PM2.5 chemical components are associated with in-hospital case fatality among acute myocardial infarction patients in China.

Recent studies have linked the cardiovascular events with the exposure to ambient fine particulate matter (PM2.5); however, the impact of PM2.5 chemical components on acute myocardial infarction (AMI) case fatality remains poorly understood. To address this gap, we included 178,340 hospitalised patients with AMI utilising the inpatient discharge database from Sichuan, Shanxi, Guangxi, and Guangdong, China spanning 2014-2019. We evaluated exposure to PM2.5 and its components (black carbon (BC), organic matter (OM), sulphate (SO42-), nitrate (NO3-), and ammonium (NH4+)) using bilinear interpolation based on the patient's residential address. We used mixed-effects logistic regression models to investigate the associations of PM2.5 and its five components with in-hospital AMI case fatality. Per interquartile range (IQR) increment in short-term exposure (7-day average) to overall PM2.5 (odds ratio (OR): 1.086, 95 % confidence interval (CI): 1.045-1.128), SO42-(1.063, 1.024-1.104), BC (1.055, 1.023-1.089), OM (1.052, 1.019-1.086, and NO3- (1.045, 1.003-1.089) were significantly associated with high risk of in-hospital AMI case fatality. The ORs per IQR increment in long-term exposure (annual average) were 1.323 (95 % CI: 1.255-1.394) for PM2.5, followed by BC (1.271, 1.210-1.335), OM (1.243, 1.188-1.300), SO42- (1.212, 1.157-1.270), NO3- (1.116, 1.075-1.159), and NH4+ (1.068, 1.031-1.106). Our study suggests that PM2.5 chemical components might be important risk factors for in-hospital AMI case fatality, highlighting the importance of targeted reduction of PM2.5 emissions, particularly BC, OM, and SO42-.

The association between cytomegalovirus infection and neurodegenerative diseases: a prospective cohort using UK Biobank data.

Background: Certain viral infections have been linked to the development of neurodegenerative diseases. This study aimed to investigate the association between cytomegalovirus (CMV) infection and five neurodegenerative diseases, spinal muscular atrophy (SMA) and related syndromes, Parkinson's disease (PD), Alzheimer's disease (AD), multiple sclerosis (MS), and disorders of the autonomic nervous system (DANS). Methods: This prospective cohort included white British individuals who underwent CMV testing in the UK Biobank from January 1, 2006 to December 31, 2021. A Cox proportional hazard model was utilized to estimate the future risk of developing five neurodegenerative diseases in individuals with or without CMV infection, adjusted for batch effect, age, sex, and Townsend deprivation index in Model 1, and additionally for type 2 diabetes, cancer, osteoporosis, vitamin D, monocyte count and leukocyte count in Model 2. Bidirectional Mendelian randomization was employed to validate the potential causal relationship between CMV infection and PD. Findings: A total of 8346 individuals, consisting of 4620 females (55.4%) and 3726 males (44.6%) who were white British at an average age of 56.74 (8.11), were included in this study. The results showed that CMV infection did not affect the risk of developing AD (model 1: HR [95% CI] = 1.01 [0.57, 1.81], P = 0.965; model 2: HR = 1.00 [0.56, 1.79], P = 0.999), SMA and related syndromes (model 1: HR = 3.57 [0.64, 19.80], P = 0.146; model 2: HR = 3.52 [0.63, 19.61], P = 0.152), MS (model 1: HR = 1.16 [0.45, 2.97], P = 0.756; model 2: HR = 1.16 [0.45, 2.97], P = 0.761) and DANS (model 1: HR = 0.65 [0.16, 2.66], P = 0.552; model 2: HR = 0.65 [0.16, 2.64], P = 0.543). Interestingly, it was found that participants who were CMV seronegative had a higher risk of developing PD compared to those who were seropositive (model 1: HR = 2.37 [1.25, 4.51], P = 0.009; model 2: HR = 2.39 [1.25, 4.54], P = 0.008) after excluding deceased individuals. This association was notably stronger in males (model 1: HR = 3.16 [1.42, 7.07], P = 0.005; model 2: HR = 3.41 [1.50, 7.71], P = 0.003), but no significant difference was observed in the female subgroup (model 1: HR = 1.28 [0.40, 4.07], P = 0.679; model 2: HR = 1.27 [0.40, 4.06], P = 0.684). However, a bidirectional Mendelian randomization analysis did not find a genetic association between CMV infection and PD. Interpretation: The study found that males who did not have a CMV infection were at a higher risk of developing PD. The findings provided a new viewpoint on the risk factors for PD and may potentially influence public health approaches for the disease. Funding: National Natural Science Foundation of China (81873776), Natural Science Foundation of Guangdong Province, China (2021A1515011681, 2023A1515010495).

