Increased Incidence Of Lung Cancer Research Articles

Influence of the atmospheric environment on spatial variation of lung cancer incidence in China.

Conducting this research contributes to a deeper understanding of the correlation between atmospheric environmental quality and lung cancer incidence, and provides the scientific basis for formulating effective environmental protection and lung cancer prevention and control strategies. Lung cancer incidence in China has strong spatial variation. However, few studies have systematically revealed the characteristics of the spatial variation in lung cancer incidence, and have explained the causes of this spatial variation in lung cancer incidence from the perspectives of multiple components of the atmospheric environment to explain this spatial variation in lung cancer incidence. To address research limitations, we first analyze the spatial variation and spatial correlation characteristics of lung cancer incidence in China. Then, we build a spatial regression model using GeoDa software with lung cancer incidence as the dependent variable, five atmospheric environment factors-particulate matter 2.5 (PM2.5) concentration, temperature, atmospheric pressure, and elevation as explanatory variables, and four socio-economic characteristics as control variables to systematically analyze the influence and intensity of these factors on lung cancer incidence. The results show that lung cancer incidence in China has apparent changes in geographical and spatial unevenness, and spatial autocorrelation characteristics. In China, the lung cancer incidence is relatively high in Northeast China, while some areas of high lung cancer incidence still exist in Central China, Southwest China and South China, although the overall lung cancer incidence is relatively low. The atmospheric environment significantly affects lung cancer incidence. Different elements of the atmospheric environment vary in the direction and extent of their influence on the development of lung cancer. A 1% increase in PM2.5 concentration is associated with a level of 0.002975 increase in lung cancer incidence. Atmospheric pressure positively affects lung cancer incidence, and an increase in atmospheric pressure by 1% increases lung cancer incidence by a level of 0.026061. Conversely, a 1% increase in temperature is linked to a level of 0.006443 decreases in lung cancer incidence, and a negative correlation exists between elevation and lung cancer incidence, where an increase in elevation by 1% correlates with a decrease in lung cancer incidence by a level of 0.000934. The core influencing factors of lung cancer incidence in the seven geographical divisions of China exhibit variations. This study facilitates our understanding of the spatial variation characteristics of lung cancer incidence in China on a finer scale, while also offering a more diverse perspective on the impact of the atmospheric environment on lung cancer incidence.

Genetic correlation and causal associations between psychiatric disorders and lung cancer risk

BackgroundPatients with certain psychiatric disorders have increased lung cancer incidence. However, establishing a causal relationship through traditional epidemiological methods poses challenges. MethodsAvailable summary statistics of genome-wide association studies of cigarette smoking, lung cancer, and eight psychiatric disorders, including attention deficit/hyperactivity disorder (ADHD), autism, depression, major depressive disorder, bipolar disorder, insomnia, neuroticism, and schizophrenia (range N: 46,350-1,331,010) were leveraged to estimate genetic correlations using Linkage Disequilibrium Score Regression and assess causal effect of each psychiatric disorder on lung cancer using two-sample Mendelian randomization (MR) models, comprising inverse-variance weighted (IVW), weighted median, MR-Egger, pleiotropy residual sum and outlier testing (MR-PRESSO), and a constrained maximum likelihood approach (cML-MR). ResultsSignificant positive correlations were observed between each psychiatric disorder and both smoking and lung cancer (all FDR < 0.05), except for the correlation between autism and lung cancer. Both univariable and the cML-MA MR analyses demonstrated that liability to schizophrenia, depression, ADHD, or insomnia was associated with an increased risk of overall lung cancer. Genetic liability to insomnia was linked specifically to squamous cell carcinoma (SCC), while genetic liability to ADHD was associated with an elevated risk of both SCC and small cell lung cancer (all P < 0.05). The later was further supported by multivariable MR analyses, which accounted for smoking. LimitationsParticipants were constrained to European ancestry populations. Causal estimates from binary psychiatric disorders may be biased. ConclusionOur findings suggest appropriate management of several psychiatric disorders, particularly ADHD, may potentially reduce the risk of developing lung cancer.

The Gap of Health Inequalities Amongst Lung Cancer Patients of Different Socioeconomic Status: A Brief Reference to the Greek Reality.

