Environmental Exposome and Atrial Fibrillation: Emerging Evidence and Future Directions.

There has been increased awareness of the linkage between environmental exposures and cardiovascular health and disease. Atrial fibrillation is the most common sustained cardiac arrhythmia, affecting millions of people worldwide and contributing to substantial morbidity and mortality. Although numerous studies have explored the role of genetic and lifestyle factors in the development and progression of atrial fibrillation, the potential impact of environmental determinants on this prevalent condition has received comparatively less attention. This review aims to provide a comprehensive overview of the current evidence on environmental determinants of atrial fibrillation, encompassing factors such as air pollution, temperature, humidity, and other meteorologic conditions, noise pollution, greenspace, and the social environment. We discuss the existing evidence from epidemiological and mechanistic studies, critically evaluating the strengths and limitations of these investigations and the potential underlying biological mechanisms through which environmental exposures may affect atrial fibrillation risk. Furthermore, we address the potential implications of these findings for public health and clinical practice and identify knowledge gaps and future research directions in this emerging field.

[Blood cadmium level and the change of cadmium exposure risk in Chinese urban school-age children in 2002 and 2012].

OBJECTIVE: To investigate the blood cadmium concentrations and the related change in Chinese urban children derived from the China Nutrition and Health Survey 2002 and 2012(CNHS 2002 and CNHS 2012). METHODS: The Chinese urban children aged 6-11 years were selected according to gender, age and regional distribution using the multi-stage stratified cluster random sampling method, as well as the corresponding whole blood samples. The blood cadmium concentration was carefully determined by the quadrupole inductively coupled plasma mass spectrometry(ICP-MS) and the percentage of blood cadmium over 2 µg/L was subsequently estimated. In addition, the upper limit values of the 95%CI of the 95th percentiles of available blood cadmium data was assessed as the threshold of cadmium exposure. RESULTS: Totally, 2182 Chinese urban children were included, and of these, 1036 children were from the CNHS 2002 and 1146 children were from the CNHS 2012. From the CNHS 2002 to the CNHS 2012, the median blood cadmium concentration was increased from 0.28 µg/L to 0.95 µg/L, and the percentage of blood cadmium with over 2 µg/L was elevated from 1.45% to 10.47%. In addition, the new estimated threshold of blood cadmium was ascended from 1.24 µg/L up to 2.89 µg/L. CONCLUSION: The risk of cadmium exposure in Chinese urban children aged 6-11 years was increasingly aggravated from the CHNS 2002 to the CNHS 2012.

Occurrence of organophosphorus flame retardants in Xiangjiang River: Spatiotemporal variations, potential affecting factors, and source apportionment.

The environmental occurrence of organophosphorus flame retardants (OPFRs) is receiving increasing attention. However, their distribution in the Xiangjiang River, an important tributary in the middle reaches of the Yangtze River, is still uncharacterized, and the potential factors influencing their distribution have not been adequately surveyed. In this study, the occurrence of OPFRs in the Xiangjiang River was comprehensively investigated from upstream to downstream seasonally. Fourteen OPFRs were detected in the sampling area, with a total concentration (∑OPFRs) ranging from 3.16 to 462 ng/L, among which tris(1-chloro-2-propyl) phosphate was identified as the primary pollutant (ND - 379 ng/L). Specifically, ∑OPFRs were significantly lower in the wet season than in the dry season, which may be due to the dilution effect of river flow and enhanced volatilization caused by higher water temperatures. Additionally, Changsha (during the dry season) and Zhuzhou (during the wet season) exhibited higher pollution levels than other cities. According to the Redundancy analysis, water quality parameters accounted for 35.7% of the variation in the occurrence of OPFRs, in which temperature, ammonia nitrogen content, dissolved oxygen, and chemical oxygen demand were identified as the potential influencing factors, accounting for 28.1%, 27.2%, 24.1%, and 11.5% of the total variation, respectively. The results of the Positive Matrix Factorization analysis revealed that transport and industrial emissions were the major sources of OPFRs in Xiangjiang River. In addition, there were no high-ecological risk cases for any individual OPFRs, although tris(2-ethylhexyl) phosphate and tributoxyethyl phosphate presented a low-to-medium risk level. And the results of mixture risk quotients indicated that medium-risk sites were concentrated in the Chang-Zhu-Tan region. This study enriches the global data of OPFRs pollution and contributes to the scientific management and control of pollution.

