Association of residential greenness with incident pneumonia: A prospective cohort study.

Residential greenness is considered beneficial to human health, and its association with respiratory function has been found in previous studies. However, its link with pneumonia remains unclear. To explore the association of residential greenness with incident pneumonia, we conducted a prospective cohort study based on participants of the UK Biobank, followed from 2006 to 2010 to the end of 2019. Residential greenness was measured by Normalized Difference Vegetation Index (NDVI) within 500 m and 1000 m buffer. Cox proportional hazard models were conducted to assess the association, and restricted cubic spline models were also constructed to estimate their exposure-response relationship. Results demonstrate that residential greenness was negatively related to the risk of incident pneumonia. An interquartile (IQR) increase in NDVI 500-m buffer was associated with 4 % [HR (95 % CI) =0.96 (0.94, 0.97), P < 0.001] lower risk of incident pneumonia. Compared to the lowest greenness quartile (Q1), the highest quartile (Q4) had a lower risk of incident pneumonia, with the HR (95 % CI) estimated to be 0.91 (0.87, 0.95) (P values <0.001). Analyses based on NDVI 1000-m buffer obtained similar results. Furthermore, a significant effect of modifications by age and income on the linkage between residential greenness and incident pneumonia was found. These findings propose a potential effective prevention of incident pneumonia and provide the scientific basis for promoting the construction of residential greenness.

Early-life exposure to tobacco, genetic susceptibility, and accelerated biological aging in adulthood.

Early-life tobacco exposure serves as a non-negligible risk factor for aging-related diseases. To understand the underlying mechanisms, we explored the associations of early-life tobacco exposure with accelerated biological aging and further assessed the joint effects of tobacco exposure and genetic susceptibility. Compared with those without in utero exposure, participants with in utero tobacco exposure had an increase in Klemera-Doubal biological age (KDM-BA) and PhenoAge acceleration of 0.26 and 0.49 years, respectively, but a decrease in telomere length of 5.34% among 276,259 participants. We also found significant dose-response associations between the age of smoking initiation and accelerated biological aging. Furthermore, the joint effects revealed that high-polygenic risk score participants with in utero exposure and smoking initiation in childhood had the highest accelerated biological aging. There were interactions between early-life tobacco exposure and age, sex, deprivation, and diet on KDM-BA and PhenoAge acceleration. These findings highlight the importance of reducing early-life tobacco exposure to improve healthy aging.

Long-term exposure to reduced specific-size ambient particulate matter and progression of arterial stiffness among Chinese adults.

To assess the associations of ambient specific-size PM with brachial-ankle pulse wave velocity (baPWV) and the progression of arterial stiffness. Participants were included from the Kailuan study, the cross-sectional study involved 36,486 participants, while the longitudinal study enrolled 16,871 participants. PM exposures was assessed through satellite-based random forest approaches at a 1 km resolution. Initial observations indicated a link between baseline baPWV and heightened levels of PM1, PM2.5, and PM10 exposure, and greater effects were observed for PM1 (ß: 22.52, 95% CI: 18.14-26.89), followed by PM2.5 (ß: 9.76, 95% CI: 7.52-12.00), and PM10 (ß: 8.88, 95% CI: 7.32-10.45). Furthermore, the growth rate of baPWV was higher in participants exposed to high levels of PM1 exposure (ß: 2.77, 95% CI: 1.19-4.35), succeeded by PM2.5 and PM10. Throughout a median follow-up period of 4.04 years, arterial stiffness was diagnosed in 1709 subjects. Long-term exposure to PM was linked with an increased risk of incident arterial stiffness, estimated HR for fixed 10 µg/m3 increments in annual average PM1 was 2.20 (95% CI: 2.01-2.42), PM2.5 was 1.48 (95% CI: 1.41-1.55), and PM10 1.32 (95% CI: 1.27-1.36). PM had a greater impact on men and older individuals (P for interaction <0.001). Long-term exposures to ambient PM1, PM2.5, and PM10 were positively associated with baPWV and an increased risk of arterial stiffness. Higher estimated effects were observed for PM1 than PM2.5 and PM10.

Air pollutants, genetic susceptibility, and abdominal aortic aneurysm risk: a prospective study.

