Background Stroke and dementia are the leading causes of neurological disease burden. Detrimental effects of air pollution on both conditions are increasingly recognised, while the impacts on the dynamic transitions have not yet been explored, and whether critical time intervals exist is unknown. Methods This prospective study was conducted based on the UK Biobank. Annual average air pollution concentrations at baseline year 2010 estimated by land-use regression models were used as a proxy for long-term air pollution exposure. Associations between multiple air pollutants (PM2.5, PM2.5-10, and NO2) indicated by air pollution score and the dynamic transitions of stroke and dementia were estimated, and the impacts during critical time intervals were explored. The date cutoff of this study was February 29, 2020. Findings During a median follow-up of 10.9 years in 413,372 participants, 6484, 3813, and 376 participants developed incident stroke, dementia, and comorbidity of stroke and dementia. For the overall transition from stroke to comorbid dementia, the hazard ratio (HR) for each interquartile range (IQR) increase in air pollution score was 1.38 (95% CI, 1.15, 1.65), and the risks were limited to two time intervals (within 1 year and over 5 years after stroke). As for the transition from dementia to comorbid stroke, increased risk was only observed during 2-3 years after dementia. Interpretation Our findings suggested that air pollution played an important role in the dynamic transition of stroke and dementia even at concentrations below the current criteria. The findings provided new evidence for alleviating the disease burden of neurological disorders related to air pollution during critical time intervals.Copyright (c) 2023 The Author(s). Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Emerging evidence has indicated the linkage of traffic noise with cardiovascular diseases, However, there's a lack of extensive studies exploring the linkage of traffic noise with cardio-metabolic risk factors such as obesity. Additionally, the role of diet in the associations remains unknown. The aim is to prospectively examine the linkage of road traffic noise with obesity, especially by focusing on evaluating the impact of meat. Participants recruited in the UK Biobank with at least one repeated measurement of obesity indicators including body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WhR), and waist-to-height ratio (WhtR) were included. The Common Noise Assessment Methods of the simplified version were used to estimate road traffic noise exposure. Participants were categorized into "less meat intake" and "more meat intake" based on the median of meat intake, assessed by the frequency of unprocessed red meat and processed meat consumption. Modified Poisson regression models were employed to evaluate the linkage of road traffic noise with obesity. Additionally, the modification effects of meat intake on this relationship were evaluated. The incidence risk ratios (IRRs) and 95% confidence interval (CI) of overall obesity, WC-based central obesity, WhR-based central obesity, and WhtR-based central obesity were 1.11 (1.02, 1.21), 1.09 (1.03, 1.14), 1.06 (1.02, 1.10), and 1.08 (1.02, 1.13), respectively, for every 10 dB(A) increase for noise. Compared with individuals with lower meat intake, those with higher meat intake exhibited a stronger linkage of road traffic noise with central obesity. The prospective study demonstrates a linkage of road traffic noise with obesity, emphasizing the significance of diet on traffic noise-related obesity risk.

Background: Exposure to air pollution may increase the risk of obesity, but living in greener space may reduce this risk. Epidemiological evidence, however, is inconsistent.Methods: Using data from the China Health and Retirement Longitudinal Study (2011-2015), we conducted a nationwide cohort study of 7424 adults. We measured overweight/obesity according to body mass index. We used annual average ground-level air pollutants, including ozone (O3), nitrogen dioxide (NO2), and particulate matter with aerodynamic diameters <= 2.5 mu m (PM2.5), to demonstrate air pollution levels. We used the Normalized difference vegetation index (NDVI) to measure greenness exposure. We used time-varying Cox proportional hazard regression models to analyze the connections among air pollution, greenness, and the development of overweight/obesity in middle-aged and older adults in China. We also conducted mediation analyses to examine the mediating effects of air pollution.Results: We found that lower risk of overweight/obesity was associated with more greenness exposure and lower levels of air pollution. We identified that an interquartile increment in NDVI was correlated with a lower hazard ratio (HR) of becoming overweight or obese (HR = 0.806, 95% confidence interval [CI]: 0.754-0.862). Although a 10 mu g/m3 increase in PM2.5 and NO2 was correlated with higher risks (HR = 1.049, 95% CI = 1.022-1.075, HR = 1.376, 95% CI = 1.264-1.499). Effects of PM2.5 on being overweight or obese were stronger in men than in women. According to the mediation analysis, PM2.5 and NO2 mediated 8.85% and 19.22% of the association between greenness and being overweight or obese. Conclusions: An increased risk of being overweight or obese in middle-aged and older adults in China was associated with long-term exposure to higher levels of PM2.5 and NO2. This risk was reduced through NDVI exposure, and the associations were partially mediated by air pollutants. To verify these findings, fine-scale studies are needed.