Lung cancer treatment and patient care are constantly improving, but it remains doubtful whether this applies equally to all socioeconomic groups. It is nowadays well established that there are socioeconomic inequalities regarding lung cancer incidence, screening, effective treatment, overall survival, and prognosis. One of the key contributing factors to low socioeconomic status is low education. Low educational level is correlated with several factors, such as smoking habits, bad lifestyle behaviors, lower paid and unhealthier occupations, polluted neighborhoods, and genetic-familial risk, that lead to increased lung cancer incidence. The disparities regarding lung cancer care are further enhanced by stigma. On this basis and inspired by the gap in health equality among the Greek population, the Greek Society of Lung Cancer initiated a campaign, "MIND THE GAP", to help increase awareness and minimize the gap associated with lung cancer, both in Greece and across Europe. The aim of this review is to explore the gap of health inequalities regarding lung cancer incidence and prognosis between patients of different SES and its root of causality. Key pivotal actions towards bridging this gap are reviewed as well.

Dental health and lung cancer risk in the Golestan Cohort Study

BackgroundPoor oral health has been linked to various systemic diseases, including multiple cancer types, but studies of its association with lung cancer have been inconclusive.MethodsWe examined the relationship between dental status and lung cancer incidence and mortality in the Golestan Cohort Study, a large, prospective cohort of 50,045 adults in northeastern Iran. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between three dental health measures (i.e., number of missing teeth; the sum of decayed, missing, or filled teeth (DMFT); and toothbrushing frequency) and lung cancer incidence or mortality with adjustment for multiple potential confounders, including cigarette smoking and opium use. We created tertiles of the number of lost teeth/DMFT score in excess of the loess adjusted, age- and sex-specific predicted numbers, with subjects with the expected number of lost teeth/DMFT or fewer as the reference group.ResultsDuring a median follow-up of 14 years, there were 119 incident lung cancer cases and 98 lung cancer deaths. Higher DMFT scores were associated with a progressively increased risk of lung cancer (linear trend, p = 0.011). Compared with individuals with the expected DMFT score or less, the HRs were 1.27 (95% CI: 0.73, 2.22), 2.15 (95% CI: 1.34, 3.43), and 1.52 (95% CI: 0.81, 2.84) for the first to the third tertiles of DMFT, respectively. The highest tertile of tooth loss also had an increased risk of lung cancer, with a HR of 1.68 (95% CI: 1.04, 2.70) compared with subjects with the expected number of lost teeth or fewer (linear trend, p = 0.043). The results were similar for lung cancer mortality and did not change substantially when the analysis was restricted to never users of cigarettes or opium. We found no associations between toothbrushing frequency and lung cancer incidence or mortality.ConclusionPoor dental health indicated by tooth loss or DMFT, but not lack of toothbrushing, was associated with increased lung cancer incidence and mortality in this rural Middle Eastern population.

THE DIRECT EFFECT OF COMMUNITY-LEVEL RISK FACTORS ON LUNG CANCER INCIDENCE IN FOUR NEW ENGLAND STATES

Abstract Lung cancer is the most common cancer globally and 70% of diagnoses are among the 65+ population. This study identifies what town-level risk factors are contributing to geographic disparities in 65+ lung cancer in N=796 towns in Connecticut, Massachusetts, New Hampshire, and Rhode Island. Multiple spatial-based analyses (e.g., Moran’s I, Getis-Ord Gi*, mapping) were conducted before running a series of spatial regression models to determine the association between town-level risk factors (i.e., environmental exposures, respiratory conditions prevalence, education rates, smoke free legislation) and lung cancer incidence. Mapping and Moran’s I test suggested the 65+ rates of lung cancer in our sample were non-randomly distributed and clusters of high and low rates were present. A hot spot analysis was conducted in ArcMap 10.8 which identified several significant clusters of 65+ lung cancer. Spatial regression models showed that community rates of comorbid respiratory conditions (65+ asthma, COPD, and tobacco use disorder (TUD)) increased lung cancer incidence by 7%, while increasing ozone emissions were directly associated with a 10% increase in incidence. Comprehensive smoke free legislation coverage was significantly associated with lung cancer incidence, but no increasing or decreasing relationship was found. No effects were found for the percentage of 65+ with low education, or 60+ who were current or former smokers. Spatial regression models allow for results which are specific to the geographic sample used and this study suggests that comorbid respiratory conditions and ozone emissions are directly associated with increased rates of 65+ lung cancer incidence in our sample.

Poor sleep quality association with higher lung cancer risk: a nested case-control study.

