PM2.5 and PM10 air pollution peaks are associated with emergency department visits for psychotic and mood disorders.
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ABSTRACT:
SUBMITTER: Pignon B
PROVIDER: S-EPMC9281271 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Long-term air pollution exposure, notably fine particulate matter, is a global contributor to morbidity and mortality and a known risk factor for coronary artery disease (CAD) and myocardial infarctions (MI). Knowledge of impacts related to source-apportioned PM2.5 is limited. New modeling methods allow researchers to estimate source-specific long-term impacts on the prevalence of CAD and MI. The Catheterization Genetics (CATHGEN) cohort consists of patients who underwent a cardiac catheterization at Duke University Medical Center between 2002 and 2010. Severity of coronary blockage was determined by coronary angiography and converted into a binary indicator of clinical CAD. History of MI was extracted from medical records. Annual averages of source specific PM2.5 were estimated using an improved gas-constrained source apportionment model for North Carolina from 2002 to 2010. We tested six sources of PM2.5 mass for associations with CAD and MI using mixed effects multivariable logistic regression with a random intercept for county and multiple adjustments. PM2.5 fractions of ammonium bisulfate and ammonium nitrate were associated with increased prevalence of CAD (odds ratio [OR] 1.20; 95% CI = 1.11, 1.22 and OR 1.18; 95% CI = 1.05, 1.32, respectively). PM2.5 from ammonium bisulfate and ammonium nitrate were also associated with increased prevalence of MI (OR 1.20; 95% CI = 1.10, 1.29 and OR 1.35; 95% CI = 1.20, 1.53, respectively). Greater PM2.5 concentrations of ammonium bisulfate and ammonium nitrate are associated with greater MI and CAD prevalence. The association with bisulfate suggests aerosol acidity may play a role. Our findings suggest analyses of source specific PM2.5 mass can reveal novel associations.
| S-EPMC8196100 | biostudies-literature
Project description:Frailty is common among older people and results in adverse health outcomes. We investigated whether exposure to PM2.5 is associated with frailty. This cross-sectional study involved 20,606 community-dwelling participants aged ≥ 65 years, residing in New Taipei City, Taiwan. Analytic data included phenotypic frailty, disease burden by Charlson Comorbidity Index (CCI), urban or rural residence, and household income. PM2.5 exposure was calculated from air quality monitoring records, with low exposure defined as the lowest quartile of the study population. 1,080 frail participants (5.2%) were older, predominantly female, had more comorbidities, lived rurally, and had low PM2.5 exposure (all p < 0.001). In multinomial logistic regression analyses, the likelihood of high PM2.5 exposure was higher in prefrail (OR 1.4, 95% CI 1.3-1.5) and frail adults (OR 1.5, 95% CI 1.2-1.9) than in robust individuals, with stronger associations in those who were male (frail: OR 2.1, 95% CI 1.5-3.1; prefrail: OR 2.2, 95% CI 1.9-2.6), ≥ 75 years old (frail: OR 1.8, 95% CI 1.3-2.4; prefrail: OR 1.5, 95% CI 1.3-1.8), non-smokers (frail: OR 1.6, 95% CI 1.3-2.0; prefrail: OR 1.4, 95% CI 1.2-1.5), had CCI ≥ 2 (frail: OR 5.1, 95% CI 2.1-12.6; prefrail: OR 2.1, 95% CI 1.2-3.8), and with low household income (frail: OR 4.0, 95% CI 2.8-5.8; prefrail: OR 2.7, 95% CI 2.2-3.3). This study revealed a significant association between PM2.5 exposure and frailty, with a stronger effect in vulnerable groups.
| S-EPMC7468121 | biostudies-literature
Project description:China's efforts to curb air pollution have drastically reduced its concentrations of fine particulate matter (PM2.5) from 2013 to 2018 nationwide. However, few studies examined the most recent changes in PM2.5 concentrations and questioned if the previous PM2.5 declining trend was sustained or not. This study took a deep dive into the PM2.5 trend for 136 northern cities of China from 2015 to early 2020 before the coronavirus disease 2019 (the COVID-19 hereafter) crisis, using ground-based PM2.5 data notably adjusted for a key measurement method change. We find that mean PM2.5 concentrations in northern China increased by 5.16 µg/m3 in 2019, offsetting 80% of the large reduction achieved in 2018. The rebound was more significant during the heating seasons (HS; Nov to next Mar) over the 2 years: 10.49 µg/m3 from the 2017 HS to the 2019 HS. A multiple linear regression analysis further revealed that anthropogenic factors contributed to around 50% of the PM2.5 rebound in northern cities of China. Such a significant role of anthropogenic factors in driving the rebound was tightly linked to deep cuts in PM2.5 concentrations in the previous year, systemic adjustment of policy targets and mitigation measures by the government, and the rising marginal cost of these measures. These findings suggest the need to chart a more sustainable path for future PM2.5 emission reductions, with an emphasis on key regions during key pollution periods.
