Effects Of Fine Particulate Matter Research Articles

The effects of fine particulate matter, solid fuel use and greenness on the risks of diabetes in middle-aged and older Chinese.

Previous studies provided clues that environmental factors were closely related to diabetes incidence. However, the evidence from high-quality and large cohort studies about the effects of PM2.5, solid fuel use and greenness on the development of diabetes among middle-aged and older adults in China was scarce. To separately investigate the independent effects of PM2.5, solid fuel use and greenness on the development of diabetes among middle-aged and older adults. A total of 9242 participants were involved in this study extracted from the China Health and Retirement Longitudinal Study. Time-varying Cox regression was applied to detect the association of diabetes with PM2.5, solid fuel use and greenness, separately. The potential interactive effect of air pollution and greenness were explored using the relative excess risk due to interaction (RERI). Per 10 μg/m3 increases in PM2.5 were associated with 6.0% (95% CI: 1.9, 10.2) increasing risks of diabetes incidence. Females seemed to be more susceptible to PM2.5. However, the effects of solid fuel use only existed in older and lower BMI populations, with hazard ratios (HRs) of 1.404 (1.116, 1.766) and 1.346 (1.057, 1.715), respectively. In addition, exposure to high-level greenness might reduce the risks of developing diabetes [HR = 0.801 (0.687, 0.934)]. Weak evidence of the interaction effect of PM2.5/solid fuel use and greenness on diabetes was found. Both PM2.5 and solid fuel use were associated with the increasing incidence of diabetes. In addition, high-level greenness might be a beneficial environmental factor for reducing the risks of developing diabetes. All in all, our findings might provide valuable references for public health apartments to formulate very fruitful policies to reduce the burden of diabetes. Both PM2.5 and solid fuel use were associated with the increasing incidence of diabetes while high-level greenness was not, which might provide valuable references for public health apartments to make policies.

The acute effects of particulate air pollution on lung function in asthmatic children: A multicenter study with intensively repeated measurements

Evidence on the comparative effects of fine particulate matter (PM2.5) and coarse particulate matter (PM10-2.5) on the lung function of asthmatic children remained limited and inconsistent. This study aims to explore the acute effect of PM2.5 and PM10-2.5 on dynamic forced expiratory volume in 1 s (FEV1) and peak expiratory flow (PEF) among asthmatic children. We conducted a multicenter study and obtained intensively repeated measurements of FEV1 and PEF of clinically diagnosed asthmatic children in 89 Chinese cities from January 2017 to May 2021. Linear mixed-effects models combined with a polynomial distributed lag model were employed to evaluate the cumulative lag effect of PM2.5 and PM10-2.5 on daily FEV1 and PEF among asthmatic children. We also evaluated the effect modifications by sex, age, testing time, season, and region. A total of 590 clinically diagnosed asthmatic children with over 0.18 million dynamic lung function records were included in this study. The adverse effect of particulate matter on lung function occurred in a short term and could last for around one week. Specifically, both PM10-2.5 and PM2.5 were associated with decreases in PEF, but only PM10-2.5 could impair the measurements of FEV1. We found that an interquartile range increase in PM10-2.5 and PM2.5 were associated with 5.40 [95% confidence interval (CI): 0.88, 9.92] mL/s and 10.48 (95%CI: 5.14, 15.81) mL/s decrease in PEF, 6.46 (95%CI: 4.53, 8.40) mL and 0.25 (95%CI: −2.03, 2.54) mL decreases in FEV1, respectively. And the estimated effect of PM10-2.5 was stronger than PM2.5 on FEV1. Besides, these changes were larger in the evening and the south region of China. In conclusion, short-term exposure to both PM2.5 and PM10-2.5 could decrease the daily lung function of asthmatic children. The impact of PM10-2.5 was more hazardous than PM2.5.