Little is known about the relationship between sleep quality and lung cancer incidence. Thus, this study was conducted to investigate the potential connection between sleep quality and lung cancer incidence. We performed and selected a nested case-control study that included 150 lung cancer cases and 150 matched controls based on the Lianyungang cohort. Univariate and multivariate logistic regression was utilized to investigate the connection between potential risk factors and lung cancer incidence risk. In this study, the average age of participants was 66.5 ± 9.1 years, with 58.7% being male, and 52.7% reportedly experiencing sleep quality problems. The results of multivariate logistic regression showed that poor sleep quality was connected to an increased lung cancer incidence risk (P = 0.033, odds ratio = 1.83, 95% confidence interval = [1.05-3.19]) compared with those with good sleep quality. The stratified analyses showed a significantly positive connection between poor sleep quality (vs. good sleep quality) and cancer risk in smokers (vs. non-smoker, P for interaction = 0.085). The combined effect analysis indicated that smokers with poor sleep quality suffered from a 2.79-fold increase in cancer incidence rates when compared with non-smokers with good sleep quality. Poor sleep quality was positively connected to an increased lung cancer incidence risk. In addition, among those individuals with poor sleep quality, smoking increased the lung cancer incidence risk.

Long-term association of air pollution and incidence of lung cancer among older Americans: A national study in the Medicare cohort

BackgroundDespite strong evidence of the association of fine particulate matter (PM2.5) exposure with an increased risk of lung cancer mortality, few studies had investigated associations of multiple pollutants simultaneously, or with incidence, or using causal methods. Disparities were also understudied. ObjectivesWe investigated long-term effects of PM2.5, nitrogen dioxide (NO2), warm-season ozone, and particle radioactivity (PR) exposures on lung cancer incidence in a nationwide cohort. MethodsWe conducted a cohort study with Medicare beneficiaries (aged ≥ 65 years) continuously enrolled in the fee-for-service program in the contiguous US from 2001 to 2016. Air pollution exposure was averaged across three years and assigned based on ZIP code of residence. We fitted Cox proportional hazards models to estimate the hazard ratio (HR) for lung cancer incidence, adjusted for individual- and neighborhood-level confounders. As a sensitivity analysis, we evaluated the causal relationships using inverse probability weights. We further assessed effect modifications by individual- and neighborhood-level covariates. ResultsWe identified 166,860 lung cancer cases of 12,429,951 studied beneficiaries. In the multi-pollutant model, PM2.5 and NO2 exposures were statistically significantly associated with increased lung cancer incidence, while PR was marginally significantly associated. Specifically, the HR was 1.008 (95% confidence interval [CI]: 1.005, 1.011) per 1-μg/m3 increase in PM2.5, 1.013 (95% CI: 1.012, 1.013) per 1-ppb increase in NO2, and 1.005 (0.999, 1.012) per 1-mBq/m3 increase in PR. At low exposure levels, all pollutants were associated with increased lung cancer incidence. Men, older individuals, Blacks, and residents of low-income neighborhoods experienced larger effects of PM2.5 and PR. DiscussionLong-term PM2.5, NO2, and PR exposures were independently associated with increased lung cancer incidence among the national elderly population. Low-exposure analysis indicated that current national standards for PM2.5 and NO2 were not restrictive enough to protect public health, underscoring the need for more stringent air quality regulations.

Quantifying emphysema in lung screening computed tomography with robust automated lobe segmentation.

Anatomy-based quantification of emphysema in a lung screening cohort has the potential to improve lung cancer risk stratification and risk communication. Segmenting lung lobes is an essential step in this analysis, but leading lobe segmentation algorithms have not been validated for lung screening computed tomography (CT). In this work, we develop an automated approach to lobar emphysema quantification and study its association with lung cancer incidence. We combine self-supervised training with level set regularization and finetuning with radiologist annotations on three datasets to develop a lobe segmentation algorithm that is robust for lung screening CT. Using this algorithm, we extract quantitative CT measures for a cohort () from the National Lung Screening Trial and analyze the multivariate association with lung cancer incidence. Our lobe segmentation approach achieved an external validation Dice of 0.93, significantly outperforming a leading algorithm at 0.90 (). The percentage of low attenuation volume in the right upper lobe was associated with increased lung cancer incidence (odds ratio: 1.97; 95% CI: [1.06, 3.66]) independent of risk factors and diagnosis of whole lung emphysema. Quantitative lobar emphysema improved the goodness-of-fit to lung cancer incidence (, ). We are the first to develop and validate an automated lobe segmentation algorithm that is robust to smoking-related pathology. We discover a quantitative risk factor, lending further evidence that regional emphysema is independently associated with increased lung cancer incidence. The algorithm is provided at https://github.com/MASILab/EmphysemaSeg.

