Associations Of PM2 Research Articles

Association of PM2.5 exposure in early pregnancy and maternal liver function: A retrospective cohort study in Shenzhen, China

ObjectiveStudies have shown that fine particulate matter (PM2.5) has adverse effects on the liver function, but epidemiological evidence is limited, especially regarding pregnant women. This study aims to investigate the association between PM2.5 exposure in early pregnancy and maternal liver function during pregnancy. MethodsThis retrospective cohort study included 13,342 pregnant participants. PM2.5 and Ozone (O3) exposure level, mean temperature, and relative humidity for each participant were assessed according to their residential address. The levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin (TBIL) were measured during the second and third trimesters. Data on PM2.5 and O3 exposure level were sourced from Tracking Air Pollution in China (TAP), while the mean temperature and relative humidity were obtained from the ERA5 dataset. The Generalized Additive Model (GAM) was used to analyze the associations between PM2.5 exposure and maternal liver function during pregnancy, adjusting for potential confounding factors. ResultsAccording to the results, each 10 μg/m3 increase in PM2.5 was associated with an increase of 3.57% (95% CI: 0.29%, 6.96%) in ALT and 4.25% (95% CI: 2.33%, 6.21%) in TBIL during the second trimester and 4.51% (95% CI: 2.59%, 6.47%) in TBIL during the third trimester, respectively. After adjusting for O3, these associations remained significant, and the effect of PM2.5 on ALT during the second trimester was further strengthened. No significant association observed between PM2.5 and AST. ConclusionsPM2.5 exposure in early pregnancy is associated with increasement of maternal ALT and TBIL, suggesting that PM2.5 exposure may have an adverse effect on maternal liver function. Although this finding indicates an association between PM2.5 exposure and maternal liver function, more research is needed to confirm our findings and explore the underlying biological mechanisms.

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.

Associations of PM2.5 exposure with long COVID severity: insights from the P4O2 COVID-19 study.

Associations of PM2.5 exposure with long COVID severity: insights from the P4O2 COVID-19 study.

Ambient particulate matter and chronic obstructive pulmonary disease mortality: a nationwide, individual-level, case-crossover study in China

Short-term exposure to particulate matter air pollution has been associated with the exacerbations of COPD, but its association with COPD mortality was not fully elucidated. We aimed to assess the association between short-term particulate matter exposure and the risk of COPD mortality in China using individual-level data. We derived 2.26 million COPD deaths from a national death registry database in Chinese mainland between 2013 and 2019. Exposures to fine particulate matter (PM2.5) and coarse particulate matter (PM2.5-10) were assessed by satellite-based models of a 1×1km resolution and assigned to each individual based on residential address. The associations of PM2.5 and PM2.5-10 with COPD mortality were examined using a time-stratified case-crossover design and conditional logistic regressions with distributed lag models. We further conducted stratified analyses by age, sex, education level, and season. Short-term exposures to both PM2.5 and PM2.5-10 were associated with increased risks of COPD mortality. These associations appeared and peaked on the concurrent day, attenuated and became nonsignificant after 5 or 7 days, respectively. The exposure-response curves were approximately linear without discernible thresholds. An interquartile range increase in PM2.5 and PM2.5-10 concentrations was associated with 4.23% (95% CI: 3.75%, 4.72%) and 2.67% (95% CI: 2.18%, 3.16%) higher risks of COPD mortality over lag 0-7d, respectively. The associations of PM2.5 andPM2.5-10 attenuated slightly but were still significant in the mutual-adjustment models. A larger association of PM2.5-10 was observed in the warm season. This individual-level, nationwide, case-crossover study suggests that short-term exposure to PM2.5 and PM2.5-10 might act as one of the environmental risk factors for COPD mortality. This study is supported by the National Key Research and Development Program of China (2023YFC3708304 and 2022YFC3702701), the National Natural Science Foundation of China (82304090 and 82030103), the 3-year Action Plan for Strengthening the Construction of the Public Health System in Shanghai (GWVI-11.2-YQ31), and the Science and Technology Commission of Shanghai Municipality (21TQ015).

Associations of PM2.5 exposure with emergency department visits and readmissions among preterm infants with bronchopulmonary dysplasia.

