Ambient Cumulative PM2.5 Exposure and the Risk of Lung Cancer Incidence and Mortality: A Retrospective Cohort Study

Smoking, sex, air pollution, lifestyle, and diet may act independently or in concert with each other to contribute to the different outcomes of lung cancer (LC). This study aims to explore their associations with the carcinogenesis of LC, which will be useful for formulating further preventive strategies. This retrospective, longitudinal follow-up cohort study was carried out by connecting to the MJ Health Database, Taiwan Cancer Registry database, and Taiwan cause of death database from 2000 to 2015. The studied subjects were persons attending the health check-ups, distributed throughout the main island of Taiwan. Cox proportional hazards regression models were used to investigate the risk factors associated with LC development and mortality after stratifying by smoking status, with a special emphasis on ambient two-year average PM2.5 exposure, using a satellite-based spatiotemporal model at a resolution of 1 km2, and on dietary habit including consumption of fruits and vegetables. After a median follow-up of 12.3 years, 736 people developed LC, and 401 people died of LC-related causes. For never smokers, the risk of developing LC (aHR: 1.32, 95%CI: 1.12–1.56) and dying from LC-related causes (aHR: 1.28, 95%CI: 1.01–1.63) rises significantly with every 10 μg/m3 increment of PM2.5 exposure, but not for ever smokers. Daily consumption of more than two servings of vegetables and fruits is associated with lowering LC risk in ever smokers (aHR: 0.68, 95%CI: 0.47–0.97), and preventing PM2.5 exposure is associated with lowering LC risk for never smokers.

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Chronic obstructive pulmonary disease and lung cancer incidence in never smokers: a cohort study

Thorax ◽

10.1136/thoraxjnl-2019-213732 ◽

2020 ◽

Vol 75 (6) ◽

pp. 506-509 ◽

Cited By ~ 3

Author(s):

Hye Yun Park ◽

Danbee Kang ◽

Sun Hye Shin ◽

Kwang-Ha Yoo ◽

Chin Kook Rhee ◽

...

Keyword(s):

Lung Cancer ◽

Chronic Obstructive Pulmonary Disease ◽

Cohort Study ◽

Pulmonary Disease ◽

Cancer Incidence ◽

Chronic Obstructive ◽

Lung Cancer Incidence ◽

Obstructive Pulmonary Disease ◽

Never Smokers

There has been limited evidence for the association between chronic obstructive pulmonary disease (COPD) and the incidence of lung cancer among never smokers. We aimed to estimate the risk of lung cancer incidence in never smokers with COPD, and to compare it with the risk associated with smoking. This cohort study involved 338 548 subjects, 40 to 84 years of age with no history of lung cancer at baseline, enrolled in the National Health Insurance Service National Sample Cohort. During 2 355 005 person-years of follow-up (median follow-up 7.0 years), 1834 participants developed lung cancer. Compared with never smokers without COPD, the fully-adjusted hazard ratios (95% CI) for lung cancer in never smokers with COPD, ever smokers without COPD, and ever smokers with COPD were 2.67 (2.09 to 3.40), 1.97 (1.75 to 2.21), and 6.19 (5.04 to 7.61), respectively. In this large national cohort study, COPD was also a strong independent risk factor for lung cancer incidence in never smokers, implying that COPD patients are at high risk of lung cancer, irrespective of smoking status.

