Effects Of PM Exposure Research Articles

Risk of De Novo Hypertensive Disorders of Pregnancy After Exposure to PM1 and PM2.5 During the Period From Preconception to Delivery: Birth Cohort Study.

Particulate matter (PM) is detrimental to the respiratory and circulatory systems. However, no study has evaluated the lag effects of weekly exposure to fine PM during the period from preconception to delivery on the risk of hypertensive disorders of pregnancy (HDPs). We set out to investigate the lag effect windows of PM on the risk of HDPs on a weekly scale. Data from women with de novo HDPs and normotensive pregnant women who were part of the Peking University Retrospective Birth Cohort, based on the hospital information system of Tongzhou district, were obtained for this study. Meteorological data and data on exposure to fine PM were predicted by satellite remote sensing data based on maternal residential address. The de novo HDP group consisted of pregnant women who were diagnosed with gestational hypertension or preeclampsia. Fine PM was defined as PM2.5 and PM1. The gestational stage of participants was from preconception (starting 12 weeks before gestation) to delivery (before the 42nd gestational week). A distributed-lag nonlinear model (DLNM) was nested in a Cox regression model to evaluate the lag effects of weekly PM exposure on de novo HDP hazard by controlling the nonlinear relationship of exposure-reaction. Stratified analyses by employment status (employed or unemployed), education level (higher or lower), and parity (primiparity or multiparity) were performed. A total of 22,570 pregnant women (mean age 29.1 years) for whom data were available between 2013 and 2017 were included in this study. The prevalence of de novo HDPs was 6.7% (1520/22,570). Our findings showed that PM1 and PM2.5 were significantly associated with an elevated hazard of HDPs. Exposure to PM1 during the 5th week before gestation to the 6th gestational week increased the hazard of HDPs. A significant lag effect of PM2.5 was observed from the 1st week before gestation to the 6th gestational week. The strongest lag effects of PM1 and PM2.5 on de novo HDPs were observed at week 2 and week 6 (hazard ratio [HR] 1.024, 95% CI 1.007-1.042; HR 1.007, 95% CI 1.000-1.015, respectively, per 10 μg/m3 increase). The stratified analyses indicated that pregnant women who were employed, had low education, and were primiparous were more vulnerable to PM exposure for de novo HDPs. Exposure to PM1 and PM2.5 was associated with the risk of de novo HDPs. There were significant lag windows between the preconception period and the first trimester. Women who were employed, had low education, and were primiparous were more vulnerable to the effects of PM exposure; more attention should be paid to these groups for early prevention of de novo HDPs.

The role of PP2A /NLRP3 signaling pathway in ambient particulate matter 2.5 induced lung injury

Ambient particulate matter 2.5 (PM2.5) exposure has been linked to pulmonary fibrosis. However, the key signaling pathways remained unclear. In the present study, we applied a mouse model with myeloid-specific deletion of Ppp2r1a gene (encoding protein phosphatase 2 A (PP2A) A subunit) to identify the key signaling pathways involved in PM2.5-induced pulmonary fibrosis. PP2A Aα−/− homozygote mice and matched wild-type (WT) littermates were exposed to filtered air (FA), unfiltered air (UA), and concentrated PM2.5 (CA) in a real-ambient PM exposure system for 8 weeks and 16 weeks, respectively. The mice exposed to PM2.5 displayed a progressive inflammation and pulmonary fibrosis. Moreover, the expressions of NLRP3, pro-caspase-1, caspase-1, ASC and IL-1β were increased in mice lung following PM2.5 exposure, indicating PM2.5 exposure caused pulmonary inflammation by the NLRP3 pathways activation. Furthermore, the effects of PM exposure on pulmonary inflammation, pulmonary fibrosis, oxidative stress, and pulmonary function damage were significantly enhanced in PP2A−/− mice compared to WT mice, indicating the role of PP2A in the regulation of pulmonary injury induced by PM exposure. In vitro study confirmed that PP2A was involved in the PM2.5-induced inflammation response and NLRP3 inflammasome activation. Importantly, we identified PP2A regulated the activation of NLRP3 pathways by direct dephosphorylating IRE1α in response to PM2.5 exposure. Taken together, our results demonstrated that PP2A-IRE1α-NLRP3 signaling pathway played a crucial role in regulating the inflammation response, triggering the lung fibrogenesis upon PM2.5 exposure. Our findings provide new insights into regulatory role of PP2A in human diseases upon the PM exposure.