BACKGROUND AND AIMS: Air pollutants are important contributors to cardiovascular diseases, but associations between long-term exposure to air pollutants and the risk of abdominal aortic aneurysm (AAA) are still unknown. METHODS: This study was conducted using a sample of 449 463 participants from the UK Biobank. Hazard ratios and 95% confidence intervals for the risk of AAA incidence associated with long-term exposure to air pollutants were estimated using the Cox proportional hazards model with time-varying exposure measurements. Additionally, the cumulative incidence of AAA was calculated by using the Fine and Grey sub-distribution hazards regression model. Furthermore, this study investigated the combined effects and interactions between air pollutants exposure and genetic predisposition in relation to the risk of AAA onset. RESULTS: Long-term exposure to particulate matter with an aerodynamic diameter <2.5 µm [PM2.5, 1.21 (1.16, 1.27)], particulate matter with an aerodynamic diameter <10 µm [PM10, 1.21 (1.16, 1.27)], nitrogen dioxide [NO2, 1.16 (1.11, 1.22)], and nitrogen oxides [NOx, 1.10 (1.05, 1.15)] was found to be associated with an elevated risk of AAA onset. The detrimental effects of air pollutants persisted even in participants with low-level exposure. For the joint associations, participants with both high levels of air pollutants exposure and high genetic risk had a higher risk of developing AAA compared with those with low concentrations of pollutants exposure and low genetic risk. The respective risk estimates for AAA incidence were 3.18 (2.46, 4.12) for PM2.5, 3.09 (2.39, 4.00) for PM10, 2.41 (1.86, 3.13) for NO2, and 2.01 (1.55, 2.61) for NOx. CONCLUSIONS: In this study, long-term air pollutants exposure was associated with an increased risk of AAA incidence.

Genetic Susceptibility Modifies Relationships Between Air Pollutants and Stroke Risk: A Large Cohort Study.

BACKGROUND: The extent to which genetic susceptibility modifies the associations between air pollutants and the risk of incident stroke is still unclear. This study was designed to investigate the separate and joint associations of long-term exposure to air pollutants and genetic susceptibility on stroke risk. METHODS: The participants of this study were recruited by the UK Biobank between 2006 and 2010. These participants were followed up from the enrollment until the occurrence of stroke events or censoring of data. Hazard ratios (HRs) and 95% CIs for stroke events associated with long-term exposure to air pollutants were estimated by fitting both crude and adjusted Cox proportional hazards models. Additionally, the polygenic risk score was calculated to estimate whether the polygenic risk score modifies the associations between exposure to air pollutants and incident stroke. RESULTS: A total of 502 480 subjects were included in this study. After exclusion, 452 196 participants were taken into the final analysis. During a median follow-up time of 11.7 years, 11 334 stroke events were observed, with a mean age of 61.60 years, and men accounted for 56.2% of the total cases. Long-term exposures to particulate matter with an aerodynamic diameter smaller than 2.5 µm (adjusted HR, 1.70 [95% CI, 1.43-2.03]) or particulate matter with an aerodynamic diameter smaller than 10 µm (adjusted HR, 1.50 [95% CI, 1.36-1.66]), nitrogen dioxide (adjusted HR, 1.10 [95% CI, 1.07-1.12]), and nitrogen oxide (adjusted HR, 1.04 [95% CI, 1.02-1.05]) were pronouncedly associated with increased risk of stroke. Meanwhile, participants with high genetic risk and exposure to high air pollutants had ≈45% (31%, 61%; particulate matter with an aerodynamic diameter smaller than 2.5 µm), 48% (33%, 65%; particulate matter with an aerodynamic diameter smaller than 10 µm), 51% (35%, 69%; nitrogen dioxide), and 39% (25%, 55%; nitrogen oxide) higher risk of stroke compared with those with low genetic risk and exposure to low air pollutants, respectively. Of note, we observed additive and multiplicative interactions between genetic susceptibility and air pollutants on stroke events. CONCLUSIONS: Chronic exposure to air pollutants was associated with an increased risk of stroke, especially in populations at high genetic risk.

Long-Term Exposure to Low Concentrations of Ambient Benzene and Mortality in a National English Cohort.