Association between Fine Particulate Matter Exposure and Cerebrospinal Fluid Biomarkers of Alzheimer's Disease among a Cognitively Healthy Population-Based Cohort.

BACKGROUND: Epidemiological evidence suggests air pollution adversely affects cognition and increases the risk of Alzheimer's disease (AD), but little is known about the biological effects of fine particulate matter (PM2.5, particulate matter with aerodynamic diameter ≤2.5µm) on early predictors of future disease risk. OBJECTIVES: We investigated the association between 1-, 3-, and 5-y exposure to ambient and traffic-related PM2.5 and cerebrospinal fluid (CSF) biomarkers of AD. METHODS: We conducted a cross-sectional analysis using data from 1,113 cognitively healthy adults (45-75 y of age) from the Emory Healthy Brain Study in Georgia in the United States. CSF biomarker concentrations of Aß42, tTau, and pTau, were collected at enrollment (2016-2020) and analyzed with the Roche Elecsys system. Annual ambient and traffic-related residential PM2.5 concentrations were estimated at a 1-km and 250-m resolution, respectively, and computed for each participant's geocoded address, using three exposure time periods based on specimen collection date. Associations between PM2.5 and CSF biomarker concentrations, considering continuous and dichotomous (dichotomized at clinical cutoffs) outcomes, were estimated with multiple linear/logistic regression, respectively, controlling for potential confounders (age, gender, race, ethnicity, body mass index, and neighborhood socioeconomic status). RESULTS: Interquartile range (IQR; IQR=0.845) increases in 1-y [ß:-0.101; 95% confidence interval (CI): -0.18, -0.02] and 3-y (ß:-0.078; 95% CI: -0.15, -0.00) ambient PM2.5 exposures were negatively associated with Aß42 CSF concentrations. Associations between ambient PM2.5 and Aß42 were similar for 5-y estimates (ß:-0.076; 95% CI: -0.160, 0.005). Dichotomized CSF variables revealed similar associations between ambient PM2.5 and Aß42. Associations with traffic-related PM2.5 were similar but not significant. Associations between PM2.5 exposures and tTau, pTau tTau/Aß42, or pTau/Aß42 levels were mainly null. CONCLUSION: In our study, consistent trends were found between 1-y PM2.5 exposure and decreased CSF Aß42, which suggests an accumulation of amyloid plaques in the brain and an increased risk of developing AD. https://doi.org/10.1289/EHP13503.

Association Between Maternal Prenatal Exposure to Household Air Pollution and Child Respiratory Health: A Systematic Review and Meta-analysis.