Estimating future PM2.5-attributed acute myocardial infarction incident cases under climate mitigation and population change scenarios in Shandong Province, China

BackgroundThe effects of fine particulate matter (PM2.5) on acute myocardial infarction (AMI) have been widely recognized. However, no studies have comprehensively evaluated future PM2.5-attributed AMI burdens under different climate mitigation and population change scenarios. We aimed to quantify the PM2.5-AMI association and estimate the future change in PM2.5-attributed AMI incident cases under six integrated scenarios in 2030 and 2060 in Shandong Province, China. MethodsDaily AMI incident cases and air pollutant data were collected from 136 districts/counties in Shandong Province from 2017 − 2019. A two-stage analysis with a distributed lag nonlinear model was conducted to quantify the baseline PM2.5-AMI association. The future change in PM2.5-attributed AMI incident cases was estimated by combining the fitted PM2.5-AMI association with the projected daily PM2.5 concentrations under six integrated scenarios. We further analyzed the factors driving changes in PM2.5-related AMI incidence using a decomposition method. ResultsEach 10 μg/m3 increase in PM2.5 exposure at lag05 was related to an excess risk of 1.3 % (95 % confidence intervals: 0.9 %, 1.7 %) for AMI incidence from 2017 − 2019 in Shandong Province. The estimated total PM2.5-attributed AMI incident cases would increase by 10.9−125.9 % and 6.4–244.6 % under Scenarios 1 − 3 in 2030 and 2060, whereas they would decrease by 0.9–5.2 % and 33.0–46.2 % under Scenarios 5 – 6 in 2030 and 2060, respectively. Furthermore, the percentage increases in PM2.5-attributed female cases (2030: −0.3 % to 135.1 %; 2060: −33.2 % to 321.5 %) and aging cases (2030: 15.2–171.8 %; 2060: −21.5 % to 394.2 %) would wholly exceed those in male cases (2030: −1.8 % to 133.2 %; 2060: −41.1 % to 264.3 %) and non-aging cases (2030: −41.0 % to 45.7 %; 2060: −89.5 % to −17.0 %) under six scenarios in 2030 and 2060. Population aging is the main driver of increased PM2.5-related AMI incidence under Scenarios 1 − 3 in 2030 and 2060, while improved air quality can offset these negative effects of population aging under the implementation of the carbon neutrality and 1.5 °C targets. ConclusionThe combination of ambitious climate policies (i.e., 1.5 °C warming limits and carbon neutrality targets) with stringent clean air policies is necessary to reduce the health impacts of air pollution in Shandong Province, China, regardless of population aging.

Association of long-term exposure to air pollution with chronic sleep deprivation in South Korea: A community-level longitudinal study, 2008–2018

Background and objectiveAlthough there are many findings about the effects of fine particulate matter (PM2.5) and sleep deprivation on health respectively, the association between PM2.5 and chronic sleep deprivation has rarely been investigated. Thus, we aimed to investigate this association using a nationwide survey in South Korea. MethodWe examined the association between long-term exposure to PM2.5 and chronic sleep deprivation using a national cross-sectional health survey covering the entire 226 districts in inland South Korea from 2008 to 2018, with a machine learning-based national air pollution prediction model with 1 km2 spatial resolution. ResultsChronic sleep deprivation was positively associated with PM2.5 in the total population (odds ratio (OR): 1.09, 95% confidence interval (CI): 1.05–1.13) and sub-population (low, middle, high population density areas with OR: 1.127, 1.09, and 1.059, respectively). The association was consistently observed in both sexes (males with OR: 1.09, females with OR: 1.09)) and was more pronounced in the elderly population (OR: 1.12) than in the middle-aged (OR: 1.07) and young (OR: 1.09) populations. ConclusionsOur results are consistent with the hypothesis regarding the relationship between long-term PM2.5 exposure and chronic sleep deprivation, and the study provides quantitative evidence for public health interventions to improve air quality that can affect chronic sleep conditions.

Chemical Composition and Transgenerational Effects on Caenorhabditis elegans of Seasonal Fine Particulate Matter.

