Effects Of Ambient Particulate Matter Research Articles

Long-term effects of ambient particulate matter on hypertension among royal Thai army officers: a retrospective cohort study

Recent research on the link between exposure to ambient particulate matter with an aerodynamic diameter up to 2.5 microns (PM2.5) and hypertension risk has primarily concentrated on spatial variation (or between-individual comparisons). Research into temporal variations (or within-individual comparisons over time) has largely been neglected. This study sought to examine the spatial–temporal effects of long-term exposure to PM2.5 on hypertension risk among military personnel in Thailand. A retrospective cohort study was conducted, encompassing 40,984 Royal Thai Army officers from 400 army units stationed across 51 provinces in Thailand. Medical check-up data from 2018 to 2021 were analyzed alongside ambient PM2.5 data from 2015 to 2017, sourced from the Geo-Informatics and Space Technology Development Agency. Two parameters, PM2.5-baseline and PM2.5-change, were introduced to assess the impact of spatial and temporal PM2.5 variations on hypertension incidence. Cox proportional hazard regression was used, with hazard ratios (HR) with 95% confidence intervals (95% CI) serving as the measure of association. The association between PM2.5-baseline and hypertension incidence yielded hazard ratios in Quartiles 2 to 4 compared to Quartile 1 of: Q2 HR: 1.19, 95% CI: 1.10–1.28; Q3 HR: 1.10, 95% CI: 1.02–1.20; Q4 HR: 1.13, 95% CI: 1.05–1.22. Additionally, the PM2.5-change showed a J-shaped association with hypertension incidence. Our findings underscore the role of both temporal and spatial factors in hypertension development and highlight the necessity for comprehensive investigations into the causal relationship between PM2.5 exposure and hypertension risk. They also provide valuable insights for devising effective strategies to mitigate the adverse health impacts of PM2.5 pollution.

The short-term effect of ambient particulate matter on suicide death

BackgroundAir pollution can cause various respiratory and neurological diseases and continuous exposure can lead to death. Previous studies have reported that particulate matter (PM) exposure increases the risk of depression, suicidal thoughts, and suicidal death; however, the results are inconsistent and limited. This study aimed to examine the relationship between short-term PM exposure and suicide deaths, as well as investigate the short-term effects of PM on suicide death within vulnerable groups based on factors such as sex, age group, suicide-related information (note, method, and cause), psychiatric disorders, and physical diseases.MethodsData on a total of 28,670 suicide deaths from 2013 to 2017, provided by the Korea Foundation for Suicide Prevention, were analyzed. The study design employed a time-series analysis with a two-stage approach. In the first step, a generalized additive model combined with a distributed lag nonlinear model was used to estimate the short-term effect of PM exposure on suicide risk specific to each city. In the second step, the estimated results from each city were pooled through a meta-analysis to derive the overall effect. We determined the effects of single lag, cumulative lag, and moving average PM concentrations from days 0–7 before suicide.ResultsWe confirmed an association between exposure to PM10 (≤ 10 μm in diameter) and deaths due to suicide. In particular, among individuals with psychiatric disorders and those who employed non-violent suicide methods, increased exposure to PM10 was associated with a higher risk of death by suicide, with percentage changes of 5.92 (95% confidence interval [CI]: 3.95–7.92) and 11.47 (95% CI: 7.95–15.11), respectively. Furthermore, in the group with psychiatric disorders, there was an observed tendency of increasing suicide risk as PM10 levels increased up to 120 µg/m3, whereas in the group with non-violent suicide deaths, there was a pronounced trend of rapid increase in suicide risk with an increase in PM10 up to 100 µg/m3.ConclusionsThese results show an association between short-term exposure to PM and suicide. Our study adds evidence for the benefits of reducing PM in preventing diseases and improving mental health.

A review on potential approach for in silico toxicity analysis of respirable fraction of ambient particulate matter.

