Ambient air pollution and lipoprotein-associated phospholipase A? in survivors of myocardial infarction.
ABSTRACT: BACKGROUND: Increasing evidence suggests a proatherogenic role for lipoprotein-associated phospholipase A? (Lp-PLA2). A meta-analysis of published cohorts has shown that Lp-PLA2 is an independent predictor of coronary heart disease events and stroke. OBJECTIVE: In this study, we investigated whether the association between air pollution and cardiovascular disease might be partly explained by increased Lp-PLA2 mass in response to exposure. METHODS: A prospective longitudinal study of 200 patients who had had a myocardial infarction was performed in Augsburg, Germany. Up to six repeated clinical examinations were scheduled every 4-6 weeks between May 2003 and March 2004. Supplementary to the multicenter AIRGENE protocol, we assessed repeated plasma Lp-PLA2 concentrations. Air pollution data from a fixed monitoring site representing urban background concentrations were collected. We measured hourly means of particle mass [particulate matter (PM) < 10 µm (PM??) and PM < 2.5 µm (PM(2.5)) in aerodynamic diameter] and particle number concentrations (PNCs), as well as the gaseous air pollutants carbon monoxide (CO), sulfur dioxide (SO?), ozone (O?), nitric oxide (NO), and nitrogen dioxide (NO?). Data were analyzed using mixed models with random patient effects. RESULTS: Lp-PLA2 showed a positive association with PM??, PM(2.5), and PNCs, as well as with CO, NO?, NO, and SO? 4-5 days before blood withdrawal (lag 4-5). A positive association with O? was much more immediate (lag 0). However, inverse associations with some pollutants were evident at shorter time lags. CONCLUSION: These preliminary findings should be replicated in other study populations because they suggest that the accumulation of acute and subacute effects or the chronic exposure to ambient particulate and gaseous air pollution may result in the promotion of atherosclerosis, mediated, at least in part, by increased levels of Lp-PLA2.
Project description:Particulate matter mass (PM), trace gaseous pollutants, and select volatile organic compounds (VOCs) with meteorological variables were measured in Logan, Utah (Cache Valley), for >4 weeks during winter 2017 as part of the Utah Winter Fine Particle Study (UWFPS). Higher PM levels for short time periods and lower ozone (O3) levels were present due to meteorological and mountain valley conditions. Nitrogenous pollutants were relatively strongly correlated with PM variables. Diurnal cycles of NOx, O3, and fine PM(PM 2.5) (aerodynamic diameter <2.5 ?m [PM2.5]) suggested formation from NOx. O3 levels increased from early morning into midafternoon, and NOx and PM2.5 increased throughout the morning, followed by sharp decreases. Toluene/benzene and xylenes/benzene ratios and VOC correlations with nitrogenous and PM species were indicative of local traffic sources. Wind sector comparisons suggested that pollutant levels were lower when winds were from nearby mountains to the east versus winds from northerly or southerly origins. Implications: The Cache Valley in Idaho and Utah has been designated a PM2.5 nonattainment area that has been attributed to air pollution buildup during winter stagnation events. To inform state implementation plans for PM2.5 in Cache Valley and other PM2.5 nonattainment areas in Utah, a state and multiagency federal research effort known as the UWFPS was conducted in winter 2017. As part of the UWFPS, the U.S. Environmental Protection Agency (EPA) measured ground-based PM species and their precursors, VOCs, and meteorology in Logan, Utah. Results reported here from the EPA study in Logan provide additional understanding of wintertime air pollution conditions and possible sources of PM and gaseous pollutants as well as being useful for future PM control strategies in this area.
Project description:Gene expression changes are linked to air pollutant exposures in in vitro and animal experiments. However, limited data are available on how these outcomes relate to ambient air pollutant exposures in humans. We performed an exploratory analysis testing whether gene expression levels were associated with air pollution exposures in a Los Angeles area cohort of elderly subjects with coronary artery disease. Candidate genes (35) were selected from published studies of gene expression-pollutant associations. Expression levels were measured weekly in 43 subjects (? 12 weeks) using quantitative PCR. Exposures included gaseous pollutants O3, nitrogen oxides (NOx), and CO; particulate matter (PM) pollutants elemental and black carbon (EC, BC); and size-fractionated PM mass. We measured organic compounds from PM filter extracts, including polycyclic aromatic hydrocarbons (PAHs), and determined the in vitro oxidative potential of particle extracts. Associations between exposures and gene expression levels were analyzed using mixed-effects regression models. We found positive associations of traffic-related pollutants (EC, BC, primary organic carbon, PM 0.25-2.5 PAH and/or PM 0.25 PAH, and NOx) with NFE2L2, Nrf2-mediated genes (HMOX1, NQO1, and SOD2), CYP1B1, IL1B, and SELP. Findings suggest that NFE2L2 gene expression links associations of traffic-related air pollution with phase I and II enzyme genes at the promoter transcription level.