While numerous studies have demonstrated the adverse effects of fine particulate matter (PM) on human health, little attention has been paid to its impact on offspring health. The multigenerational toxic effects on Caenorhabditis elegans (C. elegans) were investigated by acute exposure. PM2.5 and PM1 samples were collected and analysed for their chemical composition (inorganic ions, metals, OM, PAHs) in different seasons from April 2019 to January 2020 in Lin'an, China. A higher proportion of organic carbon components (34.3%, 35.9%) and PAHs (0.0144%, 0.0200%) occupied the PM2.5 and PM1 samples in winter, respectively. PM1 in summer was enriched with some metal elements (2.7%). Exposure to fine PM caused developmental slowing and increased germ cell apoptosis, as well as inducing intestinal autofluorescence and reactive oxygen species (ROS) production. PM1 caused stronger toxic effects than PM2.5. The correlation between PM component and F0 generation toxicity index was analysed. Body length, germ cell apoptosis and intestinal autofluorescence were all highly correlated with Cu, As, Pb, OC and PAHs, most strongly with PAHs. The highest correlation coefficients between ROS and each component are SO42- (R = 0.743), Cd (R = 0.816) and OC (R = 0.716). The results imply that OC, PAHs and some transition metals play an important role in the toxicity of fine PM to C. elegans, where the organic fraction may be the key toxicogenic component. The multigenerational studies show that PM toxicity can be passed from parent to offspring, and gradually returns to control levels in the F3-F4 generation with germ cell apoptosis being restored in the F4 generation. Therefore, the adverse effects of PM on reproductive damage are more profound.

Long-term exposure to fine particulate matter modifies the association between physical activity and the risk of hypertension.

The trade-off between the potentially detrimental effects of fine particulate matter (PM2.5) and the benefits of physical activity (PA) is unclear. We aimed to explore the independent and interaction effects between long-term PM2.5 exposure and PA on blood pressure (BP) and hypertension. A total of 8704 adults (≥45 years) without hypertension at baseline in a nationwide cohort of the China Health and Retirement Longitudinal Study (CHARLS) were followed from 2011 to 2015. The participants were selected using a four-stage, stratified, and cluster sampling procedure. The annual PM2.5 concentrations at the residential address were estimated from a two-stage machine learning model with a 10 km × 10 km resolution. A standard questionnaire collected information on PA and potential confounders, and metabolic equivalents (MET·h/wk), which combined frequency, intensity, and duration information, were used to assess PA levels. We adopted mixed-effects regression models to explore the independent and interaction effects between long-term PM2.5 exposure and PA on BP and risk of hypertension. Systolic blood pressure (SBP) decreased by -0.84 mmHg (95% CI: -1.34, -0.34) per an IQR (interquartile range, 175.5 MET·h/wk) increase in PA, and diastolic blood pressure (DBP) decreased by -0.42 mmHg (95% CI: -0.76, -0.07). Each IQR (36.1 μg/m3) increment in PM2.5 was associated with 0.48 mmHg (95% CI: -0.24, 1.20) in SBP and -0.02 mmHg (95% CI: -0.44, 0.39) in DBP. PM2.5 showed an elevated effect with risks of hypertension (odds ratio, OR = 1.01; 95% CI: 1.00, 1.03), while PA showed the inverse result (OR = 0.98; 95% CI: 0.97, 0.99). Interaction analyses indicated PA maintained the beneficial effects on BP, but the negative association was attenuated, accompanied by the increase of PM2.5. PA decreased the BP and hypertension risks, while PM2.5 showed the opposite results. PM2.5 attenuated the beneficial effects of PA on BP and modified the association between PA and the risk of hypertension.

Atorvastatin ameliorated PM2.5-induced atherosclerosis in rats

PM2.5 provokes atherosclerotic events. Atorvastatin presents anti-inflammatory and antioxidant activities, and may ameliorate PM2.5-induced atherosclerosis development. The purpose of this study was to investigate the cardiotoxic effect of fine particulate matter (PM2.5) on atherosclerosis (AS) in rats, and the intervention effects of atorvastatin (ATO) on PM2.5-induced AS development. AS model was established using 32 male Wistar rats through intraperitoneal injection of vitamin D3 combined with a high-fat diet (10% fat and 4% cholesterol). The rats were randomly divided into 4 groups: control group, PM2.5-exposed group, ATO group, and ATO treated PM2.5-exposed group. PM2.5 increased levels of TC, TG, LDL, MDA, IL-6, and TNF-α, as well as decreased SOD levels. Besides, PM2.5 also enhanced AI. After the treatment of ATO, most levels of various contents in serum, including TC, TG, LDL, MDA, IL-6, TNF-α, hS-CRP, and ox-LDL, significantly decreased compared to the PM2.5-exposed group. Moreover, after the treatment of ATO, AI was significantly reduced compared to the PM2.5-exposed group. In addition, PM2.5 exacerbated the nuclear translocation and ATO resulted in an obvious decrease in PM2.5-induced nuclear translocation. The present study suggests that PM2.5 could induce oxidative damage and systemic inflammatory response in atherosclerosis model rats, while ATO could ameliorate PM2.5-induced atherosclerosis development, possibly by lowering lipid, inhibiting inflammation, and suppressing oxidation.