Epidemiological and toxicological studies have shown the adverse effect of ambient particulate matter (PM) on respiratory and cardiovascular systems inside the human body. Various cellular and acellular assays in literature use indicators like ROS generation, cell inflammation, mutagenicity, etc., to assess PM toxicity and associated health effects. The presence of toxic compounds in respirable PM needs detailed studies for proper understanding of absorption, distribution, metabolism, and excretion mechanisms inside the body as it is difficult to accurately imitate or simulate these mechanisms in lab or animal models. The leaching kinetics of the lung fluid, PM composition, retention time, body temperature, etc., are hard to mimic in an artificial experimental setup. Moreover, the PM size fraction also plays an important role. For example, the ultrafine particles may directly enter systemic circulations while coarser PM10 may be trapped and deposited in the tracheo-bronchial region. Hence, interpretation of these results in toxicity models should be done judiciously. Computational models predicting PM toxicity are rare in the literature. The variable composition of PM and lack of proper understanding for their synergistic role inside the body are prime reasons behind it. This review explores different possibilities of in silico modeling and suggests possible approaches for the risk assessment of PM particles. The toxicity testing approach for engineered nanomaterials, drugs, food industries, etc., have also been investigated for application in computing PM toxicity.

Role of different mechanisms in pro-inflammatory responses triggered by traffic-derived particulate matter in human bronchiolar epithelial cells

BackgroundTraffic-derived particles are important contributors to the adverse health effects of ambient particulate matter (PM). In Nordic countries, mineral particles from road pavement and diesel exhaust particles (DEP) are important constituents of traffic-derived PM. In the present study we compared the pro-inflammatory responses of mineral particles and DEP to PM from two road tunnels, and examined the mechanisms involved.MethodsThe pro-inflammatory potential of 100 µg/mL coarse (PM10-2.5), fine (PM2.5-0.18) and ultrafine PM (PM0.18) sampled in two road tunnels paved with different stone materials was assessed in human bronchial epithelial cells (HBEC3-KT), and compared to DEP and particles derived from the respective stone materials. Release of pro-inflammatory cytokines (CXCL8, IL-1α, IL-1β) was measured by ELISA, while the expression of genes related to inflammation (COX2, CXCL8, IL-1α, IL-1β, TNF-α), redox responses (HO-1) and metabolism (CYP1A1, CYP1B1, PAI-2) was determined by qPCR. The roles of the aryl hydrocarbon receptor (AhR) and reactive oxygen species (ROS) were examined by treatment with the AhR-inhibitor CH223191 and the anti-oxidant N-acetyl cysteine (NAC).ResultsRoad tunnel PM caused time-dependent increases in expression of CXCL8, COX2, IL-1α, IL-1β, TNF-α, COX2, PAI-2, CYP1A1, CYP1B1 and HO-1, with fine PM as more potent than coarse PM at early time-points. The stone particle samples and DEP induced lower cytokine release than all size-fractionated PM samples for one tunnel, and versus fine PM for the other tunnel. CH223191 partially reduced release and expression of IL-1α and CXCL8, and expression of COX2, for fine and coarse PM, depending on tunnel, response and time-point. Whereas expression of CYP1A1 was markedly reduced by CH223191, HO-1 expression was not affected. NAC reduced the release and expression of IL-1α and CXCL8, and COX2 expression, but augmented expression of CYP1A1 and HO-1.ConclusionsThe results indicate that the pro-inflammatory responses of road tunnel PM in HBEC3-KT cells are not attributed to the mineral particles or DEP alone. The pro-inflammatory responses seem to involve AhR-dependent mechanisms, suggesting a role for organic constituents. ROS-mediated mechanisms were also involved, probably through AhR-independent pathways. DEP may be a contributor to the AhR-dependent responses, although other sources may be of importance.

Ambient particulate matter associates with asthma in high altitude region: A population-based study

BackgroundExposure to particulate matter (PM) has been a major public health threat, but the potentially differential effects on asthma of PM remain largely unknown in high altitude settings. We evaluated the effects of ambient PM on asthma in high altitude settings. MethodsThe study recruited a representative sample from high altitude settings using a multistage stratified sampling procedure. Asthma was defined by a self-reported history of diagnosis by a physician or by wheezing symptoms in the preceding 12 months. The annual mean PM2.5 and PM10 concentrations were calculated for each grid cell at 1-km spatial resolution based on the geographical coordinates. ResultsWe analyzed data for participants (mean age 39.1 years, 51.4% female) and 183 (3.7%, 95% confidence interval (CI): 3.2–4.2) of the participants had asthma. Prevalence was higher in women (4.3%, 95% CI 3.5–5.1) than in men (3.1%, 2.4–3.8) and increasing with higher concentration of PM exposures. For an interquartile range (IQR) difference (8.77 μg/m3) in PM2.5 exposure, the adjusted odds ratio (OR) was 1.64 (95% CI 1.46–1.83, P < 0.001) for risk of asthma. For PM10, there was evidence for an association with risk of asthma (OR 2.34, 95% CI: 1.75–3.15, P < 0.001 per IQR of 43.26 μg/m3). Further analyses showed that household mold or damp exposure may aggravate PM exposure associated risks of asthma. ConclusionsThis study identified that PM exposure could be a dominate environmental risk factor for asthma but largely unconsidered in the high-altitude areas. The association between PM exposure and asthma should be of interest for planners of national policies and encourage programs for prevention of asthma in residents living at high altitudes.