Maternal prenatal exposure to household air pollution (HAP) is a critical public health concern with potential long-term implications for child respiratory health. The objective of this study is to assess the level of association between prenatal household air pollution and child respiratory health, and to identify which HAP pollutants are associated with specific respiratory illnesses or symptoms and to what degree. Relevant studies were retrieved from PubMed databases up to April 27, 2010, and their reference lists were reviewed. Random effects models were applied to estimate summarized relative risks (RRs) and 95% confidence intervals (CIs). The analysis involved 11 studies comprising 387 767 mother-child pairs in total, assessing various respiratory health outcomes in children exposed to maternal prenatal HAP. Children with prenatal exposure to HAP pollutants exhibited a summary RR of 1.26 (95% CI=1.08-1.33) with moderate between-study heterogeneity (I²=49.22%) for developing respiratory illnesses. Specific associations were found between prenatal exposure to carbon monoxide (CO) (RR=1.11, 95% CI: 1.09-1.13), Nitrogen Oxides (NOx) (RR=1.46, 95% CI: 1.09-1.60), and particulate matter (PM) (RR=1.26, 95% CI: 1.2186-1.3152) and child respiratory illnesses (all had I² close to 0%, indicating no heterogeneity). Positive associations with child respiratory illnesses were also found with ultrafine particles (UFP), polycyclic aromatic hydrocarbons (PAH), and ozone (O3). However, no significant association was observed for prenatal exposure to sulfur dioxide (SO2). In summary, maternal prenatal exposure to HAP may contribute to a higher risk of child respiratory health issues, emphasizing the need for interventions to reduce this exposure during pregnancy. Targeted public health strategies such as improved ventilation, cleaner cooking technologies, and awareness campaigns should be implemented to minimize adverse respiratory effects on children.

Phthalate Exposure and Neurotoxicity in Children: A Systematic Review and Meta-analysis.

Objectives: This systematic review aims to assess the relationship between prenatal and childhood exposure to phthalates and neurodevelopmental outcomes, identifying periods of heightened susceptibility. Data sources considered studies examining repeated phthalate exposure during pregnancy and childhood on neurodevelopment. Methods: Evaluation included bias risk and study quality criteria. Evidence was synthesized by groups of low and high phthalate molecular weight and exposure measured prenatally and postnatally and outcome measured in childhood. Beta coefficients and their standard errors were extracted, leading to meta-analyses of various neurodevelopmental outcomes: cognition, motor skills, language, behavior, and temperament. Results: Eleven pregnancy and birth cohort studies were identified as relevant. For each phthalate group and outcome combination, there was low or very low evidence of an association, except for prenatal and postnatal phthalate exposure and behavioral development and postnatal exposure and cognition. Conclusion: The estimated effects sizes were relatively small and strong evidence for periods of heightened susceptibility could not be elucidated. No distinction between phthalates of low molecular weight and those of high molecular weight with regards to the outcomes was found.

Climate change and health: rethinking public health messaging for wildfire smoke and extreme heat co-exposures.

With the growing climate change crisis, public health agencies and practitioners must increasingly develop guidance documents addressing the public health risks and protective measures associated with multi-hazard events. Our Policy and Practice Review aims to assess current public health guidance and related messaging about co-exposure to wildfire smoke and extreme heat and recommend strengthened messaging to better protect people from these climate-sensitive hazards. We reviewed public health messaging published by governmental agencies between January 2013 and May 2023 in Canada and the United States. Publicly available resources were eligible if they discussed the co-occurrence of wildfire smoke and extreme heat and mentioned personal interventions (protective measures) to prevent exposure to either hazard. We reviewed local, regional, and national governmental agency messaging resources, such as online fact sheets and guidance documents. We assessed these resources according to four public health messaging themes, including (1) discussions around vulnerable groups and risk factors, (2) symptoms associated with these exposures, (3) health risks of each exposure individually, and (4) health risks from combined exposure. Additionally, we conducted a detailed assessment of current messaging about measures to mitigate exposure. We found 15 online public-facing resources that provided health messaging about co-exposure; however, only one discussed all four themes. We identified 21 distinct protective measures mentioned across the 15 resources. There is considerable variability and inconsistency regarding the types and level of detail across described protective measures. Of the identified 21 protective measures, nine may protect against both hazards simultaneously, suggesting opportunities to emphasize these particular messages to address both hazards together. More precise, complete, and coordinated public health messaging would protect against climate-sensitive health outcomes attributable to wildfire smoke and extreme heat co-exposures.

Speeding Up Time: New Urinary Peptide Clock Associates Greater Air Pollution Exposures with Faster Biological Aging.

A study in Belgium supports earlier findings on associations between higher air pollution exposures and markers of faster biological aging, this time by using urinary peptide levels instead of DNA-based markers.