To quantify the association of ambient air pollution (particulate matter, PM2.5) exposure with medically attended acute respiratory illness among infants with bronchopulmonary dysplasia (BPD). Single center, retrospective cohort study of preterm infants with BPD in Metropolitan Philadelphia. Multivariable logistic regression quantified associations of annual mean PM2.5 exposure (per μg/m3) at the census block group level with medically attended acute respiratory illness, defined as emergency department (ED) visits or hospital readmissions within a year after first hospital discharge adjusting for age at neonatal intensive care unit (NICU) discharge, year, sex, race, insurance, BPD severity, and census tract deprivation. As a secondary analysis, we examined whether BPD severity modified the associations. Of the 378 infants included in the analysis, 189 were non-Hispanic Black and 235 were publicly insured. Census block PM2.5 level was not significantly associated with medically attended acute respiratory illnesses, ED visits, or hospital readmissions in the full study cohort. We observed significant effect modification by BPD grade; each 1 µg/m3 higher annual PM2.5 exposure was medically attended acute respiratory illness (adjusted odds ratio [aOR] 1.65, 95% CI: 1.06-2.63) among infants with Grade 1 BPD but not among infants with grade 3 BPD (aOR 0.83, 95% CI: 0.47-1.48) (interaction p = .024). Cumulative PM2.5 exposure in the year after NICU discharge was not significantly associated with medically attended acute respiratory illness among infants with BPD. However, infants with Grade 1 BPD had significantly higher odds with higher exposures. If replicated, these findings could inform anticipatory guidance for families of these infants to avoid outdoor activities during high pollution days after NICU discharge.

Impaired thyroid hormone sensitivity exacerbates the effect of PM2.5 and its components on dyslipidemia in schizophrenia

BackgroundDyslipidemia in schizophrenia causes a serious loss of healthy life expectancy, making it imperative to explore key environmental risk factors. We aimed to assess the effect of PM2.5 and its constituents on dyslipidemia in schizophrenia, identify the critical hazardous components, and investigate the role of impaired thyroid hormones (THs) sensitivity in this association. MethodsWe collected disease data on schizophrenia from the Anhui Mental Health Center from 2019 to 2022. Logistic regression was constructed to explore the effect of average annual exposure to PM2.5 and its components [black carbon (BC), organic matter (OM), sulfate (SO42−), ammonium (NH4+), and nitrate (NO3−)] on dyslipidemia, with subgroup analyses for age and gender. The degree of impaired THs sensitivity in participants was reflected by the Thyroid Feedback Quantile-based Index (TFQI), and its role in the association of PM2.5 components with dyslipidemia was explored. ResultsA total of 5125 patients with schizophrenia were included in this study. Exposure to PM2.5 and its components (BC, OM, SO42−, NH4+, and NO3−) were associated with dyslipidemia with the odds ratios and 95 % confidence interval of 1.13 (1.04, 1.23), 1.16 (1.07, 1.26), 1.15 (1.06, 1.25), 1.11 (1.03, 1.20), 1.09 (1.00, 1.18), 1.12 (1.04, 1.20), respectively. Mixed exposure modeling indicated that BC played a major role in the effects of the mixture. More significant associations were observed in males and groups <45 years. In addition, we found that the effect of PM2.5 and its components on dyslipidemia was exacerbated as impaired THs sensitivity in the patients. ConclusionsExposure to PM2.5 and its components is associated with an increased risk of dyslipidemia in schizophrenia, which may be exacerbated by impaired THs sensitivity. Our results suggest a new perspective for the management of ambient particulate pollution and the protection of thyroid function in schizophrenia.

Association between wildfire PM2.5 and genitourinary cancer survival in California.