Short-term effects of ambient particulate matter (PM1, PM2.5 and PM10) on influenza-like illness in Guangzhou, China.

Particulate matter (PM) has been linked to respiratory infections in a growing body of evidence. Studies on the relationship between ILI (influenza-like illness) and PM1 (particulate matter with aerodynamic diameter ≤1μm) are, however, scarce. The purpose of this study was to investigate the effects of PM on ILI in Guangzhou, China. Daily ILI cases, air pollution records (PM1, PM2.5, PM10 and gaseous pollutants), and metrological data between 2014 and 2019 were gathered from Guangzhou, China. To estimate the risk of ILI linked with exposure to PM pollutants, a quasi-Poisson regression was used. Additionally, subgroup analyses stratified by gender, age and season were carried out. For each 10μg/m3 increase of PM1 and PM2.5 over the past two days (lag01), and PM10 over the past three days (lag02), the relative risks (RR) of ILI were 1.079 (95% confidence interval [CI]: 1.050, 1.109), 1.044 (95% CI: 1.027, 1.062) and 1.046 (95% CI: 1.032, 1.059), respectively. The estimated risks for men and women were substantially similar. The effects of PM pollutants between male and female were basically equivalent. People aged 15-24 years old were more susceptive to PM pollutants. It implies that PM1, PM2.5 and PM10 are all risk factors for ILI, the health impacts of PM pollutants vary by particle size. Reducing the concentration of PM1 needs to be considered when generating a strategy to prevent ILI.

Ambient particulate matter exposure plus a high-fat diet exacerbate renal injury by activating the NLRP3 inflammasome and TGF-β1/Smad2 signaling pathway in mice

BackgroundChronic kidney disease (CKD) is a public health problem of which the prevalence is increasing worldwide. Several studies have reported that ambient particulate matter (PM) causes kidney injury, which may be related to the risk of CKD. However, the underlying molecular mechanisms have not been fully clarified. In addition, whether a high-fat diet (HFD) could exacerbate ambient PM-induced nephrotoxicity has not been evaluated. This study aimed to investigate the combined effect of ambient PM and a HFD on renal injury. Methods and resultsMale C57BL/6 J mice were fed either a normal diet or a HFD and exposed to filtered air (FA) or particulate matter (PM) for 18 weeks. In the present study, we observed that renal function changed (serum blood urea nitrogen and serum creatinine), and exposure to PM and a HFD caused a synergistic effect on renal injury. Histopathological analysis showed that PM exposure induced renal fibrosis in mice, and combined exposure to PM and a HFD exacerbated these adverse effects. Moreover, ambient PM exposure activated the nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome and increased the inflammatory response, as indicated by the increases in interleukin-1β, interleukin-6 and tumor necrosis factor-α in the serum and kidney, as well as the upregulation of specific renal fibrosis-related markers (transforming growth factor-β1 and p-Smad2) in the kidney tissues of mice. Furthermore, combined exposure to PM and a HFD augmented these changes in the kidney. In vitro, inhibition of the NLRP3 inflammasome by MCC950 (an inhibitor of NLRP3) reduced the levels of proinflammatory cytokines and the expression of transforming growth factor-β1 and p-Smad2 in HK-2 cells. ConclusionTaken together, our data indicated that PM exposure caused renal inflammation and induced profibrotic effects on the kidney, and combined exposure to ambient PM and a HFD exacerbated renal injury, which may involve activation of the NLRP3 inflammasome and the TGF-β1/Smad2 signaling pathway.