Heavy metal association with chronic kidney disease of unknown cause in central India-results from a case-control study.

BACKGROUND: Chronic Kidney Disease of unknown cause (CKDu) a disease of exclusion, and remains unexplained in various parts of the world, including India. Previous studies have reported mixed findings about the role of heavy metals or agrochemicals in CKDu. These studies compared CKDu with healthy controls but lacked subjects with CKD as controls. The purpose of this study was to test the hypothesis whether heavy metals, i.e. Arsenic (As), Cadmium (Cd), Lead (Pb), and Chromium (Cr) are associated with CKDu, in central India. METHODS: The study was conducted in a case-control manner at a tertiary care hospital. CKDu cases (n = 60) were compared with CKD (n = 62) and healthy subjects (n = 54). Blood and urine levels of As, Cd, Pb, and Cr were measured by Inductively Coupled Plasma- Optical Emission Spectrometry. Pesticide use, painkillers, smoking, and alcohol addiction were also evaluated. The median blood and urine metal levels were compared among the groups by the Kruskal-Wallis rank sum test. RESULTS: CKDu had significantly higher pesticide and surface water usage as a source of drinking water. Blood As levels (median, IQR) were significantly higher in CKDu 91.97 (1.3-132.7) µg/L compared to CKD 4.5 (0.0-58.8) µg/L and healthy subjects 39.01 (4.8-67.4) µg/L (p < 0.001) On multinominal regression age and sex adjusted blood As was independently associated with CKDu[ OR 1.013 (95%CI 1.003-1.024) P < .05].Blood and urinary Cd, Pb, and Cr were higher in CKD compared to CKDu (p > .05). Urinary Cd, Pb and Cr were undetectable in healthy subjects and were significantly higher in CKDu and CKD compared to healthy subjects (P = < 0.001). There was a significant correlation of Cd, Pb and Cr in blood and urine with each other in CKDu and CKD subjects as compared to healthy subjects. Surface water use also associated with CKDu [OR 3.178 (95%CI 1.029-9.818) p < .05). CONCLUSION: The study showed an independent association of age and sex adjusted blood As with CKDu in this Indian cohort. Subjects with renal dysfunction (CKDu and CKD) were found to have significantly higher metal burden of Pb, Cd, As, and Cr as compared to healthy controls. CKDu subjects had significantly higher pesticide and surface water usage, which may be the source of differential As exposure in these subjects.

Multiple dietary patterns and the association between long-term air pollution exposure with type 2 diabetes risk: Findings from UK Biobank cohort study.

BACKGROUND: Evidence of modifying effect of various dietary patterns (DPs) on risk of type 2 diabetes (T2D) induced by long-term exposure to air pollution (AP) is still rather lacking, which therefore we aimed to explore in this study. METHODS: We included 78,230 UK Biobank participants aged 40-70 years with at least 2 typical 24-hour dietary assessments and without baseline diabetes. The annual average concentration of particulate matter with diameter micrometers ≤2.5 (PM2.5) and ≤10 (PM10), nitrogen dioxide (NO2), and nitrogen oxides (NOX) estimated by land use regression model was the alternative proxy of long-term AP exposure. Three well-known prior DPs such as Mediterranean diet (MED), dietary approaches to stop hypertension diet (DASH), and empirical dietary inflammatory pattern (EDIP), as well as three posterior DPs derived by the rank reduced regression model were used to capture participants' dietary habits. Cox regression models were used to estimate AP-T2D and DP-T2D associations. Modifying effect of DPs on AP-T2D association was assessed using stratified analysis and heterogeneity test. RESULTS: During a median follow-up 12.19 years, 1,693 participants developed T2D. PM2.5, PM10, NO2, and NOX significantly increased the T2D risk (P <0.05), with hazard ratio (HR) and 95% confidence interval (95% CI) for per interquartile range increase being 1.09 (1.02,1.15), 1.04 (1.00, 1.09), 1.11 (1.04, 1.18), and 1.08 (1.03, 1.14), respectively. Comparing high with low adherence, healthy DPs were associated with a 14-41% lower T2D risk. Participants with high adherence to MED, DASH, and anti-EDIP, alongside the posterior anti-oxidative dietary pattern (AODP) had attenuated and statistically non-significant NO2-T2D and NOX-T2D associations (Pmodify <0.05). CONCLUSIONS: Multiple forms of healthy DPs help reduce the T2D risk associated with long-term exposure to NO2 and NOX. Our findings indicate that adherence to healthy DPs is a feasible T2D prevention strategy for people long-term suffering from NO2 and NOX pollution.