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Independent effects of waist circumference and physical activity on all-cause mortality in Canadian women

Applied Physiology Nutrition and Metabolism ◽

10.1139/h05-038 ◽

2006 ◽

Vol 31 (3) ◽

pp. 271-276 ◽

Cited By ~ 24

Author(s):

Peter T Katzmarzyk ◽

Cora L Craig

Keyword(s):

Physical Activity ◽

Cohort Study ◽

Waist Circumference ◽

Physical Inactivity ◽

Proportional Hazards ◽

Leisure Time Physical Activity ◽

Smoking Status ◽

Cox Proportional Hazards ◽

Independent Effects

The purpose of this study was to determine the independent effects of waist circumference (WC) and physical inactivity on the risk of mortality in women. This prospective cohort study included 5421 female participants 20-69 years of age in the 1981 Canada Fitness Survey. WC was measured with an anthropometric tape and leisure-time physical activity levels over the previous 12 months were assessed with a questionnaire. Mortality surveillance was conducted by data linkage with the Canadian Mortality Database through 31 December, 1993. The hazard ratios (HR) of mortality were estimated using Cox proportional hazards regression with age, smoking status, and alcohol con sumption included as covariates in all models. A total of 225 deaths occurred over an average of 12.4 years of follow up (67 500 person-years of follow up). Physical activity (HR = 0.78; 95% C.I.: 0.64-0.95) and WC (HR = 1.17; 95% C.I.: 1.05-1.31) were associated with mortality when included in separate regression models. When included in the same model, both physical activity (HR = 0.79; 95% CI: 0.65-0.96) and WC (HR = 1.16; 95% C.I.: 1.04-1.30) remained independent significant predictors of mortality. In conclusion, physical inactivity and high WC have significant independent risks of premature mortality among women.Key words: death, obesity, cohort study, Canada Fitness Survey.

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Smoking and estrogen plus progestin (E+P) and lung cancer incidence and mortality.

Journal of Clinical Oncology ◽

10.1200/jco.2013.31.15_suppl.1524 ◽

2013 ◽

Vol 31 (15_suppl) ◽

pp. 1524-1524

Author(s):

Rowan T. Chlebowski ◽

Heather A. Wakelee ◽

Thomas E Rohan ◽

Jingmin Liu ◽

Michael S. Simon ◽

...

Keyword(s):

Lung Cancer ◽

Clinical Trial ◽

Cancer Incidence ◽

Smoking Status ◽

Controlled Clinical Trial ◽

Lung Cancer Incidence ◽

Lung Cancers ◽

Risk Of Death ◽

Incidence And Mortality ◽

Never Smokers

1524 Background: In the Women’s Health Initiative (WHI) randomized, placebo-controlled clinical trial, E+P increased deaths from lung cancer (those cancer-attributed) and after lung cancer (regardless of cause) (Lancet 2009:374:1243). To examine smoking status influence on this process, a cohort combining WHI clinical trial (CT) and observational study (OS) participants, the latter meeting criteria as in the CT, was identified to examine E+P associations with lung cancer incidence and outcome. Methods: 31,966 postmenopausal women (12,299 CT, 19,668 OS) with no prior hysterectomy and no prior hormone therapy use were classified at baseline as not hormone users or E+P users and as current or never smokers. Lung cancers were verified by medical record review. Multi-variant adjusted Cox proportional hazards regression, including pack-year use, calculated hazard ratios (HRs, 95% confidence intervals [CI]) for groups defined by smoking status and E+P use for lung cancer incidence, deaths from lung cancer and deaths after lung cancer. Results: After 12 years mean follow-up, 664 lung cancers were diagnosed with 444 deaths from lung cancer and 513 deaths after lung cancer. Analyzed from cohort entry; see Table. In nonusers of E+P, lung cancer incidence, deaths from lung cancer, and deaths after lung cancer were significantly and substantially greater in current smokers vs never smokers (p< .0001 for all comparisons). In current smokers, lung cancer incidence, deaths from lung cancer and deaths after lung cancer were significantly and substantially greater in E+P users vs non-users (p=.0021, .0005 and .0002, respectively). Conclusions: E+P use in current smokers nearly doubles their already high risk of death from and after lung cancer. Based on this risk, current smokers should not use E+P. [Table: see text]

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Lung Cancer Screening with Low-Dose CT in Female Never Smokers: Retrospective Cohort Study with Long-term National Data Follow-up

Cancer Research and Treatment ◽

10.4143/crt.2017.312 ◽

2018 ◽

Vol 50 (3) ◽

pp. 748-756 ◽

Cited By ~ 2

Author(s):

Hyae Young Kim ◽

Kyu-Won Jung ◽

Kun Young Lim ◽

Soo-Hyun Lee ◽

Jae Kwan Jun ◽

...