Indonesian Society of Respirology (ISR) Consensus Statement on Lung Cancer Screening and Early Detection in Indonesia

Lung cancer is the leading cause of mortality for all cancer globally and in Indonesia. In Indonesia, lung cancer contributes to 12.6% of death of all cancer, making it the number one cause of cancer death, and 8.6% of all cancer incidence in 2018, behind breast, cervical, and colorectal cancer. The total cases per year are expected to almost double from 30,023 in 2018 to 54,983 cases in 2040. Smoking is among the risk factors for lung cancer, after occupational/environmental risk factors, history of lung fibrosis, and family history of cancer. There was a tendency of younger smokers in Indonesia and increased lung cancer incidence and prevalence in the younger population. The median age of lung cancer in Indonesia was younger than in any country, probably due to the younger age of smoking, early onset of carcinogens, asbestos use, and environmental. Lung cancer screening is a voluntary measure to detect lung cancer in the earliest stage, to find cancer at curable disease before symptoms appear in high-risk individuals. Lung cancer early detection is strategies to find cancer earlier after symptoms appear (cough, hemoptysis, dyspnea, chest pain). Low-dose computerized tomography of the thorax (LDCT) screening has been known to reduce lung cancer mortality compared to a chest x-ray (CXR). This Indonesian Society of Respirology consensus statement was aimed to give recommendations on lung cancer screening and early diagnosis in Indonesia.

Disparity in Lung Cancer Screening Among Smokers and Nonsmokers in China: Prospective Cohort Study.

Low-dose computed tomography (LDCT) screening is effective in reducing lung cancer mortality in smokers; however, the evidence in nonsmokers is scarce. This study aimed to evaluate the participant rate and effectiveness of one-off LDCT screening for lung cancer among smokers and nonsmokers. A population-based prospective cohort study was performed to enroll participants aged between 40 and 74 years from 2013 to 2019 from 4 cities in Zhejiang Province, China. Participants who were evaluated as having a high risk of lung cancer from an established risk score model were recommended to undergo LDCT screening. Follow-up outcomes were retrieved on June 30, 2020. The uptake rate of LDCT screening for evaluated high-risk participants and the detection rate of early-stage lung cancer (stage 0-I) were calculated. The lung cancer incidence, lung cancer mortality, and all-cause mortality were compared between the screened and nonscreened groups. At baseline, 62.56% (18,818/30,079) of smokers and 6% (5483/91,455) of nonsmokers were identified as high risk (P<.001), of whom 41.9% (7885/18,818) and 66.31% (3636/5483) underwent LDCT screening (P<.001), respectively. After a median follow-up of 5.1 years, 1100 lung cancer cases and 456 all-cause death cases (116 lung cancer death cases) were traced. The proportion of early-stage lung cancer among smokers was 60.3% (173/287), which was lower than the proportion of 80.3% (476/593) among nonsmokers (P<.001). Among smokers, a higher proportion was found in the screened group (72/106, 67.9%) than the nonscreened group (56/114, 49.1%; P=.005), whereas no significance was found (42/44, 96% vs 10/12, 83%; P=.20) among nonsmokers. Compared with participants who were not screened, LDCT screening in smokers significantly increased lung cancer incidence (hazard ratio [HR] 1.39, 95% CI 1.09-1.76; P=.007) but reduced lung cancer mortality (HR 0.52, 95% CI 0.28-0.96; P=.04) and all-cause mortality (HR 0.47, 95% CI 0.32-0.69; P<.001). Among nonsmokers, no significant results were found for lung cancer incidence (P=.06), all-cause mortality (P=.89), and lung cancer mortality (P=.17). LDCT screening effectively reduces lung cancer and all-cause mortality among high-risk smokers. Further efforts to define high-risk populations and explore adequate lung cancer screening modalities for nonsmokers are needed.