Ambient air pollution exposure and the risk of probable sarcopenia: A prospective cohort study.

BACKGROUND: Sarcopenia is characterized by decreased muscle mass and strength, posing threat to quality of life. Air pollutants are increasingly recognized as risk factors for diseases, while the relationship between the two remains to be elucidated. This study investigated whether exposure to ambient air pollution contributes to the development of sarcopenia. METHODS: We employed the data from the UK Biobank with 303,031 eligible participants. Concentrations of PM2·5, NO2, and NOx were estimated. Cox proportional hazard regression models were applied to investigate the associations between pollutants and sarcopenia. RESULTS: 30,766 probable sarcopenia cases was identified during the follow-up. We observed that exposure to PM2.5 (HR, 1.232; 95% CI, 1.053-1.440), NO2 (HR, 1.055; 95% CI, 1.032-1.078) and NOx (HR, 1.016; 95% CI, 1.007-1.026) were all significantly associated with increased risk for probable sarcopenia for each 10 µg/m3 increase in pollutant concentration. In comparison with individuals in the lowest quartiles of exposure, those in the upper quartiles had significantly increased risk of probable sarcopenia. Sarcopenia-related factors, e.g., reduced lean muscle mass, diminished walking pace, and elevated muscle fat infiltration ratio, also exhibited positive associations with exposure to ambient air pollution. On the contrary, high level physical activity significantly mitigated the influence of air pollutants on the development of probable sarcopenia. CONCLUSIONS: Air pollution exposure elevated the risk of developing sarcopenia and related manifestations in a dose-dependent manner, while physical activity maintained protective under this circumstance. Efforts should be made to control air pollution and emphasize the importance of physical activity for skeletal muscle health under this circumstance.

Association of ambient air pollution with hemoglobin levels and anemia in the general population of Korean adults.

BACKGROUND: Emerging evidence has suggested significant associations between ambient air pollution and changes in hemoglobin levels or anemia in specific vulnerable groups, but few studies have assessed this relationship in the general population. This study aimed to evaluate the association between long-term exposure to air pollution and hemoglobin concentrations or anemia in general adults in South Korea. METHODS: A total of 69,830 Korean adults from a large-scale nationwide survey were selected for our final analysis. Air pollutants included particulate matter with an aerodynamic diameter less than or equal to 10 micrometers (PM10), particulate matter with an aerodynamic diameter less than or equal to 2.5 micrometers, nitrogen dioxide, sulfur dioxide (SO2), and carbon monoxide (CO). We measured the serum hemoglobin concentration to assess anemia for each participant. RESULTS: In the fully adjusted model, exposure levels to PM10, SO2, and CO for one and two years were significantly associated with decreased hemoglobin concentrations (all p < 0.05), with effects ranging from 0.15 to 0.62% per increase in interquartile range (IQR) for each air pollutant. We also showed a significant association of annual exposure to PM10 with anemia (p = 0.0426); the odds ratio (OR) [95% confidence interval (CI)] for anemia per each increase in IQR in PM10 was estimated to be 1.039 (1.001-1.079). This association was also found in the 2-year duration of exposure (OR = 1.046; 95% CI = 1.009-1.083; adjusted Model 2). In addition, CO exposure during two years was closely related to anemia (OR = 1.046; 95% CI = 1.004-1.091; adjusted Model 2). CONCLUSIONS: This study provides the first evidence that long-term exposure to air pollution, especially PM10, is significantly associated with reduced hemoglobin levels and anemia in the general adult population.