Oxidative stress generated by polycyclic aromatic hydrocarbons from ambient particulate matter enhance vascular smooth muscle cell migration through MMP upregulation and actin reorganization

BackgroundEpidemiological studies have suggested that elevated concentrations of particulate matter (PM) are strongly associated with the incidence of atherosclerosis, however, the underlying cellular and molecular mechanisms of atherosclerosis by PM exposure and the components that are mainly responsible for this adverse effect remain to be established. In this investigation, we evaluated the effects of ambient PM on vascular smooth muscle cell (VSMC) behavior. Furthermore, the effects of polycyclic aromatic hydrocarbons (PAHs), major components of PM, on VSMC migration and the underlying mechanisms were examined.ResultsVSMC migration was significantly increased by treatment with organic matters extracted from ambient PM. The total amount of PAHs contained in WPM was higher than that in SPM, leading to higher ROS generation and VSMC migration. The increased migration was successfully inhibited by treatment with the anti-oxidant, N-acetyl-cysteine (NAC). The levels of matrix metalloproteinase (MMP) 2 and 9 were significantly increased in ambient PM-treated VSMCs, with MMP9 levels being significantly higher in WPM-treated VSMCs than in those treated with SPM. As expected, migration was significantly increased in all tested PAHs (anthracene, ANT; benz(a)anthracene, BaA) and their oxygenated derivatives (9,10-Anthraquinone, AQ; 7,12-benz(a)anthraquinone, BAQ, respectively). The phosphorylated levels of focal adhesion kinase (FAK) and formation of the focal adhesion complex were significantly increased in ambient PM or PAH-treated VSMCs, and these effects were blocked by administration of NAC or α-NF, an inhibitor of AhR, the receptor that allows PAH uptake. Subsequently, the levels of phosphorylated Src and NRF, the downstream targets of FAK, were altered with a pattern similar to that of p-FAK.ConclusionsPAHs, including oxy-PAHs, in ambient PM may have dual effects that lead to an increase in VSMC migration. One is the generation of oxidative stress followed by MMP upregulation, and the other is actin reorganization that results from the activation of the focal adhesion complex.

Fine particulate matter measured by satellites predicts the risk of age-related macular degeneration in a longitudinal cohort study.

Although studies have revealed that ambient particulate matter (PM) has detrimental effects on the ocular surface, there have been limited reports detailing the effect of ambient PM on the posterior segment of the eye. A large-scale longitudinal cohort study evaluating the association between fine PM, especially PM2.5, and the retina could elucidate the risk of ambient pollutants for retinal diseases. We investigated the association between PM2.5 and the development of age-related macular degeneration (AMD). We conducted a population-based cohort study of 4,284,128 participants in Taiwan between 2001 and 2011. PM2.5 was continuously measured by satellites and subsequently assigned to each geographic district along with its postcode. A time-dependent Cox proportional-hazard model was used to assess the overall effects of average PM2.5. We used distributed lag non-linear models to evaluate the dose-response relationship between PM2.5 and AMD development. The annual mean of PM2.5 exposure was 34.23 ± 7.17μg/m3. The PM2.5 concentrations were highest in spring, followed by those in winter, autumn, and summer. Twelve thousand ninety-five new AMD cases were reported during the study period. After adjusting for covariates, the AMD risk increased by 19% (95% confidence interval 1.13-1.25) for a 10μg/m3 PM2.5 increase. The present study demonstrated that chronic exposure to PM2.5 increases the risk of AMD. Almost half of the Taiwanese live in a polluted area where the PM2.5 levels are higher than the World Health Organization recommended air quality guideline of 10μg/m3 had a 1.4-fold risk, which significantly increases concern about their visual health and social burden.

Glucose Metabolic Disorders Enhance Vascular Dysfunction Triggered by Particulate Air Pollution: a Panel Study.

Vascular dysfunction is a biological pathway whereby particulate matter (PM) exerts deleterious cardiovascular effects. The effects of ambient PM on vascular function in prediabetic individuals are unclear. A panel study recruited 112 Beijing residents with and without prediabetes. Multiple vascular function indices were measured up to 7 times. The associations between vascular function indices and short-term exposure to ambient PM, including fine particulate matter (PM2.5), ultrafine particles, accumulation mode particles, and black carbon, and the modification of these associations by glucose metabolic status were examined using linear mixed-effects models. Increases in brachial artery pulse pressure, central aortic pulse pressure, and ejection duration, and decreases in subendocardial viability ratio and reactive hyperemia index were significantly associated with at least one PM pollutant in all participants, indicating increased vascular dysfunction. For example, for an interquartile range increment in 5-day moving average ultrafine particles, brachial artery pulse pressure, and central aortic pulse pressure increased 5.4% (0.8%-10.4%) and 6.2% (1.2%-11.5%), respectively. Additionally, PM-associated changes in vascular function differed according to glucose metabolic status. Among participants with high fasting blood glucose levels (≥6.1 mmol/L), PM exposure was significantly associated with increased brachial artery systolic blood pressure, central aortic systolic blood pressure, brachial artery pulse pressure, central aortic pulse pressure, and augmentation pressure normalized to a heart rate of 75 bpm and decreased subendocardial viability ratio and reactive hyperemia index. Weaker or null associations were observed in the low-fasting blood glucose group. Glucose metabolic disorders may exacerbate vascular dysfunction associated with short-term ambient PM exposure.