Exposure to combustion derived particulate matter exacerbates influenza infection in neonatal mice by inhibiting IL22 production

BackgroundParticulate matter (PM) containing environmentally persistent free radicals (EPFRs) are formed during various combustion processes, including the thermal remediation of hazardous wastes. Exposure to PM adversely affects respiratory health in infants and is associated with increased morbidity and mortality due to acute lower respiratory tract infections. We previously reported that early-life exposure to PM damages the lung epithelium and suppresses immune responses to influenza virus (Flu) infection, thereby enhancing Flu severity. Interleukin 22 (IL22) is important in resolving lung injury following Flu infection. In the current study, we determined the effects of PM exposure on pulmonary IL22 responses using our neonatal mouse model of Flu infection.ResultsExposure to PM resulted in an immediate (0.5–1-day post-exposure; dpe) increase in IL22 expression in the lungs of C57BL/6 neonatal mice; however, this IL22 expression was not maintained and failed to increase with either continued exposure to PM or subsequent Flu infection of PM-exposed mice. This contrasts with increased IL22 expression in age-matched mice exposed to vehicle and Flu infected. Activation of the aryl hydrocarbon receptor (AhR), which mediates the induction and release of IL22 from immune cells, was also transiently increased with PM exposure. The microbiome plays a major role in maintaining epithelial integrity and immune responses by producing various metabolites that act as ligands for AhR. Exposure to PM induced lung microbiota dysbiosis and altered the levels of indole, a microbial metabolite. Treatment with recombinant IL22 or indole-3-carboxaldehyde (I3A) prevented PM associated lung injury. In addition, I3A treatment also protected against increased mortality in Flu-infected mice exposed to PMs.ConclusionsTogether, these data suggest that exposure to PMs results in failure to sustain IL22 levels and an inability to induce IL22 upon Flu infection. Insufficient levels of IL22 may be responsible for aberrant epithelial repair and immune responses, leading to increased Flu severity in areas of high PM.

Seasonal effects of ambient PM2.5 on the cardiovascular system of hyperlipidemic mice

ABSTRACTPeople in polluted communities are often exposed to both PM and ozone (O3), albeit not always simultaneously; an important question is whether exposure to particles with seasonal compositional differences can influence biological outcomes. We addressed this question using a mouse model of cardiovascular disease by contrasting the health outcomes of exposures to particles formed or aged during periods of relatively high photochemical activity (i.e. spring/summer), which has increased ambient O3 concentrations, with outcomes of exposures to fall/winter particles which are associated with lower O3 concentrations. Electrocardiographs (ECGs) and blood pressures (BPs) were acquired following exposures to concentrated ambient particles (CAPs). ECGs were analyzed to changes in specific waveform parameters and changes in heart rate variability (HRV). Exposures elicited several types of waveform abnormalities that were associated with seasonal differences in particle constituents. Alterations in R-R interval and P-R interval were seen following exposure to summer CAPs but not fall CAPs and differential responses were seen in the corrected Q-T interval following the two seasonal exposures. Measures of HRV increased after exposure to summer CAPs compared to air-exposed controls but not following the winter CAPs exposure. There were chemical differences with respect to the organic constituents in ambient particles between summer and fall aerosol. The oxygen to carbon ratios (O:C) were generally higher in the spring and summer than in the fall, consistent with seasonal differences in atmospheric photochemical activity. Seasonal differences in atmospheric photochemical activity can modify ambient aerosol composition and can alter biological responses in the cardiovascular system. The results from this study confirm that ambient photochemical activity can alter the toxicity of ambient PM. Regional and seasonal differences in PM2.5 composition should be important considerations when evaluating the effects of PM exposure on cardiovascular health.Implications: Particles formed during periods of high photochemical activity (e.g. spring/summer) elicit more adverse cardiovascular health effects than particles formed during periods of low photochemical activity (e.g. fall/winter). Seasonal differences in atmospheric photochemical activity modified ambient aerosol composition and worsened cardiovascular responses. These results can inform regulatory agencies and may help design air quality regulations for PM2.5 that consider seasonal and regional variations.

Proteomic changes driven by urban pollution suggest particulate matter as a deregulator of energy metabolism, mitochondrial activity, and oxidative pathways in the rat brain

The adverse effects of air pollution have been long studied in the lung and respiratory systems, but the molecular changes that this causes at the central nervous system level have yet to be fully investigated and understood. To explore the evolution with time of protein expression levels in the brain of rats exposed to particulate matter of different sizes, we carried out two-dimensional gel electrophoresis followed by determination of dysregulated proteins through Coomassie blue staining-based densities (SameSpots software) and subsequent protein identification using MALDI-based mass spectrometry. Expression differences in dysregulated proteins were found to be statistically significant with p-value <0.05. A systems biology-based approach was utilized to determine critical biochemical pathways involved in the rats' brain response. Our results suggest that rats' brains have a particulate matter size dependent-response, being the mitochondrial activity and the astrocyte function severely affected. Our proteomic study confirms the dysregulation of different biochemical pathways involving energy metabolism, mitochondrial activity, and oxidative pathways as some of the main effects of PM exposure on the rat brain. SignificanceRat brains exposed to particulate matter with origin in car engines are affected in two main areas: mitochondrial activity, by the dysregulation of many pathways linked to the respiratory chain, and neuronal and astrocytic function, which stimulates brain changes triggering tumorigenesis and neurodegeneration.