The mortality impact of fine particulate matter in China: Evidence from trade shocks

We use county-level panel data to estimate the long-run effect of fine particulate matter (PM 2.5 ) pollution on mortality in China. Our causal inference relies on changes in local pollution via wind transport and demand shocks of Chinese products from export destinations amid the global economic crisis during the late 2000s. We find an economically and statistically significant impact of long-term exposure to PM 2.5 on cardiovascular and respiratory mortality, and the effect is the largest for those 65 years and older. Using the substantial variation in pollution levels both across time and space in China, we provide evidence of a concave dose-response function, with diminishing marginal mortality impacts of pollution at levels beyond those in developed nations.

Real-time, single-particle chemical composition, volatility and mixing state measurements of urban aerosol particles in southwest China

To investigate the volatility of atmospheric particulates and the evolution of other particulate properties (chemical composition, particle size distribution and mixing state) with temperature, a thermodenuder coupled with a single particle aerosol mass spectrometer was used to conduct continuous observations of atmospheric fine particles in Chengdu, southwest China. Because of their complex sources and secondary reaction processes, the average mass spectra of single particles contained a variety of chemical components (including organic, inorganic and metal species). When the temperature rose from room temperature to 280°C, the relative areas of volatile and semi-volatile components decreased, while the relative areas of less or non-volatile components increased. Most (> 80%) nitrate and sulfate existed in the form of NH4NO3 and (NH4)2SO4, and their volatilization temperatures were 50–100°C and 150–280°C, respectively. The contribution of biomass burning (BB) and vehicle emission (VE) particles increased significantly at 280°C, which emphasized the important role of regional biomass burning and local motor vehicle emissions to the core of particles. With the increase in temperature, the particle size of the particles coated with volatile or semi-volatile components was reduced, and their mixing with secondary inorganic components was significantly weakened. The formation of K-nitrate (KNO3) and K-sulfate (KSO4) particles was dominated by liquid-phase processes and photochemical reactions, respectively. Reducing KNO3 and BB particles is the key to improving visibility. These new results are helpful towards better understanding the initial sources, pollution formation mechanisms and climatic effects of fine particulate matter in this megacity in southwest China.

Di-(2-ethylhexyl) phthalate aggravates fine particulate matter-induced asthma in weanling mice due to T follicular helper cell-dependent response

Environmental pollutants fine particulate matter and di-(2-ethylhexyl) phthalate (DEHP) are believed to be the risk factors for childhood asthma. Allergic asthma is basically an immediate hypersensitivity mediated by IgE, the product of humoral immune response. T follicular helper cells (Tfh) have been newly identified as the crucial T helper cells for supporting B cells to produce immunoglobulins in humoral immunity. Tfh cells are therefore potentially to serve as the diagnostic marker and therapeutic target of immune diseases. In this study, we examined the joint effects of fine particulate matter and DEHP on the initiation and progression of asthma and explored the fundamental role of Tfh cells during the process. Weanling C57BL/6 mice (both sexes) were concurrently exposed to DEHP (intragastric administration at 300 μg/kg) and fine atmospheric particulate matter (mean particle diameter < 4 µm, PM4) (oropharyngeal instillation at 2 mg/kg) once every three days for 30 days (10 times). We found that DEHP displayed adjuvant effects to potentiate PM4 allergen-induced expansion of Tfh and plasma cells, production of serum IgE and IgG1, and occurrence of airway hyper-responsiveness and inflammation. Then PM4 and DEHP co-exposure was performed to Cd4 knock-out mice reconstituted with normal wild-type adoptive Tfh cells or non-Tfh cells. The results of immune adoptive transfusion indicated that the joint immunotoxic effects of PM4 and DEHP were dependent on Tfh cells. We further proved that DEHP could adjuvantly boost PM4-induced expression of BCL-6 and c-MAF and secretion of IL-13 and IL-4 in Tfh cells. In conclusion, these data suggest that DEHP metabolites act in an adjuvant-like manner to aggravate PM4 allergen-induced asthma based on anaphylactic IgE response, resulting from excessive IL-13 and IL-4 synthesized by abnormally differentiated Tfh cells.

