Risk Of Lung Cancer Mortality Research Articles

Cancer mortality risk in the Urals Cohort of Exposed Population Offspring

The objective of the study is to analyze solid cancer mortality and estimate the risk value of solid cancer mortality in the offspring of parents irradiated in the Southern Urals, depending on the dose to the parents' gonads as well as to conduct a preliminary assessment of the mortality risk from cancer of individual locations depending on the gonadal dose. The issue of the transgenerational effects of the human gonad exposure is still very important. There exists conclusive evidence of the presence of such effects in experimental animals. However, there is no proof of the existence of these effects in humans despite a great number of research on this subject. International scientific community and international organizations, UNSCEAR and ICRP being among them, regard this issue as the one that has not been solved yet and requires further studies. Urals Cohort of offspring of the population exposed on the Techa River and on the territory of the East Ural radioactive trace was established in the Urals research Center for Radiation medicine in 2022. The key feature of the cohort is the exclusion of the offspring with postnatal exposure. The size of the cohort as of September 2023 is 31,154 persons. The number of person-years over the whole follow-up period from 1950 through 2020 is 1 226 380. Mean dose to the gonads of mothers of all the cohort members is 41 mGy, to those of the fathers' — 35 mGy, mean combined gonad dose is 76 mGy. Over the whole follow-up period 3,774 deaths from all causes including 284 deaths from solid cancers were registered in the cohort. The mean age of the cohort members at the end of the follow-up period was 42 years. The risk of death was analyzed using Poisson regression by the programs of the EPICURE statistical software package. Three models of dose dependence were tested: linear, quadratic, and linear-quadratic models of paternal gonadal dose, maternal gonadal dose, and total gonadal dose. Mortality risk analysis of all solid cancers in the offspring cohort showed no statistically significant effect with parental gonadal dose (we have obtained positive although statistically insignificant values of solid cancers mortality risk) which is consistent with the results of other studies in human populations. At the same time, the analysis for the first time obtained a statistically significant linear dependence of the solid cancer mortality risk in offspring with father's age over 45 years depending on the dose to the father's gonads. The excess relative risk of death was 8.09/Gy, (0.51-22.93), p < 0.05. Also, for the first time, evidence of dose dependence of the mortality risk of lung cancer in male offspring on maternal gonadal dose, paternal gonadal dose, and combined gonadal dose was obtained. The values of excess relative risk of lung cancer and 95% confidence intervals according to the linear model were 5.39/Gy (0.46; 15.56) from paternal gonad dose, 4.36/Gy (0.15; 13.48) from maternal gonad dose, and - 3.95/Gy (0.55; 12.14) from combined gonad dose. Point risk estimates of lung cancer at this stage are characterized by wide confidence intervals and require additional studies to assess the influence of possible effect modifiers, but with a high degree of probability indicate the presence of dose dependence of this effect. Increasing the follow-up period and attained age, will increase the number of cancers in the future and will reduce dose response uncertainties and provide more accurate estimates of the risk of death in the offspring cohort.

Association between family history with lung cancer incidence and mortality risk in the Asia Cohort Consortium.

Family history of lung cancer (FHLC) has been widely studied but most prospective cohort studies have primarily been conducted in non-Asian countries. We assessed the association between FHLC with risk of lung cancer (LC) incidence and mortality in a population of East Asian individuals. A total of 478,354 participants from 11 population-based cohorts in the Asia Cohort Consortium were included. A Cox proportional hazards regression model was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). A total of 7,785 LC incident cases were identified. FHLC (any LC subtype) was associated with an increased risk of LC incidence (HR = 1.45, 95% CI = 1.30-1.63). The positive association was observed in men and women (HR = 1.44, 95% CI = 1.26-1.66 in men; HR = 1.47, 95% CI = 1.22-1.79 in women), and in both never-smokers and ever-smokers (HR = 1.43, 95% CI = 1.18-1.73 in never-smokers; HR = 1.46, 95% CI =1.27-1.67 in ever-smokers). FHLC was associated with an increased risk of lung adenocarcinoma (HR = 1.63, 95% CI: 1.36-1. 94),squamous cell carcinoma (HR = 1.88, 95% CI: 1.46-2.44), and other non-small cell LC (HR = 1.94, 95% CI: 1.02-3.68). However, we found no evidence of significant effect modification by sex, smoking status, and ethnic groups. In conclusion, FHLC was associated with increased risk of LC incidence and mortality, and the associations remained consistent regardless of sex, smoking status and ethnic groups among the East Asian population.