Associations of ambient air pollution with incidence and dynamic progression of atrial fibrillation.

The influence of air pollution on dynamic changes in clinical state from healthy to atrial fibrillation (AF), further AF-related complications and ultimately, death are unclear. We aimed to investigate the relationships between air pollution and the occurrence and progression trajectories of AF. We retrieved 442,150 participants free of heart failure (HF), myocardial infarction (MI), stroke and dementia at baseline from UK Biobank. Exposures to air pollution for each transition stage were estimated at the geocoded residential address of each participant using the bilinear interpolation approach. The outcomes were incident AF, complications, and death. Multi-stage models were used to evaluate the associations between air pollution and dynamic progression of AF. Over a 12.6-year median follow-up, a total of 21,670 incident AF patients were identified, of whom, 4103 developed complications and 1331 died. PM2.5, PM10, NOx and NO2 were differentially positively associated, while O3 was negatively associated with risks of progression trajectories of AF. PM2.5 exposure was significantly associated with an increased risk of progression. The associations of PM2.5, PM10, NOx, and NO2 on incident AF were generally more pronounced compared to other transitions. The cumulative transition probabilities were generally higher in individuals with higher exposure levels of PM2.5, PM10, NOx, and NO2 and lower exposure to O3. Air pollution could potentially have a role in increasing the risk of both the occurrence and progression of AF, emphasizing the significance of air pollution interventions in both the primary prevention of AF and the management of AF-related outcomes.

Air pollution associated with cardiopulmonary disease and mortality among participants with preserved ratio impaired spirometry.

BACKGROUND: Epidemiological evidence regarding the association between air pollutants and cardiopulmonary disease, mortality in individuals with preserved ratio impaired spirometry (PRISm), and their combined effects remains unclear. METHODS: We followed 36,149 participants with PRISm in the UK Biobank study. Annual concentrations of PM2.5, PM10, NO2, NOx, and SO2 at residential addresses were determined using a bilinear interpolation method, accounting for address changes. A multistate model assessed the dynamic associations between air pollutants and cardiopulmonary diseases and mortality in PRISm. Quantile g-computation was used to investigate the joint effects of air pollutants. RESULTS: Long-term exposure to PM2.5, PM10, NO2, NOx, and SO2 was significantly associated with the risk of cardiopulmonary disease in PRISm. The corresponding hazard ratios (HRs) [95 % confidence intervals (95 % CIs)] per interquartile range (IQR) were 1.49 (1.43, 1.54), 1.52 (1.46, 1.57), 1.34 (1.30, 1.39), 1.30 (1.26, 1.34), and 1.44 (1.41, 1.48), respectively. For mortality, the corresponding HRs (95 % CIs) per IQR were 1.36 (1.25, 1.47), 1.35 (1.24, 1.46), 1.27 (1.18, 1.36), 1.23 (1.15, 1.31), and 1.29 (1.20, 1.39), respectively. In PRISm, quantile g-computation analysis demonstrated that a quartile increase in exposure to a mixture of all air pollutants was positively associated with the risk of cardiopulmonary disease and mortality, with HRs (95 % CIs) of 1.84 (1.76, 3.84) and 1.45 (1.32, 1.57), respectively. CONCLUSION: Long-term individual and joint exposure to air pollutants (PM2.5, PM10, NO2, NOx, and SO2) might be an important risk factor for cardiopulmonary disease and mortality in high-risk populations with PRISm.

Air Pollution Metabolomic Signatures and Chronic Respiratory Diseases Risk: A Longitudinal Study.