Association between Particulate Matter Pollution Concentration and Hospital Admissions for Hypertension in Ganzhou, China.

Fine particulate matter (PM2.5) and respirable particulate matter (PM10) are two major air pollutants with toxic effects on the cardiovascular system. Hypertension, as a chronic noncommunicable cardiovascular disease, is also a risk factor for several diseases. We applied generalized linear models with a quasi-Poisson link to assess the effect of air pollution exposure on the number of daily admissions for patients with hypertension. In addition, we established a two-pollutant model to evaluate PM2.5 and PM10 hazard effect stability by adjusting the other gaseous pollutants. Results showed that during the study period, 24 h mean concentrations of ambient PM2.5 and PM10 at 38.17 and 59.84 μg/m3, respectively, and a total of 2,611 hypertension hospital admissions were recorded. Air pollution concentrations significantly affected the number of hospitalizations for hypertension approximately 2 months after exposure. For each 10 μg/m3 increase in PM2.5 and PM10 in single-pollutant models, the number of hospitalizations for hypertension increased by 7.92% (95% CI: 5.48% to 10.42%) and 4.46% (95% CI: 2.86% to 5.65%), respectively, at the lag day with the strongest effect. NO2, O3, CO, and SO2 had different significant effects on the number of hospitalizations over the same time period, and PM2.5 and PM10 still showed robust significant effects after adjustment of gas pollutants through a two-pollutant model. These findings may contribute to a better understanding of the health effects of ambient particulate matter.

Prenatal and early postnatal exposure to ambient particulate matter and early childhood neurodevelopment: A birth cohort study

Adverse impacts of prenatal or postnatal ambient particulate matter exposure have been identified on offspring neurodevelopment. However, it is unclear whether the effect in the two exposure periods is different for early childhood neurodevelopment. This study aimed to evaluate and compare the associations of prenatal and early postnatal exposure to ambient particulate matter with offspring neurodevelopment at 2 years of age and to identify which period was more sensitive to the effects of ambient particulate matter on offspring neurodevelopment. A total of 1331 mother-child pairs from a birth cohort were included in this study from October 2013 to September 2014 in Wuhan, China. The concentrations of ambient daily fine particulate matter (PM2.5) and particulate matter less than 10μm in aerodynamic diameter (PM10) at each participant's home address during pregnancy and the first two years after birth were estimated by land-use regression models (LUR). Offspring neurodevelopment was measured by the Chinese revision of Bayley Scale of Infant Development (BSID-CR) for each child at 2 years of age. Mental developmental index (MDI) and psychomotor developmental index (PDI) from the BSID-CR were used as outcome variables. A generalized estimating equation (GEE) model was used to estimate the associations of prenatal and postnatal PM2.5 and PM10 exposure with offspring neurodevelopment. After adjusting for potential confounders, we found that both prenatal and early postnatal exposure to PM2.5 and PM10 were associated with decreased offspring MDI and PDI scores. Compared with prenatal exposure, the associations of early postnatal exposure to PM2.5 and PM10 with offspring MDI and PDI were stronger. This study indicates that exposure to ambient particulate matters, mainly during early postnatal period and to a lesser extent prenatally, is associated with impaired offspring neurodevelopment.

Effects of Dust Event Days on Influenza: Evidence from Arid Environments in Lanzhou

Airborne aerosol is believed to be an important pathway for infectious disease transmissions like COVID-19 and influenza. However, the effects of dust event days on influenza have been rarely explored, particularly in arid environments. This study explores the effects of ambient particulate matter (PM) and dust events on laboratory-confirmed influenza in a semi-arid city. A descriptive analysis of daily laboratory-confirmed influenza (influenza) cases, PM (PM10 and PM2.5), meteorological parameters, and dust events were conducted from 2014 to 2019 in Lanzhou, China. The case-crossover design combined with conditional Poisson regression models was used to estimate the lagging effects of PM and dust events on influenza. In addition, a hierarchical model was used to quantitatively evaluate the interactive effect of PM with ambient temperature and absolute humidity on influenza. We found that PM and dust events had a significant effect on influenza. The effects of PM10 and PM2.5 on influenza became stronger as the cumulative lag days increased. The greatest estimated relative risks (RRs) were 1.018 (1.011,1.024) and 1.06 1(1.034,1.087), respectively. Compared with the non-dust days, the effects of dust events with duration ≥ 1 day and with duration ≥ 2 days on influenza were the strongest at lag0 day, with the estimated RRs of 1.245 (95% CI: 1.061-1.463) and 1.483 (95% CI: 1.232-1.784), respectively. Subgroup analysis showed that pre-school children and school-aged children were more sensitive to PM and dust events exposure. Besides, we also found that low humidity and temperature had an interaction with PM to aggravate the risk of influenza. In summary, ambient PM and dust events exposure may increase the risk of influenza, and the risk of influenza increases with the dust events duration. Therefore, more efforts from the government as well as individuals should be strengthened to reduce the effect of PM on influenza, particularly in cold and dry weather.