Long-term exposure to ambient air pollution and risk of lung cancer – A comparative analysis of incidence and mortality in four administrative cohorts in the ELAPSE study

BackgroundStudies have linked air pollution to lung cancer incidence and mortality, but few have compared these associations, which may differ due to cancer survival variations. We aimed to evaluate the association between long-term air pollution exposure and lung cancer incidence and compare findings with previous lung cancer mortality analyses within the same cohorts. MethodsWe analyzed four population-based administrative cohorts in Denmark (2000–2015), England (2011–2017), Norway (2001–2016) and Rome (2001–2015). We assessed residential exposure to annual average fine particulate matter (PM2.5), nitrogen dioxide (NO₂), black carbon (BC), and warm-season ozone (O3) using Europe-wide land use regression models. We used Cox proportional hazard models to evaluate cohort-specific hazard ratios (HRs) and 95% confidence intervals (CIs) for lung cancer incidence identified using hospital admission records (English and Roman cohorts) or cancer registries (Danish and Norwegian cohorts). We evaluated the associations at low exposure levels using subset analyses and natural cubic splines. Cohort-specific HRs were pooled using random-effects meta-analyses, separately for incidence and mortality. ResultsOver 93,733,929 person-years of follow-up, 111,949 incident lung cancer cases occurred. Incident lung cancer was positively associated with PM2.5, NO2 and BC, and negatively associated with O3. The negative O3 association became positive after adjustment for NO2. Associations were almost identical or slightly stronger for lung cancer incidence than mortality in the same cohorts, with respective meta-analytic HRs (95% CIs) of 1.14 (1.06, 1.22) and 1.12 (1.02, 1.22) per 5 μg/m3 increase in PM2.5, and 1.10 (1.04, 1.16) and 1.09 (1.02, 1.16) per 10 μg/m3 increase in NO2. Positive associations persisted for both incidence and mortality at low pollution levels with similar magnitude. ConclusionsWe found similarly elevated risks of lung cancer incidence and mortality in association with residential exposure to PM2.5, NO2 and BC in meta-analyses of four European administrative cohorts, which persisted at low pollution levels.

Space and space-time cluster at high risk of lung cancer mortality in the south-central macrozone, Chile (1990-2019)

Space and space-time cluster at high risk of lung cancer mortality in the south-central macrozone, Chile (1990-2019)

Breastfeeding may reduce the effects of maternal smoking on lung cancer mortality in adult offspring: a prospective cohort study.

Although previous research has indicated a correlation between smoking and the mortality rate in patients with lung cancer, the impact of early life factors on this relationship remains unclear and requires further investigation. This study aimed to investigate the hypothesis that breastfeeding reduces the risk of lung cancer-related death. The authors conducted a prospective cohort study involving 501859 participants recruited from the United Kingdom Biobank to explore the potential association between breastfeeding and the risk of lung cancer mortality using a Cox proportional hazards model. Subsequently, the polygenic risk score for lung cancer was calculated to detect interactions between genes and the environment. Over a median follow-up duration of 11.8 years, encompassing a total of 501859 participants, breastfeeding was found to reduce the risk of lung cancer-related death and the impact of maternal smoking on lung cancer mortality in adult offspring. This association remained consistent after stratification. Furthermore, the influence of maternal smoking and breastfeeding on the risk of lung cancer mortality was significant at a high genetic risk level. Breastfeeding can reduce the risk of lung cancer-related death and the impact of maternal smoking on lung cancer mortality in adult offspring. This correlation has the potential to reduce the probability of lung-cancer-related deaths in subsequent generations.