Background: Benzene affects human health through environmental exposure in addition to occupational contact. However, few studies have examined the associations between long-term exposure to low concentrations of ambient benzene and mortality risks in nonoccupational settings.Methods: This prospective cohort study consists of 393,042 participants without stroke, myocardial infarction, or cancer at baseline from the UK Biobank. Annual average concentrations of benzene for each year during follow-up were measured using air dispersion models. The main outcomes were all-cause mortality and mortality from specific causes. Cox proportional-hazards models with time-varying exposure measurements were used to estimate the hazard ratios and 95% confidence intervals (CIs) for mortality risks. Restricted cubic spline models were used to estimate exposure-response relationships.Measurements and Main Results: With each interquartile range increase in the average annual concentration of benzene, the adjusted hazard ratios of mortality risk from all causes, cardiovascular disease, cancer, and respiratory disease were 1.26 (95% CI, 1.24-1.27), 1.24 (95% CI, 1.21-1.28), 1.27 (95% CI, 1.25-1.29), and 1.25 (95% CI, 1.20-1.30), respectively. The monotonically increasing exposure-response curves showed no threshold and plateau within the observed concentration range. Furthermore, the effect of benzene exposure on mortality persisted across different subgroups and was somewhat stronger in younger and White people (P for interaction < 0.05).Conclusions: Long-term exposure to low concentrations of ambient benzene significantly increases mortality risk in the general population. Ambient benzene represents a potential threat to public health, and further investigations are needed to support timely pollution regulation and health protection.

Residential greenness and incident idiopathic pulmonary fibrosis: A prospective study.

BACKGROUND: The impact of residential greenness on incident idiopathic pulmonary fibrosis (IPF) is unknown. We aimed to assess the association between residential greenness and incident IPF, identify underlying pathways, and further evaluate the effect among different genetic subgroups. METHODS: 469,348 participants in the UK Biobank were included and followed until December 2020. Normalized difference vegetation index (NDVI) within 300-, 500-, 1000-, and 1500-m buffers (NDVI300m, NDVI500m, NDVI1000m, and NDVI1500m) were employed as indicators of greenness. The polygenic risk score (PRS) was constructed based on 13 independent SNPs. Cox models were fitted to assess the association of residential greenness with incident IPF. Casual mediation analyses were applied to evaluate potential mediators. FINDINGS: After a median follow-up of 11.85 years, 1574 IPF cases were identified. We found residential greenness inversely associated with incident IPF. The HRs (95%CIs) for each interquartile increase of NDVI300m, NDVI500m, NDVI1000m, NDVI1500m were 0.93 (0.87, 0.99), 0.92 (0.86, 0.98), 0.89 (0.83, 0.95), and 0.89 (0.83, 0.95), respectively. The association was stronger among individuals with intermediate or high genetic risk. In mediation analyses, the main mediators identified were PM2.5 and NO2, with proportion mediated estimated to be 31.92% and 40.61% respectively for NDVI300m. INTERPRETATION: Residential greenness was associated with reduced risk of incident IPF.

The association between telomere length and non-alcoholic fatty liver disease: a prospective study.

BACKGROUND: Research on the association between telomere length (TL) and incident non-alcoholic fatty liver disease (NAFLD) is limited. This study examined this association and further assessed how TL contributes to the association of NAFLD with its known risk factors. METHODS: Quantitative PCR (polymerase chain reaction) was employed to assess leucocyte telomere length. Polygenic risk score (PRS) for NAFLD, air pollution score, and lifestyle index were constructed. Cox proportional hazard models were conducted to estimate the hazard ratios (HRs) and 95% confidence intervals. RESULTS: Among 467,848 participants in UK Biobank, we identified 4809 NAFLD cases over a median follow-up of 12.83 years. We found that long TL was associated with decreased risk of incident NAFLD, as each interquartile range increase in TL resulted in an HR of 0.93 (95% CI 0.89, 0.96). TL partly mediated the association between age and NAFLD (proportion mediated: 15.52%). When assessing the joint effects of TL and other risk factors, the highest risk of NAFLD was found in participants with low TL and old age, low TL and high air pollution score, low TL and unfavorable lifestyle, and low TL and high PRS, compared to each reference group. A positive addictive interaction was observed between high PRS and low TL, accounting for 14.57% (2.51%, 27.14%) of the risk of NAFLD in participants with low telomere length and high genetic susceptibility. CONCLUSIONS: Long telomere length was associated with decreased risk of NAFLD incidence. Telomere length played an important role in NAFLD.

Long-term exposure to ambient air pollution, genetic susceptibility, and the incidence of bipolar disorder: A prospective cohort study.