Keyword(s):

Lung Cancer ◽

Cohort Study ◽

Cancer Screening ◽

Retrospective Cohort ◽

Low Dose ◽

Lung Cancer Screening ◽

National Data ◽

Never Smokers

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Pre-diagnosis neutrophil-to-lymphocyte ratio and mortality in individuals who develop lung cancer

Cancer Causes & Control ◽

10.1007/s10552-021-01469-3 ◽

2021 ◽

Author(s):

Laurie Grieshober ◽

Stefan Graw ◽

Matt J. Barnett ◽

Gary E. Goodman ◽

Chu Chen ◽

...

Keyword(s):

Lung Cancer ◽

Proportional Hazards ◽

Smoking Status ◽

Cox Proportional Hazards ◽

Neutrophil To Lymphocyte Ratio ◽

Blood Draw ◽

Lymphocyte Ratio ◽

Cox Proportional Hazards Models ◽

Inflammatory Profile ◽

Heavy Smokers

Abstract Purpose The neutrophil-to-lymphocyte ratio (NLR) is a marker of systemic inflammation that has been reported to be associated with survival after chronic disease diagnoses, including lung cancer. We hypothesized that the inflammatory profile reflected by pre-diagnosis NLR, rather than the well-studied pre-treatment NLR at diagnosis, may be associated with increased mortality after lung cancer is diagnosed in high-risk heavy smokers. Methods We examined associations between pre-diagnosis methylation-derived NLR (mdNLR) and lung cancer-specific and all-cause mortality in 279 non-small lung cancer (NSCLC) and 81 small cell lung cancer (SCLC) cases from the β-Carotene and Retinol Efficacy Trial (CARET). Cox proportional hazards models were adjusted for age, sex, smoking status, pack years, and time between blood draw and diagnosis, and stratified by stage of disease. Models were run separately by histotype. Results Among SCLC cases, those with pre-diagnosis mdNLR in the highest quartile had 2.5-fold increased mortality compared to those in the lowest quartile. For each unit increase in pre-diagnosis mdNLR, we observed 22–23% increased mortality (SCLC-specific hazard ratio [HR] = 1.23, 95% confidence interval [CI]: 1.02, 1.48; all-cause HR = 1.22, 95% CI 1.01, 1.46). SCLC associations were strongest for current smokers at blood draw (Interaction Ps = 0.03). Increasing mdNLR was not associated with mortality among NSCLC overall, nor within adenocarcinoma (N = 148) or squamous cell carcinoma (N = 115) case groups. Conclusion Our findings suggest that increased mdNLR, representing a systemic inflammatory profile on average 4.5 years before a SCLC diagnosis, may be associated with mortality in heavy smokers who go on to develop SCLC but not NSCLC.

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Hemoglobin A1c in Patients with Diabetes Predict Long-Term Mortality Following Coronary Artery Surgery

Journal of Clinical Medicine ◽

10.3390/jcm10122739 ◽

2021 ◽

Vol 10 (12) ◽

pp. 2739

Author(s):

Muhammad Abu Tailakh ◽

Shlomo-yaron Ishay ◽

Jenan Awesat ◽

Liat Poupko ◽

Gidon Sahar ◽

...

