Long-term exposure to ambient PM2.5 and stroke mortality among urban residents in northern China.
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ABSTRACT:
SUBMITTER: Yang X
PROVIDER: S-EPMC8150861 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Evidence of associations between exposure to ambient air pollution and health outcomes are sparse in the South Asian region due to limited air pollution exposure and quality health data. This study investigated the potential impacts of ambient particulate matter (PM) on respiratory disease hospitalization in Kandy, Sri Lanka for the year 2019. The Generalized Additive Model (GAM) was applied to estimate the short-term effect of ambient PM on respiratory disease hospitalization. As the second analysis, respiratory disease hospitalizations during two distinct air pollution periods were analyzed. Each 10 μg/m3 increase in same-day exposure to PM2.5 and PM10 was associated with an increased risk of respiratory disease hospitalization by 1.95% (0.25, 3.67) and 1.63% (0.16, 3.12), respectively. The effect of PM2.5 or PM10 on asthma hospitalizations were 4.67% (1.23, 8.23) and 4.04% (1.06, 7.11), respectively (p < 0.05). The 65+ years age group had a higher risk associated with PM2.5 and PM10 exposure and hospital admissions for all respiratory diseases on the same day (2.74% and 2.28%, respectively). Compared to the lower ambient air pollution period, higher increased hospital admissions were observed among those aged above 65 years, males, and COPD and pneumonia hospital admissions during the high ambient air pollution period. Active efforts are crucial to improve ambient air quality in this region to reduce the health effects.
| S-EPMC8466407 | biostudies-literature
Project description:Fine-particulate pollution is a major public health concern in China. Accurate assessment of the population exposed to PM2.5 requires high-resolution pollution and population information. This paper assesses China's potential population exposure to PM2.5, maps its spatiotemporal variability, and simulates the effects of the recent air pollution control policy. We relate satellite-based Aerosol Optical Depth (AOD) retrievals to ground-based PM2.5 observations. We employ block cokriging (BCK) to improve the spatial interpolation of PM2.5 distribution. We use the subdistrict level population data to estimate and map the potential population exposure to PM2.5 pollution in China at the subdistrict level, the smallest administrative unit with public demographic information. During 8 April 2013 and 7 April 2014, China's population-weighted annual average PM2.5 concentration was nearly 7 times the annual average level suggested by the World Health Organization (WHO). About 1322 million people, or 98.6% of the total population, were exposed to PM2.5 at levels above WHO's daily guideline for longer than half a year. If China can achieve its Action Plan on Prevention and Control of Air Pollution targets by 2017, the population exposed to PM2.5 above China's daily standard for longer than half a year will be reduced by 85%.
| S-EPMC6313548 | biostudies-literature
Project description:BackgroundStudies suggested that PM2.5 exposure could lead to adverse reproductive effects on male animals. However, the underlying mechanism is still not clear. Besides, animals in the majority of previous studies were exposed to PM2.5 through intratracheal instillation which should be improved. In addition, limited amount of research has been conducted in China where the PM2.5 concentration is higher and the PM2.5 components are different. The aim of this work is to explore the effects of concentrated ambient PM2.5 (CAP) on mice sperm quality and testosterone biosynthesis.MethodsA total of 12 male C57BL/6 mice were exposed to filtered air (FA) or CAP for 125 days using the Shanghai Meteorological and Environmental Animal Exposure System. The mice sperm concentration, sperm motility, DNA fragmentation index, high DNA stainability and plasma testosterone were analyzed. Testicular histology and sperm morphology were observed through optical microscope. Testosterone biosynthesis related gene expressions were analyzed using real-time PCR, including cytochrome P450 CHOL side-chain cleavage enzyme (P450scc), steroidogenic acute regulatory protein (StAR), 3β-hydroxysteroid dehydrogenase (3β HSD), 17β-hydroxysteroid dehydrogenase, cytochrome P450 aromatase (P450arom), estrogen receptor (ER), androgen receptor (AR) and follicle stimulating hormone receptor (FSHR).ResultsExposure to CAP resulted in disturbance of various stages of spermatogenesis and significant higher percentage of abnormal sperm (FA vs. CAP: 24.37% vs. 44.83%) in mice testis. CAP exposure significantly decreased sperm concentration (43.00 × 106 vs. 25.33 × 106) and motility (PR: 63.58% vs. 55.15%; PR + NP: 84.00% vs. 77.08%) in epididymis. Plasma testosterone concentration were significantly declined (0.28 ng/ml vs. 0.69 ng/ml) under CAP exposure. Notably, the levels of testosterone biosynthesis related genes, StAR, P450scc, P450arom, ER and FSHR were significantly decreased with CAP exposure.ConclusionConcentrated ambient PM2.5 exposure altered mice sperm concentration, motility and morphology, which might be mediated primarily by the decline in testosterone concentration and testosterone biosynthesis process.