Targeting transitioning lung monocytes/macrophages as treatment strategies in lung disease related to environmental exposures.

BACKGROUND: Environmental/occupational exposures cause significant lung diseases. Agricultural organic dust extracts (ODE) and bacterial component lipopolysaccharide (LPS) induce recruited, transitioning murine lung monocytes/macrophages, yet their cellular role remains unclear. METHODS: CCR2 RFP+ mice were intratracheally instilled with high concentration ODE (25%), LPS (10 µg), or gram-positive peptidoglycan (PGN, 100 µg) for monocyte/macrophage cell-trafficking studies. CCR2 knockout (KO) mice and administration of intravenous clodronate liposomes strategies were employed to reduce circulating monocytes available for lung recruitment following LPS exposure. Lung tissues and bronchoalveolar lavage fluid (BALF) were collected. Pro-inflammatory and/or pro-fibrotic cytokines, chemokines, and lung extracellular matrix mediators were quantitated by ELISA. Infiltrating lung cells including monocyte/macrophage subpopulations, neutrophils, and lymphocytes were characterized by flow cytometry. Lung histopathology, collagen content, vimentin, and post-translational protein citrullination and malondialdehyde acetaldehyde (MAA) modification were quantitated. Parametric statistical tests (one-way ANOVA, Tukey'smultiple comparison) and nonparametric statistical (Kruskal-Wallis, Dunn's multiple comparison) tests were used following Shapiro-Wilk testing for normality. RESULTS: Intratracheal instillation of ODE, LPS, or PGN robustly induced the recruitment of inflammatory CCR2+ CD11cintCD11bhi monocytes/macrophages and both CCR2+ and CCR2- CD11c-CD11bhi monocytes at 48 h. There were also increases in CCR2+ CD4+ and CD8+ T cells and NK cells. Despite reductions in LPS-induced lung infiltrating CD11cintCD11bhi cells (54% reduction), CCR2 knockout (KO) mice were not protected against LPS-induced inflammatory and pro-fibrotic consequences. Instead, compensatory increases in lung neutrophils and CCL2 and CCL7 release occurred. In contrast, the depletion of circulating monocytes through the administration of intravenous clodronate (vs. vehicle) liposomes 24 h prior to LPS exposure reduced LPS-induced infiltrating CD11cintCD11bhi monocyte-macrophage subpopulation by 59% without compensatory changes in other cell populations. Clodronate liposome pre-treatment significantly reduced LPS-induced IL-6 (66% reduction), matrix metalloproteinases (MMP)-3 (36%), MMP-8 (57%), tissue inhibitor of metalloproteinases (61%), fibronectin (38%), collagen content (22%), and vimentin (40%). LPS-induced lung protein citrullination and MAA modification, post-translational modifications implicated in lung disease, were reduced (39% and 48%) with clodronate vs. vehicle liposome. CONCLUSION: Highly concentrated environmental/occupational exposures induced the recruitment of CCR2+ and CCR2- transitioning monocyte-macrophage and monocyte subpopulations and targeting peripheral monocytes may reduce the adverse lung consequences resulting from exposures to LPS-enriched inhalants.

Air Pollutants and Mortality Risk in Patients with Aortic Dissection: Evidence from a Clinical Cohort, Single-Cell Sequencing, and Proteomics.