10567 Background: Aerosolized particulate matter (PM) 2.5 (i.e., particles ≤ 2.5 µm in diameter or fine particles), including those that emanate from wildfires, has been previously associated with cancer risk and survival. While prior studies have focused primarily on etiology, little is known about the effects of wildfire PM2.5 on cancer prognosis. We sought to explore the effects of wildfire PM2.5 on genitourinary (GU) cancer survival in the state of California where episodic wildfires are considered a component of its climate. Methods: Using the California Cancer Registry, we identified incident prostate (n=81,261), urothelial (n=26,689), and kidney (n=26,303) cancers diagnosed between 2017-2020. Daily PM2.5 was estimated over the same period. Random forests regression was used to fuse diverse datasets (official air quality monitoring, satellite observations, meteorological modeling, predictive smoke modeling, and low-cost sensor networks [PurpleAir]) and produce a consensus estimate of PM2.5 for each centroid of a 1-square kilometer grid across California. We used home address at the time of cancer diagnosis to map each cancer case to the nearest centroid, and averaged PM2.5 exposures over the 6 months preceding cancer diagnosis for each case. Cox-proportional hazards regression was used to quantify the hazard ratio (HR) for death from any cause following cancer diagnosis associated with PM2.5, adjusting for key covariates including age, sex, race/ethnicity, neighborhood socioeconomic status, comorbidity, smoking status, rural/urban residence, and stage at diagnosis. Results: In patients with prostate cancer, a 10 µg/m³ increase in PM2.5 concentration was associated with an 18% increased hazard of death (HR=1.18; 95% confidence interval (CI)= 1.02-1.36, p=0.023). When stratified by stage at diagnosis, the association of PM2.5 and survival was limited to stages I, II, and III (HR=1.39; CI= 1.11-1.74, p=0.005) versus stage IV (HR=1.06; CI= 0.87-1.27, p=0.566). For urothelial cancer, a 10 µg/m³ increase in PM2.5 concentration was associated with a non-statistically significant 11% increased hazard of death (HR=1.11; CI= 0.96-1.29, p=0.151), which did not differ by stage at diagnosis. Kidney cancer survival was not associated with PM2.5 (HR= 0.94; CI= 0.79-1.11, p= 0.44). Conclusions: These findings suggest that higher PM2.5 exposure could influence prostate and urothelial cancer prognosis, perhaps through alteration of physiological pathways relevant to cancer aggressiveness or impairing response to treatment, including cellular immune response, inflammation, angiogenesis, or cell-signaling pathways. Further studies should look into the mechanisms and design mitigating strategies in patients diagnosed with these high-risk cancers who have been exposed to wildfire PM2.5.

Association of PM2.5 chemical constituents with general, abdominal and visceral obesity and mediation roles of physical activity

BackgroundThe association between exposure to PM2.5 chemical constituents and obesity remains to be elucidated, as most studies have used a single measure of obesity. This study aimed to investigate the associations of exposure to PM2.5 chemical constituents with general, abdominal, and visceral obesity, and the mediation effect of physical activity (PA) in the associations.MethodsBased on a total of 49,819 adults from the baseline of the Yunnan Behavior and Disease Surveillance cohort (YBDS) in southern China in 2021, we used multiple linear regression, weighted quantile sum regression, and quantile regression to estimate independent and joint effects of PM2.5 chemical constituents on elevated BMI, waist circumference (WC) and visceral adiposity index (VAI) and whether these effects changed in quantiles. Mediation analysis was used to examine whether physical activity acts as a mediator in these pathways.ResultsPer IQR μg/m3 increase in all PM2.5 chemical constituents was significantly associated with the elevated BMI (β [95% CI]: 0.170 [0.127, 0.214]), WC (0.316 [0.217, 0.415]) and VAI (0.102 [0.075, 0.129]), with the largest weights from OM (53.89, 81.67, and 89.82%, respectively). The effects of PM2.5 chemical constituents on obesity showed an overall upward trend from quantiles 1–4 of BMI, WC, and VAI, especially with a rapid upward trend from the sixth decile of VAI. Reduced PA mediated 3.16, 7.08, and 3.78% of the associations between PM2.5 chemical constituents and elevated BMI, WC, and VAI, respectively.ConclusionsExposure to PM2.5 chemical constituents, especially OM, was significantly associated with increased risks for obesity in adults. The effects of associations increased with obesity severity, with PA playing a mediation role.

Long-term exposure to air pollution and road traffic noise and incidence of dementia in the Danish Nurse Cohort.

