifted into non-significance after adjusting for IGF-II. Conclusion: An increased level of IGF-II was significantly associated with decreased risk of cancer mortality, whereas the association between IGF-I and all cancer mortality was not significant. The inverse association of IGFBP-3 level with all cancer mortality was affected when adjusting for IGF-II levels, shifting from significant to non-significant. Confirmation of these results from further cohort studies may aid in identifying the potential association between these molecules and the risk of cancer among the general Japanese population.     

Actinic skin damage and mortality--the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study

Background

Exposure to sunlight may decrease the risk of several diseases through the synthesis of vitamin D, whereas solar radiation is the main cause of some skin and eye diseases. However, to the best of our knowledge, the association of sun-induced skin damage with mortality remains unknown.

Methodology/Principal Findings

Subjects were 8472 white participants aged 25–74 years in the First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. Cardiovascular disease mortality, cancer mortality, and all-cause mortality were obtained by either a death certificate or a proxy interview, or both. Actinic skin damage was examined and recorded by the presence and severity (absent, minimal, moderate, or severe) of overall actinic skin damage and its components (i.e., fine telangiectasia, solar elastosis, and actinic keratoses). Cox regression and Kaplan-Meier methods were applied to explore the associations. A total of 672 cancer deaths, 1500 cardiovascular disease deaths, and 2969 deaths from all causes were documented through the follow-up between 1971 and 1992. After controlling for potential confounding variables, severe overall actinic skin damage was associated with a 45% higher risk for all-cause mortality (95% CI: 1.22, 1.72; P<0.001), moderate overall skin damage with a 20% higher risk (95% CI: 1.08., 1.32; P<0.001), and minimal overall skin damage with no significant mortality difference, when compared to those with no skin damage. Similar results were obtained for all-cause mortality with fine telangiectasia, solar elastosis, and actinic keratoses. The results were similar for cancer and cardiovascular disease mortality.

Conclusions

The present study gives an indication of an association of actinic skin damage with cardiovascular disease, cancer and all-cause mortality in white subjects. Given the lack of support in the scientific literature and potential unmeasured confounding factors, this finding should be interpreted with caution. More independent studies are needed before any practical recommendations can be made.     

Overall and recurrence-free survival among black and white bladder cancer patients in an equal-access health system

BackgroundWhile the incidence of bladder cancer is twice as high among whites than among blacks, mortality is higher among blacks than whites. Unequal access to medical care may be an important factor. Insufficient access to care could delay cancer detection and treatment, which can result in worse survival. The purpose of this study was to evaluate whether survival differed between black and white bladder cancer patients in the Department of Defense (DoD), which provides universal healthcare to all beneficiaries regardless of racial background.MethodsThis study was based on data from the U.S. DoD Automated Central Tumor Registry (ACTUR). White and black patients histologically diagnosed with bladder cancer between 1990 and 2004 were included in the study and followed to the end of 2007. The outcomes were all-cause mortality and recurrence. We assessed the relationship between race and outcomes of interest using Cox proportional hazard ratios (HRs) for all, non-muscle invasive (NMIBC), and muscle invasive (MIBC) bladder cancers, separately.ResultsThe survival of black and white individuals did not differ statistically. No significant racial differences in survival (HR: 0.96, 95% CI: 0.76–1.22) or recurrence-free survival (HR: 0.94, 95% CI: 0.69–1.30) were observed after adjustment for demographic variables, tumor characteristics, and treatment. Similar findings were observed for NMIBC and MIBC patients, respectively.ConclusionBlack patients were more likely to present with MIBC than white patients. However, white and black patients with bladder cancer were not significantly different in overall and recurrence-free survival regardless of muscle invasion. Our study suggests the importance of equal access to healthcare in reducing racial disparities in bladder cancer survival.     

Sex differences in the proportion of esophageal squamous cell carcinoma cases attributable to tobacco smoking and alcohol consumption

Objective: Alcohol and tobacco are the two major established environmental factors associated with squamous cell carcinoma of the esophagus (ESCC). However, the prevalence of these exposures differs substantially between men and women. Moreover, the prevalence of smoking has declined in recent years, whereas per capita consumption of alcohol has remained steady in both sexes. Quantifying the burden of ESCC attributable to these causal factors is necessary to inform potential preventive strategies. Methods: We estimated the population attributable fraction (PAF) of ESCC due to smoking and alcohol, using data from an Australian population based case–control study (305 ESCC cases, 1554 controls). Results: Estimated PAF for ESCC were 49% (95% CI: 38–60) and 32% (95% CI: 25–40) due to smoking and heavy alcohol consumption respectively. More than 75% of the ESCC burden in men could be attributed to smokers with heavy alcohol consumption. The highest burden was among ≥30 pack years smokers who also consumed alcohol heavily (>17 drinks/week); this differed significantly between men (PAF 36%, 95% CI 29–44) and women (PAF 5%, 95% CI 2–10). Among women only, low intakes of fruit and vegetables accounted for about 9% of the ESCC burden. Conclusion: The burden of ESCC attributable to smoking combined with heavy alcohol consumption is remarkably high in men. In women, the burden of ESCC due to these factors is lower, and poor nutrition may also play a role.