There is mounting recent evidence showing that air pollution exposure may be related to the risk of mental health, yet the association between long-term exposure to air pollution and the risk of incident bipolar disorder (BD) remains unclear. Thus we aim to identify associations between air pollution and the incidence of BD in a prospective population-based cohort. In total, 482,726 participants who were free of BD from the UK Biobank were included in this prospective study. We applied time-varying Cox proportional hazards models, accounting for relevant confounders, and used annual-year moving averages of air pollution as time-varying exposures. The genetic risk for BD was categorized into three categories (low, intermediate, and high) according to the tertiles of polygenic risk score. During a median of 10.79-year follow-up, 923 incident BD events were recorded. Long-term exposures to PM2.5, PM10, NO2, and NOx were associated with increased BD risk. Estimated HRs (95% CIs) for each interquartile range increase in PM2.5, PM10, NO2, and NOx concentrations were 1.31 (1.18-1.45), 1.19 (1.09-1.31), 1.19 (1.08-1.30), and 1.16 (1.07-1.26), respectively. Associations were still observed and even stronger at pollutant concentrations lower than WHO air quality guideline. In subgroup analysis stratified by genetic risk, we observed consistent associations between all pollutants and BD risk in intermediate and high genetic risk groups, but not in low genetic risk group. For example, the HRs (95% CIs) for PM2.5 were 1.00 (0.94-1.53), 1.30 (1.06-1.59), and 1.34 (1.16-1.54) in low, intermediate, and high genetic groups, respectively. In conclusion, long-term exposure to air pollution was significantly associated with an elevated risk of BD. Associations of air pollution with BD occurred only within intermediate and high genetic risk categories and were even stronger at the pollutants levels below WHO air quality guidelines. These findings could help inform policy makers regarding ambient air quality standards and BD management.

Air pollution, genetic susceptibility, and the risk of atrial fibrillation: A large prospective cohort study.

To date, no study has explored the extent to which genetic susceptibility modifies the effects of air pollutants on the risk of atrial fibrillation (AF). This study was designed to investigate the separate and joint effects of long-term exposure to air pollutants and genetic susceptibility on the risk of AF events. This study included 401,251 participants without AF at baseline from UK Biobank. We constructed a polygenic risk score and categorized it into three categories. Cox proportional hazards models were fitted to assess the separate and joint effects of long-term exposure to air pollutants and genetics on the risk of AF. Additionally, we further evaluated the effect modification of genetic susceptibility. The hazard ratios and corresponding 95% confidence intervals of incident AF for per interquartile range increase in particulate matter with an aerodynamic diameter smaller than 2.5 µm (PM2.5) or 10 µm (PM10), nitrogen dioxide (NO2), and nitrogen oxide (NOx) were 1.044 (1.025, 1.063), 1.063 (1.044, 1.083), 1.061 (1.042, 1.081), and 1.039 (1.023, 1.055), respectively. For the combined effects, participants exposed to high air pollutants levels and high genetic risk had approximately 149.2% (PM2.5), 181.7% (PM10), 170.2% (NO2), and 157.2% (NOx) higher risk of AF compared to those with low air pollutants levels and low genetic risk, respectively. Moreover, the significant additive interactions between PM10 and NO2 and genetic risk on AF risk were observed, with around 16.4% and 35.1% of AF risk could be attributable to the interactive effects. In conclusion, long-term exposure to air pollutants increases the risk of AF, particularly among individuals with high genetic susceptibility.

Unmet chronic care needs and insufficient nurse staffing to achieve universal health coverage in China: Analysis of the Global Burden of Disease Study 2019.

BACKGROUND: Although China has made impressive progress towards Universal Health Coverage through the health system reform plan since 2009, chronic disease prevention and control implementations are still inadequate to meet the need at large. This study aims to quantify the acute and chronic care needs in China and examine the human resources for health and financial protection for the population to achieve Universal Health Coverage. METHODS: The data on disability-adjusted life years, years lived with disability, and years of life lost in China were disaggregated from the Global Burden of Diseases Study 2019 by age and sex based on acute care need or chronic care need. An auto-regressive integrated moving average model was deployed to predict the supply gap of physicians, nurses and midwives from 2020 to 2050. Out-of-pocket health expenditure was compared among China, Russia, Germany, the US, and Singapore to examine the current status of financial protection. RESULTS: In 2019, conditions requiring chronic care accounted for 86.4% of all-cause, all-age disability-adjusted life years in China, while acute-care-need conditions accounted for 11.3%. Approximate 25.57% of disability-adjusted life years in communicable diseases and 94.32% in non-communicable diseases were caused by chronic care need conditions. Chronic care-need conditions accounted for more than 80% of both man and woman's disease burden. The proportion of disability-adjusted life years and years of life lost attributable to chronic care was greater than 90% in people aged 25 and up. The nurse and midwife supply will be in absolute shortage and unable to achieve effective universal health coverage effective coverage of 80% or 90% from 2020 to 2050, while the physician supply will be sufficient to maintain effective universal health coverage of 80% and reach 90% from 2036. The out-of-pocket health expenditure decreased with time but was still relatively higher than that of Germany, the US, and Singapore. CONCLUSIONS: The present study demonstrates the chronic care needs outweigh those for acute care in China. Nurse supply and the financial protection for the poor were still inadequate to achieve Universal Health Coverage. Better workforce planning and concerted actions on chronic care prevention and control should be taken to meet the population's chronic care needs.