We examined the association of long-term exposure to air pollution and road traffic noise with dementia incidence in the Danish Nurse Cohort. Female nurses were followed for dementia incidence (hospital contact or medication prescription) from 1993/1999 to 2020. Air pollution and road traffic noise levels were estimated at nurses' residences, and their associations with dementia were examined using Cox regression models. Of 25,233 nurses 1409 developed dementia. Particulate matter with a diameter of ≤2.5µm (PM2.5) was associated with dementia incidence, after adjusting for lifestyle, socioeconomic status, and road traffic noise (hazard ratio [95% confidence interval] 1.35 [1.15-1.59] per interquartile range of 2.6µg/m3). There was no association of PM2.5 with dementia in physically active nurses. Association with road traffic noise diminished after adjusting for PM₂.₅ (1.02 [0.93-1.11] per 7.6dB). Long-term exposure to air pollution increases risk of dementia, and physical activity may moderate this risk. Long-term exposure to air pollution was associated with increased risk of dementia among female nurses from the Danish Nurse Cohort. Association of air pollution with dementia was independent of road traffic noise. Association of road traffic noise with dementia diminished after adjusting for air pollution. Physical activity moderated adverse effects of air pollution on dementia.

Differential associations of fine and coarse particulate air pollution with cause-specific pneumonia mortality: A nationwide, individual-level, case-crossover study

BackgroundThe connections between fine particulate matter (PM2.5) and coarse particulate matter (PM2.5-10) and daily mortality of viral pneumonia and bacterial pneumonia were unclear. ObjectivesTo distinguish the connections between PM2.5 and PM2.5-10 and daily mortality due to viral pneumonia and bacterial pneumonia. MethodsUsing a comprehensive national death registry encompassing all areas of mainland China, we conducted a case-crossover investigation from 2013 to 2019 at an individual level. Residential daily particle concentrations were evaluated using satellite-based models with a spatial resolution of 1 km. To analyze the data, we employed the conditional logistic regression model in conjunction with polynomial distributed lag models. ResultsWe included 221,507 pneumonia deaths in China. Every interquartile range (IQR) elevation in concentrations of PM2.5 (lag 0–2 d, 37.6 μg/m3) was associated with higher magnitude of mortality for viral pneumonia (3.03%) than bacterial pneumonia (2.14%), whereas the difference was not significant (p-value for difference = 0.38). An IQR increase in concentrations of PM2.5-10 (lag 0–2 d, 28.4 μg/m3) was also linked to higher magnitude of mortality from viral pneumonia (3.06%) compared to bacterial pneumonia (2.31%), whereas the difference was not significant (p-value for difference = 0.52). After controlling for gaseous pollutants, their effects were all stable; however, with mutual adjustment, the associations of PM2.5 remained, and those of PM2.5-10 were no longer statistically significant. Greater magnitude of associations was noted in individuals aged 75 years and above, as well as during the cold season. ConclusionThis nationwide study presents compelling evidence that both PM2.5 and PM2.5-10 exposures could increase pneumonia mortality of viral and bacterial causes, highlighting the more robust effects of PM2.5 and somewhat higher sensitivity of viral pneumonia.

Association between long-term exposure to fine particulate matter and its chemical constituents and premature death in individuals living with HIV/AIDS

Long-term exposure to fine particulate matter (PM2.5) is associated with an increased total mortality. However, the association of PM2.5 with mortality in people living with human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS, PLWHA) and the relationship between its constituents and adverse outcomes remain unknown. In this cohort study, 28,140 PLWHA were recruited from the HIV/AIDS Comprehensive Response Information Management System of the Hubei Provincial Centre for Disease Control and Prevention in China between 2001 and 2020. The annual PM2.5 chemical composition data, including sulfate (SO42−), nitrate (NO3−), ammonium (NH4+), black carbon (BC), and organic matter (OM), was extracted from the Tracking Air Pollution (TAP) dataset in China. A Cox proportional hazard model with time-varying exposure and time-to-event quantile-based generalized (g) computation was used to assess the associations between PM2.5 chemical constituents, and mortality in PLWHA. A multivariate Cox proportional hazard model estimated an excess hazard ratio (eHR) of 0.32% [95% confidence interval (CI): (0.01%, 0.64%)] for AIDS-related death (ARD), associated with 1 μg/m3 rise in PM2.5 exposure. An increase of 1 μg/m3 in NH4+ was associated with 5.13% [95% CI: (2.89%, 7.43%)] and 2.97% [95% CI: (1.52%, 4.44%)] increase in the risk of ARD and all-cause deaths (ACD), respectively. When estimated using survival-based quantile g-computation, the eHR for ARD with a joint change in a decile increase in all five components was 6.10% [95% CI: 3.77%, 8.48%)]. Long-term exposure to PM2.5 chemical composition, particularly NH4+ increased the risk of death in PLWHA. This study provides epidemiological evidence that SO42− and NH4+ increased the risk of ARD and that NH4+ increased the risk of ACD in PLWHA. Multi-constituent analyses further suggested that NH4+ may be a key component in increasing the risk of premature death in patients with HIV/AIDS. Individuals aged ≥65 with HIV/AIDS are more vulnerable to SO42−, and consequent ACD.