BACKGROUND: Although evidence has documented the associations of ambient air pollution with chronic respiratory diseases (CRDs) and lung function, the underlying metabolic mechanisms remain largely unclear. RESEARCH QUESTION: How does the metabolomic signature for air pollution relate to CRD risk, respiratory symptoms, and lung function? STUDY DESIGN AND METHODS: We retrieved 171,132 participants free of COPD and asthma at baseline from the UK Biobank, who had data on air pollution and metabolomics. Exposures to air pollutants (particulate matter with diameter ≤ 2.5 µm [PM2.5], particulate matter with a diameter ≤ 10 µm, nitrogen oxide [NOX], and NO2) were assessed for 4 years before baseline considering residential address histories. We used 10-fold cross-validation elastic net regression to identify air pollution-associated metabolites. Multivariable Cox models were used to assess the associations between metabolomic signatures and CRD risk. Mediation and pathway analysis were conducted to explore the metabolic mechanism underlying the associations. RESULTS: During a median follow-up of 12.51 years, 8,951 and 5,980 incident COPD and asthma cases were recorded. In multivariable Cox regressions, air pollution was positively associated with CRD risk (eg, hazard ratio per interquartile range increment in PM2.5, 1.09; 95% CI, 1.06-1.13). We identified 103, 86, 85, and 90 metabolites in response to PM2.5, particulate matter with a diameter ≤ 10 µm, NOX, and NO2 exposure, respectively. The metabolomic signatures showed significant associations with CRD risk (hazard ratio per SD increment in PM2.5 metabolomic signature, 1.11; 95% CI, 1.09-1.14). Mediation analysis showed that peripheral inflammatory and erythrocyte-related markers mediated the effects of metabolomic signatures on CRD risk. We identified 14 and 12 perturbed metabolic pathways (energy metabolism and amino acid metabolism pathways, etc) for PM2.5 and NOX metabolomic signatures. INTERPRETATION: Our study identifies metabolomic signatures for air pollution exposure. The metabolomic signatures showed significant associations with CRD risk, and inflammatory- and erythrocyte-related markers partly mediated the metabolomic signatures-CRD links.

Regular use of fish oil supplements and course of cardiovascular diseases: prospective cohort study.

Objective: To examine the effects of fish oil supplements on the clinical course of cardiovascular disease, from a healthy state to atrial fibrillation, major adverse cardiovascular events, and subsequently death. Design: Prospective cohort study. Setting: UK Biobank study, 1 January 2006 to 31 December 2010, with follow-up to 31 March 2021 (median follow-up 11.9 years). Participants: 415 737 participants, aged 40-69 years, enrolled in the UK Biobank study. Main outcome measures: Incident cases of atrial fibrillation, major adverse cardiovascular events, and death, identified by linkage to hospital inpatient records and death registries. Role of fish oil supplements in different progressive stages of cardiovascular diseases, from healthy status (primary stage), to atrial fibrillation (secondary stage), major adverse cardiovascular events (tertiary stage), and death (end stage). Results: Among 415 737 participants free of cardiovascular diseases, 18 367 patients with incident atrial fibrillation, 22 636 with major adverse cardiovascular events, and 22 140 deaths during follow-up were identified. Regular use of fish oil supplements had different roles in the transitions from healthy status to atrial fibrillation, to major adverse cardiovascular events, and then to death. For people without cardiovascular disease, hazard ratios were 1.13 (95% confidence interval 1.10 to 1.17) for the transition from healthy status to atrial fibrillation and 1.05 (1.00 to 1.11) from healthy status to stroke. For participants with a diagnosis of a known cardiovascular disease, regular use of fish oil supplements was beneficial for transitions from atrial fibrillation to major adverse cardiovascular events (hazard ratio 0.92, 0.87 to 0.98), atrial fibrillation to myocardial infarction (0.85, 0.76 to 0.96), and heart failure to death (0.91, 0.84 to 0.99). Conclusions: Regular use of fish oil supplements might be a risk factor for atrial fibrillation and stroke among the general population but could be beneficial for progression of cardiovascular disease from atrial fibrillation to major adverse cardiovascular events, and from atrial fibrillation to death. Further studies are needed to determine the precise mechanisms for the development and prognosis of cardiovascular disease events with regular use of fish oil supplements.

Associations of serum glucocorticoid levels on hypertension and blood pressure-related indicators: a nested case-control study in rural China.