BACKGROUND Evidence on road traffic noise and heart failure (HF) is limited, and little is known on the potential mediation roles of acute myocardial infarction (AMI), hypertension, or diabetes.OBJECTIVES The purpose of this study was to evaluate the impacts of long-term road traffic noise exposure on the risk of incident HF considering air pollution, and explore the mediations of the previously mentioned diseases. METHODS This prospective study included 424,767 participants without HF at baseline in UK Biobank. The residential-level noise and air pollution exposure was estimated, and the incident HF was identified through linkages with medical records. Cox proportional hazard models were used to estimate HRs. Furthermore, time-dependent mediation was performed.RESULTS During a median 12.5 years of follow-up, 12,817 incident HF were ascertained. The HRs were 1.08 (95% CI: 1.00-1.16) per 10 dB[A] increase in weighted average 24-hour road traffic noise level (L-den), and 1.15 (95% CI: 1.02-1.31) for exposure to L-den >65 dB[A] compared with the reference category (L-den #55 dB[A]), respectively. Furthermore, the strongest combined effects were found in those with both high exposures to road traffic noise and air pollution including fine particles and nitrogen dioxide. Prior AMI before HF within 2 years' time interval mediated 12.5% of the association of road traffic noise with HF. CONCLUSIONS More attention should be paid and a preventive strategy should be considered to alleviate the disease burden of HF related to road traffic noise exposure, especially in participants who survived AMI and developed HF within 2 years.

Background In recent years, muscle strength in children and adolescents has continued to decline, especially in rural areas. Executive function as a higher function of the brain, is closely related to the future achievement of children and adolescents. For this reason, this study analyzed the correlation between muscle strength and executive function in children and adolescents in rural areas of China to better promote the development of muscle strength and executive function. Methods Demographic factors, muscle strength, and executive function were tested in 1,335 children and adolescents in rural China using a three-stage stratified whole-group sampling method. One-way ANOVA and chi-square test were used to compare the differences in executive function among children and adolescents with different muscle strengths. Multiple linear regression analysis and logistic regression analysis were used to analyze the association that exists between muscle strength and executive function. Results When comparing the inconsistently, congruent, 1back, 2back, conversion, size parity, and cognitive flexibility response times of children and adolescents with different muscle strength indexes in rural China, the differences were statistically significant (F = 46.592, 45.610, 10.809, 32.068, 24.095, 19.260, 11.501, p < 0.001). Logistic regression analysis was performed using children and adolescents with muscle strength index >P80 as the control group. The results showed that the risk of 1back dysfunction was higher (OR = 1.764, 95% CI:1.094, 2.843) in children and adolescents with muscle strength index P80. The muscle strength index