The Use of a Tailored Decision Aid to Improve Understanding of Lung Cancer Screening in People With HIV

People with HIV are at increased risk for lung cancer and multimorbidity, complicating the balance of risks and benefits of lung cancer screening. We previously adapted Decision Precision (screenlc.com) to guide shared decision-making for lung cancer screening in people with HIV. Does an HIV-adapted and personally tailored decision aid improve shared decision-making regarding lung cancer screening in people with HIV as measured by knowledge, decisional conflict, and acceptability? This was a single-arm pilot trial of the decision aid in 40 participants with HIV eligible for lung cancer screening. The decision aid included personalized screening recommendations and HIV-specific, five-year risk estimates of lung cancer and all-cause mortality. Participants reviewed the decision aid at shared decision-making visits and completed pre- and post-visit surveys with measures of knowledge about lung cancer screening, acceptability, and decisional conflict. The 40 enrolled participants were a median 62 years old and 60% were currently smoking with median five-year risks of lung cancer and all-cause mortality of 2.0% (IQR 1.4-3.3%) and 4.1% (IQR 3.3-7.9%). Personalized recommendations included "Encourage Screening" for 53% of participants and "Preference Sensitive" recommendations for the remainder. Participants showed improvement in two validated knowledge measures with relative improvement of 60% (p<0.001) on the LCS-12 and 27% (p<0.001) on the LKS-7, with significant improvement on questions regarding false-positive and false-negative findings, incidental findings, lung cancer-specific mortality benefit, and the possible harms of screening. Participants reported low scores on the decisional conflict scale (median score 0, IQR 0-5) and high acceptability. Ninety percent ultimately underwent screening within one month of the visit. This HIV-adapted and personally tailored decision aid improved participants' knowledge of risks, benefits, and characteristics of screening with low decisional conflict and high acceptability. This decision aid can enable high-quality shared decision-making in this high-risk population.

Glycemic status, insulin resistance, and mortality from lung cancer among individuals with and without diabetes

BackgroundThe effects of glycemic status and insulin resistance on lung cancer remain unclear. We investigated the associations between both glycemic status and insulin resistance, and lung cancer mortality, in a young and middle-aged population with and without diabetes.MethodsThis cohort study involved individuals who participated in routine health examinations. Lung cancer mortality was identified using national death records. Cox proportional hazards models were used to calculate hazard ratios (HRs) with 95% CIs for lung cancer mortality risk.ResultsAmong 666,888 individuals (mean age 39.9 ± 10.9 years) followed for 8.3 years (interquartile range, 4.6–12.7), 602 lung cancer deaths occurred. Among individuals without diabetes, the multivariable-adjusted HRs (95% CI) for lung cancer mortality comparing hemoglobin A1c categories (5.7–5.9, 6.0–6.4, and ≥ 6.5% or 39–41, 42–46, and ≥ 48 mmol/mol, respectively) with the reference (< 5.7% or < 39 mmol/mol) were 1.39 (1.13–1.71), 1.72 (1.33–2.20), and 2.22 (1.56–3.17), respectively. Lung cancer mortality was associated with fasting blood glucose categories in a dose–response manner (P for trend = 0.001) and with previously diagnosed diabetes. Insulin resistance (HOMA-IR ≥ 2.5) in individuals without diabetes was also associated with lung cancer mortality (multivariable-adjusted HR, 1.41; 95% CI, 1.13–1.75). These associations remained after adjusting for changing status in glucose, hemoglobin A1c, insulin resistance, smoking status, and other confounders during follow-up as time-varying covariates.ConclusionsGlycemic status within both diabetes and prediabetes ranges and insulin resistance were independently associated with an increased risk of lung cancer mortality.

Identifying Populations at Risk for Lung Cancer Mortality from the National Health and Nutrition Examination Survey (2001-2018) Using the 2021 USPSTF Screening Guidelines.