BACKGROUND: The relationship between glucocorticoids and hypertension has shown inconsistent findings in previous studies. To address this, our study employed a nested case-control design in rural areas to further investigate the association between serum glucocorticoid levels and hypertension, and blood pressure-related indicators. METHODS: This study employed a nested case-control design, involving 560 pairs of hypertensive cases and matched controls. The concentrations of serum cortisol (F), cortisone (E) and 11-deoxycortisol (S) were determined using liquid chromatography-tandem mass spectrometry. We employed various methods, including generalized linear model (GLM), conditional logistic regression model, restricted cubic spline regression, subgroup analysis, interaction, and joint effects, with adjustments for multiple covariates to analyze the relationships between glucocorticoids, hypertension, and blood pressure-related indicators. RESULTS: After multivariable adjustments, ln-F, ln-F/E, and ln-S were positively associated with SBP, DBP, pulse pressure (PP), and mean arterial pressure (MAP), while ln-E was negatively associated with DBP and MAP ( P  < 0.05). Interestingly, ln-S showed no statistically significant association with hypertension prevalence ( P  > 0.05), whereas ln-F and ln-F/E were positively associated with it ( P  < 0.05). The adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were 1.153 (1.011-1.315) for ln-F and 2.072 (1.622-2.645) for ln-F/E, respectively. In contrast, ln-E exhibited a negative association with hypertension prevalence (adjusted OR = 0.837, 95% CI 0.714-0.982). Moreover, a significant association was observed between the combined use of high-dose F/E and high-dose S with hypertension prevalence (adjusted OR = 3.273, 95% CI 2.013-5.321). Blood pressure indicators and hypertension prevalence significantly increased with elevated serum F and F/E concentrations ( P  < 0.05). Interaction analysis further revealed that among women, the positive association between F/E and hypertension prevalence was more pronounced than in men ( P  < 0.05), and S exhibited a more significant positive association with hypertension prevalence in the overweight population ( P  < 0.05). CONCLUSION: Serum F/E and S levels demonstrated positive associations with hypertension and blood pressure-related indicators, and their combined influence exhibited a synergistic effect on hypertension. Notably, F, F/E, and S were associated with heightened hypertension risk, warranting particular attention in women and overweight populations.

Long-term exposure to ambient ozone and adult-onset asthma: A prospective cohort study.

BACKGROUND: The association between long-term exposure to ozone (O3) and adult-onset asthma (AOA) remains inconclusive, and analysis of causality is lacking. OBJECTIVES: To examine the causal association between long-term O3 exposure and AOA. METHODS: A prospective cohort study of 362,098 participants was conducted using the UK Biobank study. Incident cases of AOA were identified using health administrative data of the National Health Services. O3 exposure at participants' residential addresses was estimated by a spatio-temporal model. Instrumental variable (IV) modelling was used to analyze the causal association between O3 exposure and AOA, by incorporating wind speed and planetary boundary layer height as IVs into time-dependent Cox model. Negative control outcome (accidental injury) was also used to additionally evaluate unmeasured confounding. RESULTS: During a mean follow-up of 11.38 years, a total of 10,973 incident AOA cases were identified. A U-shaped concentration-response relationship was observed between O3 exposure and AOA in the traditional Cox models with HR of 0.916 (95% CI: 0.888, 0.945) for O3 at low levels (<38.17 ppb), and 1.204 (95% CI: 1.168, 1.242) for O3 at high levels (≥38.17 ppb). However, in the IV analysis we only found a statistically significant association between high-level O3 exposure and AOA risk, but not for low-level O3 exposure. No significant associations between O3 exposure and accidental injury were observed. CONCLUSION: Our findings suggest a potential causal relationship between long-term exposure to high-level ambient O3 and increased risks of AOA.

Dietary Inflammatory Index and Dietary Diversity Score Associated with Sarcopenia and Its Components: Findings from a Nationwide Cross-Sectional Study.

Little is known about the independent and joint effects of the energy-adjusted dietary inflammatory index (E-DII) and dietary diversity score (DDS) on sarcopenia and its components (low muscle mass, low muscle strength, and low physical performance). A total of 155,669 UK Biobank participants with ≥1 (maximum 5) 24 h dietary assessments were included in this cross-sectional analysis. We used logistic regression models to investigate the associations of E-DII and DDS with sarcopenia and its three components. We further examined the joint effects of E-DII and DDS on sarcopenia and its components using additive and multiplicative interaction analyses. We observed that lower E-DII and higher DDS were associated with lower odds of sarcopenia and its components. There were significant joint associations of E-DII and DDS with sarcopenia and low physical performance (p-interaction < 0.05) on the multiplicative interactive scale. Our study suggests that lower dietary inflammatory potential and higher dietary diversity might be important protective factors against sarcopenia and its components. More cases of sarcopenia and low physical performance might be preventable by adherence to a more anti-inflammatory diet combined with a higher dietary diversity.

Causal association between long-term exposure to air pollution and incident Parkinson's disease.