Particulate matter exposure is associated with inflammatory gene methylation in obese subjects

BackgroundOverweight and obesity are becoming more widespread with alarming projections for the coming years. Obesity may increase susceptibility to the adverse effects of PM exposure, exacerbating the effects on cardiovascular diseases and altering the biomarkers of vascular inflammation. The associated biological mechanisms have not been fully understood yet; the common denominator in the pathogenesis of the co-morbidities of obesity is the presence of an active, low-grade inflammatory process. DNA methylation has been shown to regulate inflammatory pathways that are responsible for the development of cardiovascular diseases. ObjectivesThe aim of the study was to investigate, in a population of overweight/obese subjects, the effects of PM on blood DNA methylation in genes associated to inflammatory response. MethodsUsing bisulfite pyrosequencing, we measured DNA methylation in peripheral blood mononuclear cells from 186 overweighted/obese subjects. In particular, we quantified DNA methylation in a set of 3 candidate genes, including CD14, TLR4 and TNF-α, because of the important roles that these genes play in the inflammatory pathway. Personal exposure to PM10 was estimated for each subject based on the local PM10 concentrations, measured by monitoring stations at residential address. Repeated measure models were used to evaluate the association of PM10 with each genes, accounting for possible correlations among the genes that regulate the same inflammatory pathway. ResultsWe found an inverse association between the daily PM10 exposure and the DNA methylation of inflammatory genes, measured in peripheral blood of healthy overweight/obese subjects. Considering different exposure time-windows, the effect on CD14 and TLR4 methylation was observed, respectively, in days 4–5-6, and days 6–7-8. TNF-α methylation was not associated to PM10. ConclusionsOur findings support a picture in which PM10 exposure and transcriptional regulation of inflammatory gene pathway in obese subjects are associated.

Particulate matter components and subclinical atherosclerosis: common approaches to estimating exposure in a Multi-Ethnic Study of Atherosclerosis cross-sectional study

BackgroundConcentrations of outdoor fine particulate matter (PM2.5) have been associated with cardiovascular disease. PM2.5 chemical composition may be responsible for effects of exposure to PM2.5.MethodsUsing data from the Multi-Ethnic Study of Atherosclerosis (MESA) collected in 2000–2002 on 6,256 US adults without clinical cardiovascular disease in six U.S. metropolitan areas, we investigated cross-sectional associations of estimated long-term exposure to total PM2.5 mass and PM2.5 components (elemental carbon [EC], organic carbon [OC], silicon and sulfur) with measures of subclinical atherosclerosis (coronary artery calcium [CAC] and right common carotid intima-media thickness [CIMT]). Community monitors deployed for this study from 2007 to 2008 were used to estimate exposures at baseline addresses using three commonly-used approaches: (1) nearest monitor (the primary approach), (2) inverse-distance monitor weighting and (3) city-wide average.ResultsUsing the exposure estimate based on nearest monitor, in single-pollutant models, increased OC (effect estimate [95% CI] per IQR: 35.1 μm [26.8, 43.3]), EC (9.6 μm [3.6,15.7]), sulfur (22.7 μm [15.0,30.4]) and total PM2.5 (14.7 μm [9.0,20.5]) but not silicon (5.2 μm [−9.8,20.1]), were associated with increased CIMT; in two-pollutant models, only the association with OC was robust to control for the other pollutants. Findings were generally consistent across the three exposure estimation approaches. None of the PM measures were positively associated with either the presence or extent of CAC. In sensitivity analyses, effect estimates for OC and silicon were particularly sensitive to control for metropolitan area.ConclusionEmploying commonly-used exposure estimation approaches, all of the PM2.5 components considered, except silicon, were associated with increased CIMT, with the evidence being strongest for OC; no component was associated with increased CAC. PM2.5 chemical components, or other features of the sources that produced them, may be important in determining the effect of PM exposure on atherosclerosis. These cross-sectional findings await confirmation in future work employing longitudinal outcome measures and using more sophisticated approaches to estimating exposure.

Can mortality displacement mask thresholds in the concentration-response relation between particulate matter air pollution and mortality?