The Role of Trees in Winter Air Purification on Children’s Routes to School

Air pollution is now considered to be the world’s largest environmental health threat, accounting for millions of deaths globally each year. The social group that is particularly exposed to the harmful effects of air pollution is children. Their vulnerability results from higher breathing frequency and being subject to concentration peaks just above the ground. The negative effects of ambient particulate matter also depend on the time of exposure. A daily route to school can constitute an important component of children’s physical activity, but air pollution can pose a threat to their health. Numerous studies have proved that high loads of PM can be effectively reduced by vegetation. Little is known, however, on whether vegetation can also reduce PM during leaf dormancy. In this study we investigated the role of trees in air purification during the leafless period in children’s routes to selected schools located in Warsaw during winter. The results obtained show a weak impact of the tree canopy in winter.

Respiratory and cardiovascular effects of ambient particulate matter from dust storm and non-dust storm periods in Kuwait

Epidemiological studies demonstrate a positive association between daily changes in concentrations of ambient airborne particulate matter (PM) and adverse respiratory and cardiovascular health effects. However, physicochemical properties of PM can vary greatly across geographical, atmospheric, and temporal conditions and influence the relative toxicity of airborne PM. The purpose of this study was to investigate the adverse pulmonary and cardiovascular health effects of ambient PM collected from discrete sampling sites in Kuwait during dust storm (DS) and non-dust storm (NDS) conditions. Collected dust samples were characterized for their chemical composition using atomic absorption, GC–MS, and HPLC–MS analyses. Male BALB/cJ mice were exposed to 100 µg of either NDS or dust storm (DS) PM in 50 µl of PBS by oropharyngeal aspiration. Lung function was measured and bronchoalveolar lavage was conducted at 1, 7, and 14 days post-exposure. Ischemia–reperfusion injury was performed 24 h after exposures by obstructing the left main coronary artery approximately 4 mm distal to its origin for 20 min, followed by 2 h. of reperfusion. Exposure to either NDS or DS PM resulted in airway hyperresponsiveness to acetylcholine compared to PBS controls. Total protein and cells in BAL fluid were elevated in both dust groups one day after exposure; however, DS PM induced a greater increase in cell numbers than did NDS PM, particularly in neutrophils, eosinophils, and lymphocytes. Representative lung sections exhibited positive staining for mucus in large airways at 7 days which resolved by 14 days in dust storm-exposed mice but persisted in NDS-exposed animals. Our findings suggest that NDS PM may be more effective in producing an adaptive immune response, while the early inflammation induced by DS PM may better resolve. We also observed a prolonged airway mucus response after exposure to NDS PM, suggesting it may produce more asthma-like features than dust storm PM. PM-induced changes to cardiac ischemia–reperfusion injury were not observed in this study. The lack of cardiovascular response may have been due to the limited exposure and single time point used in this study.

Greenness alleviates the effects of ambient particulate matter on the risks of high blood pressure in children and adolescents