Epidemiological evidence for long-term air pollution exposure and Parkinson's disease (PD) is controversial, and analysis of causality is limited. We identified 293,888 participants who were free of PD at baseline in the UK Biobank (2006-2010). Time-varying air pollution [fine particulate (PM2.5) and ozone (O3)] exposures were estimated using spatio-temporal models. Incident cases of PD were identified using validated algorithms. Four methods were used to investigate the associations between air pollution and PD, including (1) standard time-varying Cox proportional-hazard model; (2) Cox models weighted by generalized propensity score (GPS) and inverse-probability weights (IPW); (3) instrumental variable (IV) analysis; and (4) negative control outcome analysis. During a median of 11.6 years of follow-up, 1822 incident PD cases were identified. Based on standard Cox regression, the hazard ratios (95% confidence interval) for a 1 µg/m3 or ppb increase in PM2.5 and O3 were 1.23 (1.17, 1.30) and 1.02 (0.98, 1.05), respectively. Consistent results were found in models weighted by GPS and IPW, and in IV analysis. There were no significant associations between air pollution and negative control outcomes. This study provides evidence to support a causal association between PM2.5 exposure and PD. Mitigation of air pollution could be a protective measure against PD.

High Dietary Intake of Iron Might Be Harmful to Atrial Fibrillation and Modified by Genetic Diversity: A Prospective Cohort Study.

Some studies suggest an association between iron overload and cardiovascular diseases (CVDs). However, the relationship between dietary iron intake and atrial fibrillation (AF) remains uncertain, as does the role of genetic loci on this association. The study involved 179,565 participants from UK Biobank, tracking incident atrial fibrillation (AF) cases. Iron intake was categorized into low, moderate, and high groups based on dietary surveys conducted from 2009 to 2012. The Cox regression model was used to estimate the risk of AF in relation to iron intake, assessing the hazard ratio (HR) and 95% confidence interval (95% CI). It also examined the impact of 165 AF-related and 20 iron-related genetic variants on this association. Pathway enrichment analyses were performed using Metascape and FUMA. During a median follow-up period of 11.6 years, 6693 (3.97%) incident AF cases were recorded. A total of 35,874 (20.0%) participants had high iron intake. High iron intake was associated with increased risk of AF [HR: 1.13 (95% CI: 1.05, 1.22)] in a fully adjusted model. Importantly, there were 83 SNPs (11 iron-related SNPs) that could enhance the observed associations. These genes are mainly involved in cardiac development and cell signal transduction pathways. High dietary iron intake increases the risk of atrial fibrillation, especially when iron intake exceeds 16.95 mg. The association was particularly significant among the 83 SNPs associated with AF and iron, the individuals with these risk genes. Gene enrichment analysis revealed that these genes are significantly involved in cardiac development and cell signal transduction processes.

Air pollution, APOE genotype and risk of dementia among individuals with cardiovascular diseases: A population-based longitudinal study.

Individuals with cardiovascular disease (CVD) are particularly vulnerable to dementia, but it remains unclear whether air pollution exposure links with higher risk of dementia among those with CVD. The data were derived from the UK Biobank study (UKB). Dementia-free participants with CVD at baseline were included. Air pollution exposure was assessed through land use regression models, including particulate matter (PM2.5, PM2.5-10, and PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX). A Cox proportional hazards model was used to investigate the associations between air pollution exposure and incident dementia among individuals with CVD. Air pollution was associated with dementia among individuals with CVD, and the hazard ratios of dementia associated with each interquartile range (IQR) µg/m3 increase in air pollution were 1.07 (95% CI: 1.02, 1.12) for PM2.5, 1.10 (95% CI: 1.04, 1.15) for PM10, 1.08 (95% CI: 1.03, 1.14) for NO2 and 1.05 (95% CI: 1.00, 1.09) for NOx. Associations between air pollution and all-cause dementia were found to be significant among individuals with hypertension. Adverse effects of air pollution were also observed for Alzheimer's dementia (AD) and vascular dementia (VaD), with a higher effect for AD. Observed associations remained similar in subgroups of APOE ε4 carriers and noncarriers, although there was a higher risk difference across different air pollution concentration among these individuals carrying APOE ε4. Air pollution emerges as a critical risk factor for dementia among individuals with CVD, regardless of genetic susceptibility indicated by the APOE genotype. Notably, individuals with hypertension might be susceptible to the adverse effects of air pollution, leading to a higher incidence of dementia. Understanding these impacts on dementia among individuals with CVD may promote better targeted prevention and clinical management strategies.

Fresh fruit, dried fruit, raw vegetables, and cooked vegetables consumption associated with progression trajectory of type 2 diabetes: a multi-state analysis of a prospective cohort.