Lung cancer (LC) is the leading cause of cancer mortality in the United States. To combat this predicament, early screening and critically assessing its risk factors remain crucial. The aim of this study was to identify the value of specific factors from the National Health and Nutrition Examination Survey (NHANES) from 2001-2018, as they relate to lung cancer mortality in the US Preventive Services Task Force (USPSTF)-eligible population. A total of 3545 adults who met USPSTF criteria were extracted from 81,595 NHANES participants. The LC Death Risk Assessment Tool was used to calculate the number of deaths per 1000 individuals. The Mann-Whitney U test and one-way ANOVA determined the statistical significance of the factors involved in LC mortality. Male sex, African and Hispanic ethnicity, lower education attainment, and secondhand exposure to cigarette smoke correlated with an increased risk of LC mortality. Additionally, the factor of emotional support from NHANES data was analyzed and did not show any benefit to reducing risk. By identifying individuals at high-risk, preventative measures can be maximized to produce the best possible outcome.

Three-year follow-up study reveals improved survival rate in NSCLC patients underwent guideline-concordant diagnosis and treatment.

No studies in China have assessed the guideline-concordance level of the first-course of non-small cell lung cancer (NSCLC) diagnosis and treatment and its relationship with survival. This study comprehensively assesses the current status of guideline-concordant diagnosis (GCD) and guideline-concordant treatment (GCT) of NSCLC in China and explores its impact on survival. First course diagnosis and treatment data for NSCLC patients in Liaoning, China in 2017 and 2018 (n=1828) were used and classified by whether they underwent GCD and GCT according to Chinese Society of Clinical Oncology (CSCO) guidelines. Pearson's chi-squared test was used to determine unadjusted associations between categorical variables of interest. Logistic models were constructed to identify variables associated with GCD and GCT. Kaplan-Meier analysis and log-rank tests were used to estimate and compare 3-year survival rates. Multivariate Cox proportional risk models were constructed to assess the risk of cancer mortality associated with guideline-concordant diagnosis and treatment. Of the 1828 patients we studied, 48.1% underwent GCD, and 70.1% underwent GCT. The proportions of patients who underwent both GCD and GCT, GCD alone, GCT alone and neither GCD nor GCT were 36.7%, 11.4%, 33.5% and 18.4%, respectively. Patients in advanced stage and non-oncology hospitals were significantly less likely to undergo GCD and GCT. Compared with those who underwent neither GCD nor GCT, patients who underwent both GCD and GCT, GCD alone and GCT alone had 35.2%, 26.7% and 35.7% higher 3-year survival rates; the adjusted lung cancer mortality risk significantly decreased by 29% (adjusted hazard ratio[aHR], 0.71; 95% CI, 0.53-0.95), 29% (aHR, 0.71; 95% CI, 0.50-1.00) and 32% (aHR, 0.68; 95% CI, 0.51-0.90). The 3-year risk of death is expected to be reduced by 29% if patients with NSCLC undergo both GCD and GCT. There is a need to establish an oncology diagnosis and treatment data management platform in China to monitor, evaluate, and promote the use of clinical practice guidelines in healthcare settings.

Greenness, air pollution, and mortality risk: a retrospective cohort study of patients with lung cancer in China

ABSTRACT The association between long-term exposure to air pollution and mortality from lung cancer has been established, yet evaluations of the potential mitigating effects of greenness on this impact are scarce. We conducted a cohort study in Pingyi County. A two-level Cox proportional hazards regression model was used to examine the associations among long-term exposure to air pollution, residential greenness, and lung cancer mortality. Among the examined pollutants, nitrogen dioxide exhibited the most significant adverse effects and highest risk of lung cancer mortality, with hazard ratio (HR) = 2.783 (95% confidence interval [CI]: 1.885–4.107) for all-cause mortality, HR = 2.492 (95%CI: 1.659–3.741) for tumour-related mortality, and HR = 2.431 (95%CI: 1.606–3.678) for lung cancer mortality. Higher greenness values were associated with a reduced risk of lung cancer mortality. These findings suggest the importance of implementing strategies for increasing greenness to reduce the health impacts of air pollution.