| S-EPMC6885350 | biostudies-literature
Project description:Background Air pollution has been recognized as an untraditional risk factor for myocardial infarction (MI). However, the MI risk attributable to long-term exposure to fine particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5) is unclear, especially in younger populations, and few studies have represented the general population or had power to examine comorbidities. Methods and Results We applied the difference-in-differences approach to estimate the relationship between annual PM2.5 exposure and hospitalizations for MI among US residents and further identified potential susceptible subpopulations. All hospital admissions for MI in 10 US states over the period 2002 to 2016 were obtained from the Healthcare Cost and Utilization Project State Inpatient Database. In total, 1 914 684 MI hospital admissions from 8106 zip codes were included in this study. We observed a 1.35% (95% CI, 1.11-1.59) increase in MI hospitalization rate for 1-μg/m3 increase in annual PM2.5 exposure. The estimate was robust to adjustment for surface pressure, relative humidity, and copollutants. In the population exposed to ≤12 μg/m3, there was a larger increment of 2.17% (95% CI, 1.79-2.56) in hospitalization rate associated with 1-μg/m3 increase in PM2.5. Young people (0-34 years of age) and elderly people (≥75 years of age) were the 2 most susceptible age groups. Residents living in more densely populated or poorer areas and individuals with comorbidities were observed to be at a greater risk. Conclusions This study indicates long-term residential exposure to PM2.5 could increase risk of MI among the general US population, people with comorbidities, and poorer individuals. The association persists below current standards.
| S-EPMC10547266 | biostudies-literature
Project description:BackgroundThe metabolomic signatures of short- and long-term exposure to PM2.5 have been reported and linked to inflammation and oxidative stress. However, little is known about the relative contribution of the specific PM2.5 species (hence sources) that drive these metabolomic signatures.ObjectivesWe aimed to determine the relative contribution of the different species of PM2.5 exposure to the perturbed metabolic pathways related to changes in the plasma metabolome.MethodsWe performed mass-spectrometry based metabolomic profiling of plasma samples among men from the Normative Aging Study to identify metabolic pathways associated with PM2.5 species. The exposure windows included short-term (one, seven-, and thirty-day moving average) and long-term (one year moving average). We used linear mixed-effect regression with subject-specific intercepts while simultaneously adjusting for PM2.5, NO2, O3, temperature, relative humidity, and covariates and correcting for multiple testing. We also used independent component analysis (ICA) to examine the relative contribution of patterns of PM2.5 species.ResultsBetween 2000 and 2016, 456 men provided 648 blood samples, in which 1158 metabolites were quantified. We chose 305 metabolites for the short-term and 288 metabolites for the long-term exposure in this analysis that were significantly associated (p-value < 0.01) with PM2.5 to include in our PM2.5 species analysis. On average, men were 75.0 years old and their body mass index was 27.7 kg/m2. Only 3% were current smokers. In the adjusted models, ultrafine particles (UFPs) were the most significant species of short-term PM2.5 exposure followed by nickel, vanadium, potassium, silicon, and aluminum. Black carbon, vanadium, zinc, nickel, iron, copper, and selenium were the significant species of long-term PM2.5 exposure. We identified several metabolic pathways perturbed with PM2.5 species including glycerophospholipid, sphingolipid, and glutathione. These pathways are involved in inflammation, oxidative stress, immunity, and nucleic acid damage and repair. Results were overlapped with the ICA.ConclusionsWe identified several significant perturbed plasma metabolites and metabolic pathways associated with exposure to PM2.5 species. These species are associated with traffic, fuel oil, and wood smoke. This is the largest study to report a metabolomic signature of PM2.5 species' exposure and the first to use ICA.