Early-Life Exposure to Air Pollution and Childhood Asthma Cumulative Incidence in the ECHO CREW Consortium

Exposure to outdoor air pollution contributes to childhood asthma development, but many studies lack the geographic, racial and ethnic, and socioeconomic diversity to evaluate susceptibility by individual-level and community-level contextual factors. To examine early life exposure to fine particulate matter (PM2.5) and nitrogen oxide (NO2) air pollution and asthma risk by early and middle childhood, and whether individual and community-level characteristics modify associations between air pollution exposure and asthma. This cohort study included children enrolled in cohorts participating in the Children's Respiratory and Environmental Workgroup consortium. The birth cohorts were located throughout the US, recruited between 1987 and 2007, and followed up through age 11 years. The survival analysis was adjusted for mother's education, parental asthma, smoking during pregnancy, child's race and ethnicity, sex, neighborhood characteristics, and cohort. Statistical analysis was performed from February 2022 to December 2023. Early-life exposures to PM2.5 and NO2 according to participants' birth address. Caregiver report of physician-diagnosed asthma through early (age 4 years) and middle (age 11 years) childhood. Among 5279 children included, 1659 (31.4%) were Black, 835 (15.8%) were Hispanic, 2555 (48.4%) where White, and 229 (4.3%) were other race or ethnicity; 2721 (51.5%) were male and 2596 (49.2%) were female; 1305 children (24.7%) had asthma by 11 years of age and 954 (18.1%) had asthma by 4 years of age. Mean values of pollutants over the first 3 years of life were associated with asthma incidence. A 1 IQR increase in NO2 (6.1 μg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.25 [95% CI, 1.03-1.52]) and children younger than 11 years (HR, 1.22 [95% CI, 1.04-1.44]). A 1 IQR increase in PM2.5 (3.4 μg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.31 [95% CI, 1.04-1.66]) and children younger than 11 years (OR, 1.23 [95% CI, 1.01-1.50]). Associations of PM2.5 or NO2 with asthma were increased when mothers had less than a high school diploma, among Black children, in communities with fewer child opportunities, and in census tracts with higher percentage Black population and population density; for example, there was a significantly higher association between PM2.5 and asthma incidence by younger than 5 years of age in Black children (HR, 1.60 [95% CI, 1.15-2.22]) compared with White children (HR, 1.17 [95% CI, 0.90-1.52]). In this cohort study, early life air pollution was associated with increased asthma incidence by early and middle childhood, with higher risk among minoritized families living in urban communities characterized by fewer opportunities and resources and multiple environmental coexposures. Reducing asthma risk in the US requires air pollution regulation and reduction combined with greater environmental, educational, and health equity at the community level.

Association of PM2.5 Exposure and Alzheimer Disease Pathology in Brain Bank Donors-Effect Modification by APOE Genotype.