Effects of fine ambient particulate matters on de novo hypertensive disorders of pregnancy and blood pressure before 20 weeks

The effects of fine particulate matter (PM) on de novo hypertensive disorders of pregnancy (HDP) were inconsistent during the first and second trimesters. This study aimed to assess the trimester-specific effects of PM2.5 and PM1 prior to diagnosis of de novo HDP. The exposure of fine PM was predicted by satellite remote sensing data according to maternal residential addresses. De novo HDP was defined as gestational hypertension and preeclampsia during the current pregnancy. A logistic regression model was performed to assess the association of PM2.5 and PM1 with HDP during the first and early second trimesters (0–13 weeks and 14–20 weeks). The generalized estimating equation model was conducted to assess the effect of PM2.5 and PM1 on blood pressure. The present study included 22,821 pregnant women (mean age, 29.1 years) from 2013 to 2017. PM2.5 and PM1 were significantly associated with an increased risk of de novo HDP during the first trimester (OR = 1.070, 95% CI: 1.013–1.130; OR = 1.264, 95% CI: 1.058–1.511 for per 10 μg/m3) and early second trimester (OR = 1.045, 95% CI: 1.003–1.088; OR = 1.170, 95% CI: 1.002–1.366 for per 10 μg/m3). Significant trends of increased de novo HDP risk was also observed with the increment of PM (all P for trend <0.05). The stratified analyses demonstrated that the associations between exposure to fine PM and the risk of HDP were more pronounced among the pregnant women with maternal age above 35 and low maternal education level (all OR >1.047). Each 10 μg/m3 increase of PM1 and PM2.5 before diagnosis of de novo HDP elevated 0.204 (95% CI: 0.098–0.310) and 0.058 (95%CI: 0.033–0.083) mmHg of systolic blood pressure. Exposure to PM2.5 and PM1 during the first and early second trimester were positively associated with the risk of de novo HDP. The fine PM before diagnosis of de novo HDP elevated the systolic blood pressure.

The effects of fine particulate matter on the blood-testis barrier and its potential mechanisms.

With the rapid expansion of industrial scale, an increasing number of fine particulate matter (PM2.5) has bringing health concerns. Although exposure to PM2.5 hasbeen clearly associated with male reproductive toxicity, the exact mechanisms are still unclear. Recent studies demonstrated that exposure to PM2.5 can disturb spermatogenesis through destroying the blood-testis barrier (BTB), consisting of different junction types, containing tight junctions (TJs), gap junctions (GJs), ectoplasmic specialization (ES) and desmosomes. The BTB is one of the tightest blood-tissue barriers among mammals, which isolating germ cells from hazardous substances and immune cell infiltration during spermatogenesis. Therefore, once the BTB is destroyed, hazardous substances and immune cells will enter seminiferous tubule and cause adversely reproductive effects. In addition, PM2.5 also has shown to cause cells and tissuesinjury via inducing autophagy, inflammation, sex hormones disorder, and oxidative stress. However, the exact mechanisms of the disruption of the BTB, induced by PM2.5, are still unclear. It is suggested that more research is required to identify the potential mechanisms. In this review, we aim to understand the adverse effects on the BTB after exposure to PM2.5 and explore its potential mechanisms, which provides novel insight into accounting for PM2.5-induced BTB injury.