Incidence trends and spatial distributions of lung adenocarcinoma and squamous cell carcinoma in Taiwan

Lung cancer is the second most common cancer in Taiwan. After Taiwan implemented the Tobacco Hazards Prevention Act in 1997, smoking rates declined. However, the incidence rates of lung cancer for both sexes are still increasing, possibly due to risk factors other than smoking. We used age–period–cohort analysis to examine the secular trends of lung cancer incidence rates by histological type in Taiwan. A stabilized kriging method was employed to map these lung cancer incidence rates. Lung adenocarcinoma incidence rates increased, but lung squamous cell carcinoma incidence rates decreased, for both the sexes in recent birth cohorts, particularly in women. In Taiwan, the hotspots of lung adenocarcinoma incidence rates were in the northern, northeastern, and western coastal areas; the incidence rates increased rapidly in the western and southern coastal regions and southern mountainous regions. The high incidence rates of lung squamous cell carcinoma in men were in the southwestern and northeastern coastal areas. The incidence rates rapidly increased in the central and southern coastal and mountainous regions. For both sexes in Taiwan, lung squamous cell carcinoma incidence rates declined from 1997 to 2017, but lung adenocarcinoma increased. The increased incidence rates of lung adenocarcinoma may be related to indoor and outdoor air pollution. Some areas in Taiwan have increasing lung cancer incidence rates, including the northwestern and southern coasts and mountains, and warrant particular attention.

Air pollution and lung cancer survival in Pennsylvania

ObjectiveLung cancer is a leading cause of cancer death in the United States. Exposure to outdoor air pollution (OAP) is associated with increased lung cancer incidence, however little is known about the association of OAP and survival after diagnosis. MethodsWe investigated the effects of OAP and lung cancer survival in Pennsylvania using data from Pennsylvania Cancer Registry. The study population consisted of 252,123 patients diagnosed between 1990 and 2017. The Environmental Protection Agency’s ambient air monitoring network provided information on OAP exposure of NO2, O3, PM2.5, and PM10. Mean OAP exposures were calculated by interpolating exposure concentrations from the five nearest monitors within a 50-kilometer radius of each patient’s residential address from date of diagnosis to date of death or last contact. Cox proportional-hazards models were used to estimate the hazard ratios (HR) for OAP exposures for overall and lung cancer-specific survival. Statistical analyses were stratified by SEER cancer stage groupings (localized, regional, and distant) and adjusted for individual-level and area-level covariates. ResultsMedian survival time was 0.76 [CIs: 0.75, 0.77] years for the study population and for localized, regional, and distant site diagnosis were 2.2 [CIs: 2.17, 2.23], 1.13 [CIs: 1.12, 1.15], and 0.42 [CIs: 0.41, 0.43] years, respectively. NO2 indicated the greatest HR which increased with increasing magnitude of exposure across all cancer staging groups for deaths before 2-years post-diagnosis. HRs varied by stage and magnitude of OAP exposure with greatest overall effects shown in NO2 followed by PM2.5, O3, and PM10. A subgroup analysis of patients with treatment status information (2010–2017) showed similar associations of increasing HRs with increasing exposure. ConclusionThese findings supported the hypotheses that OAP can influence the carcinogenic process, impairing chemotherapy treatment, and provide important public health implications since environmental factors are not often considered in prognosis of survival after diagnosis.

Abstract A026: Altered immune landscape in aging lungs contributes to malignant evolution