Fine particulate matter (PM2.5) exposure has been found to be associated with Alzheimer disease (AD) and is hypothesized to cause inflammation and oxidative stress in the brain, contributing to neuropathology. The APOE gene, a major genetic risk factor of AD, has been hypothesized to modify the association between PM2.5 and AD. However, little prior research exists to support these hypotheses. This study investigates the association between traffic-related PM2.5 and AD hallmark pathology, including effect modification by APOE genotype, in an autopsy cohort. A cross-sectional study was conducted using brain tissue donors enrolled in the Emory Goizueta AD Research Center who died before 2020 (n = 224). Donors were assessed for AD pathology including the Braak stage, Consortium to Establish a Registry for AD (CERAD) score, and combined AD neuropathologic change (ABC) score. Traffic-related PM2.5 concentrations were modeled for the metro-Atlanta area during 2002-2019 with a spatial resolution of 200-250 m. One-year, 3-year, and 5-year average PM2.5 concentrations before death were matched to participants' home address. We assessed the association between traffic-related PM2.5 and AD hallmark pathology and effect modification by APOE genotype, using adjusted ordinal logistic regression models. Among the 224 participants, the mean age of death was 76 years, and 57% had at least 1 APOE ε4 copy. Traffic-related PM2.5 was significantly associated with the CERAD score for the 1-year exposure window (odds ratio [OR] 1.92; 95% CI 1.12-3.30) and the 3-year exposure window (OR 1.87; 95% CI 1.01-3.17). PM2.5 was also associated with higher Braak stage and ABC score albeit nonsignificantly. The strongest associations between PM2.5 and neuropathology markers were among those without APOE ε4 alleles (e.g., for the CERAD score and 1-year exposure window, OR 2.31; 95% CI 1.36-3.94), though interaction between PM2.5 and APOE genotype was not statistically significant. Our study found traffic-related PM2.5 exposure was associated with the CERAD score in an autopsy cohort, contributing to epidemiologic evidence that PM2.5 affects β-amyloid deposition in the brain. This association was particularly strong among donors without APOE ε4 alleles. Future studies should further investigate the biological mechanisms behind this association.

Association between ambient PM1 and the prevalence of chronic kidney disease in China: A nationwide study

Particulate of diameter ≤ 1 µm (PM1) presents a novel risk factor of adverse health effects. Nevertheless, the association of PM1 with the risk of chronic kidney disease (CKD) in the general population is not well understood, particularly in regions with high PM1 levels like China. Based on a nationwide representative survey involving 47,204 adults and multi-source ambient air pollution inversion data, the present study evaluated the association of PM1 with CKD prevalence in China. The two-year average PM1, particulate of diameter ≤ 2.5 µm (PM2.5), and PM1–2.5 values were accessed using a satellite-based random forest approach. CKD was defined as estimated glomerular filtration rate < 60 ml/min/1.73 m2 or albuminuria. The results suggested that a 10 μg/m3 rise in PM1 was related to a higher CKD risk (odds ratio [OR], 1.13; 95% confidence interval [CI] 1.08–1.18) and albuminuria (OR, 1.11; 95% CI, 1.05–1.17). The association between PM1 and CKD was more evident among urban populations, older adults, and those without comorbidities such as diabetes or hypertension. Every 1% increase in the PM1/PM2.5 ratio was related to the prevalence of CKD (OR, 1.03; 95% CI, 1.03–1.04), but no significant relationship was found for PM1–2.5. In conclusion, the present study demonstrated long-term exposure to PM1 was associated with an increased risk of CKD in the general population and PM1 might play a leading role in the observed relationship of PM2.5 with the risk of CKD. These findings provide crucial evidence for developing air pollution control strategies to reduce the burden of CKD.

Correlation of time trends of air pollutants, greenspaces and tracheal, bronchus and lung cancer incidence and mortality among the adults in United States.

Tracheal, Bronchus, and Lung (TBL) cancer continues to represent the majority of cancer-related incidence and mortality in United States (U.S.). While air pollutants are considered essential risk factors, both global and national average concentrations of major harmful air pollutants have significantly decreased over the decades. Green space may have a beneficial effect on human health. We obtained data on national and state-level burden of TBL cancer, the annual average concentration of main air pollutants, and levels of green spaces in 2007, 2013, and 2019. According to generalized estimating equation (GEE), we examine the associations among incidence and mortality of TBL cancer, air pollutants, and greenspaces, represented by the Normalized Difference Vegetation Index (NDVI) in different age groups with models adjusted with meteorological, and socio-demographic. We observed additional effects of the interaction between the NDVI, Ozone, PM2.5, and other factors, which helped us to interpret and understand our results. Also, we collated states that witnessed net increments in forest coverage and conducted the same analysis separately. In our analysis, the majority of associations between NDVI and air pollutants with TBL cancer remained significantly positive, particularly noticeable among individuals aged 20 to 54. However, our findings did not explore air pollution as a potential mediator between greenspace exposure and TBL cancer. While the associations of PM2.5 with TBL cancer remained positive, the other four pollutants showed positive but statistically insignificant associations. Our interaction analysis yielded that there were positive associations between NDVI and ozone, PM2.5, and tobacco use. Max NDVI acts as a protective factor along with high HDI. Additionally, PM2.5 and HDI also showed a negative association. In 18 states with more forest, NDVI acts as a protective factor along with higher health care coverage, better health status, and participation in physical activities. In the state-level of U.S., the effects of total greenspace with TBL cancer are mixed and could be modified by various socio-economic factors. PM2.5 has a direct correlation with TBL cancer and the effects can be influenced by underlying socioeconomic conditions.