BACKGROUND:Epidemiologic evidence on whether iron accumulation in brain modified the association between artificial light at night (ALAN) and incident mental disorders is lacking. The authors aims to investigate modification of brain iron deposition on the associations of ALAN with multiple mental disorders in the middle-aged and older adults. METHODS:This prospective study used data from the UK Biobank. ALAN was drawn from satellite datasets. Susceptibility-weighted magnetic resonance imaging was used to ascertain iron content of each brain region. T2* signal loss was used as indices of iron deposition. The main outcomes are impacts of ALAN exposure on onset of wide spectrum of physician-diagnosed mental disorders, which was estimated by time-varying Cox proportional hazard model. The authors further conducted stratified analyses by levels of iron brain deposition to examine the potential modifying effects. RESULTS:Among 298,283 participants followed for a median of 10.91 years, higher ALAN exposure was associated with increased risk of mental disorders. An IQR (11.37 nW/cm2/sr) increase in annual levels of ALAN was associated with an HR of 1.050 (95 % CI: 1.034,1.066) for any mental disorder, 1.076 (95 % CI: 1.053,1.099) for substance use disorder, and 1.036 (95 % CI: 1.004,1.069) for depression disorder in fully adjusted models. The exposure-response curves showed steeper trends at lower ALAN levels and a plateau at higher exposures. The associations were stronger in participants with high iron deposition in left hippocampus, left accumbens and left pallidum. CONCLUSIONS:ALAN was associated with multiple mental disorders in the middle-aged and older adults, and the findings indicated stricter standards of ALAN is needed and targeted preventive measures are warranted, especially with high brain iron deposition.

Objectives: Recent studies have linked exposure to road traffic noise or air pollution with incident type 2 diabetes (T2D), but investigation on their co-exposure was limited and underlying mechanisms remain unclear. We hy-pothesized that long-term co-exposure to road traffic noise and air pollution increases the risk of incident T2D via the development of metabolic syndrome (MetS). Methods: This prospective study included 390,834 participants in UK Biobank. Cumulative risk index (CRI), the health-based weighted levels of multiple exposures, was applied to characterize the co-exposure to 24-hour road traffic noise (Lden), particulate matter with aerodynamic diameter <= 2.5 mu m (PM2.5), and nitrogen dioxide (NO2). Lden was modeled by the Common Noise Assessment Methods in Europe and air pollutant levels were measured by the Land Use Regression model at participants' residential addresses. Incident T2D was ascertained through linkages to inpatient hospital records. MetS was defined by five (central obesity, triglycerides, HDL cholesterol, glucose, and blood pressure) or six factors (C-reactive protein additionally). Cox proportional hazard models were used to assess the association between environmental exposures and incident T2D, and mediation analyses were applied to investigate the role of MetS.Results: After a median of 10.9 years of follow-up, 13,214 (3.4%) incident T2D cases were ascertained. The exposure to Lden, PM2.5, and NO2, as well as their co-exposure, were significantly associated with an elevated risk of incident T2D, with HRs of 1.03 (95%CI: 1.00, 1.05) per 3.5 dB(A) increase in Lden, 1.05 (95%CI: 1.01, 1.10) per 1.3 mu g/m3 increase in PM2.5, 1.07 (95%CI: 1.02, 1.11) per 9.8 mu g/m3 increase in NO2, and 1.06 (95%CI: 1.02, 1.09) per interquartile range increase in CRI. MetS significantly mediated 43.5%-54.7% of the CRI-T2D relationship.Conclusions: Long-term co-exposure to road traffic noise and air pollution is associated with an elevated risk of incident T2D, which may partly be mediated by MetS.

BACKGROUND:Stroke and dementia are major neurological disorders that contribute significantly to disease burden and are interlinked in terms of risk. Nevertheless, there is currently no study investigating the influence of residential greenspace on the trajectory of these neurological disorders. METHODS:This longitudinal study utilized data from the UK Biobank. Exposure to residential greenspace was measured by the percentage of total greenspace coverage within a 300-meter buffer zone surrounding the participants' residences. A multistate model was employed to illustrate the trajectory of major neurological disorders, and a piecewise Cox regression model was applied to explore the impact of residential greenspace on different time courses of disease transitions. RESULTS:With 422,649 participants and a median follow-up period of 12.5 years, 8568 (2.0 %), 5648 (1.3 %), and 621 (0.1 %) individuals developed incident stroke, dementia, and comorbidity of both conditions, respectively. An increase in residential greenspace by one interquartile range was associated with reduced risks of transitions from baseline to stroke, dementia, and death, as well as from stroke to comorbidity. The corresponding hazard ratios (HRs) were 0.967 (95 % CI: 0.936, 0.998), 0.928 (0.892, 0.965), 0.925 (0.907, 0.942), and 0.799 (0.685, 0.933), respectively. Furthermore, the protective effect of residential greenspace on the transition from stroke or dementia to comorbidity was particularly pronounced within the first year and over 5 years after stroke and during the 2 to 3 years after dementia onset, with HRs of 0.692 (0.509, 0.941), 0.705 (0.542, 0.918), and 0.567 (0.339, 0.949), respectively. CONCLUSION:This study observed a protective role of residential greenspace in the trajectory of major neurological disorders and contributed to identifying critical progression windows. These findings underscore the significance of environment-health interactions in the prevention of neurological disorders.