Acute effect of fine particulate matter and respiratory mortality in Changsha, China: a time-series analysis

BackgroundPrevious studies have confirmed that exposure to fine particulate matter (PM2.5) is associated with respiratory disease mortality. However, due to the differences in PM2.5 concentration, composition and population susceptibility within different regions, the estimates of the association between PM2.5 concentration and mortality are different. Moreover, few studies have examined the potential hazard of excessive PM2.5 exposure in terms of respiratory disease mortality.MethodsDaily recorded data on meteorological indices, environmental pollutants, and causes of death data in Changsha from January 2015 to December 2018 were obtained. The potential relationship between PM2.5 concentrations and respiratory disease mortality was determined using distributed lag nonlinear model (DLNM), which includes the relative risk (RR) and cumulative relative risk (CRR) of the lagged effect. The synergistic effects of other air pollutants were also considered.ResultsA total of 8,825 cases of respiratory disease mortality occurred in Changsha between 2015 and 2018. The acute effect of PM2.5 concentration was associated with an increased risk of respiratory disease mortality. Regarding the lag specific effect, a 10 μg/m3 increase in PM2.5 concentration on respiratory disease mortality was statistically significant at lag day 0 and lag day 7 with a relative risk of 1.019 (95% CI 1.007- 1.031) and 1.013(95%CI: 1.002-1.024). As for the cumulative lag effect, a 4-day moving average of PM2.5 concentrations was significantly associated with a cumulative relative risk of 1.027 (95%CI: 1.011-1.031). The single-day lag effect and cumulative 4-day lag effect for male individuals were more significant than those observed in females. The effect of PM2.5 concentrations and respiratory disease mortality remained statistically significant in the multi-pollutant models (SO2, NO2, and O3). A higher risk was observed in the cold season than in the warm season.ConclusionsOur findings show a potential association between exposure to PM2.5 concentration and respiratory disease mortality in Changsha, with male individuals observed to have particularly higher risk.

Association of Short-Term Exposure to PM2.5 with Blood Lipids and the Modification Effects of Insulin Resistance: A Panel Study in Wuhan.

Results of previous studies about the acute effects of fine particulate matter (PM2.5) on blood lipids were inconsistent. This study aimed to quantify the short-term effects of PM2.5 on blood lipids and estimate the modifying role of insulin resistance, reflected by the homeostasis model assessment of insulin resistance (HOMA-IR). From September 2019 to January 2020, the study recruited 70 healthy adults from Wuhan University for a total of eight repeated data collections. At each visit, three consecutive days were monitored for personal exposure to PM2.5, and then a physical examination was carried out on the fourth day. The linear mixed-effect models were operated to investigate the impact of PM2.5 over diverse exposure windows on blood lipids. With the median of the HOMA-IR 1.820 as the cut-off point, participants were assigned to two groups for the interaction analyses. We found the overall mean level (standard deviation, SD) of PM2.5 was 38.34 (18.33) μg/m3. Additionally, with a 10 μg/m3 rise in PM2.5, the corresponding largest responses in triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), as well as high-density lipoprotein cholesterol (HDL-C), were -0.91% (95% confidence interval (CI): -1.63%, -0.18%), -0.33% (95% CI: -0.64%, -0.01%,), -0.94% (95% CI: -1.53%, -0.35%), and 0.67% (95% CI: 0.32%, 1.02%), respectively. The interaction analyses revealed that a significantly greater reduction in the four lipids corresponded to PM2.5 exposure when in the group with the lower HOMA-IR (&lt;1.820). In conclusion, short-term PM2.5 exposure over specific time windows among healthy adults was associated with reduced TG, TC, as well as LDL-C levels, and elevated HDL-C. Additionally, the association of PM2.5-lipids may be modulated by insulin resistance.

Associations of personal PM2.5 and PM2.5-Bound polycyclic aromatic hydrocarbons exposure with blood lipid profiles: A panel study from middle-aged Chinese adults

Adverse effects of fine particulate matter (particulate matter ≤2.5 μm aerodynamic diameter, PM2.5) and PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) on blood lipid profiles remain uncertain. We designed a panel study with repeated measures. In this panel study, we enrolled 215 adult residents who participated in two study periods from the Wuhan-Zhuhai cohort. Personal 24-h PM2.5, sixteen kinds of 24-h PM2.5-bound PAHs, and blood lipid profiles were repeatedly measured across two study periods. We observed that an interquartile-range increase in four-ring or five-ring PAHs was linked with a 0.112 and 0.108 mmol/l increase in triglyceride, respectively in single-constituent models. These associations remained robust in both constituent-PM2.5 joint models and single-constituent residual models. Additionally, we observed that the significant relationships of four/five-ring PAHs with triglycerides were stronger among females, non-smokers, and participants without hypertension and diabetes. Bayesian kernel machine regression models further revealed that combining sixteen kinds of PM2.5-bound PAHs as a mixture of pollutants could result in a cumulative toxic effect on total cholesterol and triglycerides. No significant relationships were observed between personal PM2.5 exposure and blood lipid changes. Our findings suggest that exposure to PM2.5-bound PAHs may adversely affect lipid metabolism, which provides new evidence for formulating pollution abatement strategies for cardiovascular health.