Lifestyle, Genetic Susceptibility, and the Risk of Idiopathic Pulmonary Fibrosis: A Large Prospective Cohort Study.

BACKGROUND: Lifestyle is an important contributor of age-related chronic disease, but the association between lifestyle and the risk of idiopathic pulmonary fibrosis (IPF) remains unknown. The extent to which genetic susceptibility modifies the effects of lifestyle on IPF also remains unclear. RESEARCH QUESTION: Is there a joint effect or interaction of lifestyle and genetic susceptibility on the risk of developing IPF? STUDY DESIGN AND METHODS: This study included 407,615 participants from the UK Biobank study. A lifestyle score and a polygenic risk score were constructed separately for each participant. Participants were then classified into three lifestyle categories and three genetic risk categories based on the corresponding score. Cox models were fitted to assess the association of lifestyle and genetic risk with the risk of incident IPF. RESULTS: With favorable lifestyle as the reference group, intermediate lifestyle (hazard ratio, 1.384; 95% CI, 1.218-1.574) and unfavorable lifestyle (hazard ratio, 2.271; 95% CI, 1.852-2.785) were significantly associated with an increased risk of IPF. For the combined effect of lifestyle and polygenic risk score, participants with unfavorable lifestyle and high genetic risk had the highest risk of IPF (hazard ratio, 7.796; 95% CI, 5.482-11.086) compared with those with favorable lifestyle and low genetic risk. Moreover, approximately 32.7% (95% CI, 11.3-54.1) of IPF risk could be attributed to the interaction of an unfavorable lifestyle and high genetic risk. INTERPRETATION: Exposure to unfavorable lifestyle significantly increased the risk of IPF, particularly in those with high genetic risk.

Exposure to various ambient air pollutants and 9 cardiovascular conditions among individuals with diabetes: A prospective analysis of the UK Biobank.

BACKGROUND AND AIMS: The adverse effects of air pollutants on the risk of most cardiovascular diseases (CVDs) are well-established, but the risk of CVDs such as deep vein thrombosis, pulmonary embolism, or aortic valve stenosis have been underappreciated, especially in the diabetic population. This study aimed to evaluate associations between long-term air pollutants exposure and the risk of incident CVDs among participants with diabetes. METHODS: This study included 27,827 participants with baseline diabetes from the UK Biobank. We then estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for CVDs associated with chronic air pollutant exposure in the diabetic population by fitting the Cox proportional hazards model. Moreover, we investigated the cardiovascular effects of air pollutants at concentrations below WHO guideline limits. RESULTS: After multivariable adjustment, long-term NO2 and NOx exposures were positively associated with the development of 8 and 6 types of CVDs in participants with diabetes, respectively. In term of particulate matters, the effect estimates ranged from 1.51 (1.13, 2.03) (coronary artery disease) to 4.65 (2.73, 7.92) (peripheral arterial disease) per 10 µg/m3 increase in PM2.5. Whereas, the effect estimates ranged from 1.15 (1.04, 1.27) (arterial hypertension) to 2.28 (1.40, 3.69) (pulmonary embolism) per 10 µg/m3 increase in PM10. In addition, our study discovered that for most of the cardiovascular events (8 of 9), the deleterious effects of air pollutants persisted even when participants were exposed to air pollutants concentrations below WHO guideline limits. CONCLUSIONS: Long-term exposure to ambient NO2, NOx, PM2.5, and PM10, either at normal or low level, increased risk of various cardiovascular outcomes in the diabetic population.

Long-term Exposure to Ambient Air Pollutants and Increased Risk of Pneumonia in the UK Biobank.