Abstract Aging is a major risk factor in increased lung cancer incidence. While most research has focused on age-associated mutation accumulation to explain the late-life increase in cancer incidence, there are tissue environmental forces that both impede and promote cancer evolution. Just as organismal evolution is known to be driven by environmental changes, cellular (somatic) evolution in our bodies is similarly driven by changes in tissue environments. Environmental change promotes selection for new phenotypes that are adaptive to the new context. In our tissues, aging or insult-driven alterations in tissues drives selection for adaptive mutations, and some of these mutations can confer malignant phenotypes. Chronic, low-level inflammation has been associated with aging, termed inflammaging, yet how age-associated changes in lung tissue microenvironments contribute to increased lung cancer incidence has remained largely unknown. Since chronic inflammation has been shown to contribute to tumor development, we hypothesized that inflammaging contributes to increased oncogenic adaptation in the lung. Using either viral delivery of CRISPR constructs to mediate EML4-ALK translocations or ectopic expression of KRAS-G12D, we showed increased adenoma formation in old mice. Importantly, in the EML4-ALK model, we showed that the overexpression of alpha-1 antitrypsin (AAT) in old mice resulted in lower adenoma counts compared to their old wild type counterparts. Flow cytometric analysis of immune cells isolated from bronchoalveolar fluid of young and old mice showed an altered immune landscape, such as increased neutrophils, gamma delta T cells, and Foxp3+ regulatory T cells. Furthermore, analysis of the single-cell RNAseq data from Tabula Muris Consortium demonstrated increased exhaustion markers in the CD8+ T cells and regulatory T cells. Separately, Gene Set Enrichment Analysis (GSEA) of the differential gene expressions of lung epithelial cells isolated from young and old mice revealed enriched pathways related to immune activation and inflammatory response, and immune-suppression markers. Lastly, bulk RNA-seq from lungs of young, old, and old mice overexpressing AAT revealed increased immune cell exhaustion markers and that the overexpression of AAT partially reversed this increase. Finally, analysis of Genotype-Tissue Expression (GTEx) data comparing gene expressions in lungs of young and old humans similarly showed enriched pathways related to immune activation and increased T cell exhaustion markers in the elderly. In addition, using deconvolution methods CiberSort and xCell, we demonstrated altered innate and adaptive immune cell populations, for example, increased neutrophils and regulatory T cells, that are associated with advanced age, similar to aging mice. In conclusion, we showed that there is an exhausted immune microenvironment in aging lungs, that inflammation contributes to the increased tumor initiation, and that decreasing inflammation could decrease the lung tumor incidence by reactivating the immune system. Citation Format: Shi Biao Chia, Catherine Pham-Danis, Hannah Scarborough, Nathaniel Little, Etienne P. Danis, Andrew E. Goodspeed, Charles Dinarello, James DeGregori. Altered immune landscape in aging lungs contributes to malignant evolution [abstract]. In: Proceedings of the AACR Special Conference on the Evolutionary Dynamics in Carcinogenesis and Response to Therapy; 2022 Mar 14-17. Philadelphia (PA): AACR; Cancer Res 2022;82(10 Suppl):Abstract nr A026.

Long-term Exposure to PM10 Increases Lung Cancer Risks: A Cohort Analysis.

PurposeAlthough lung cancer incidences in female never-smokers have increased, few studies focus on explicit investigation. We aimed to investigate the relationship between long-term exposure to ambient particulate matter sized 10 μm or less in diameter (PM10) and the incidence of lung cancer within different genders and smoking status populations.Materials and MethodsWe included Seoul metropolitan residents, aged between 20 and 65 years, who underwent a national health screening examination from 2005–2007 and were followed up until 2015. Individual-level long-term exposure to PM10 was assessed based on subject home addresses. To assess the relationship between PM10 and lung cancer, we estimated hazard ratios (HRs) for increased lung cancer incidence from a 10 μg/m3 increase in PM10.ResultsAmong 5,831,039 individuals, 36,225 (0.6%) developed lung cancer within the 7 years observed. In females, the majority (94.4%) of lung cancer development was found in never-smokers. In adjusted analyses, a significant relationship between lung cancer development and PM10 was observed in males, regardless of smoking status (never-smoker: HR, 1.14 [95% confidence interval (CI), 1.13 to 1.15]; ex-smoker: HR, 1.16 [95% CI, 1.14 to 1.17]; current smoker: HR, 1.18 [95% CI, 1.17 to 1.19]). We also found significant associations in female never- or ex-smokers with smaller HRs (never-smoker: HR, 1.06 [95% CI, 1.05 to 1.07]; ex-smoker: HR, 1.13 [95% CI, 1.02 to 1.23]; current smoker: HR, 1.04 [95% CI, 0.99 to 1.10]).ConclusionOur findings suggest that long-term exposure to PM10 is associated with lung cancer development. A novel approach to lung cancer screening needs to be considered depending on the exposed PM10 level.

Relationship between lung function and lung cancer risk: a pooled analysis of cohorts plus Mendelian randomization study.