| S-EPMC8731191 | biostudies-literature
Project description:Epidemiologic observations suggest that exposure to ambient fine particulate matter (PM2.5) is associated with increased risk of chronic kidney disease (CKD) and diabetes, a causal driver of CKD. We evaluated whether diabetes mediates the association between PM2.5 and CKD. A cohort of 2,444,157 United States veterans were followed over a median 8.5 years. Environmental Protection Agency data provided PM2.5 exposure levels. Regression models assessed associations and their proportion mediated. A 10 µg/m3 increase in PM2.5 was associated with increased odds of having a diabetes diagnosis (odds ratio: 1.18, 95% CI: 1.06-1.32), use of diabetes medication (1.22, 1.07-1.39), and increased risk of incident eGFR <60 ml/min/1.73 m2 (hazard ratio:1.20, 95% CI: 1.13-1.29), incident CKD (1.28, 1.18-1.39), ≥30% decline in eGFR (1.23, 1.15-1.33), and end-stage renal disease (ESRD) or ≥50% decline in eGFR (1.17, 1.05-1.30). Diabetes mediated 4.7% (4.3-5.7%) of the association of PM2.5 with incident eGFR <60 ml/min/1.73 m2, 4.8% (4.2-5.8%) with incident CKD, 5.8% (5.0-7.0%) with ≥30% decline in eGFR, and 17.0% (13.1-20.4%) with ESRD or ≥50% decline in eGFR. Diabetes minimally mediated the association between PM2.5 and kidney outcomes. The findings will help inform more accurate estimates of the burden of diabetes and burden of kidney disease attributable to PM2.5 pollution.
| S-EPMC7067761 | biostudies-literature
Project description:BackgroundAsthma affects millions of people worldwide. Lima, Peru is one of the most polluted cities in the Americas but has insufficient ground PM2.5 (particulate matter that are 2.5 μm or less in diameter) measurements to conduct epidemiologic studies regarding air pollution. PM2.5 estimates from a satellite-driven model have recently been made, enabling a study between asthma and PM2.5.ObjectiveWe conducted a daily time-series analysis to determine the association between asthma emergency department (ED) visits and estimated ambient PM2.5 levels in Lima, Peru from 2010 to 2016.MethodsWe used Poisson generalized linear models to regress aggregated counts of asthma on district-level population weighted PM2.5. Indicator variables for hospitals, districts, and day of week were included to account for spatial and temporal autocorrelation while assessing same day, previous day, day before previous and average across all 3-day exposures. We also included temperature and humidity to account for meteorology and used dichotomous percent poverty and gender variables to assess effect modification.ResultsThere were 103,974 cases of asthma ED visits during the study period across 39 districts in Lima. We found a 3.7% (95% CI: 1.7%-5.8%) increase in ED visits for every interquartile range (IQR, 6.02 μg/m3) increase in PM2.5 same day exposure with no age stratification. For the 0-18 years age group, we found a 4.5% (95% CI: 2.2%-6.8%) increase in ED visits for every IQR increase in PM2.5 same day exposure. For the 19-64 years age group, we found a 6.0% (95% CI: 1.0%-11.0%) increase in ED visits for every IQR in average 3-day exposure. For the 65 years and up age group, we found a 16.0% (95% CI: 7.0%-24.0%) decrease in ED visits for every IQR increase in PM2.5 average 3-day exposure, although the number of visits in this age group was low (4,488). We found no effect modification by SES or gender.DiscussionResults from this study provide additional literature on use of satellite-driven exposure estimates in time-series analyses and evidence for the association between PM2.5 and asthma in a low- and middle-income (LMIC) country.