BACKGROUND: Short-term exposure to air pollution has been linked to pneumonia risk. However, evidence on the long-term effects of air pollution on pneumonia morbidity is scarce and inconsistent. We investigated the associations of long-term air pollutant exposure with pneumonia and explored the potential interactions with smoking. RESEARCH QUESTION: Is long-term exposure to ambient air pollution associated with the risk of pneumonia, and does smoking modify the associations? STUDY DESIGN AND METHODS: We analyzed data in 445,473 participants without pneumonia within 1 year before baseline from the UK Biobank. Annual average concentrations of particulate matter (particulate matter with a diameter < 2.5 µm [PM2.5] and particulate matter with a diameter < 10 µm [PM10]), nitrogen dioxide (NO2), and nitrogen oxides (NOx) were estimated using land-use regression models. Cox proportional hazards models were used to assess the associations between air pollutants and pneumonia incidence. Potential interactions between air pollution and smoking were examined on both additive and multiplicative scales. RESULTS: The hazard ratios of pneumonia for each interquartile range increase in PM2.5, PM10, NO2, and NOx concentrations were 1.06 (95% CI, 1.04-1.08), 1.10 (95% CI, 1.08-1.12), 1.12 (95% CI, 1.10-1.15), and 1.06 (95% CI, 1.04-1.07), respectively. There were significant additive and multiplicative interactions between air pollution and smoking. Compared with individuals who had never smoked with low air pollution exposure, individuals who had ever smoked with high air pollution exposure had the highest pneumonia risk (PM2.5: hazard ratio [HR], 1.78; 95% CI, 1.67-1.90; PM10: HR, 1.94; 95% CI, 1.82-2.06; NO2: HR, 2.06; 95% CI, 1.93-2.21; NOx: HR, 1.88; 95% CI, 1.76-2.00). The associations between air pollutants and pneumonia risk persisted in participants exposed to air pollutants concentrations meeting the European Union limits. INTERPRETATION: Long-term exposure to air pollutants was associated with an increased risk of pneumonia, especially in individuals who smoke.

Temporal trends in lung cancer mortality and years of life lost in Wuhan, China, 2010-2019.

Objective: Lung cancer is responsible for millions of deaths yearly, and its burden is severe worldwide. This study aimed to investigate the burden of lung cancer in the population of Wuhan based on the surveillance data from 2010 to 2019. Methods: Data of this study was obtained from the Mortality Register System established by the Wuhan Center for Disease Control and Prevention. The study systematically analyzed the burden of lung cancer deaths in the population of Wuhan and its 13 administrative regions from 2010 to 2019 via the Joinpoint regression models, Age-Period-Cohort (APC) models, and decomposition analysis. Results: This study found the upward and downward trends in the age-standardized mortality rates (ASMRs) and age-standardized years of life lost rates (ASYLLRs) of lung cancer from 2010 to 2019. In Joinpoint regression models, the corresponding estimated annual percentage change (EAPC) were 1.00% and -1.90%, 0.60%, and -3.00%, respectively. In APC models, lung cancer mortality tended to increase with age for both sexes in Wuhan, peaking at the 85-89 age group; The period effects for different populations have started to gradually decline in recent years. In addition, the cohort effects indicated that the risk of lung cancer death was highest among those born in the 1950s-1955s, at 1.08 (males) and 1.01 (females). Among all administrative districts in Wuhan, the ASMR of lung cancer in the Xinzhou District has remained the highest over the study period. In decomposition analysis, both population aging (P<0.01) and population growth (P<0.01) aggravated (Z>0) lung cancer deaths in the Wuhan population. Conclusions: The burden of lung cancer death in the Wuhan population has shown a gradual decline in recent years, but the impact of aging and population growth on lung cancer mortality should not be ignored. Therefore, lung cancer surveillance must be strengthened to reduce the burden of lung cancer in Wuhan.

The Global Burden of Type 2 Diabetes Attributable to Tobacco: A Secondary Analysis From the Global Burden of Disease Study 2019.