Impact of OLD/Emphysema in LC Mortality Risk in Screening Programs: An Analysis of NLST and P-IELCAP

IntroductionThe impact of obstructive lung disease (OLD) and emphysema on lung cancer (LC) mortality in patients undergoing LC screening is controversial. MethodsPatients with spirometry and LC diagnosed within the first three rounds of screening were selected from the National Lung Screening Trial (NLST) and from the Pamplona International Early Lung Cancer Detection Program (P-IELCAP). Medical and demographic data, tumor characteristics, comorbidities and presence of emphysema were collected. The effect of OLD and emphysema on the risk of overall survival was assessed using unadjusted and adjusted Cox models, competing risk regression analysis, and propensity score matching. ResultsData from 353 patients with LC, including 291 with OLD and/or emphysema and 62 with neither, were analyzed. The median age was 67.3 years-old and 56.1% met OLD criteria, predominantly mild (1: 28.3%, 2: 65.2%). Emphysema was present in 69.4% of the patients. Patients with OLD and/or emphysema had worse survival on univariate analysis (HR: 1.40; 95% CI: 0.86–2.31; p=0.179). However, after adjusting for LC stage, age, and sex, the HR was 1.02 (95% CI: 0.61–1.70; p=0.952). Specific LC survival between both groups showed an adjusted HR of 0.90 (95% CI: 0.47–1.72; p=0.76). Propensity score matching found no statistically significant difference in overall survival (HR: 1.03; 95% CI: 0.59–1.9; p=0.929). ConclusionThe survival of LC patients diagnosed in the context of screening is not negatively impacted by the coexistence of mild OLD and/or emphysema.

Estimated Doses to the Heart, Lungs and Oesophagus and Risks From Typical UK Radiotherapy for Early Breast Cancer During 2015–2023

PurposeBreast cancer radiotherapy can increase the risks of heart disease, lung cancer and oesophageal cancer. At present, the best dosimetric predictors of these risks are mean doses to the whole heart, lungs and oesophagus, respectively. We aimed to estimate typical doses to these organs and resulting risks from UK breast cancer radiotherapy. MethodsA systematic review and meta-analysis was conducted of planned or delivered mean doses to the whole heart, lungs or oesophagus from UK breast cancer radiotherapy in studies published during 2015–2023. Average mean doses were summarised for combinations of laterality and clinical targets. Heart disease and lung cancer mortality risks were then estimated using established models. ResultsFor whole heart, thirteen studies reported 2893 doses. Average mean doses were higher in left than in right-sided radiotherapy and increased with extent of clinical targets. For left-sided radiotherapy, average mean heart doses were: 2.0 Gy (range 1.2–8.0 Gy) breast/chest wall, 2.7 Gy (range 0.6–5.6 Gy) breast/chest wall with either axilla or supraclavicular nodes and 2.9 Gy (range 1.3–4.7 Gy) breast/chest wall with nodes including internal mammary. For right-sided radiotherapy, average mean heart doses were: 1.0 Gy (range 0.3–1.0 Gy) breast/chest wall and 1.2 Gy (range 1.0–1.4 Gy) breast/chest wall with either axilla or supraclavicular nodes. There were no whole heart dose estimates from right internal mammary radiotherapy. For whole lung, six studies reported 2230 doses. Average mean lung doses increased with extent of targets irradiated: 2.6 Gy (range 1.4–3.0 Gy) breast/chest wall, 3.0 Gy (range 0.9–5.1 Gy) breast/chest wall with either axilla or supraclavicular nodes and 7.1 Gy (range 6.7–10.0 Gy) breast/chest wall with nodes including internal mammary. For whole oesophagus, two studies reported 76 doses. Average mean oesophagus doses increased with extent of targets irradiated: 1.4 Gy (range 1.0–2.0 Gy) breast/chest wall with either axilla or supraclavicular nodes and 5.8 Gy (range 1.9–10.0 Gy) breast/chest wall with nodes including internal mammary. ConclusionsThe typical doses to these organs may be combined with dose-response relationships to estimate radiation risks. Estimated 30-year absolute lung cancer mortality risks from modern UK breast cancer radiotherapy for patients irradiated when aged 50 years were 2–6% for long-term continuing smokers, and <1% for non-smokers. Estimated 30-year mortality risks for heart disease were <1%.

Impaired lung function and lung cancer risk in 461 183 healthy individuals: a cohort study

BackgroundIt has been known that smoking and various lung diseases including lung cancer can cause lung function impairment. However, the impact of different types of lung function impairments, such as...