We aimed to evaluate the association between air pollutants and mortality risk in patients with acute aortic dissection (AAD) in a longitudinal cohort and to explore the potential mechanisms of adverse prognosis induced by fine particulate matter (PM2.5). Air pollutants data, including PM2.5, PM10.0, nitrogen dioxide (NO2), carbon monoxide (CO), sulfur dioxide (SO2), and ozone (O3), were collected from official monitoring stations, and multivariable Cox regression models were applied. Single-cell sequencing and proteomics of aortic tissue were conducted to explore the potential mechanisms. In total, 1,267 patients with AAD were included. Exposure to higher concentrations of air pollutants was independently associated with an increased mortality risk. The high-PM2.5 group carried approximately 2 times increased mortality risk. There were linear associations of PM10, NO2, CO, and SO2 exposures with long-term mortality risk. Single-cell sequencing revealed an increase in mast cells in aortic tissue in the high-PM2.5 exposure group. Enrichment analysis of the differentially expressed genes identified the inflammatory response as one of the main pathways, with IL-17 and TNF signaling pathways being among the top pathways. Analysis of proteomics also identified these pathways. This study suggests that exposure to higher PM2.5, PM10, NO2, CO, and SO2 are associated with increased mortality risk in patients with AAD. PM2.5-related activation and degranulation of mast cells may be involved in this process.

The impact of co-exposure to air and noise pollution on the incidence of metabolic syndrome from a health checkup cohort.

Previous studies have found associations between the incidence of metabolic syndrome (MetS) and exposure to air pollution or road traffic noise. However, investigations on environmental co-exposures are limited. This study aimed to investigate the association between co-exposure to air pollution and road traffic noise and MetS and its subcomponents. Participants living in Taipei City who underwent at least two health checkups between 2010 and 2016 were included in the study. Data were sourced from the MJ Health database, a longitudinal, large-scale cohort in Taiwan. The monthly traffic noise exposure (Lden and Lnight) was computed using a dynamic noise map. Monthly fine particulate data at one kilometer resolution were computed from satellite imagery data. Cox proportional hazards regression models with month as the underlying time scale were used to estimate hazard ratios (HRs) for the impact of PM2.5 and road traffic noise exposure on the risk of developing MetS or its subcomponents. Data from 10,773 participants were included. We found significant positive associations between incident MetS and PM2.5 (HR: 1.88; 95% CI 1.67, 2.12), Lden (HR: 1.10; 95% CI 1.06, 1.15), and Lnight (HR: 1.07; 95% CI 1.02, 1.13) in single exposure models. Results further showed significant associations with an elevated risk of incident MetS in co-exposure models, with HRs of 1.91 (95% CI 1.69, 2.16) and 1.11 (95% CI 1.06, 1.16) for co-exposure to PM2.5 and Lden, and 1.90 (95% CI 1.68, 2.14) and 1.08 (95% CI 1.02, 1.13) for co-exposure to PM2.5 and Lnight. The HRs for the co-exposure models were higher than those for models with only a single exposure. This study provides evidence that PM2.5 and noise exposure may elevate the risk of incident MetS and its components in both single and co-exposure models. Therefore, preventive approaches to mitigate the risk of MetS and its subcomponents should consider reducing exposure to PM2.5 and noise pollution.

Relationship between phthalates exposures and metabolic dysfunction-associated fatty liver disease in United States adults.

As a new definition for the evidence of hepatic steatosis and metabolic dysfunctions, the relationship between phthalates (PAEs) and metabolic dysfunction-associated fatty liver disease (MAFLD) remains virtually unexplored. This study included 3,137 adults from the National Health and Nutrition Examination Survey spanning 2007-2018. The diagnosis of MAFLD depended on the US Fatty Liver Index (US FLI) and evidence of metabolic dysregulation. Eleven metabolites of PAEs were included in the study. Poisson regression, restricted cubic spline (RCS), and weighted quantile sum (WQS) regression were used to assess the associations between phthalate metabolites and MAFLD. After adjusting for potential confounders, Poisson regression analysis showed that mono-2-ethyl-5-carboxypentyl phthalate (MECPP), mono-n-butyl phthalate, mono-(3-carboxypropyl) phthalate, mono-ethyl phthalate (MEP), mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl-5-oxohexyl) phthalate were generally significant positively associated with MAFLD (P<0.05). Furthermore, the WQS index constructed for the eleven phthalates was significantly related to MAFLD (OR:1.43; 95%CI: 1.20, 1.70), MEHHP (33.30%), MEP (20.84%), MECPP (15.43%), and mono-isobutyl phthalate (11.78%) contributing the most. This study suggests that exposure to phthalates, individually or in combination, may be associated with an increased risk of MAFLD.