| S-EPMC7994935 | biostudies-literature
Project description:It has been posited that populations being exposed to long-term air pollution are more susceptible to COVID-19. Evidence is emerging that long-term exposure to ambient PM2.5 (particulate matter with aerodynamic diameter 2.5 ?m or less) associates with higher COVID-19 mortality rates, but whether it also associates with the speed at which the disease is capable of spreading in a population is unknown. Here, we establish the association between long-term exposure to ambient PM2.5 in the United States (US) and COVID-19 basic reproduction ratio R0- a dimensionless epidemic measure of the rapidity of disease spread through a population. We inferred state-level R0 values using a state-of-the-art susceptible, exposed, infected, and recovered (SEIR) model initialized with COVID-19 epidemiological data corresponding to the period March 2-April 30. This period was characterized by a rapid surge in COVID-19 cases across the US states, implementation of strict social distancing measures, and a significant drop in outdoor air pollution. We find that an increase of 1 ?g/m3 in PM2.5 levels below current national ambient air quality standards associates with an increase of 0.25 in R0 (95% CI: 0.048-0.447). A 10% increase in secondary inorganic composition, sulfate-nitrate-ammonium, in PM2.5 associates with ?10% increase in R0 by 0.22 (95% CI: 0.083-0.352), and presence of black carbon (soot) in the ambient environment moderates this relationship. We considered several potential confounding factors in our analysis, including gaseous air pollutants and socio-economical and meteorological conditions. Our results underscore two policy implications - first, regulatory standards need to be better guided by exploring the concentration-response relationships near the lower end of the PM2.5 air quality distribution; and second, pollution regulations need to be continually enforced for combustion emissions that largely determine secondary inorganic aerosol formation.
| S-EPMC7651233 | biostudies-literature
Project description:BackgroundAccumulated researches revealed that both fine particulate matter (PM2.5) and sunlight exposure may be a risk factor for obesity, while researches regarding the potential effect modification by sunlight exposure on the relationship between PM2.5 and obesity are limited. We aim to investigate whether the effect of PM2.5 on obesity is affected by sunlight exposure among the general population in China.MethodsA sample of 47,204 adults in China was included. Obesity and abdominal obesity were assessed based on body mass index, waist circumference and waist-to-hip ratio, respectively. The five-year exposure to PM2.5 and sunlight were accessed using the multi-source satellite products and a geochemical transport model. The relationship between PM2.5, sunshine duration, and the obesity or abdominal obesity risk was evaluated using the general additive model.ResultsThe proportion of obesity and abdominal obesity was 12.6% and 26.8%, respectively. Levels of long-term PM2.5 ranged from 13.2 to 72.1 μg/m3 with the mean of 46.6 μg/m3. Each 10 μg/m3 rise in PM2.5 was related to a higher obesity risk [OR 1.12 (95% CI 1.09-1.14)] and abdominal obesity [OR 1.10 (95% CI 1.07-1.13)]. The association between PM2.5 and obesity varied according to sunshine duration, with the highest ORs of 1.56 (95% CI 1.28-1.91) for obesity and 1.66 (95% CI 1.34-2.07) for abdominal obesity in the bottom quartile of sunlight exposure (3.21-5.34 hours/day).ConclusionLong-term PM2.5 effect on obesity risk among the general Chinese population are influenced by sunlight exposure. More attention might be paid to reduce the adverse impacts of exposure to air pollution under short sunshine duration conditions.