| S-EPMC8195863 | biostudies-literature
Project description:BackgroundPrenatal exposure to ambient air pollution is linked to a higher risk of unfavorable pregnancy outcomes. However, the association between pregnancy complications and exposure to indoor air pollution remains unclear. The Air Pollution on Pregnancy Outcomes research is a hospital-based prospective cohort research created to look into the effects of aerodynamically exposed particulate matter (PM)10 and PM2.5 on pregnancy outcomes.MethodsThis prospective multicenter observational cohort study was conducted from January 2021 to June 2023. A total of 662 women with singleton pregnancies enrolled in this study. An AirguardK® air sensor was installed inside the homes of the participants to measure the individual PM10 and PM2.5 levels in the living environment. The time-activity patterns and PM10 and PM2.5, determined as concentrations from the time-weighted average model, were applied to determine the anticipated exposure levels to air pollution of each pregnant woman. The relationship between air pollution exposure and pregnancy outcomes was assessed using logistic and linear regression analyses.ResultsExposure to elevated levels of PM10 throughout the first, second, and third trimesters as well as throughout pregnancy was strongly correlated with the risk of pregnancy problems according to multiple logistic regression models adjusted for variables. Except for in the third trimester of pregnancy, women exposed to high levels of PM2.5 had a high risk of pregnancy complications. During the second trimester and entire pregnancy, the risk of preterm birth (PTB) increased by 24% and 27%, respectively, for each 10 μg/m3 increase in PM10. Exposure to high PM10 levels during the second trimester increased the risk of gestational diabetes mellitus (GDM) by 30%. The risk of GDM increased by 15% for each 5 μg/m3 increase in PM2.5 during the second trimester and overall pregnancy, respectively. Exposure to high PM10 and PM2.5 during the first trimester of pregnancy increased the risk of delivering small for gestational age (SGA) infants by 96% and 26%, respectively.ConclusionExposure to high concentrations of PM10 and PM2.5 is strongly correlated with the risk of adverse pregnancy outcomes. Exposure to high levels of PM10 and PM2.5 during the second trimester and entire pregnancy, respectively, significantly increased the risk of PTB and GDM. Exposure to high levels of PM10 and PM2.5 during the first trimester of pregnancy considerably increased the risk of having SGA infants. Our findings highlight the need to measure individual particulate levels during pregnancy and the importance of managing air quality in residential environment.
| S-EPMC11004777 | biostudies-literature
Project description:Estimating the health burden of air pollution against the background of population aging is of great significance for achieving the Sustainable Development Goal 3.9 which aims to substantially reduce the deaths and illnesses from air pollution. Here, we estimated spatiotemporal changes in deaths attributable to PM2.5 air pollution in China from 2000 to 2035 and examined the drivers. The results show that from 2019 to 2035, deaths were projected to decease 15.4% (6.6%-20.7%, 95% CI) and 8.4% (0.6%-13.5%) under the SSP1-2.6 and SSP5-8.5 scenario, respectively, but increase 10.4% (5.1%-20.5%) and 18.1% (13.0%-28.3%) under SSP2-4.5 and SSP3-7.0 scenarios. Population aging will be the leading contributor to increased deaths attributable to PM2.5 air pollution, which will counter the positive gains achieved by improvements in air pollution and healthcare. Region-specific measures are required to mitigate the health burden of air pollution and this requires long-term efforts and mutual cooperation among regions in China.
| S-EPMC10460422 | biostudies-literature
Project description:Background: Exposure to 2.5-micron diameter air pollutants (PM 2.5) has been associated with an increased risk of illness and death worldwide; however, in Latin American health impacts assessment of this risk factor is scarce. Medellín is one of the most polluted cities in the region, with a population growth rate that is twice as high as that of other Colombian cities, which implies a growing population at risk. Methods: A descriptive study of the disease burden was carried out using the city as the unit of observation. Health events were selected based on epidemiologic evidence and the availability of the population attributable fraction associated with PM 2.5. The mortality records were taken from the module of deceased of the Single Registry of Affiliates of the Health System; the morbidity records were taken from the Individual Health Services Registries. For the estimation of the burden of disease, the current Global Burden of Disease guidelines were followed. Results: Attributable disability-adjusted life years to exposure to ambient PM 2.5 pollution (DALYs PM2.5) constituted 13.8% of total burden of the city. Males showed the greatest loss of DALYs PM2.5 due to acute events, while in women the greatest loss was due to chronic events. Ischemic heart disease, chronic diseases of the lower respiratory tract, and influenza and pneumonia were the events that contributed the most to DALYs PM2.5. 71.4% of the DALYs PM2.5 corresponded to mortality, mainly in the population over 65 years of age. Regarding attributable morbidity, acute events were more prevalent in both sexes, especially due to respiratory diseases Conclusion: Premature death among the elderly population has the greatest weight on burden of disease attributable to ambient PM 2.5 pollution, mainly due to respiratory and cardiovascular diseases, without significant differences according to gender.