Confounder-dependent Bayesian mixture model: Characterizing heterogeneity of causal effects in air pollution epidemiology.

Several epidemiological studies have provided evidence that long-term exposure to fine particulate matter (pm2.5) increases mortality rate. Furthermore, some population characteristics (e.g., age, race, and socioeconomic status) might play a crucial role in understanding vulnerability to air pollution. To inform policy, it is necessary to identify groups of the population that are more or less vulnerable to air pollution. In causal inference literature, the group average treatment effect (GATE) is a distinctive facet of the conditional average treatment effect. This widely employed metric serves to characterize the heterogeneity of a treatment effect based on some population characteristics. In this paper, we introduce a novel Confounder-Dependent Bayesian Mixture Model (CDBMM) to characterize causal effect heterogeneity. More specifically, our method leverages the flexibility of the dependent Dirichlet process to model the distribution of the potential outcomes conditionally to the covariates and the treatment levels, thus enabling us to: (i) identify heterogeneous and mutually exclusive population groups defined by similar GATEs in a data-driven way, and (ii) estimate and characterize the causal effects within each of the identified groups. Through simulations, we demonstrate the effectiveness of our method in uncovering key insights about treatment effects heterogeneity. We apply our method to claims data from Medicare enrollees in Texas. We found six mutually exclusive groups where the causal effects of pm2.5 on mortality rate are heterogeneous.

Seasonal extreme temperatures and short-term fine particulate matter increases pediatric respiratory healthcare encounters in a sparsely populated region of the intermountain western United States.

BACKGROUND: Western Montana, USA, experiences complex air pollution patterns with predominant exposure sources from summer wildfire smoke and winter wood smoke. In addition, climate change related temperatures events are becoming more extreme and expected to contribute to increases in hospital admissions for a range of health outcomes. Evaluating while accounting for these exposures (air pollution and temperature) that often occur simultaneously and may act synergistically on health is becoming more important. METHODS: We explored short-term exposure to air pollution on children's respiratory health outcomes and how extreme temperature or seasonal period modify the risk of air pollution-associated healthcare events. The main outcome measure included individual-based address located respiratory-related healthcare visits for three categories: asthma, lower respiratory tract infections (LRTI), and upper respiratory tract infections (URTI) across western Montana for ages 0-17 from 2017-2020. We used a time-stratified, case-crossover analysis with distributed lag models to identify sensitive exposure windows of fine particulate matter (PM2.5) lagged from 0 (same-day) to 14 prior-days modified by temperature or season. RESULTS: For asthma, increases of 1 µg/m3 in PM2.5 exposure 7-13 days prior a healthcare visit date was associated with increased odds that were magnified during median to colder temperatures and winter periods. For LRTIs, 1 µg/m3 increases during 12 days of cumulative PM2.5 with peak exposure periods between 6-12 days before healthcare visit date was associated with elevated LRTI events, also heightened in median to colder temperatures but no seasonal effect was observed. For URTIs, 1 unit increases during 13 days of cumulative PM2.5 with peak exposure periods between 4-10 days prior event date was associated with greater risk for URTIs visits that were intensified during median to hotter temperatures and spring to summer periods. CONCLUSIONS: Delayed, short-term exposure increases of PM2.5 were associated with elevated odds of all three pediatric respiratory healthcare visit categories in a sparsely population area of the inter-Rocky Mountains, USA. PM2.5 in colder temperatures tended to increase instances of asthma and LRTIs, while PM2.5 during hotter periods increased URTIs.