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.

Associations of residential greenness with bone mineral density and osteoporosis: the modifying effect of genetic susceptibility.

OBJECTIVES: To investigate the associations of residential greenness with bone mineral density and incident osteoporosis, and further evaluate the potential modifying effect of genetic susceptibility. METHODS: We used the Normalised Difference Vegetation Index (NDVI) at various buffer distances, including 300 m (NDVI300m), 500 m (NDVI500m), 1000 m (NDVI1000m) and 1500 m (NDVI1500m), to serve as indicators of greenness. We fitted linear regression, logistic regression and Cox proportional hazard models to assess the associations of residential greenness with estimated bone mineral density (eBMD), prevalent osteoporosis and incident osteoporosis, respectively. With the Polygenic Risk Score (PRS) for osteoporosis, we further assessed the joint effects of genetic risk and greenness on the risk of osteoporosis. We conducted causal mediation analyses to explore potential mediators. RESULTS: Each IQR increase in NDVI300m was associated with 0.0007 (95% CI 0.0002 to 0.0013) increase in eBMD, 6% lower risk of prevalent osteoporosis (OR 0.94; 95% CI 0.92 to 0.97) and 5% lower risk of incident osteoporosis (HR 0.95; 95% CI 0.93 to 0.98). The joint effects of greenness and PRS on the risk of osteoporosis displayed a clear dose-response pattern. Compared with individuals exposed to low NDVI levels and high genetic risk, those exposed to high NDVI levels and low genetic risk had a 56% (95% CI 51% to 61%) lower risk of osteoporosis. The primary mediators in the association between greenness and incident osteoporosis were identified as PM2.5 and NO2. CONCLUSIONS: Residential greenness was associated with higher bone mineral density and decreased risk of incident osteoporosis.

Greenness, Genetic Predisposition, and Tinnitus.

This study aimed to investigate the association between residential greenness and tinnitus and the potential interaction between greenness and genetic predisposition to tinnitus. The normalized difference vegetation index (NDVI) is used to measure residential greenness. The tinnitus is defined based on self-reported. In the cross-sectional analyses, logistic regression models are used for the baseline sample of the United Kingdom Biobank cohort. In the secondary analysis, a Cox proportional hazard model is used for a subsample of participants who completed the tinnitus questionnaire at follow-up. In the cross-sectional analysis including 106471 participants, higher residential greenness is associated with lower odds of tinnitus for each interquartile range increase in continuous NDVI, with an adjusted odds ratio of 0.97 (95% confidence interval: 0.95 to 0.99) for tinnitus. A similar association is observed in the longitudinal analysis, with an adjusted hazard ratio of 0.92 (95% confidence interval: 0.86 to 0.98) for the association of NDVI increased per interquartile range with incident tinnitus. Moreover, there is a significant interaction between greenness and genetic predisposition to tinnitus (P < 0.05). This study suggested that residential greenness is negatively associated with tinnitus. Greenness and genetic predisposition to tinnitus are found to have a significant interaction.

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.

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.

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.

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.

HLA-C*07:01 and HLA-DQB1*02:01 protect against white matter hyperintensities and deterioration of cognitive function: A population-based cohort study.

BACKGROUND: Neuroinflammation and aberrant immune regulation are increasingly implicated in the pathophysiology of white matter hyperintensities (WMH), an imaging marker of cerebrovascular pathologies and predictor of cognitive impairment. The role of human leukocyte antigen (HLA) genes, critical in immunoregulation and associated with susceptibility to neurodegenerative diseases, in WMH pathophysiology remains unexplored. METHODS: We performed association analyses between classical HLA alleles and WMH volume, derived from MRI scans of 38 302 participants in the UK Biobank. To identify independent functional alleles driving these associations, we conducted conditional forward stepwise regression and lasso regression. We further investigated whether these functional alleles showed consistent associations with WMH across subgroups characterized by varying levels of clinical determinants. Additionally, we validated the clinical relevance of the identified alleles by examining their association with cognitive function (n = 147 549) and dementia (n = 460 029) in a larger cohort. FINDINGS: Four HLA alleles (DQB1*02:01, DRB1*03:01, C*07:01, and B*08:01) showed an association with reduced WMH volume after Bonferroni correction for multiple comparisons. Among these alleles, DQB1*02:01 exhibited the most significant association (ß = -0.041, 95 % CI: -0.060 to -0.023, p = 1.04 × 10-5). Forward selection and lasso regression analyses indicated that DQB1*02:01 and C*07:01 primarily drove this association. The protective effect against WMH conferred by DQB1*02:01 and C*07:01 persisted in clinically relevant subgroups, with a stronger effect observed in older participants. Carrying DQB1*02:01 and C*07:01 was associated with higher cognitive function, but no association with dementia was found. INTERPRETATION: Our population-based findings support the involvement of immune-associated mechanisms, particularly both HLA class I and class II genes, in the pathogenesis of WMH and subsequent consequence of cognitive functions.