Keyword(s):

Coronary Artery ◽

Coronary Artery Bypass ◽

Hemoglobin A1c ◽

Smoking Status ◽

Artery Bypass ◽

Cox Proportional Hazards ◽

Chronic Obstructive ◽

Hba1c Levels

Objective: to estimate the association between preoperative hemoglobin A1c (HbA1c) levels below and above 7%, and the rate of all-cause mortality (ACM) in diabetes mellitus (DM) patients after coronary artery bypass grafting (CABG) within a ten-year follow-up period. Methods: we collected data on patient HbA1c levels that were measured up to 3 months prior to isolated CABG in consecutive patients with DM, and analyzed the rates of ACM over a median of a 5.9-year post-operative period. Results: preoperative HbA1c levels were collected in 579 DM patients. The mean HbA1c was 8.0 ± 1.7%, where 206 (35.6%) patients had an HbA1c ≤ 7% and 373 (64.4%) had an HbA1c > 7%. During the follow-up period, mortality rates were 20.4% and 28.7% in the HbA1c ≤ 7% and HbA1c > 7% groups, respectively (Kaplan-Meier estimates, log-rank p = 0.01). Multivariable Cox proportional hazards regression, adjusted for age, gender, smoking status, chronic obstructive pulmonary disease, hypertension, chronic renal failure, old myocardial infarction, number of coronary artery bypass surgeries, and post-operative glycemic control, showed a hazard ratio of 2.67 for long-term ACM (p = 0.001) in patients with HbA1c > 7%. Conclusions: DM patients with high HbA1c levels prior to CABG are at higher risk for long-term complications, especially late ACM.

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Self-reported and cotinine-verified smoking and increased risk of incident hearing loss

Scientific Reports ◽

10.1038/s41598-021-87531-1 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Woncheol Lee ◽

Yoosoo Chang ◽

Hocheol Shin ◽

Seungho Ryu

Keyword(s):

Smoking Status ◽

Objective Measure ◽

Self Report ◽

Urinary Cotinine ◽

Increased Risk ◽

Former Smokers ◽

Never Smokers ◽

Time Varying Covariates ◽

New Onset

AbstractWe examined the associations of smoking status and urinary cotinine levels, an objective measure of smoking, with the development of new-onset HL. This cohort study was performed in 293,991 Korean adults free of HL who underwent a comprehensive screening examination and were followed for up to 8.8 years. HL was defined as a pure-tone average of thresholds at 0.5, 1.0, and 2.0 kHz ≥ 25 dB in both ears. During a median follow-up of 4.9 years, 2286 participants developed new-onset bilateral HL. Self-reported smoking status was associated with an increased risk of new-onset bilateral HL. Multivariable-adjusted HRs (95% CIs) for incident HL comparing former smokers and current smokers to never-smokers were 1.14 (1.004–1.30) and 1.40 (1.21–1.61), respectively. Number of cigarettes, pack-years, and urinary cotinine levels were consistently associated with incident HL. These associations were similarly observed when introducing changes in smoking status, urinary cotinine, and other confounders during follow-up as time-varying covariates. In this large cohort of young and middle-aged men and women, smoking status based on both self-report and urinary cotinine level were independently associated with an increased incidence of bilateral HL. Our findings indicate smoking is an independent risk factor for HL.

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Abstract P196: Bidirectional Association Between Hypertension and Gout: The Singapore Chinese Health Study

Circulation ◽

10.1161/circ.131.suppl_1.p196 ◽

2015 ◽

Vol 131 (suppl_1) ◽

Author(s):

An Pan ◽

Gim Gee Teng ◽

Jian-Min Yuan ◽

Woon-Puay Koh

Keyword(s):