Introduction: There is an increasing interest in understanding whether air pollutants modify the quantitative relationships between temperature and health outcomes. The results of available studies were, however, inconsistent. This study aims to sum up the current evidence and provide a comprehensive understanding of this topic. Methods: We conducted an electronic search in PubMed (MEDLINE), EMBASE, Web of Science Core Collection, and ProQuest Dissertations and Theses. The modified Navigation Guide was applied to evaluate the quality and strength of evidence. We calculated pooled temperature-related mortality at low and high pollutant levels respectively, using the random-effects model.Results: We identified 22 eligible studies, eleven of which were included in the meta-analysis. Significant effect modification was observed on heat effects for all-cause and non-accidental mortality by particulate matter with an aerodynamic diameter of <10 mu m (PM10) and ozone (O3) (p < 0.05). The excess risks (ERs) for all-cause and non-accidental mortality were 5.4% (4.4%, 6.4%) and 6.3% (4.8%, 7.8%) at the low PM10 level, 8.8% (7.5%, 10.1%) and 11.4% (8.7%, 14.2%) at the high PM10 level, respectively. As for O3, the ERs for all-cause and nonaccidental mortality were 5.1% (3.9%, 6.3%) and 3.6% (0.1%, 7.2%) at the low O3 level, 7.6% (6.3%, 9.0%) and 12.5% (4.7%, 20.9%) at the high O3 level, respectively. Surprisingly, the heat effects on cardiovascular mortality were found to be lower at high carbon monoxide (CO) levels [ERs = 5.4% (3.9%, 6.9%)] than that at low levels [ERs = 9.4% (7.0%, 11.9%)]. The heterogeneity varied, but the results of sensitivity analyses were generally robust. Significant effect modification by air pollutants was not observed for heatwave or cold effects.Conclusions: PM10 and O3 modify the heat-related all-cause and non-accidental mortality, indicating that policymakers should consider air pollutants when establishing heat-health warning systems. Future studies with comparable designs and settings are needed.

Although the lockdown policy implemented during the COVID-19 pandemic indeed improved the air quality and reduced the related health risks, the real effects of the lockdown and its resulting health risks remain unclear considering the effects of unobserved confounders and the longstanding efforts of the government regarding air pollution. We compared air pollution between the lockdown period and the period before the lockdown using a difference-in-differences (DID) model and estimated the mortality burden caused by the number of deaths related to air pollution changes. The NO2 and CO concentrations during the lockdown period (17 days) declined by 8.94 μg/m3 (relative change: 16.94%; 95% CI: 3.71, 14.16) and 0.20 mg/m3 (relative change: 16.95%; 95% CI: 0.04, 0.35) on an average day, respectively, and O3 increased by 8.41 μg/m3 (relative change: 32.80%; 95% CI: 4.39, 12.43); no meaningful impacts of the lockdown policy on the PM2.5, PM10, SO2, or the AQI values were observed. Based on the three clearly changed air pollutants, the lockdown policy prevented 8.22 (95% CI: 3.97, 12.49) all-cause deaths. Our findings suggest that the overall excess deaths caused by air pollution during the lockdown period declined. It is beneficial for human health when strict control measures, such as upgrading industry structure and promoting green transportation, are taken to reduce emissions, especially in cities with serious air pollution in China, such as Shijiazhuang.