Objectives: Growing epidemiological studies have reported the relationship between tobacco and health loss among patients with type 2 diabetes (T2D). This study aimed to explore the secular trend and spatial distribution of the T2D burden attributable to tobacco on a global scale to better understand regional disparities and judge the gap between current conditions and expectations. Methods: As a secondary analysis, we extracted data of tobacco-attributable T2D burden from the 2019 Global Burden of Disease Study (GBD). Joinpoint regression was adopted to determine the secular trend of age-standardized rates (ASR), with average annual percentage change (AAPC). Gaussian process regression (GPR) was used to explore the average expected relationship between ASRs and the socio-demographic index (SDI). Spatial autocorrelation was used to indicate if there is clustering of age-standardized DALY rate (ASDR) with Moran's I value. Multi-scale geographically weighted regression (MGWR) was to investigate the spatial distribution and scales of influencing factors in ASDR attributable to tobacco, with the regression coefficients for each influencing factor among 204 countries. Results: Tobacco posed a challenge to global T2D health, particularly for the elderly and men from lower SDI regions. For women, mortality attributable to secondhand smoke was higher than smoking. A downward trend in age-standardized mortality rate (ASMR) of T2D attributable to tobacco was observed (AAPCs= -0.24; 95% CI -0.30 to -0.18), while the ASDR increased globally since 1990 (AAPCs= 0.19; 0.11 to 0.27). Oceania, Southern Sub-Saharan Africa, and Southeast Asia had the highest ASMRs and ASDRs, exceeding expectations based on the SDI. Also, "high-high" clusters were mainly observed in South Africa and Southeast Asian countries, which means a high-ASDR country is surrounded by high-ASDR neighborhoods in the above areas. According to MGWR model, smoking prevalence was the most sensitive influencing factor, with regression coefficients from 0.15 to 1.80. Conclusion: The tobacco-attributable burden of T2D should be considered as an important health issue, especially in low-middle and middle-SDI regions. Meanwhile, secondhand smoke posed a greater risk to women. Regional disparities existed, with hot spots mainly concentrated in South Africa and Southeast Asian countries.

Eliciting national and subnational sets of disability weights in mainland China: Findings from the Chinese disability weight measurement study.

Background: The disability weight (DW) quantifies the severity of health states from disease sequela and is a pivotal parameter for disease burden calculation. We conducted a national and subnational DW measurement in China. Methods: In 2020-2021, we conducted a web-based survey to assess DWs for 206 health states in 31 Chinese provinces targeting health workers via professional networks. We fielded questions of paired comparison (PC) and population health equivalence (PHE). The PC data were analysed by probit regression analysis, and the regression results were anchored by results from the PHE responses on the DW scale between 0 (no loss of health) and 1 (health loss equivalent to death). Findings: We used PC responses from 468,541 respondents to estimate DWs of health states. Eight of 11 domains of health had significantly negative coefficients in the regression of the difference between Chinese and Global Burden of Disease (GBD) DWs, suggesting lower DW values for health states with mention of these domains in their lay description. We noted considerable heterogeneity within domains, however. After applying these Chinese DWs to the 2019 GBD estimates for China, total years lived with disability (YLDs) increased by 14·9% to 177 million despite lower estimates for musculoskeletal disorders, cardiovascular diseases, mental disorders, diabetes and chronic kidney disease. The lower estimates of YLDs for these conditions were more than offset by higher estimates of common, low-severity conditions. Interpretation: The differences between the GBD and Chinese DWs suggest that there might be some contextual factors influencing the valuation of health states. While the reduced estimates for mental disorders, alcohol use disorder, and dementia could hint at a culturally different valuation of these conditions in China, the much greater shifts in YLDs from low-severity conditions more likely reflects methodological difficulty to distinguish between health states that vary a little in absolute DW value but a lot in relative terms. Funding: This work was supported by the National Natural Science Foundation of China [grant number 82173626], the National Key Research and Development Program of China [grant numbers 2018YFC1315302], Wuhan Medical Research Program of Joint Fund of Hubei Health Committee [grant number WJ2019H304], and Ningxia Natural Science Foundation Project [grant number 2020AAC03436].

Mixed exposure to phenol, parabens, pesticides, and phthalates and insulin resistance in NHANES: A mixture approach.