Project description:In time-series studies of ambient air pollution and health in large urban areas, measurement errors associated with instrument precision and spatial variability vary widely across pollutants. In this paper, we characterize these errors for selected air pollutants and estimate their impacts on epidemiologic results from an ongoing study of air pollution and emergency department visits in Atlanta. Error was modeled for daily measures of 12 air pollutants using collocated monitor data to characterize instrument precision and data from multiple study area monitors to estimate population-weighted spatial variance. Time-series simulations of instrument and spatial error were generated for each pollutant, added to a reference pollutant time-series, and used in a Poisson generalized linear model of air pollution and cardiovascular emergency department visits. Reductions in risk ratio due to instrument precision error were less than 6%. Error due to spatial variability resulted in average risk ratio reductions of less than 16% for secondary pollutants (O(3), PM(2.5) sulfate, nitrate and ammonium) and between 43% and 68% for primary pollutants (NO(x), NO(2), SO(2), CO, PM(2.5) elemental carbon); pollutants of mixed origin (PM(10), PM(2.5), PM(2.5) organic carbon) had intermediate impacts. Quantifying impacts of measurement error on health effect estimates improves interpretation across ambient pollutants.
Project description:To review the evidence for the short term association between air pollution and stroke.Systematic review and meta-analysis of observational studiesMedline, Embase, Global Health, Cumulative Index to Nursing and Allied Health Literature (CINAHL), and Web of Science searched to January 2014 with no language restrictions.Studies investigating the short term associations (up to lag of seven days) between daily increases in gaseous pollutants (carbon monoxide, sulphur dioxide, nitrogen dioxide, ozone) and particulate matter (<2.5 µm or <10 µm diameter (PM2.5 and PM10)), and admission to hospital for stroke or mortality.Admission to hospital and mortality from stroke.From 2748 articles, 238 were reviewed in depth with 103 satisfying our inclusion criteria and 94 contributing to our meta-estimates. This provided a total of 6.2 million events across 28 countries. Admission to hospital for stroke or mortality from stroke was associated with an increase in concentrations of carbon monoxide (relative risk 1.015 per 1 ppm, 95% confidence interval 1.004 to 1.026), sulphur dioxide (1.019 per 10 ppb, 1.011 to 1.027), and nitrogen dioxide (1.014 per 10 ppb, 1.009 to 1.019). Increases in PM2.5 and PM10 concentration were also associated with admission and mortality (1.011 per 10 ?g/m(3) (1.011 to 1.012) and 1.003 per 10 µg/m(3) (1.002 to 1.004), respectively). The weakest association was seen with ozone (1.001 per 10 ppb, 1.000 to 1.002). Strongest associations were observed on the day of exposure with more persistent effects observed for PM(2·5).Gaseous and particulate air pollutants have a marked and close temporal association with admissions to hospital for stroke or mortality from stroke. Public and environmental health policies to reduce air pollution could reduce the burden of stroke.PROSPERO-CRD42014009225.
Project description:Ambient air pollution has been implicated in the development of hypertensive disorders of pregnancy (HDP). However, evidence of the association between air pollution and HDP is still limited, and the effects of gaseous air pollutants on HDP and their time windows of exposure have not been well studied.We used the Florida birth registry data to investigate the associations between air pollutants (NO2, SO2, PM(2.5), O3 and CO) and the risks of HDP in 22,041 pregnant women in Jacksonville, Florida, USA from 2004 to 2005. Further, we examined whether air pollution exposure during different time windows defined by trimesters and the entire pregnancy had different effects on HDP.The single-pollutant logistic regression model showed that exposure to four pollutants during the full pregnancy period was significantly associated with prevalence of HDP after adjusting for covariates: NO2 (OR=1.21, 95% CI 1.09 to 1.35), PM2.5 (OR=1.24, 95% CI 1.08 to 1.43), SO2 (OR=1.13, 95% CI 1.01 to 1.25) and CO (OR=1.12, 95% CI 1.03 to 1.22) per IQR increase. Similar effects were observed when first trimester exposure to NO2, SO2 and CO, and second trimester exposures to PM2.5 were examined. Consistent results were confirmed in multiple-pollutant models.This study suggests that exposure to high levels of air pollution during early pregnancy and the full gestational period was associated with increased prevalence of HDP in Florida, USA.