Ambient fine particulate matter exposures and human early placental inflammation

The effect of fine particulate matter (PM2.5) on human early maternal–fetal interface is unknown. We explored the association between maternal exposure to ambient PM2.5 and inflammation in placental villus of 114 women with clinically recognized early pregnancy loss (CREPL) and 114 women with normal early pregnancy (NEP). Temporally-adjusted land use regression models were used to estimate maternal daily PM2.5 exposure during pregnancy. Villus interleukin-1beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were measured using multiplex cytokines detection platform. Single-day lag effect of PM2.5 exposure within ten days before early placental villus collection was estimated using multivariable linear regression model. Distributed lag and net cumulative effects of PM2.5 exposures within ten and 30 days before villus collection, as well as five single weeks during the periovulatory period, were estimated using distributed lag non-linear models. In all 228 subjects, after adjusting for group (CREPL or NEP), temporal confounders, and demographic characteristics, both single-day and distributed lag effects of PM2.5 exposure at lag 8 significantly increased villus IL-6; distributed lag effects of PM2.5 exposure in the first and second weeks before ovulation increased IL-1β, and PM2.5 exposure in the third week after ovulation increased IL-6 and TNF-α. In CREPL, single-day lag effect significantly increased IL-1β (at lag 1), IL-6 (at lag 8), and TNF-α (at lag 5); distributed lag effect increased IL-6 (at lag 4–lag 8) and TNF-α (at lag 4–lag 6); and cumulative effect within ten days before villus collection increased IL-6. There was no statistically significant cumulative effect in NEP. In summary, maternal PM2.5 exposure was associated with placental inflammation in human early pregnancy, particularly with increased villus IL-6 in CREPL. Whether maternal–fetal interface inflammation related to PM2.5 exposure during the periovulatory period or later contributes to CREPL or other adverse pregnancy outcomes requires further study.

Synergistic Effects of Particle Radioactivity (Gross β Activity) and Particulate Matter ≤2.5 μm Aerodynamic Diameter on Cardiovascular Disease Mortality.

Background Although the effects of fine particulate matter (particulate matter ≤2.5 μm aerodynamic diameter [PM2.5]) on cardiovascular disease (CVD) morbidity and mortality are well established, little is known about the CVD health effects of particle radioactivity. In addition, there are still questions about which of the PM2.5 physical, chemical, or biological properties are mostly responsible for its toxicity. Methods and Results We investigated the association between particle radioactivity, measured as gross β activity from highly resolved spatiotemporal predictions, and mortality for CVD, myocardial infarction, stroke, and all-cause nonaccidental mortality in Massachusetts (2001-2015). Within both difference-in-differences model and generalized linear mixed model frameworks, we fit both single-exposure and 2-exposure models adjusting for PM2.5 and examined the interaction between PM2.5 and gross β activity. We found significant associations between gross β activity and PM2.5 and each mortality cause. Using difference-in-differences and adjusting for PM2.5, we found the highest associations with myocardial infarction (rate ratio, 1.16 [95% CI, 1.08-1.24]) and stroke (rate ratio, 1.11 [95% CI, 1.04-1.18]) for an interquartile range increase (0.055millibecquerels per cubic meter) in gross β activity. We found a significant positive interaction between PM2.5 and gross β activity, with higher associations between PM2.5 and mortality at a higher level of gross β activity. We also observed that the associations varied across age groups. The results were comparable between the 2 statistical methods also with and without adjusting for PM2.5. Conclusions This is the first study that, using highly spatiotemporal predictions of gross β-activity, provides evidence that particle radioactivity increases CVD mortality and enhances PM2.5 CVD mortality. Therefore, particle radioactivity can be an important property of PM2.5 that must be further investigated. Addressing this important question can lead to cost-effective air-quality regulations.