Both ambient particulate matter (PM) and decrease of greenness have been suggested as risk factors for high blood pressure (HBP) in children and adolescents. But most evidence were from cross-sectional studies with limited data from prospective cohorts. In this cohort study, we included 588,004 children and adolescents aged 7 to 18 years without HBP from 2005 to 2018 in Beijing (240,081) and Zhongshan (347,923) city of China. The cumulative incidence of HBP was 32.04%, and incidence rate was 14.86 per 100 person-year. After adjustment for confounders, the ten-unit increase in PM1, PM2.5, and PM10 exposure was significantly associated with 43%, 70%, and 43%- higher risks of HBP, respectively, but the 0.1-unit increase in NDVI exposure was significantly associated with a 25% lower risk of HBP. The HRs of PM1 on the HBP risk were 1.486 and 1.150 in the low and the high-level of greenness, and they were 2.635 and 2.507 for PM2.5, and for PM10 1.367 and 1.702 in the two groups. The attributable fraction (AFs) of PM1, PM2.5, and PM10 on HBP incidents were 13.74%, 40.08%, and 15.47% in the low-level of greenness, which simultaneously was higher than those in the high-level of greenness (AF = 4.62%, 17.28%, and 9.96%). The exposure to higher ambient PM air pollution and lower greenness around schools were associated with a higher risk of HBP in children and adolescents, but higher greenness alleviated the adverse effects of ambient PM1 and PM2.5 on the HBP risks. Our findings highlighted a synergic strategy in preventing childhood HBP by decreasing air pollution reduction and improving greenness concurrently.

PM10 exposure interacts with abdominal obesity to increase blood triglycerides: a cross-sectional linkage study.

BackgroundBlood lipids and glucose levels dysregulation represent potential mechanisms intermediating the adverse cardiovascular effects of ambient particulate matter (PM) exposure. This study aims to estimate the effect of long-term PM10 exposure on blood lipids and glucose levels and to assess the potential mediation and/or modification action of abdominal obesity (AO) (waist-to-height ratio).MethodsOur study was based on 2,390 participants of the first Portuguese Health Examination Survey (INSEF, 2015) with available data on blood lipids and glucose parameters and living within a 30-km radius of an air quality monitoring station with available PM10 measurements. PM10 concentrations were acquired from the air quality monitoring network of the Portuguese Environment Agency. Generalized linear models were used to assess the effect of 1-year PM10 exposure on blood lipids and glucose levels. An interaction term was introduced in the models to test the modification action of AO.ResultsWe found an association between PM10 and non-fasting blood triglycerides (TG) after adjustment for age, sex, education, occupation, lifestyles-related variables and temperature but only in participants with AO. Per each 1 µg/m3 PM10 increment, there was a 1.84% (95% confidence interval: 0.02–3.69) increase in TG. For the remaining blood lipid and glucose parameters, no associations were found.ConclusionsOur study demonstrates that even at low levels of exposure, long-term PM10 exposure interacts with AO to increase blood TG. Our findings suggest that reducing both AO prevalence and PM10 below current standards would result in additional health benefits for the population.

Ambient particulate matter exposure interacts with abdominal obesity to increase blood triglycerides

Abstract Background Blood lipids levels dysregulation represent potential mechanism intermediating the adverse cardiovascular effects of ambient particulate matter (PM) exposure. The present study aims to estimate the effect of particulate matter (PM10) exposure on blood lipid levels (TC, Total Cholesterol; HDL-C, High-Density Lipoprotein Cholesterol; LDL-C, Low-Density Lipoprotein Cholesterol; TG, Triglycerides) in the adult Portuguese mainland population and to assess the potential mediation and/or modification action of abdominal obesity on this effect. Methods We used data from 2390 participants of the 1st Portuguese Health Examination Survey (INSEF, 2015) with available data on blood lipids parameters and living within a 30km radius of an air quality monitoring station with available PM10 measurements. PM10 concentrations were acquired from the air quality monitoring network of the Portuguese Environment Agency. Generalized linear models were used to assess the effect of 1-year PM10 exposure on blood lipids values. An interaction term was introduced in the models to test the modification action of abdominal obesity. Results We found an association between long-term exposure to PM10 and non-fasting blood TG levels after adjustment for age, sex, education, occupation, lifestyles related variables and temperature but only in participants with abdominal obesity (1.84% TG increase per each 1 µg/m3 PM10 increment, 95% CI: 0.02%; 3.69%) which is well supported by the sensitivity analysis. Conclusions Our study demonstrate that even at low levels of exposure, long-term PM10 exposure interacts with abdominal obesity to increase blood TG levels. To the best of our knowledge, this is the first study showing the modification action of abdominal obesity regarding the PM10 effect on a blood lipid parameter. Our findings suggest that reducing both abdominal obesity prevalence and PM10 below current standards would result in additional health benefits for the population. Key messages Long-term PM10 exposure interacts with abdominal obesity to increase non-fasting blood triglycerides levels by about 2% per each 1 µg/m3 PM10 increase. Reducing both abdominal obesity prevalence and PM10 below current standards would result in additional health benefits for the population.