Associations between PM2.5 and O3 exposures and new onset type 2 diabetes in regional and national samples in the United States

BackgroundExposure to particulate matter ≤2.5 μm in diameter (PM2.5) and ozone (O3) has been linked to numerous harmful health outcomes. While epidemiologic evidence has suggested a positive association with type 2 diabetes (T2D), there is heterogeneity in findings. We evaluated exposures to PM2.5 and O3 across three large samples in the US using a harmonized approach for exposure assignment and covariate adjustment. MethodsData were obtained from the Veterans Administration Diabetes Risk (VADR) cohort (electronic health records [EHRs]), the Reasons for Geographic and Racial Disparities in Stroke (REGARDS) cohort (primary data collection), and the Geisinger health system (EHRs), and reflect the years 2003–2016 (REGARDS) and 2008–2016 (VADR and Geisinger). New onset T2D was ascertained using EHR information on medication orders, laboratory results, and T2D diagnoses (VADR and Geisinger) or report of T2D medication or diagnosis and/or elevated blood glucose levels (REGARDS). Exposure was assigned using pollutant annual averages from the Downscaler model. Models stratified by community type (higher density urban, lower density urban, suburban/small town, or rural census tracts) evaluated likelihood of new onset T2D in each study sample in single- and two-pollutant models of PM2.5 and O3. ResultsIn two pollutant models, associations of PM2.5, and new onset T2D were null in the REGARDS cohort except for in suburban/small town community types in models that also adjusted for NSEE, with an odds ratio (95% CI) of 1.51 (1.01, 2.25) per 5 μg/m3 of PM2.5. Results in the Geisinger sample were null. VADR sample results evidenced nonlinear associations for both pollutants; the shape of the association was dependent on community type. ConclusionsAssociations between PM2.5, O3 and new onset T2D differed across three large study samples in the US. None of the results from any of the three study populations found strong and clear positive associations.

Association of PM2.5 mass and its components with ovarian reserve in a northern peninsular province, China: The critical exposure period and components

BackgroundA possible role of PM2.5 components on ovarian reserve has not been adequately unexplored. ObjectiveTo evaluate the association between PM2.5 components and women’ ovarian reserve over critical exposure periods in northern China, where the level of air pollution is among the nation’s highest. MethodsWe included 15,102 women with serum anti-Müllerian hormone (AMH) measurements from the Center for Reproductive Medicine of Shandong University during 2015–2019. Concentrations of PM2.5 and its five major components (0.1° × 0.1°), including sulfate, nitrate, ammonium, organic matter, and black carbon, were assigned to each residential address. Multivariable linear mixed effect models combined with constituent-residual models were performed to estimate the effect sizes of essential components over six short- to long-term exposure periods. ResultsThe strength of association was stronger during the process from primary to small antral follicle compared with other longer windows. For every interquartile range increase in PM2.5 mass was associated with − 8.7% (95%CI: −12.3%, −4.9%) change in AMH and the effect size was greatest for sulfate. Women with the lower level of attained education and those living inland were more susceptible compared with other population subgroups. ConclusionExposure to specific components of air pollution during critical exposure windows is associated with a decline in ovarian reserve. These data add to the growing body of evidence that environmental factors have adverse effects on reproductive health, particularly for vulnerable population subgroups.