Project description:Cardiovascular disease is the number one cause of death globally and air pollution can be a contributing cause. Acute myocardial infarction and cardiac arrest are frequent manifestations of coronary heart disease. The objectives of the study were to investigate the association between 4 657 out-of-hospital cardiac arrests (OHCA) and hourly and daily outdoor levels of PM(10), PM(2.5), coarse fraction of PM (PM(10-2.5)), ultrafine particle proxies, NO(x), NO(2), O(3) and CO in Copenhagen, Denmark, for the period 2000-2010. Susceptible groups by age and sex was also investigated. A case-crossover design was applied. None of the hourly lags of any of the pollutants were significantly associated with OHCA events. The strongest association with OHCA events was observed for the daily lag4 of PM(2.5), lag3 of PM(10), lag3 of PM(10-2.5), lag3 of NO(x) and lag4 of CO. An IQR increase of PM(2.5) and PM(10) was associated with a significant increase of 4% (95% CI: 0%; 9%) and 5% (95% CI: 1%; 9%) in OHCA events with 3 days lag, respectively. None of the other daily lags or other pollutants was significantly associated with OHCA events. Adjustment for O(3) slightly increased the association between OHCA and PM(2.5) and PM(10). No susceptible groups were identified.
Project description:In the previous studies regarding the effects of exposure to ambient air pollution on biological markers and/or behavior of animals, the gaseous pollutants are not separated from the particulate matter (PM). Hence the synergetic effect of gaseous pollutants and PM was not considered. In this regard, current study was aimed to devolve a new method for separation of PM from gaseous pollutants. Also, the effect of exposure to fine particulate matter (PM2.5) on the Alzheimer and depressive cognitive-like behaviors in rats after 3 and 6 months were investigated. Three chambers were designed including exposure group 1 (PM2.5 plus gaseous pollutants alone), exposure group 2 (gaseous pollutants alone) and control group (clean air). Exposure time was 5 h per day (9.00 a.m.-2.00 p.m.) for 4 days per week. The concentration of PM2.5 and gaseous pollutants (O3, NO2, and SO2) were monitored in the exposure hours, continuously. Concentration of PM2.5 by beta attenuation method and concentration of O3, NO2, and SO2 by UV fluorescence was monitored. Also, the concentration of metals including Al, Cr, Mn, Pb, Cd, Ni, Fe, and Cu and 16-polycyclic aromatic hydrocarbons (PAHs) bound PM2.5 by inductively coupled plasma mass spectrometry (ICP-MS) and gas chromatography-mass spectrometry (GC-MS) were analyzed, respectively. Cognitive-like behavior related to Alzheimer and depressive behaviors were determined by Y maze and Force swimming. The concentration of PM2.5 in the 3 and 6 months exposure was higher than WHO guideline, significantly (p-value <0.05). The concentration of O3, NO2 and SO2 in the 3 and 6 months exposure was lower than WHO guideline, significantly (p-value <0.05). The order of metals in the PM2.5 according to mean concentration Al > Ca > Cu > Cd > Na > Fe > Cr > Ni > Mn > Pb. Also, the sum concentration of 16-PAHs in the PM2.5 in the 3 and 6 months exposure was 45.7 ± 37.15 ng/m3 and 30.04 ± 25.27 ng/m3, respectively. Exposure to PM2.5 cannot significantly increase Alzheimer and depressive cognitive-like behaviors in the rats. Also, a significant difference between male and female in Alzheimer and depressive cognitive-like behaviors not observed. •A new method for separation of PM2.5 from other PM in the ambient air by ECO-PM sampler was presented.•A new method for separation of PM2.5 from gaseous pollutants in the ambient air by HEPA filter and active carbon was presented.•Tow exposure groups including exposure 1: PM2.5 plus gaseous pollutants and exposure 2: gaseous pollutants only were designed for increased accuracy of the in-vivo study.•Exposure to PM2.5 cannot cause significant increased Alzheimer and depressive cognitive-like behaviors in the rats.