Abstract Two critical issues for public health assessment and regulation of exposure to particulate matter air pollution (PM) are whether there is a threshold in the concentration-response relation between PM and mortality and whether there is mortality displacement. In this vein, a number of time-series studies have concluded that a linear relation without a threshold is appropriate for describing the concentration-response relation, and a number of other studies have concluded that the mortality effects of PM exposure cannot be attributed to mortality displacement alone. Using three-state (healthy, frail, dead) population models that incorporate actual time series data from Cook County, Illinois for the period 1987–2000, the author investigates the shape of the concentration-response relation between PM and mortality, as observable from time-series data, in the presence of mortality displacement. It is found that thresholds in the concentration-response relation can be masked, or hidden, by linear concentration-response relations if some of the effect of PM exposure is attributable to mortality displacement. This is an important finding that has implications for studies that have found a linear concentration-response relation appropriate, particularly given the markedly different implications for public health assessment and regulation of a linear versus threshold concentration-response relation.

Acute exposure to elevated PM2.5 generated by traffic and cardiopulmonary health effects in healthy older adults

There are evidences for exposure to vehicular emissions and adverse cardiopulmonary health effects. This study attempted to further explore these effects on elderly. This study monitored personal PM(2.5) concentrations and ambulatory electrocardiograms continuously for 24 h on 1 working day in 3 separate weeks for 11 school crossing guards. Spirometry was also performed before and after the morning shift. The traffic at each work location was video recorded during one of the three morning shifts. The increases in the average personal PM(2.5) concentrations (baseline PM(2.5) was subtracted) of 1.2-87 and 1.1-98 microg/m(3) were observed during the 1-h morning (DeltaPM(2.5-ave-m)) and afternoon shift (DeltaPM(2.5-ave-a)), respectively. Traffic count was not a significant predictor of the DeltaPM(2.5-ave-m) (P=0.78). Mean heart rate variability (HRV), measured as 5-min standard deviation of normal-to-normal (SDNN) beats during the 10-min rest periods, decreased 18-26% (P<0.02) 15 min, 2 and 4 h after the morning shift, but changes in SDNN (DeltaSDNN) were insignificant post-afternoon exposure (-0.3 to -7% with P>0.53). DeltaSDNN were negatively associated with DeltaPM(2.5-ave-m), with the strongest association at 2 h after the morning shift (P<0.01) but insignificant 4 h after the morning exposure. The peak PM(2.5) concentration (DeltaPM(2.5-peak), baseline PM(2.5) was subtracted) was not a significant predictor for DeltaSDNN, and no clear effect of PM(2.5) exposure on heart rate was observed. There was no effect of PM exposure on lung function (P>0.16), either. In conclusion, acute exposure to the PM(2.5) resulting from mobile sources can cause acute decline in HRV in healthy older adults, suggesting one of the biological mechanisms for the adverse cardiovascular health effects associated with traffic-related air pollution. Traffic count may not be an appropriate surrogate measure of acute personal exposure to vehicular emission in traffic congested areas.

Performance evaluation of the active-flow personal DataRAM PM2.5 mass monitor (Thermo Anderson pDR-1200) designed for continuous personal exposure measurements

The need for continuous personal monitoring for exposure to particulate matter has been demonstrated by recent health studies showing effects of PM exposure on time scales of less than a few hours. Filter-based methods cannot measure this short-term variation of PM levels, which can be quite significant considering human activity patterns. The goal of this study was to evaluate the active-flow personal DataRAM for PM 2.5 (MIE pDR-1200; Thermo Electron Corp., Franklin, MA) designed as a wearable monitor to continuously measure particle exposure. The instrument precision was found to be good (2.1%) and significantly higher than the passive pDR configuration tested previously. A comparison to other proven continuous monitors resulted in good agreement at low relative humidities. Results at higher humidity followed predictable trends and provided a correction scheme that improved the accuracy of pDR readings. The pDR response to particle size also corresponded to previously observed and theoretical errors. The active flow feature of the pDR allows collection of the sampled particles on a back-up filter. The 24-h mass measured on this filter was found to compare very well with a Federal Reference Method for PM 2.5 mass.

Performance evaluation of the active-flow personal DataRAM PM2.5 mass monitor (Thermo Anderson pDR-1200) designed for continuous personal exposure measurements

Abstract The need for continuous personal monitoring for exposure to particulate matter has been demonstrated by recent health studies showing effects of PM exposure on time scales of less than a few hours. Filter-based methods cannot measure this short-term variation of PM levels, which can be quite significant considering human activity patterns. The goal of this study was to evaluate the active-flow personal DataRAM for PM2.5 (MIE pDR-1200; Thermo Electron Corp., Franklin, MA) designed as a wearable monitor to continuously measure particle exposure. The instrument precision was found to be good (2.1%) and significantly higher than the passive pDR configuration tested previously. A comparison to other proven continuous monitors resulted in good agreement at low relative humidities. Results at higher humidity followed predictable trends and provided a correction scheme that improved the accuracy of pDR readings. The pDR response to particle size also corresponded to previously observed and theoretical errors. The active flow feature of the pDR allows collection of the sampled particles on a back-up filter. The 24-h mass measured on this filter was found to compare very well with a Federal Reference Method for PM2.5 mass.