Time series analysis of short-term effects of particulate matter pollution on the circulatory system disease mortality risk in Lishui District, China.

Epidemiological evidence has shown a significant association between short-term exposure to air pollution and mortality risk for circulatory system diseases (CSD). However, informative insights on the significance and magnitude of its relationship in the process of government interventions on abating air pollution are still lacking, particularly in a burgeoning Chinese city. In this study, we conducted a time series study in Lishui District, Nanjing, to examine the effect of ambient particulate matter (PM), e.g., PM2.5 and PM10, on daily death counts of CSD which included cardiovascular disease (CVD), cerebrovascular disease (CEVD), and arteriosclerotic heart disease (ASHD) mortality from January 1, 2015, to December 31, 2019. The results revealed that each 10μg/m3 increase in PM2.5 and PM10 concentration at lag0 day was associated with an increase of 1.33% (95% confidence interval, 0.08%, 2.60%) and 1.12% (0.43%, 1.82%) in CSD mortality; 2.42% (0.44%, 4.43%) and 1.43% (0.32%, 2.55%) in CVD mortality; 1.20% (- 0.31%, 2.73%) and 1.21% (0.38%, 2.05%) in CEVD mortality; and 2.78% (0.00%, 5.62%) and 1.66% (0.14%, 3.21%) in ASHD mortality, respectively. For cumulative risk, the corresponding increase in daily mortality for the same change in PM2.5 concentration at lag03 day was significantly associated with 1.94% (0.23%, 3.68%), 3.17% (0.58%, 5.84%), 2.38% (0.17%, 4.63%), and 4.92% (1.18%, 8.81%) for CSD, CVD, CEVD, and ASHD, respectively. The exposure-response curves were approximately nonlinear over the entire exposure range of the PM concentrations. We also analyzed the effect modifications by season (warm or cold), age group (0-64years, 65-74years, or ≥ 75years), and sex (male or female). Although not statistically significant, stratified analysis showed greater vulnerability to PM exposure for cold season, population over 65years of age, and female group.

Effects of ambient particulate matter (PM10) on prevalence of diabetes and fasting plasma glucose

Objective: To explore the effect of long-term exposure to ambient particulate matter (PM10) on the prevalence of diabetes and fasting plasma glucose (FPG). Methods: The subjects of the study were from the baseline population of "Jinchang Cohort", and 24 285 subjects were finally included after excluding incomplete home address information and diabetic diagnosis information. The demographic characteristics, lifestyle and health status of the survey subjects were collected through questionnaire, physical examination and laboratory tests. ArcGIS software was used to match the nearest environmental monitoring stations for each subject according to residential address. Two-year average concentrations of PM10 were calculated to estimate exposure level. The logistic regression and the multiple linear regression were conducted to assess the effects of ambient PM10 on the prevalence of diabetes and FPG. The restricted cubic spline was used to quantify the dose-response relationship. Stratified analysis and effect modification analysis were also performed. Results: The age of 24 285 participants was (49.32±8.60) years, and the BMI was (24.22±6.09) kg/m2. There were 13 950 (57.44%) males and 2 066 (8.51%) diabetic patients. After adjusting for confounders, for every 10 μg/m3 increase in the average PM10 concentration in the first two years of the survey, the prevalence of diabetes increased [OR (95%CI) =1.05 (1.01-1.09)]and the FPG level elevated [β (95%CI) = 0.061 (0.047-0.076) mmol/L]. The results of the restricted cubic spline analysis showed a nonlinear relationship between PM10 concentration and FPG level (P<0.001). Further subgroup analysis showed that female [OR (95%CI) =1.10 (1.03-1.18)], people over 50 years old [OR (95%CI) =1.06 (1.02-1.11) ], subjects with family history of diabetes [OR (95%CI) = 1.13 (1.04-1.23) ], and with hypertension [OR (95%CI) = 1.07 (1.02-1.12) ] had a stronger association between the prevalence of diabetes and PM10 exposure (all P interaction values were<0.05). The effects of PM10 on FPG were more significant in people older than 50 years[β (95%CI) = 0.080 (0.050-0.109) mmol/L], with family history of diabetes [β (95%CI) = 0.087 (0.036-0.137) mmol/L], and hypertension [β (95%CI) = 0.077 (0.046-0.108) mmol/L] (all P interaction values were<0.05). Conclusions: Long-term exposure to ambient PM10 increases the diabetes prevalence and FPG. People older than 50 years old, with family history of diabetes and hypertension could be more sensitive to the effects of PM10 exposure.