| S-EPMC8777285 | biostudies-literature
Project description:BackgroundFine particulate matter (PM2.5) is an important environmental risk factor for cardiopulmonary diseases. However, the association between PM2.5 and risk of CKD remains under-recognized, especially in regions with high levels of PM2.5, such as China.MethodsTo explore the association between long-term exposure to ambient PM2.5 and CKD prevalence in China, we used data from the China National Survey of CKD, which included a representative sample of 47,204 adults. We estimated annual exposure to PM2.5 before the survey date at each participant's address, using a validated, satellite-based, spatiotemporal model with a 10 km×10 km resolution. Participants with eGFR <60 ml/min per 1.73 m2 or albuminuria were defined as having CKD. We used a logistic regression model to estimate the association and analyzed the influence of potential modifiers.ResultsThe 2-year mean PM2.5 concentration was 57.4 μg/m3, with a range from 31.3 to 87.5 μg/m3. An increase of 10 μg/m3 in PM2.5 was positively associated with CKD prevalence (odds ratio [OR], 1.28; 95% confidence interval [CI], 1.22 to 1.35) and albuminuria (OR, 1.39; 95% CI, 1.32 to 1.47). Effect modification indicated these associations were significantly stronger in urban areas compared with rural areas, in males compared with females, in participants aged <65 years compared with participants aged ≥65 years, and in participants without comorbid diseases compared with those with comorbidities.ConclusionsThese findings regarding the relationship between long-term exposure to high ambient PM2.5 levels and CKD in the general Chinese population provide important evidence for policy makers and public health practices to reduce the CKD risk posed by this pollutant.
| S-EPMC8054885 | biostudies-literature
Project description:Previous studies have shown that long-term exposure to fine particulate matter (PM2.5) increases the morbidity and mortality of pulmonary diseases such as asthma, chronic obstructive pulmonary disease and pulmonary emphysema. Oxidative stress and inflammation play key roles in pulmonary damage caused by PM2.5. Nuclear factor erythroid 2-related factor 2 (Nrf2) could regulate the expression of antioxidant and anti-inflammatory genes and is pivotal for protection against PM2.5-induced oxidative stress. In this study, a real-ambient exposure system was constructed with the outdoor ambient air in north China. Wild-type (WT) and Nrf2-/- (KO) mice were exposed to the real-ambient system for six weeks. After PM2.5 exposure, our data showed that the levels of inflammatory factors and malondialdehyde were significantly increased in WT and KO mice. Moreover, the lung function and pathological phenotype of the WT mice were altered but there was no obvious change in the Nrf2-/- mice. To further explore the potential molecular mechanisms, we performed RNA-sequencing. The RNA-sequence analysis results showed that the CYP450 pathway in the first ten pathways of KEGG was related to the metabolism of PM2.5. In WT and KO mice, the expression of CYP2E1 in the CYP450 pathway showed opposite trends after PM2.5 exposure. The data showed that the expression of the CYP2E1 gene in WT-PM mice increased while it decreased in KO-PM; the expression of the CYP2E1 protein showed a similar trend. CYP2E1 is primarily distributed in the endoplasmic reticulum (ER) where it could metabolize various exogenous substances attached to PM2.5 and produce highly toxic oxidation products closely related to ER stress. Consistently, the expression level of GRP94, a biomarker of ER stress, was increased in WT mice and reduced in KO mice under PM2.5 exposure. Persistent ER stress is a mechanism that causes lung damage under PM2.5 exposure. Nrf2 facilitates lung injury during PM2.5 exposure and CYP2E1 metabolism is involved in this process.
| S-EPMC8104929 | biostudies-literature
Project description:COVID-19 has escalated into one of the most serious crises in the 21st Century. Given the rapid spread of SARS-CoV-2 and its high mortality rate, here we investigate the impact and relationship of airborne PM2.5 to COVID-19 mortality. Previous studies have indicated that PM2.5 has a positive relationship with the spread of COVID-19. To gain insights into the delayed effect of PM2.5 concentration (μgm-3) on mortality, we focused on the role of PM2.5 in Wuhan City in China and COVID-19 during the period December 27, 2019 to April 7, 2020. We also considered the possible impact of various meteorological factors such as temperature, precipitation, wind speed, atmospheric pressure and precipitation on pollutant levels. The results from the Pearson's correlation coefficient analyses reveal that the population exposed to higher levels of PM2.5 pollution are susceptible to COVID-19 mortality with a lag time of >18 days. By establishing a generalized additive model, the delayed effect of PM2.5 on the death toll of COVID-19 was verified. A negative correction was identified between temperature and number of COVID-19 deaths, whereas atmospheric pressure exhibits a positive correlation with deaths, both with a significant lag effect. The results from our study suggest that these epidemiological relationships may contribute to the understanding of the COVID-19 pandemic and provide insights for public health strategies.
| S-EPMC8553633 | biostudies-literature