Since little consensus has been reached on whether milder reduction in forced expiratory volume in 1s (FEV1) increases lung cancer incidence, we conducted a meta-analysis and performed Mendelian randomization (MR) analysis to explore the association and causal relationship between FEV1 and lung cancer incidence. We conducted a comprehensive search from PubMed, Medline, EMBASE, and Cochrane Library databases as of February 2020. MR analysis was performed using summary data obtained from two large consortia [International Lung Cancer Consortium (ILCCO) and Neale Lab] to assess the possible causality between FEV1 and lung cancer risk. Eight studies involving 88,743 cases were included. The incidence of lung cancer increased with decreasing FEV1.The combined odds ratio (OR) of decreased FEV1 for lung cancer incidence was 1.91 [95% confidence interval (CI) 1.67-2.19; P < 0.001]. Compared with the highest quintile of FEV1 (quintile 5, > 100% of predicted), the OR was 3.06 (95% CI 2.20-4.24; P < 0.001) for quintile 1 (< 70% of predicted), 1.89 (95% CI 1.50-2.38; P < 0.001) for quintile 2 (70-80% of predicted), 1.53 (95% CI 1.31-1.79; P < 0.001) for quintile 3 (80-90% of predicted), and 1.64 (95% CI 1.18-2.28; P = 0.003) for quintile 4 (90-100% of predicted). In subgroup meta-analysis, the correlation between FEV1 and lung cancer risk was different among men (OR = 1.74; 95% CI 1.49-2.03; P < 0.001) and women (OR = 2.80; 95% CI 1.87-4.19; P < 0.001). However, MR analysis showed no causality between the FEV1 and lung cancer risk (OR = 1.199; 95% CI 0.958-1.500; P = 0.114). FEV1 is likely to be a predictor of lung cancer, especially for women. However, genetically decreased FEV1 is not causally correlated with lung cancer incidence.

Relationships between sleep traits and lung cancer risk: a prospective cohort study in UK Biobank.

To prospectively investigate the association between sleep traits and lung cancer risk, accounting for the interactions with genetic predisposition of lung cancer. We included 469 691 individuals free of lung cancer at recruitment from UK Biobank, measuring sleep behaviors with a standardized questionnaire and identifying incident lung cancer cases through linkage to national cancer and death registries. We estimated multivariable-adjusted hazard ratios (HRs) for lung cancer (2177 incident cases) across four sleep traits (sleep duration, chronotype, insomnia, and snoring) and examined the interaction and joint effects with a lung cancer polygenic risk score. A U-shaped association was observed for sleep duration and lung cancer risk, with an 18% higher risk (95% confidence interval [CI]: 1.07 to 1.30) for short sleepers and a 17% higher risk (95% CI: 1.02 to 1.34) for long sleepers compared with normal sleepers (7-8 h/day). Evening preference was associated with elevated lung cancer risk compared with morning preference (HR: 1.25; 95% CI: 1.07 to 1.46), but no association was found for insomnia or snoring. Compared with participants with favorable sleep traits and low genetic risk, those with both unfavorable sleep duration (<7 hours or >8 hours) or evening preference and high genetic risk showed the greatest lung cancer risk (HRsleep duration: 1.83; 95% CI: 1.47 to 2.27; HRchronotype: 1.85; 95% CI: 1.34 to 2.56). Both unfavorable sleep duration and evening chronotype were associated with increased lung cancer incidence, especially for those with low to moderate genetic risk. These results indicate that sleep behaviors as modifiable risk factors may have potential implications for lung cancer risk.

Asthma and asthma symptom control in relation to incidence of lung cancer in the HUNT study

Large prospective studies on asthma, especially asthma symptom control, as a potential risk factor for lung cancer are limited. We followed up 62,791 cancer-free Norwegian adults from 1995–1997 to 2017. Self-reported doctor-diagnosed asthma was categorized into active and non-active asthma. Levels of asthma symptom control were classified into controlled and partially controlled (including partly controlled and uncontrolled) according to the Global Initiative for Asthma guidelines. Incident lung cancer cases were ascertained from the Cancer Registry of Norway. Cox regression models were used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) for possible associations. Totally, 984 participants developed lung cancer during a median follow-up of 21.1 years. After adjustment for smoking and other potential confounders, an increased incidence of lung cancer was found for adults with partially controlled asthma (HR 1.39, 95% CI 1.00–1.92) compared with those without asthma at baseline. Adults with active asthma had a tendency of increased lung cancer incidence (HR 1.29, 95% CI 0.95–1.75). Sensitivity analyses indicated that the observed associations were less likely resulted from reverse causation or residual confounding by smoking. Our findings suggested that proper control of asthma symptoms might contribute to a reduced incidence of lung cancer.

Sex Difference and Smoking Effect of Lung Cancer Incidence in Asian Population.