| S-EPMC8564742 | biostudies-literature
Project description:BackgroundNonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. Particulate matter air pollution <2.5 μm in diameter (PM2.5) is a ubiquitous exposure primarily produced from fossil fuel combustion. Previous epidemiologic studies have been mixed. The objective of this study was to examine the association between ambient PM2.5 exposure and NAFLD among hospitalized patients in the Nationwide Inpatient Sample (NIS).MethodsWe conducted a cross-sectional analysis of hospitalizations from 2001 to 2011 using the NIS, the largest nationally representative all-payer inpatient care administrative database in the United States. Average annual PM2.5 exposure was estimated by linking census tracts (based on NIS-provided hospital ZIP Codes) with a spatiotemporal exposure model. Clinical conditions were identified using hospital discharge diagnosis codes. Multivariable logistic regression incorporating discharge weights was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between PM2.5 exposure and odds of NAFLD among hospitalized patients adjusting for age, sex, race/ethnicity, year, individual- and area-level socioeconomic status, urbanicity, region, obesity, diabetes, metabolic syndrome, impaired fasting glucose, dyslipidemia, hypertension, obstructive sleep apnea, and smoking.ResultsThere were 269,705 hospitalized patients with NAFLD from 2001 to 2011 (total unweighted n = 45,433,392 hospitalizations). Higher ambient PM2.5 exposure was associated with increased odds of NAFLD among hospitalized patients (adjusted OR: 1.24 per 10 μg/m3 increase, 95% CI 1.15-1.33, p < 0.01). There were statistically significant interactions between PM2.5 exposure and age, race/ethnicity, diabetes, smoking, and region, with stronger positive associations among patients who were aged ≥45 years, non-Hispanic White or Asian/Pacific Islander, non-diabetics, non-smokers, or in the Midwest and West regions, respectively.ConclusionsIn this nationwide cross-sectional analysis of the NIS database, there was a positive association between ambient PM2.5 exposure and odds of NAFLD among hospitalized patients. Future research should examine the effects of long-term historical PM2.5 exposure and incident NAFLD cases.
| S-EPMC9378584 | biostudies-literature
Project description:Air pollution, via ambient PM2.5, is a big threat to public health since it associates with increased hospitalisation, incidence rate and mortality of cardiopulmonary injury. However, the potential mediators of pulmonary injury in PM2.5 -induced cardiovascular disorder are not fully understood. To investigate a potential cross talk between lung and heart upon PM2.5 exposure, intratracheal instillation in vivo, organ culture ex vivo and human bronchial epithelial cells (Beas-2B) culture in vitro experiments were performed respectively. The exposed supernatants of Beas-2B were collected to treat primary neonatal rat cardiomyocytes (NRCMs). Upon intratracheal instillation, subacute PM2.5 exposure caused cardiac dysfunction, which was time-dependent secondary to lung injury in mice, thereby demonstrating a cross-talk between lungs and heart potentially mediated via small extracellular vesicles (sEV). We isolated sEV from PM2.5 -exposed mice serum and Beas-2B supernatants to analyse the change of sEV subpopulations in response to PM2.5 . Single particle interferometric reflectance imaging sensing analysis (SP-IRIS) demonstrated that PM2.5 increased CD63/CD81/CD9 positive particles. Our results indicated that respiratory system-derived sEV containing miR-421 contributed to cardiac dysfunction post-PM2.5 exposure. Inhibition of miR-421 by AAV9-miR421-sponge could significantly reverse PM2.5 -induced cardiac dysfunction in mice. We identified that cardiac angiotensin converting enzyme 2 (ACE2) was a downstream target of sEV-miR421, and induced myocardial cell apoptosis and cardiac dysfunction. In addition, we observed that GW4869 (an inhibitor of sEV release) or diminazene aceturate (DIZE, an activator of ACE2) treatment could attenuate PM2.5 -induced cardiac dysfunction in vivo. Taken together, our results suggest that PM2.5 exposure promotes sEV-linked miR421 release after lung injury and hereby contributes to PM2.5 -induced cardiac dysfunction via suppressing ACE2.
| S-EPMC9089227 | biostudies-literature