PURPOSE: To examine the effects of fresh fruit, dried fruit, raw vegetables, and cooked vegetables on type 2 diabetes (T2D) progression trajectory. METHODS: We included 429,886 participants in the UK Biobank who were free of diabetes and diabetes complications at baseline. Food groups were determined using a validated food frequency questionnaire. Outcomes were T2D incidence, complications, and mortality. Multi-state model was used to analyze the effects of food groups on T2D progression. RESULTS: During a follow-up of 12.6 years, 10,333 incident T2D cases were identified, of whom, 3961 (38.3%) developed T2D complications and 1169 (29.5%) died. We found that impacts of four food groups on T2D progression varied depending on disease stage. For example, compared to participants who ate less than one piece of dried fruit per day, the hazard ratios and 95% confidence intervals for those who ate ≥ 2 pieces of dried fruit per day were 0.82 (0.77, 0.87), 0.88 (0.85, 0.92), and 0.86 (0.78, 0.95) for transitions from diabetes-free state to incident T2D, from diabetes-free state to total death, and from incident T2D to T2D complications, respectively. Higher intake of fresh fruit was significantly associated with lower risk of disease progression from diabetes-free state to all-cause death. Higher intake of raw and cooked vegetables was significantly associated with lower risks of disease progression from diabetes-free state to incident T2D and to total death. CONCLUSIONS: These findings indicate that higher intake of fresh fruit, dried fruit, raw vegetables, and cooked vegetables could be beneficial for primary and secondary prevention of T2D.

Ambient fine particulate matter chemical composition associated with in-hospital case fatality, hospital expenses, and length of hospital stay among patients with heart failure in China.

*Joint senior authorship. BACKGROUND: Previous studies have observed the adverse effects of ambient fine particulate matter pollution (PM2.5) on heart failure (HF). However, evidence regarding the impacts of specific PM2.5 components remains scarce. METHODS: We included 58 129 patients hospitalised for HF between 2013 and 2017 in 11 cities of Shanxi, China from inpatient discharge database. We evaluated exposure to PM2.5 and its components ((sulphate (SO42-), nitrate (NO3-), ammonium (NH4+), organic matter (OM) and black carbon (BC)), along with meteorological factors using bilinear interpolation at each patients' residential address. We used multivariable logistic and linear regression models to assess the associations of these components with in-hospital case fatality, hospital expenses, and length of hospital stay. RESULTS: Increase equivalents to the interquartile range (IQR) in OM (odds ratio (OR) = 1.13; 95% confidence interval (CI) = 1.02, 1.26) and BC (OR = 1.14; 95% CI = 1.02, 1.26) were linked to in-hospital case fatality. Per IQR increments in PM2.5, SO42-, NO3-, OM, and BC were associated with cost increases of 420.62 (95% CI = 285.75, 555.49), 221.83 (95% CI = 96.95, 346.71), 214.93 (95% CI = 68.66, 361.21), 300.06 (95% CI = 176.96, 423.16), and 303.09 (95% CI = 180.76, 425.42) CNY. Increases of 1 IQR in PM2.5, SO42-, OM, and BC were associated with increases in length of hospital stay of 0.10 (95% CI = 0.02, 0.19), 0.09 (95% CI = 0.02, 0.17), 0.10 (95% CI = 0.03, 0.17), and 0.16 (95% CI = 0.08, 0.23) days. CONCLUSIONS: Our findings suggest that ambient SO42-, OM, and BC might be significant risk factors for HF, emphasising the importance of formulating customised guidelines for the chemical constituents of PM and controlling the emissions of the most dangerous components.

Mapping multi-omics characteristics related to short-term PM2.5 trajectory and their impact on type 2 diabetes in middle-aged and elderly adults in Southern China.

The relationship between PM2.5 and metabolic diseases, including type 2 diabetes (T2D), has become increasingly prominent, but the molecular mechanism needs to be further clarified. To help understand the mechanistic association between PM2.5 exposure and human health, we investigated short-term PM2.5 exposure trajectory-related multi-omics characteristics from stool metagenome and metabolome and serum proteome and metabolome in a cohort of 3267 participants (age: 64.4 ± 5.8 years) living in Southern China. And then integrate these features to examine their relationship with T2D. We observed significant differences in overall structure in each omics and 193 individual biomarkers between the high- and low-PM2.5 groups. PM2.5-related features included the disturbance of microbes (carbohydrate metabolism-associated Bacteroides thetaiotaomicron), gut metabolites of amino acids and carbohydrates, serum biomarkers related to lipid metabolism and reducing n-3 fatty acids. The patterns of overall network relationships among the biomarkers differed between T2D and normal participants. The subnetwork membership centered on the hub nodes (fecal rhamnose and glycylproline, serum hippuric acid, and protein TB182) related to high-PM2.5, which well predicted higher T2D prevalence and incidence and a higher level of fasting blood glucose, HbA1C, insulin, and HOMA-IR. Our findings underline crucial PM2.5-related multi-omics biomarkers linking PM2.5 exposure and T2D in humans.