Project description:BACKGROUND:Epidemiological studies have reported associations between elevated air pollution and autism spectrum disorders (ASD). However, we hypothesized that exposure to air pollution that mimics real world scenarios, is a potential contributor to ASD. The exact etiology and molecular mechanisms underlying ASD are not well understood. Thus, we assessed whether changes in OXTR levels may be part of the mechanism linking PM2.5/gaseous pollutant exposure and ASD. The current in-vivo study investigated the effect of exposure to fine particulate matter (PM2.5) and gaseous pollutants on ASD using behavioral and molecular experiments. Four exposure groups of Wistar rats were included in this study: 1) particulate matter and gaseous pollutants exposed (PGE), 2) gaseous pollutants only exposed (GE), 3) autism-like model (ALM) with VPA induction, and 4) clean air exposed (CAE) as the control. Pregnant dams and male pups were exposed to air pollutants from embryonic day (E0) to postnatal day (PND21). RESULTS:The average?±?SD concentrations of air pollutants were: PM2.5: 43.8?±?21.1??g/m3, CO: 13.5?±?2.5?ppm, NO2: 0.341?±?0.100?ppm, SO2: 0.275?±?0.07?ppm, and O3: 0.135?±?0.01?ppm. The OXTR protein level, catalase activity (CAT), and GSH concentrations in the ALM, PGE, and GE rats were lower than those in control group (CAE). However, the decrements in the GE rats were smaller than other groups. Also in behavioral assessments, the ALM, PGE, and GE rats demonstrated a repetitive /restricted behavior and poor social interaction, but the GE rats had weaker responses compared to other groups of rats. The PGE and GE rats showed similar trends in these tests compared to the VPA rats. CONCLUSIONS:This study suggested that exposure to ambient air pollution contributed to ASD and that OXTR protein may serve as part of the mechanism linking them.
Project description:BACKGROUND: There are limited studies on the role of interaction between exposure to ambient air pollution and glutathione-S-transferase (GST) P1 on the risk of asthma/wheezing among children, which provided suggestive, but inconclusive results. METHODS: To assess the joint effect of air pollutants and GSTP1 on asthma/wheezing, we conducted a nationwide cross-sectional study of 3,825 children in Taiwan Children Health Study. The studied determinants were three GSTP1 Ile105Val (rs 1695) genotypes (Ile-Ile; Ile-Val and Val-Val) and expoure to ambient air pollutants. We used routine air-pollution monitoring data for ozone (O(3)) and particles with an aerodynamic diameter of 2.5 µm or less (PM(2.5)). The effect estimates were presented as odds ratios (ORs) per interquartile changes for PM(2.5) and O(3). FINDINGS: In a two-stage hierarchical model adjusting for confounding, the risk of asthma was negatively associated with PM(2.5) (adjusted odds ratio (OR) 0.60; 95% confidence interval (CI) 0.45, 0.82) and O(3) (OR 0.74; 95% CI 0.60, 0.90) among Ile105 homozygotes, but positively associated with PM(2.5) (OR 1.52; 95% CI 1.01, 2.27) and O(3) (OR 1.19; 95% CI 0.91, 1.57) among those with at least one val105 allele (interaction p value = 0.001 and 0.03, respectively). A similar tendency of effect modification between PM(2.5) and O(3) and GSTP1 on wheezing was found. CONCLUSION: Children who carried Ile105 variant allele and exposed to PM(2.5) and O(3) may be less likely to occurrence of asthma/wheezing.
Project description:There is now a large body of literature supporting a linkage between exposure to air pollutants and asthma morbidity. However, the extent and significance of this relationship varies considerably between pollutants, location, scale of analysis, and analysis methods. Our primary goal is to evaluate the relationship between asthma hospitalizations, levels of ambient air pollution, and weather conditions in Los Angeles (LA) County, California, an area with a historical record of heavy air pollution. County-wide measures of carbon monoxide (CO), nitrogen dioxide (NO(2)), ozone (O(3)), particulate matter<10 ?m (PM(10)), particulate matter<2.5 ?m (PM(2.5)), maximum temperature, and relative humidity were collected for all months from 2001 to 2008. We then related these variables to monthly asthma hospitalization rates using Bayesian regression models with temporal random effects. We evaluated model performance using a goodness of fit criterion and predictive ability. Asthma hospitalization rates in LA County decreased between 2001 and 2008. Traffic-related pollutants, CO and NO(2), were significant and positively correlated with asthma hospitalizations. PM(2.5) also had a positive, significant association with asthma hospitalizations. PM(10), relative humidity, and maximum temperature produced mixed results, whereas O(3) was non-significant in all models. Inclusion of temporal random effects satisfies statistical model assumptions, improves model fit, and yields increased predictive accuracy and precision compared to their non-temporal counterparts. Generally, pollution levels and asthma hospitalizations decreased during the 9 year study period. Our findings also indicate that after accounting for seasonality in the data, asthma hospitalization rate has a significant positive relationship with ambient levels of CO, NO(2), and PM(2.5).