Associations of PM2.5 composition and green space with metabolic syndrome in a Chinese essential hypertensive population

BackgroundMetabolic syndrome (MetS) has emerged as a significant global public health concern. While environmental factors, including PM2.5, have been identified as important risk factors for MetS in the general population, limited studies have investigated their impact on individuals with essential hypertension. Therefore, our study aims to explore the relationship between PM2.5 composition, green space, and their combined effects on MetS among a Chinese essential hypertensive population. MethodA total of 20,131 participants diagnosed with essential hypertension from 10 provinces in China were included in this study. Individual level exposure to various environmental factors (including PM2.5, PM2.5 composition, green space and temperature) were evaluated using spatiotemporal models based on satellites data. Participants were defined as MetS according to the definition issued by the International Diabetes Federation. Generalized additive mixed models were used to analyze the individual air pollutants, green space and their interaction on MetS. ResultThe prevalence of MetS in this population was 44.33%. The adjusted odd ratio (OR) of MetS, with each one unit increase in SO42−, BC and NO3− were 1.077 (1.049, 1.106), 1.126 (1.077, 1.177) and 0.977 (0.958, 0.996) respectively. Additionally, each unit increase of the Normalized Difference Vegetation Index (NDVI) was associated with a decreased risk of MetS (OR: 0.988, 95% CI: 0.984–0.993). In particular, green space was found to mitigate the adverse impacts of PM2.5 on MetS (OR: 0.988, 95% CI: 0.984–0.993). ConclusionOur results suggested that there was a positive association between PM2.5 and its composition (SO42−, BC) with MetS in the essential hypertensive population, while green space might play a protective role. Moreover, green space could effectively weaken the positive relationship between air pollutants and MetS, especially in males and participants younger than 60 years old.

Long-term exposure to ambient PM2.5 and its constituents is associated with MAFLD

Existing evidence suggests that long-term exposure to ambient fine particulate pollution (PM2.5) may increase metabolic dysfunction-associated fatty liver disease (MAFLD) risk. However, there is still limited evidence on the association of PM2.5 constituents with MAFLD. Therefore, this study explores the associations between the five main chemical constituents of PM2.5 and MAFLD to provide more explicit information on the liver exposome. A total of 76,727 participants derived from the China Multi-Ethnic Cohort, a large-scale epidemic survey in southwest China, were included in this study. Multiple linear regression models were used to estimate the pollutant-specific association with MAFLD. Weighted quantile sum regression was used to evaluate the joint effect of the pollutant-mixture on MAFLD and identify which constituents contribute most to it. Three-year exposure to PM2.5 constituents was associated with a higher MAFLD risk and more severe liver fibrosis. Odds ratios for MAFLD were 1.480, 1.426, 1.294, 1.561, 1.618, and 1.368 per standard deviation increase in PM2.5, black carbon, organic matter, ammonium, sulfate, and nitrate, respectively. Joint exposure to the five major chemical constituents was also positively associated with MAFLD (odds ratio 1.490, 95% CI 1.360-1.632). Nitrate contributed most to the joint effect of the pollutant-mixture. Further stratified analyses indicate that males, current smokers, and individuals with a high-fat diet might be more susceptible to ambient PM2.5 exposure than others. Long-term exposure to PM2.5 and its five major chemical constituents may increase the risk of MAFLD. Nitrate might contribute most to MAFLD, which may provide new clues for liver health. Males, current smokers, and participants with high-fat diets were more susceptible to these associations. This large-scale epidemiologic study explored the associations between constituents of fine particulate pollution (PM2.5) and metabolic dysfunction-associated fatty liver disease (MAFLD), and further revealed which constituents play a more important role in increasing the risk of MAFLD. In contrast to previous studies that examined the effects of PM2.5 as a whole substance, this study carefully explored the health effects of the individual constituents of PM2.5. These findings could (1) help researchers to identify the specific particles responsible for hepatotoxicity, and (2) indicate possible directions for policymakers to efficiently control ambient air pollution, such as targeting the sources of nitrate pollution.

Differences in association of PM2.5 and PM10 with respiratory hospitalization in Korea from 2006 to 2019

Differences in association of PM2.5 and PM10 with respiratory hospitalization in Korea from 2006 to 2019