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.

Age-Period-Cohort Analysis on Long-Term Mortality Trend of Genitourinary Diseases - China, 1987-2021.

What is already known about this topic?: There has been a lack of attention to genitourinary diseases for an extended period, resulting in limited research on the mortality trends of genitourinary diseases in China. What is added by this report?: This study examines the long-term trend of genitourinary diseases' mortality across Chinese individuals of all genders and in various urban and rural regions. Additionally, it investigates the impact of age-period-cohort effects on this trend. What are the implications for public health practice?: It is imperative to address genitourinary diseases, particularly among vulnerable populations such as rural older men. Policymakers should prioritize these individuals by providing necessary policy interventions and healthcare support.

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.

Trends and Patterns of Respiratory Tuberculosis Mortality in Rural and Urban - China, 1987-2021.

What is already known about this topic?: In China, an estimated 780,000 individuals contract tuberculosis (TB) every year. With TB ranked as the second most prevalent disease in terms of the morbidity and mortality rates for legally infectious diseases, it imparts a substantial disease burden on families and society. What is added by this report?: This study identifies specific periods and cohort effects related to trends in respiratory TB mortality in both rural and urban regions of China. The mortality rates have been found to decrease at an annual rate of 5.5% in urban regions and 6.6% in rural ones, with a more marked decline evident in rural areas. These findings represent a significant milestone in the prevention and treatment of respiratory TB in China, especially in its rural locales. What are the implications for public health practice?: This research contributes to policymakers' comprehension, assisting in the early formulation of cogent optimization policies, thereby further supporting the United Nations Sustainable Development Goals (SDGs) and the Endeavor to End Respiratory TB Strategy. It is recommended that policymakers prioritize key groups such as children, young adults aged 20-30 in rural areas, and older men (60 years and over) in urban areas when developing these astute optimization policies.

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.

Short-term exposure to reduced specific-size ambient particulate matter increase the risk of cause-specific cardiovascular disease: A national-wide evidence from hospital admissions.

Evidence for the health effects of ambient PM1 (particulate matter with an aerodynamic diameter ≤ 1 µm) pollution is limited, and it remains unclear whether a smaller particulate matter has a greater impact on human health. We conducted a time-series study in 184 major cities by extracting daily hospital data on admissions for ischemic heart disease, heart failure, heart rhythm disturbances, and stroke between 2014 and 2017 from a medical insurance claims database of 0.28 billion beneficiaries. City-specific associations were estimated with over-dispersed generalized additive models. A random-effects meta-analysis was used to estimate regional and national average associations. We conducted stratified and meta-regression analyses to explore potential effect modifiers of the association. We recorded 8.83 million cardiovascular admissions during the study period. At the national-average level, a 10-µg/m3 increase in same-day PM1, PM2.5(particulate matter with an aerodynamic diameter ≤ 2.5 µm) and PM10(particulate matter with an aerodynamic diameter ≤ 10 µm) concentrations corresponded to a 1.14% (95% confidence interval 0.88-1.41%), 0.55% (0.40-0.70%), and 0.45% (0.36-0.55%) increase in cardiovascular admissions, respectively. PM1 exposure was also positively associated with all cardiovascular disease subtypes, including ischemic heart disease (1.28% change; 0.99-1.56%), heart failure (1.30% change; 0.70-1.91%), heart rhythm disturbances (1.11% change; 0.65-1.58%), and ischemic stroke (1.29% change; 0.88-1.71%). The associations between PM1 and cardiovascular admissions were stronger in cities with lower PM1 levels, higher air temperatures and relative humidity, as well as in subgroups with elder age (all P < 0.05). This study provides robust evidence of short-term associations between PM1 concentrations and increased hospital admissions for all major cardiovascular diseases in China. Our findings suggest a greater short-term impact on cardiovascular risk from PM1 in comparison to PM2.5 and PM10.

Ambient air pollution, genetic risk and telomere length in UK biobank.