Smoking Status ◽

Final Analysis ◽

Normal Weight ◽

Cox Proportional Hazards ◽

Health Study ◽

Increased Risk ◽

Bidirectional Association ◽

Singapore Chinese ◽

Incident Cases

Introduction: Although it has been hypothesized that the hypertension-gout relation is bidirectional, few studies have addressed this hypothesis in a prospective setting, particularly in the Asian populations. Methods: We analyzed data from the Singapore Chinese Health Study (SCHS), a cohort of 63,257 Chinese aged 45-74 years at recruitment from 1993-98. The information about self reports of physician-diagnosed hypertension and gout was enquired at follow-ups I (1999-2004) and II (2006-2010). We included participants with complete data for both follow-ups and who were free of heart disease, stroke and cancer at follow-up I. For the analysis of hypertension and risk of incident gout, participants with prevalent gout were further excluded and the final analysis included 31,694 participants. For the analysis of gout and risk of incident hypertension, participants with prevalent hypertension were further excluded and the final analysis included 20,490 participants. Cox proportional hazards models were used to estimate multivariable-adjusted relative risks (RRs) and 95% confidence intervals (CIs) with adjustment for age, sex, years of interview, dialect group, education, smoking status, alcohol intake, physical activity, body mass index (BMI) and history of diabetes. Results: The mean age of the participants at baseline was 60.1 (SD 7.3) years, and the average follow-up year was 6.8 (SD 1.4) years. In the analysis of hypertension and risk of gout, 836 incident cases were identified. Compared to normotensive participants, hypertensive patients had a 93% increased risk of developing gout (RR 1.93; 95% CI 1.66-2.24). The association was slightly stronger in women (RR 2.09; 95% CI 1.69-2.58) compared to men (RR 1.72; 95% CI 1.39-2.14; P for interaction=0.056). The association was also stronger in normal weight adults (BMI <24 kg/m2; RR 2.25; 95% CI 1.82-2.77) compared to overweight/obese individuals (BMI ≥24 kg/m2; RR 1.66; 95% CI 1.34-2.04; P for interaction=0.03). In the parallel analysis of gout and risk of hypertension, 5491 participants reported to have newly diagnosed hypertension during the follow-up. Compared to participants without gout, those with gout had a 17% increased risk of developing hypertension (RR 1.17; 95% CI 1.01-1.35). The association was evident in men (RR 1.29; 95% CI 1.07-1.55) but not in women (RR 0.94; 95% CI 0.73-1.20; P for interaction=0.03). The association was present in normal weight adults (RR 1.34; 95% CI 1.09-1.64) but not among overweight/obese individuals (RR 0.99; 95% CI 0.80-1.23; P for interaction=0.03). Conclusions: Our results provide compelling evidence that the hypertension-gout association is bidirectional in Chinese population. The potential interactions of the bidirectional association with sex and obesity deserve further investigations.

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Abstract 43: Association of Plasminogen Activator Inhibitor-1 with Prevalent and Incident Obesity is Independent of Inflammatory Markers: The Multi-Ethnic Study of Atherosclerosis (MESA)

Circulation ◽

10.1161/circ.131.suppl_1.43 ◽

2015 ◽

Vol 131 (suppl_1) ◽

Author(s):

Sadiya S Khan ◽

Donald M Lloyd-Jones ◽

Cheelin Chan ◽

Kiang Liu ◽

Mary Cushman ◽

...

Keyword(s):