Updated Analysis of Radon Exposure and Lung Cancer Mortality in the Cohort of Newfoundland Fluorspar Miners (1950-2016).

The commercial mining of fluorspar in St. Lawrence Newfoundland began in 1933. Miners who worked underground were exposed to high levels of radon progeny, especially before ventilation was introduced into the mines in 1960. The mean cumulative radon exposure for underground miners in this cohort was 380.9 working level months (WLM). A series of studies of this cohort have characterized the increased risks of lung cancer mortality due to radon. We have extended the follow-up of this cohort an additional 15 years to provide additional insights on the risks of low levels of radon exposure, and the modifying effects of time since exposure, age at first exposure, attained age, duration of exposure, and cigarette smoking. The cohort consisted of 1,735 underground and 315 male surface miners who, combined, accrued 81,650 person-years of follow-up. The mortality experience of the cohort was determined from 1950-2016 through record linkage to Canadian national death data. Individual-level estimates of exposure to radon progeny, in WLMs, were determined for each year of employment. We compared the mortality experience of the underground miners to Newfoundland men using the standardized mortality ratio (SMR). Poisson regression models were fit to estimate excess relative risks (ERR) per 100 WLM. There were 236 lung cancer deaths identified, and of these, 221 occurred among underground workers. The SMR for lung cancer among underground miners compared to Newfoundland men was 2.67 (95% CI: 2.33, 3.04). The ERR per 100 WLM for lung cancer mortality, assuming a 5-year exposure lag, was 0.41 (95% CI: 0.23, 0.59). Attained age and time since exposure were important modifiers to the radon-lung cancer relationship. The joint relationship between smoking and radon on lung cancer risk was sub-additive, however, the smoking data were limited and available for only half of the cohort.

Ultra-processed food consumption and risk of chronic respiratory diseases mortality among adults: evidence from a prospective cohort study

PurposeThe purpose of the study was to determine the relationships between ultra-processed food (UPF) consumption and risk of mortality due to chronic respiratory diseases (CRDs) overall, chronic obstructive pulmonary disease (COPD), and lung cancer.MethodsA total of 96,607 participants aged 55 years and over were included from the Prostate, Lung, Colorectal and Ovarian (PLCO) cancer trial. Dietary intake was measured using food frequency questionnaire. Cox regression was fitted to estimate the risk of all-cause mortality and mortality due to CRDs overall, COPD and lung cancer associated with UPF intake. Competing risk regression was used to account for deaths from other causes and censoring.ResultsDuring the follow-up of 1,379,655.5 person-years (median 16.8 years), 28,700 all-cause, 4092 CRDs, 2015 lung cancer and 1,536 COPD mortality occurred. A higher intake of UPF increased the risk of mortality from CRDs overall by 10% (HR 1.10; 95% CI 1.01, 1.22) and COPD by 26% (HR 1.26; 95% CI 1.06, 1.49) but not associated with lung cancer mortality risk (HR 0.97; 95% CI 0.84, 1.12). However, the risk of lung cancer increased by 16% (HR 1.16; 95% CI 1.01, 1.34) in the highest UPF intake after multiple imputation. Dose–response relationships existed for CRDs and COPD mortality but not lung cancer.ConclusionUPF consumption was associated with an increased risk of CRD mortality. The association between UPF consumption and lung cancer mortality is inconclusive and only significant when multiple imputation was applied.

Association between reproductive factors with lung cancer incidence and mortality: A pooled analysis of over 308,000 females in the Asia cohort consortium.