BACKGROUND: Telomere length (TL) is a biomarker of genomic aging. The evidence on the association between TL and air pollution was inconsistent. Besides, the modification effect of genetic susceptibility on the air pollution-TL association remains unknown. OBJECTIVE: We aimed to evaluate the association of ambient air pollution with TL and further assess the modification effect of genetic susceptibility. METHODS: 433,535 participants with complete data of TL and air pollutants in UK Biobank were included. Annual average exposure of NO2, NOx, PM10 and PM2.5 was estimated by applying land use regression models. Genetic risk score (GRS) was constructed using reported telomere-related SNPs. Leukocyte TL was measured by quantitative polymerase chain reaction (qPCR). Multivariable linear regression models were employed to conduct associational analyses. RESULTS: Categorical exposure models and RCS models both indicated U-shaped (for NO2 and NOx) and L-shaped (for PM10 and PM2.5) correlations between air pollution and TL. In comparison to the lowest quartile, the 2nd and 3rd quartile of NO2 (q2: -1.3% [-2.1%, -0.4%]; q3: -1.2% [-2.0%, -0.3%], NOx (q2: -1.3% [-2.1%, -0.5%]; q3: -1.4% [-2.2%, -0.5%]), PM2.5 (q2: -0.8% [-1.7%, 0.0%]; q3: -1.3% [-2.2%, -0.5%]), and the third quartile of PM10 (q3: -1.1% [-1.9%, -0.2%]) were inversely associated with TL. The highest quartile of NO2 was positively correlated with TL (q4: 1.0% [0.0%, 2.0%]), whereas the negative correlation between the highest quartile of other pollutants and TL was also attenuated and no longer significant. In the genetic analyses, synergistic interactions were observed between the 4th quartile of three air pollutants (NO2, NOx, and PM2.5) and genetic risk. IMPACT STATEMENT: Our study for the first time revealed a non-linear trend for the association between air pollution and telomere length. The genetic analyses suggested synergistic interactions between air pollution and genetic risk on the air pollution-TL association. These findings may shed new light on air pollution's health effects, offer suggestions for identifying at-risk individuals, and provide hints regarding further investigation into gene-environment interactions.

Air pollution, alcohol consumption, and the risk of elevated liver enzyme levels: a cross-sectional study in the UK Biobank.

Evidences on the association between exposure to air pollution and liver enzymes was scarce in low pollution area. We aimed to investigate the association between air pollution and liver enzyme levels and further explore whether alcohol intake influence this association. This cross-sectional study included 425,773 participants aged 37 to 73 years from the UK Biobank. Land Use Regression was applied to assess levels of PM2.5, PM10, NO2, and NOx. Levels of liver enzymes including AST, ALT, GGT, and ALP were determined by enzymatic rate method. Long-term low-level exposure to PM2.5 (per 5-µg/m3 increase) was significantly associated with AST (0.596% increase, 95% CI, 0.414 to 0.778%), ALT (0.311% increase, 0.031 to 0.593%), and GGT (1.552% increase, 1.172 to 1.933%); The results were similar for PM10; NOX and NO2 were only significantly correlated with AST and GGT Significant modification effects by alcohol consumption were found (P-interaction < 0.05). The effects of pollutants on AST, ALT, and GGT levels gradually increased along with the weekly alcohol drinking frequency. In conclusion, long-term low-level air pollutants exposure was associated with elevated liver enzyme levels. And alcohol intake may exacerbate the effect of air pollution on liver enzymes.

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.

Brachial-ankle pulse wave velocity is a stronger predictor than blood pressure for atherosclerotic cardiovascular diseases and all-cause mortality: a cohort study.

Whether brachial-ankle pulse wave velocity (baPWV) is a better predictive indicator than blood pressure (BP) for atherosclerotic cardiovascular diseases (ASCVD) events and all-cause mortality in the general population has not yet been established. The current study included 47,659 participants from the Kailuan cohort in China, who underwent the baPWV test and were free of ASCVD, atrial fibrillation, and cancer at baseline. The hazard ratios (HRs) of ASCVD and all-cause mortality were evaluated using the Cox proportional hazards model. The predictive ability of baPWV, systolic BP (SBP), and diastolic BP (DBP) for ASCVD and all-cause mortality was evaluated using the area under the curve (AUC) and concordance index (C-index). Within the median follow-up period of 3.27 and 3.32 person-years, 885 ASCVD events and 259 deaths occurred, respectively. The HRs of ASCVD and all-cause mortality increased with the increase of baPWV, SBP, and DBP. When baPWV, SBP, and DBP were analyzed as continuous variables, the adjusted HRs were 1.29 (95% CI, 1.22-1.37), 1.28 (95% CI, 1.20-1.37), and 1.26 (95% CI, 1.17-1.34) for each standard deviation increase, respectively. The AUC and C-index for baPWV in predicting ASCVD and all-cause mortality were 0.744 and 0.750, respectively, while those for SBP were 0.697 and 0.620, those for DBP were 0.666 and 0.585. The AUC and C-index of baPWV were higher than those of SBP and DBP (P < 0.001). Therefore, baPWV is an independent predictor of ASCVD and all-cause mortality in the general Chinese population, and its predictive ability is superior to that of BP. baPWV is a more ideal screening method for ASCVD in large-scale population.