Simple SummaryThis study analyzed the sex difference in the effect of smoking exposure on lung cancer in terms of absolute and relative risks despite the increasing lung cancer incidence in Asian female never smokers. Lung cancer risk is positively associated with the duration of smoking, quantity of smoking, and pack-years of smoking, and negatively associated with the number of years since smoking cessation for both sexes. However, higher lung cancer incidence in men than in women with the same level of smoking exposure was observed, suggesting a higher susceptibility for lung cancer in men. Sex should be considered in combination with smoking history in the selection of a lung cancer screening target population.This study analyzed the sex difference in the effect of smoking exposure on lung cancer in terms of absolute and relative risks despite the increasing lung cancer incidence in Asian female never smokers. A retrospective cohort study was conducted on individuals aged 40–79 years who participated in the national health screening program in 2007 and 2008 with linkage to the Korea Central Cancer Registry records. We evaluated sex differences in the age-standardized incidence rate (ASR) of lung cancer by smoking history and the hazard ratio (HR) after adjusting for potential confounders. ASRs for male and female never smokers were 92.5 and 38.3 per 100,000 person-years, respectively (rate ratio (RR) = 2.4; 95% confidence interval (CI) = 2.3–2.5). ASRs for male and female current smokers with a 30 pack-year smoking history were 305.3 and 188.4 per 100,000 person-years, respectively (RR = 1.6; 95% CI = 1.3–2.0). Smoking was significantly associated with lung cancer risk for both sexes. HRs for former smokers versus never smokers were 1.27 (95% CI = 1.23–1.33) for men and 1.43 (95% CI = 1.16–1.81) for women. HRs for current smokers versus never smokers were 2.71 (95% CI = 2.63–2.79) for men and 2.70 (95% CI = 2.48–2.94) for women. HRs for lung cancer increased similarly in both men and women according to smoking status. However, among Korean individuals with comparable smoking statuses, lung cancer incidence is higher in men than in women. Sex should be considered in combination with smoking history in the selection of a lung cancer screening target population.

Gender-related trends&#x0D; in key epidemiological indicators of lung cancer&#x0D; in the Republic of Kazakhstan, 2014-2018

Relevance: Over the past decades, lung cancer (LC) incidence worldwide is adding about 1.5% each year. The risk of LC&#x0D; development increases 4-5 times with age. The mortality-to-incidence ratio (MIR) in LC is the most unfavorable – up to 95.6%&#x0D; of patients die.&#x0D; The purpose of this study was to analyze the epidemiological situation with lung cancer in the Republic of Kazakhstan&#x0D; over the past five years, with the assessment of key epidemiological indicators by gender.&#x0D; Results: In the previous five years (2014-2018), the men to women ratio among LC patients was equal to 4.2:1 and remained&#x0D; stable. A gradual decline in mortality (16‰ in 2014 to 12.9‰ in 2018) correlated with the MIR dynamic pattern (67.5% in&#x0D; 2014 to 60.0% in 2018). The standardized LC incidence in men was declining steadily (46.8‰ in 2014 to 43.0‰ in 2018). A&#x0D; more evident decrease in male mortality from LC (32.0‰ in 2014 to 24.2‰ in 2018) was due to the progress recently achieved&#x0D; in LC diagnostics and treatment in the Republic of Kazakhstan. On the contrary, the LC incidence in women increased by 2.6% a&#x0D; year (7.6‰ in 2014 to 7.8‰ in 2018). The female mortality from LC was declining steadily (4.6‰ in 2014 to 3.5‰ in 2018),&#x0D; with a negative growth rate of minus 31.4%.&#x0D; Conclusion: The analysis of epidemiologic indicators for LC in the Republic of Kazakhstan showed a general downward&#x0D; trend in incidence and mortality regardless of gender. However, we can expect an increase in the female incidence of LC in sync&#x0D; with the global trend. The study period has witnessed the improvement in both the primary diagnostics (due to the renewal of&#x0D; diagnostic equipment in the country) and treatment of LC (through the introduction in the Republic of methods of molecular&#x0D; genetic studies which are the basis for the state-financed personalized drug therapy with targeted agents).

Characteristics of lung cancer in idiopathic pulmonary fibrosis with single lung transplant versus non-transplanted patients: a retrospective observational study

BackgroundPatients with idiopathic pulmonary fibrosis (IPF) have significantly higher incidence of lung cancer (LC) relative to the general population. There is a further increase in LC incidence in patients with...