Previous studies have investigated the association between reproductive factors and lung cancer risk; however, findings have been inconsistent. In order to assess this association among Asian women, a total of 308,949 female participants from 11 prospective cohorts and four Asian countries (Japan, Korea, China, and Singapore) were included. Cox proportional hazards regression models were used to estimate the hazard ratios (HR) and 95% confidence intervals (CIs). A total of 3,119 primary lung cancer cases and 2247 lung cancer deaths were identified with a mean follow-up of 16.4 years. Parous women had a lower risk of lung cancer incidence and mortality as compared with nulliparous women, with HRs of 0.82 (95% CI = 0.70-0.96) and 0.78 (95% CI = 0.65-0.94). The protective association of parity and lung cancer incidence was greater among ever-smokers (HR = 0.66, 95% CI = 0.49-0.87) than in never-smokers (HR = 0.90, 95% CI = 0.74-1.09) (P-interaction = 0.029). Compared with age at first delivery ≤20 years, older age at first delivery (21-25, ≥26 years) was associated with a lower risk of lung cancer incidence and mortality. Women who ever used hormone replacements had a higher likelihood of developing non-small cell lung cancer (HR = 1.31, 95% CI = 1.02-1.68), compared to those who never used hormone replacements. Future studies are needed to assess the underlying mechanisms, the relationships within these female reproductive factors, and the potential changes in smoking habits over time.

A Comprehensive Analysis of Risk Assessment of Particulate Matter in Five Health Centers in Akure, Nigeria

This study presents a comprehensive assessment of indoor particulate matter (PM) concentrations, focusing on PM1, PM2.5, and PM10 in five primary health centers (PHCs): Arakale (Urban), the Federal College of Agriculture (FECA) (Urban), Iju (semi-urban), Oba-Ile (semi-urban), and Owode (Rural) within Akure local government areas in Nigeria. The primary novelty of this research lies in its detailed exploration of the toxicity potential of these PM fractions, providing valuable insights into the local air quality and associated health risks. This study assesses the health implications by calculating the toxicity potential (TP), relative risk (RR), excess risk (ER), and attributable fractions (Afs) for cardiopulmonary and lung cancer mortality. The results reveal varying RR values for all-cause mortality, with Arakale showing a slight elevation (RR: 1.061), indicating potential health risks. ER values for cardiopulmonary mortality range from 14.728 ± 7.25 to 19.04 ± 0.38, emphasizing the substantial excess risk associated with long-term PM2.5 exposure. The study also uncovers Afs for cardiopulmonary mortality ranging between 11.03 ± 0.31 and 19.22 ± 0.04, underscoring the significant contribution of PM to cardiovascular and respiratory health risks. Similarly, Afs for lung cancer mortality range from 10.03 ± 0.012 to 17.13 ± 0.10, highlighting the substantial association between PM2.5 exposure and lung cancer risk. These findings underscore the urgent need for targeted air quality management strategies and public health interventions in the studied locations to mitigate the heightened health risks associated with particulate matter pollution. The calculated RR, ER, and AF values offer crucial insights into the complex relationship between PM exposure and adverse health outcomes, providing a foundation for informed decision-making and future research endeavors.

Cardiovascular health, sleeping duration, and risk of mortality in current and former smokers

Background and aimsTo investigate the associations of ideal cardiovascular health metrics (ICVHMs) with all-cause mortality among former and current smokers compared with never smokers. Methods and resultsA total of 378,147 participants [mean age (SD) years: 56.3 (8.1); 47.2 % men] were included from the UK Biobank cohort. The ICVHMs were combined Life's simple 7 from the American Heart Association and sleep duration time. The association was explored using COX regression models. During a median follow-up of 13.3 years, we documented 24,594 deaths. Compared with never smokers, among former smokers, the multivariable-adjusted hazard ratio (HR) for all-cause mortality was 1.82 (95%CI 1.71–1.92) for participants who had ≤2 ICVHMs and 1.03 (0.97–1.10) for participants who had ≥6 ICVHMs; among current smokers, the HRs for mortality were 2.74 (2.60–2.89) and 2.18 (1.78–2.67). The phenomenon was more pronounced among participants younger than 60 years [HR (95%CI), 1.82 (1.71–1.95) for ≤2 ICVHMs vs 1.04 (0.96–1.12) for ≥6 ICVHMs with age ≥60 years and 1.83 (1.62–2.06) vs 0.98 (0.88–1.11) with age <60 years among former smokers; 2.66 (2.49–2.85) vs 2.44 (1.84–3.24) with age ≥60 years and 2.85 (2.62–3.10) vs 1.96 (1.47–2.61) with age <60 years among current smokers]. In addition, the HR for mortality of each 1-number increment in ICVHMs was 0.87 (0.86–0.89) among former smokers and 0.91 (0.89–0.94) among current smokers. ConclusionOur findings indicated the importance of adherence to have more ICVHMs in the mortality risk among former smokers, and priority of smoking cessation in current smokers. ImplicationsStudies have found that former smokers still have higher risks of lung cancer and all-cause mortality than never-smokers. The next question is whether the effects of previous or current smoking could be ameliorated by eight ideal cardiovascular health metrics (ICVHMs). We aim to explore whether ICVHMs may counteract the risk of all-cause mortality among former and current smokers. The results showed that only former smokers with ≥6 ICVHMs exhibited a comparable risk of all-cause mortality with never smokers. Furthermore, current smokers even having ≥6 ICVHMs still exhibited a higher risk of all-cause mortality compared with never smokers.