Plasminogen Activator ◽

Inflammatory Markers ◽

Smoking Status ◽

Plasminogen Activator Inhibitor ◽

Cox Proportional Hazards ◽

Plasminogen Activator Inhibitor 1 ◽

Ethnic Study ◽

Activator Inhibitor ◽

Pai 1

Background: In experimental animal models, deficiency of plasminogen activator inhibitor-1 (PAI-1) protects against development of obesity. In addition, elevated circulating levels of PAI-1 are associated in cross-sectional studies with prevalent obesity in humans. However, no studies have investigated the prospective association between PAI-1 and incident obesity. Methods: Plasma PAI-1 levels were measured in a random sample of men and women at baseline (2000-2002) in the Multi-Ethnic Study of Atherosclerosis. Obesity was defined as body mass index (BMI) > 30kg/m2. Incident obesity was identified at four follow-up exams (2002-2011) among those who were not obese at baseline. Logistic regression was used to examine the odds ratios (OR) and 95% confidence intervals (CI) of prevalent obesity at baseline. Cox proportional hazards regression was used to estimate hazard ratios (HR) for time to incident obesity. The covariates used for adjustment included baseline demographics (age, race, sex, center), lifestyle risk factors (physical activity, dietary energy intake, smoking status, alcohol consumption, education), and inflammatory markers (CRP and IL-6). Results: In 839 participants mean age was 59 years old; 59% and 47% of the cohort were female and white, respectively. At baseline, each standard deviation (SD) increase in log(PAI-1) level was associated with an odds ratio (OR) for adjusted prevalent obesity of 2.70 (95% CI: 2.21 - 3.30, p<0.001. This association remained significant after further adjustment for IL-6 and CRP with OR 2.39 (95% CI: 1.94-2.94, p<0.001). Over a median follow-up of 8.5 years, 16% of participants developed obesity. The multivariable adjusted hazard ratio for incident obesity was 1.36 (95% CI 1.09-1.69, p<0.001) per 1 SD increase in log(PAI-1). (Table). Conclusions: Elevated PAI-1 levels are associated with prevalent and incident obesity. These findings are consistent with results from murine studies and provide evidence suggesting a potential role of PAI-1 in the pathogenesis of obesity.

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No difference in reoperation rates for nonunions (operative nonunions) in posterior cervical fusions stopping at C7 versus T1/2: a cohort of 875 patients

Journal of Neurosurgery Spine ◽

10.3171/2021.10.spine211085 ◽

2021 ◽

pp. 1-7

Keyword(s):

Proportional Hazards ◽

Smoking Status ◽

Incidence Rates ◽

Cox Proportional Hazards ◽

Adjacent Segment ◽

Spine Registry ◽

Age At Surgery ◽

Significant Difference ◽

Reoperation Rates

OBJECTIVE The challenges of posterior cervical fusions (PCFs) at the cervicothoracic junction (CTJ) are widely known, including the development of adjacent-segment disease by stopping fusions at C7. One solution has been to cross the CTJ (T1/T2) rather than stopping at C7. This approach may have undue consequences, including increased reoperations for symptomatic nonunion (operative nonunion). The authors sought to investigate if there is a difference in operative nonunion in PCFs that stop at C7 versus T1/T2. METHODS A retrospective analysis identified patients from the authors’ spine registry (Kaiser Permanente) who underwent PCFs with caudal fusion levels at C7 and T1/T2. Demographics, diagnoses, operative times, lengths of stay, and reoperations were extracted from the registry. Operative nonunion was adjudicated via chart review. Patients were followed until validated operative nonunion, membership termination, death, or end of study (March 31, 2020). Descriptive statistics and 2-year crude incidence rates and 95% confidence intervals for operative nonunion for PCFs stopping at C7 or T1/T2 were reported. Time-dependent crude and adjusted multivariable Cox proportional hazards models were used to evaluate operative nonunion rates. RESULTS The authors identified 875 patients with PCFs (beginning at C3, C4, C5, or C6) stopping at either C7 (n = 470) or T1/T2 (n = 405) with a mean follow-up time of 4.6 ± 3.3 years and a mean time to operative nonunion of 0.9 ± 0.6 years. There were 17 operative nonunions, and, after adjustment for age at surgery and smoking status, the cumulative incidence rates were similar between constructs stopping at C7 and those that extended to T1/T2 (C7: 1.91% [95% CI 0.88%–3.60%]; T1/T2: 1.98% [95% CI 0.86%–3.85%]). In the crude model and model adjusted for age at surgery and smoking status, no difference in risk for constructs extended to T1/T2 compared to those stopping at C7 was found (adjusted HR 1.09 [95% CI 0.42–2.84], p = 0.86). CONCLUSIONS In one of the largest cohort of patients with PCFs stopping at C7 or T1/T2 with an average follow-up of > 4 years, the authors found no statistically significant difference in reoperation rates for symptomatic nonunion (operative nonunion). This finding shows that there is no added risk of operative nonunion by extending PCFs to T1/T2 or stopping at C7.

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