Associations of glycosylated hemoglobin, pre-diabetes, and type 2 diabetes with incident lung cancer: A large prospective cohort study.

BACKGROUND: The association of pre-diabetes and type 2 diabetes (T2D) with incident lung cancer is uncertain, and the incident risk across the glycemic spectrum is unclear. We aimed to explore the associations of glycosylated hemoglobin (HbA1c), pre-diabetes, and T2D with incident lung cancer in a large prospective cohort. METHODS: Leveraging a total of 210,779 cancer-free adults recruited in the UK Biobank between 2006 and 2010. We performed multivariable Cox proportional hazards models and restricted cubic spline methods to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs) for the associations of HbA1c, pre-diabetes, and T2D with incident lung cancer. RESULTS: During a median follow-up of 11.06 years, 1738 incident lung cancer cases were ascertained. The incidence of lung cancer was 20% higher among people with diabetes (HR: 1.20, 95% CI: 1.02 to 1.42) and 38% higher among people with pre-diabetes (HR: 1.38, 95% CI: 1.15 to 1.65). After dividing people with diabetes by whether taking antidiabetic medications, the incidence was 28% higher among people with diabetes without medications (HR: 1.28, 95% CI: 1.02 to 1.61) and 15% higher among people with diabetes with medications (HR: 1.15, 95% CI: 0.93 to 1.41). The increased risk of incident lung cancer for each standard deviation (6.45 mmol/mol) increase in HbA1c was more pronounced across HbA1c values of 32-42 mmol/mol (HR: 1.37, 95% CI: 1.18 to 1.59). The risk was more pronounced among participants <60 years. CONCLUSIONS: Pre-diabetes and T2D are associated with an increased incidence of lung cancer. The increased risk of incident lung cancer is more pronounced across HbA1c values of 32-42 mmol/mol, which are currently considered normal values.

Short-Term Exposure to PM2.5 Chemical Components and Depression Outpatient Visits: A Case-Crossover Analysis in Three Chinese Cities.

BACKGROUND: The association between specific chemical components of PM2.5 and depression remains largely unknown. METHODS: We conducted a time-stratified case-crossover analysis with a distributed lag nonlinear model (DLNM) to evaluate the relationship of PM2.5 and its chemical components, including black carbon (BC), organic matter (OM), sulfate (SO42-), nitrate (NO3-), and ammonium (NH4+), with the depression incidence. Daily depression outpatients were enrolled from Huizhou, Shenzhen, and Zhaoqing. RESULTS: Among 247,281 outpatients, we found the strongest cumulative effects of PM2.5 and its chemical components with the odd ratios (ORs) of 1.607 (95% CI: 1.321, 1.956) and 1.417 (95% CI: 1.245, 1.612) at the 50th percentile of PM2.5 and OM at lag 21, respectively. Furthermore, the ORs with SO42- and NH4+ at the 75th percentile on the same lag day were 1.418 (95% CI: 1.247, 1.613) and 1.025 (95% CI: 1.009, 1.140). Relatively stronger associations were observed among females and the elderly. CONCLUSIONS: Our study suggests that PM2.5 and its chemical components might be important risk factors for depression. Reducing PM2.5 emissions, with a particular focus on the major sources of SO42- and OM, might potentially alleviate the burden of depression in South China.

Green Space Morphology and School Myopia in China.