Identification of key genes in chronic intermittent hypoxia-induced lung cancer progression based on transcriptome sequencing

BackgroundObstructive sleep apnea (OSA) is associated with increased risk of lung cancer mortality. Nevertheless, little is known about the underlying molecular mechanisms. This research aimed to investigate differentially expressed genes (DEGs) and explore their function in Lewis lung carcinoma (LLC)-bearing mice exposed to chronic intermittent hypoxia (CIH) by transcriptome sequencing.MethodsLung cancer tissues in LLC-bearing mice exposed to CIH or normoxia were subjected for transcriptome sequencing to examine DEGs. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses were employed to explore the function of DEGs. To evaluate the prognostic value of DEGs, the Kaplan–Meier survival analysis in combination with Cox proportional hazard model were applied based on The Cancer Genome Atlas.ResultsA total of 388 genes with 207 up-regulated and 181 down-regulated genes were differentially expressed between the CIH and normoxia control groups. Bioinformatics analysis revealed that the DEGs were related to various signaling pathways such as chemokine signaling pathway, IL-17 signaling pathway, TGF-β signaling pathway, transcriptional misregulation in cancer, natural killer cell mediated cytotoxicity, PPAR signaling pathway. In addition, the DEGs including APOL1, ETFB, KLK8, PPP1R3G, PRL, SPTA1, PLA2G3, PCP4L1, NINJ2, MIR186, and KLRG1 were proven to be significantly correlated with poorer overall survival in lung adenocarcinoma.ConclusionsCIH caused a significant change of gene expression profiling in LLC-bearing mice. The DEGs were found to be involved in various physiological and pathological processes and correlated with poorer prognosis in lung cancer.

Lifetime excess absolute risk for lung cancer due to exposure to radon: results of the pooled uranium miners cohort study PUMA

The Pooled Uranium Miners Analysis (PUMA) study is the largest uranium miners cohort with 119,709 miners, 4.3 million person-years at risk and 7754 lung cancer deaths. Excess relative rate (ERR) estimates for lung cancer mortality per unit of cumulative exposure to radon progeny in working level months (WLM) based on the PUMA study have been reported. The ERR/WLM was modified by attained age, time since exposure or age at exposure, and exposure rate. This pattern was found for the full PUMA cohort and the 1960 + sub-cohort, i.e., miners hired in 1960 or later with chronic low radon exposures and exposure rates. The aim of the present paper is to calculate the lifetime excess absolute risk (LEAR) of lung cancer mortality per WLM using the PUMA risk models, as well as risk models derived in previously published smaller uranium miner studies, some of which are included in PUMA. The same methods were applied for all risk models, i.e., relative risk projection up to <95 years of age, an exposure scenario of 2 WLM per year from age 18–64 years, and baseline mortality rates representing a mixed Euro-American-Asian population. Depending upon the choice of model, the estimated LEAR per WLM are 5.38 × 10−4 or 5.57 × 10−4 in the full PUMA cohort and 7.50 × 10−4 or 7.66 × 10−4 in the PUMA 1960 + sub-cohort, respectively. The LEAR per WLM estimates derived from risk models reported for previously published uranium miners studies range from 2.5 × 10−4 to 9.2 × 10−4. PUMA strengthens knowledge on the radon-related lung cancer LEAR, a useful way to translate models for policy purposes.