Causal modeling of the effects of fine particulate matter and nitrogen dioxide on natural-cause mortality within the ELAPSE project

Causal modeling of the effects of fine particulate matter and nitrogen dioxide on natural-cause mortality within the ELAPSE project

The synergistic effects of Particle Radioactivity (Gross Beta Activity) and PM2.5 on Cardiovascular Diseases Mortality

BACKGROUND: Although the effects of fine particulate matter (particulate matter &amp;#x2264;2.5 &amp;#x3bc;m aerodynamic diameter; PM₂.₅) on cardiovascular diseases (CVD) morbidity and mortality are well established, little is known about CVD health effects of particle radioactivity (PR). In addition, there are still questions about which of the PM₂.₅ physical, chemical, or biological properties are mostly responsible for its toxicity. METHODS: We investigated the association between PR, measured as gross β-activity from highly resolved spatiotemporal predictions, and mortality for CVD, myocardial infarction, stroke, and all-cause non-accidental mortality in Massachusetts (2001-2015). Within both difference-in-difference (DID) approach and generalized linear mixed-effect model frameworks, we fit gross β-activity-alone, PM2.5 alone, gross β-activity&amp;#x26;PM₂.₅ models and examined the interaction between PM₂.₅ and gross β-activity. RESULTS: We found significant associations between gross β-activity/PM₂.₅ and each mortality cause. Using the DID approach and adjusting for PM₂.₅, we found the highest associations with MI (RR=1.16, 95% CI: 1.08, 1.24) and stroke (RR=1.11, 95% CI: 1.04, 1.18) for an IQR increase (0.055 mBq/m3) in gross β-activity. We found a significant positive interaction between PM₂.₅ and gross β-activity, with higher associations between PM₂.₅ and mortality at a higher level of gross β-activity. We also observed that the associations varied across age groups. The results were comparable between the two statistical methods with and without adjusting for PM₂.₅. CONCLUSIONS: This is the first study that, using highly spatiotemporal predictions of gross β-activity, provides evidence that PR increases CVD mortality and enhances PM₂.₅ CVD mortality. Therefore, PR can be an important property of PM₂.₅ that must be further investigated. Addressing this important question can lead to cost-effective air quality regulations. KEYWORDS: cardiovascular disease; death; particle radioactivity; death

Comparison of the Chemical Characteristics and Toxicity of PM2.5 Collected Using Different Sizes of Cyclones

Cyclone sampling devices have been helpful in assessing the toxic effects of fine particulate matter (PM2.5). The particle collection efficiency of sampling devices is critical. This study investigated the effect of cyclone size on particle size, chemical composition, and particle toxicity. Three cyclones with different inner diameters (12–68 mm) were tested for penetration using an aerodynamic particle sizer, fluorescent polystyrene latex, and a differential mobility analyzer. The elemental and water-soluble ion compositions of the particles collected by different cyclones were compared. An evaluation of the particles’ toxicity was conducted by comparing the results of dithiothreitol (DTT), limulus amebocyte lysate (LAL), and cell exposure assays. The experimental evaluation showed a 50% cut-size of the cyclones between 0.17–0.28, 0.34–0.36, and 0.70 μm for the small, medium, and large cyclones, respectively. To collect PM2.5 and evaluate separation performance in the real environment, the small and large cyclones were selected according to the particle penetration and flow rate. A comparison of chemical composition and enrichment factor values found that the particles in the small cyclone samples contained smaller and more anthropogenic sources than those in the large cyclone samples. The oxidative potential (OP) measured by the DTT assay of the samples collected using the small and large cyclones differed across sampling periods and associated with the transition metals. The viability of human epithelial A549 cells after exposure to the collected particles using the cyclones was different across sampling periods and associated with OP. The endotoxin concentrations measured in the LAL assay were found only in the large cyclone samples; they affected the estimated level of cytokine based on IL(interleukin)-6 release from human leukemia monocytic (THP-1) cells derived macro-phage-like cells. Regardless of the size, the cyclone techniques used in this study to collect aerosol particles would be a powerful tool for a detailed evaluation of particle toxicity.