Importance: China has experienced both rapid urbanization and major increases in myopia prevalence. Previous studies suggest that green space exposure reduces the risk of myopia, but the association between myopia risk and specific geometry and distribution characteristics of green space has yet to be explored. These must be understood to craft effective interventions to reduce myopia. Objective: To evaluate the associations between myopia and specific green space morphology using novel quantitative data from high-resolution satellite imaging. Design, Setting, and Participants: This prospective cohort study included students grades 1 to 4 (aged 6 to 9 years) in Shenzhen, China. Baseline data were collected in 2016-2017, and students were followed up in 2018-2019. Data were analyzed from September 2020 to January 2022. Exposures: Eight landscape metrics were calculated using land cover data from high-resolution Gaofen-2 satellite images to measure area, aggregation, and shape of green space. Main Outcome and Measures: The 2-year cumulative change in myopia prevalence at each school and incidence of myopia at the student level after 2 years were calculated as main outcomes. The associations between landscape metrics and school myopia were assessed, controlling for geographical, demographic, and socioeconomic factors. Principal component analyses were performed to further assess the joint effect of landscape metrics at the school and individual level. Results: A total of 138 735 students were assessed at baseline. Higher proportion, aggregation, and better connectivity of green space were correlated with slower increases in myopia prevalence. In the principal component regression, a 1-unit increase in the myopia-related green space morphology index (the first principal component) was negatively associated with a 1.7% (95% CI, -2.7 to -0.6) decrease in myopia prevalence change at the school level (P = .002). At the individual level, a 1-unit increase in myopia-related green space morphology index was associated with a 9.8% (95% CI, 4.1 to 15.1) reduction in the risk of incident myopia (P < .001), and the association remained after further adjustment for outdoor time, screen time, reading time, and parental myopia (adjusted odds ratio, 0.88; 95% CI, 0.80 to 0.97; P = .009). Conclusions and Relevance: Structure of green space was associated with a decreased relative risk of myopia, which may provide guidance for construction and renovation of schools. Since risk estimates only indicate correlations rather than causation, further interventional studies are needed to assess the effect on school myopia of urban planning and environmental designs, especially size and aggregation metrics of green space, on school myopia.

Associations between air pollution and the risk of first admission and multiple readmissions for cardiovascular diseases.

OBJECTIVES: We aimed to investigate the associations between air pollutants and the risk of admission and multiple readmission events for cardiovascular disease (CVD). METHODS: A total of 285 009 participants free of CVD at baseline from the UK Biobank were included in this analysis. Four major cardiovascular admission events were identified during the follow-up: chronic ischaemic heart disease (CIHD), cerebrovascular disease, atrial fibrillation and heart failure. We used Prentice, Williams and Peterson-Total Time model to examine the association between ambient air pollution and first admission, as well as multiple readmissions for these CVDs. RESULTS: During a median follow-up of 12 years, 17 176 (6.03%) participants were hospitalised with CVDs, and 6203 (36.11%) patients with CVD had subsequent readmission events for CVDs. We observed significant associations between air pollution and both first admission and readmission for CVDs, with generally stronger associations on readmission for cardiovascular events. For example, the adjusted HRs for the first admission and subsequent readmission for cerebrovascular disease were 1.130 (95% CI 1.070 to 1.194) and 1.270 (95% CI 1.137 to 1.418) for each IQR increase of particulate matter with a diameter ≤2.5 µm. The corresponding HRs for CIHD were 1.060 (95% CI 1.008 to 1.114) and 1.120 (95% CI 1.070 to 1.171). Sex stratified analyses showed that the associations were generally more pronounced among females than males. CONCLUSION: This study provides evidence that ambient air pollutants might play an important role in both first admission and readmission for cardiovascular events. In addition, patients with pre-existing CVDs may be more vulnerable to air pollution compared with healthy population.

Interactive effects of physical activity and sarcopenia on incident ischemic heart disease: Results from a nation-wide cohort study.

BACKGROUND AND AIMS: Lack of physical activity (PA) and sarcopenia is a known risk factors for ischemic heart disease (IHD). However, considering their coexistence in the middle-aged and elderly population, the interaction of these two factors remains uncertain. Here, we investigated the interactive effects of PA and sarcopenia on IHD. METHODS: We extracted 344,688 participants free of IHD at baseline from the UK Biobank. PA was classified into low, moderate, and high according to the International Physical Activity Questionnaire. Sarcopenia was identified in accordance with the European Working Group on Sarcopenia in Older People 2. Cox proportional hazard models were applied to estimate the effect of PA and sarcopenia on incident IHD and its subtypes. We also used objective PA data measured by wrist-worn devices to repeat these analyses. RESULTS: Over a median follow-up of 11.7 years, 24,809 (7.2%) participants developed incident IHD. Lack of PA was associated with a higher risk of IHD after adjusting for potential confounders. The hazard ratio (HR) was 1.09 (95% CI: 1.05-1.13) for individuals without sarcopenia and 1.29 (95% CI: 1.17-1.42) for those with sarcopenia. Regarding the joint effect, the combination of low PA and sarcopenia was associated with the highest risk of IHD, with an HR of 1.54 (95% CI: 1.44-1.66), and both additive and multiplicative interactions were significant (RERI 0.27, 95% CI: 0.14-0.39, p-interaction <0.01). For subtypes of IHD, the interaction was pronounced in acute myocardial infarction and chronic ischemic heart disease. CONCLUSIONS: These results suggest a synergistic interaction between lack of PA and sarcopenia on the risk of IHD. Findings from this study may help facilitate more effective primary prevention of IHD.