PURPOSE: The effects of environmental chemicals on insulin resistance have attracted extensive attention. Previous studies typically focused on the single chemical effects. This study adopted three different models to analyze the mixed effects of nine common chemicals (one phenol, two parabens, two chlorophenols and four phthalates) on insulin resistance. METHODS: Urinary concentrations of chemicals were extracted from National Health and Nutrition Examination Survey (NHANES) 2009-2016. Insulin resistance was assessed using homeostatic model assessment (HOMA) and defined as HOMA-IR >2.6. The generalized linear regression (GLM), weighted quantile sum regression (WQS) and Bayesian kernel machine regression models (BKMR) were applied to assess the relationship between chemical mixture and HOMA-IR or insulin resistance. RESULTS: Of the 2067 participants included, 872 (42.19 %) were identified as insulin resistant. In single-chemical GLM model, di-2-ethylhexyl phthalate (DEHP) had the highest parameter (ß/OR, 95 % CIs) of 0.21 (quartile 4, 0.12- 0.29) and 1.95 (quartile 4, 1.39- 2.74). Similar results were observed in the multi-chemical models, with DEHP (quartile 4) showing the positive relationship with HOMA-IR (0.18, 0.08- 0.28) and insulin resistance (1.76, 1.17- 2.64). According to WQS models, the WQS indices were significantly positively correlated with both HOMA-IR (ß: 0.07, 95 % CI: 0.03- 0.12) and insulin resistance (OR: 1.25, 95 % CI: 1.03- 1.53). DEHP was the top-weighted chemical positively correlated with both HOMA-IR and insulin resistance. In the BKMR model, the joint effect was also positively correlated with both outcomes. DEHP remained the main contributor to the joint effect, consistent with WQS analysis. CONCLUSION: Our findings suggested that these chemical mixtures had the positive joint effects on both HOMA-IR and insulin resistance, with DEHP being the potentially predominant driver. The inter-validation of the three models may indicate that reducing the DEHP concentration could improve glucose homeostasis and reduce the risk of insulin resistance. However, further studies are recommended to deepen our findings and elucidate the mechanisms of insulin resistance and chemical mixture.

Trends of ischemic heart disease mortality attributable to household air pollution during 1990-2019 in China and India: an age-period-cohort analysis.

Cardiovascular diseases (CVD) caused by household air pollution (HAP) have sparked widespread concern globally in the recent decade. Meanwhile, increased ischemic heart disease (IHD) mortality has been the leading cause of worldwide CVD deaths. Both China and India experienced a high IHD burden and high exposure to HAP. The present study aimed to estimate and compare the long-term trends of HAP-attributable IHD mortality in the two countries. The data of this study were extracted from the Global Burden of Diseases (GBD) Study 2019. The age-period-cohort (APC) analysis was utilized to estimate the independent trends of the age, period, and cohort effects from 1990 to 2019. The age-standardized mortality rates (ASMRs) of HAP-attributable IHD have fallen faster in China than in India for both sexes. The local drift and net drift values were < 0 for all age groups in both countries. The age effects in both countries and sexes increased with time, suggesting age is a risk factor for IHD; conversely, period and cohort effects in China demonstrated a faster decline in both genders than in India. It indicated that China has been more successful than India in decreasing HAP-attributable IHD mortality.

Association Between Physical Activity Intensity and the Risk for Depression Among Adults From the National Health and Nutrition Examination Survey 2007-2018.

Objective: Whether vigorous physical activities (VPA) bring additional benefits to depression prevention in comparison with moderate physical activity (MPA) remains unclear. The aim of this study was to find the correlation between the proportion of VPA to moderate-to-VPA (MVPA) (a combination of VPA and MPA) and the risk for depression, as well as to explore whether correlations differ among subgroups separated by age and sex. Methods: The data originating from the National Health and Nutrition Examination Survey (NHANES) 2007-2018 were applied. The total amount of PA per week was obtained by multiplying frequency and duration. The proportion of VPA to MVPA was obtained among the participants who performed any MVPA. Depression was set for those who scored 10 and above in the Patient Health Questionnaire-9 (PHQ-9). The odds ratios (ORs) and 95% confidence intervals (95% CIs) for depression were evaluated using logistic regression. Results: Among 26,849 participants of this study, only 12,939 adults were found with any MVPA, in which 748 participants with depression were detected. Logistic regression was conducted among 12,939 participants. The participants with higher than 66.7-100% of MVPA as VPA were inversely correlated with a 30% (OR = 0.70, 95% CI = 0.50, 0.99) lower risk for depression. The subgroup analyses revealed that significant correlations were only found in men and those aged 45 years and above. Conclusion: This study suggested that a higher proportion of VPA to MVPA might be correlated with a lower risk for depression in men and those aged 45 years and above. Besides the recommendation, adults should perform 150 min MVPA per week, more time should be spent in performing VPA in MVPA among men and older adults.