Complex Mixture Of Particulate Matter Research Articles

Trend Analysis of Occupational Lung Cancer from Coke Oven Emission Exposure - China, 2008-2019.

What is already known about this topic?Coke oven emissions are a complex mixture of particulate matter and gases, some with carcinogenicity, released during coke production. Lung cancer caused by coke oven emissions has been listed as a statutory occupational cancer in China and many countries.What is added by this report?In this study, coke oven emissions-induced lung cancer was mainly found in the manufacturing industries. Coke oven workers exposed to higher levels of polycyclic aromatic hydrocarbons in different workplaces had a high risk of occupational lung cancer.What are the implications for public health practice?It is necessary to take efforts to greatly reduce emissions from coke production and effectively monitor the health of workers.

Black Carbon - A Silent Contributor to Climate Change

Black carbon is a potent climate-warming component of particulate matter formed by the incomplete combustion of fossil-fuels, wood and other fuels. Complete combustion would turn all the carbon in the fuel into carbon dioxide, but combustion is never complete, and CO2, CO, volatile organic compounds, organic compounds, and black carbon particles are formed in the process. It contributes to warming by converting incoming solar radiation to heat. When deposited on ice and snow, BC and co-emitted particles reduce surface albedo thereby melting the glaciers. The complex mixture of particulate matter resulting from incomplete combustion is referred as soot. When suspended in the atmosphere, black carbon contributes to warming by converting incoming solar radiations to heat. It also influences cloud formation and impacts regional circulation and rainfall pattern. The Artic and the glaciated regions such as Himalayas are particularly vulnerable to melting as a result. The present paper aims to review the work done on black carbon and its mitigation measure.

Associations between Ambient Particulate Matter (PM2.5), Endothelial Dysfunction and Inflammation

TPS 683: Short-term health effects of air pollutants 2, Exhibition Hall, Ground floor, August 28, 2019, 3:00 PM - 4:30 PM Ambient air pollution is a complex mixture of particulate matter (PM2.5), gases and metals. Epidemiological evidence suggests that exposure to air pollution is one of the leading risk factors for cardiovascular disease (CVD). While the association between PM2.5 exposure and CVD is particularly strong, the pathophysiologic mechanisms underlying this association are not completely understood. We conducted a cross-sectional study of 100 participants, recruited from the University of Louisville. Peripheral endothelial function in these subjects was assessed by calculating a reactive hyperemia index (RHI) using the EndoPAT device. Urine samples were used to measure isoprostanes (n=90) while 14 cytokines, 2 adhesion molecules, and 2 matrix metalloproteinases were measured in plasma using a Luminex (n=77). Ambient levels of PM2.5 were obtained by calculating the daily average of all regional EPA-validated monitoring stations in the Louisville, KY region. Adjusted associations with ambient PM2.5 levels were tested using generalized linear models. The average age of our participants was 48 years, with 44% male, 62% white, 52% with diagnosed hypertension, and 44% having Type-2 diabetes. Average daily PM2.5 levels were 11.5 ± 5.1 μg/m3. We found that there was a 12.4% decrease in RHI with every 10μg/m3 PM2.5 increase (95% CI: -21.0, -2.7). F-2 isoprostane metabolite, a measure of oxidative stress, showed a positive association of 28.4% (95% CI: 2.7, 60.3) per 10μg/m3 PM2.5. We also observed positive associations with angiopoietin 1 (17.4%; 95% CI: 2.8, 33.8), VEGF (10.4%; 95% CI: 0.6, 21.0), PiGf (31.7%; 95% CI: 12.2, 54.5), ICAM-1 (24.6%; 95% CI: 1.6, 52.8), and MMP-9 (30.3%; 95% CI: 8.0, 57.5) per 10μg/m3 PM2.5. Additionally, we observed a negative association between PM2.5 and VCAM-1 of -15.9% per 10μg/m3 (95% CI:-28.3, -1.3). Exposure to PM2.5 was associated with impaired vascular function, which may result from oxidative stress and inflammation, and lead to a pro-atherogenic state.

Ambient Particulate Matter and Acrolein Co-Exposure Increases Myocardial Dyssynchrony in Mice via TRPA1.

Air pollution is a complex mixture of particulate matter and gases linked to adverse clinical outcomes. As such, studying responses to individual pollutants does not account for the potential biological responses resulting from the interaction of various constituents within an ambient air shed. We previously reported that exposure to high levels of the gaseous pollutant acrolein perturbs myocardial synchrony. Here, we examined the effects of repeated, intermittent co-exposure to low levels of concentrated ambient particulates (CAPs) and acrolein on myocardial synchrony and the role of transient receptor potential cation channel A1 (TRPA1), which we previously linked to air pollution-induced sensitization to triggered cardiac arrhythmia. Female B6129 and Trpa1-/- mice (n = 6/group) were exposed to filtered air (FA), CAPs (46 µg/m3 of PM2.5), Acrolein (0.42 ppm), or CAPs+Acrolein for 3 h/day, 2 days/week for 4 weeks. Cardiac ultrasound was conducted to assess cardiac synchronicity and function before and after the first exposure and after the final exposure. Heart rate variability (HRV), an indicator of autonomic tone, was assessed after the final exposure. Strain delay (time between peak strain in adjacent cardiac wall segments), an index of myocardial dyssynchrony, increased by 5-fold after the final CAPs+Acrolein exposure in B6129 mice compared with FA, CAPs, or Acrolein-exposed B6129 mice, and CAPs+Acrolein-exposed Trpa1-/- mice. Only exposure to acrolein alone increased the HRV high frequency domain (5-fold) in B6129 mice, but not in Trpa1-/- mice. Thus, repeated inhalation of pollutant mixtures may increase risk for cardiac responses compared with single or multiple exposures to individual pollutants through TRPA1 activation.

The human circulating miRNome reflects multiple organ disease risks in association with short-term exposure to traffic-related air pollution

Traffic-related air pollution is a complex mixture of particulate matter (PM) and gaseous pollutants, such as nitrogen dioxide (NO2). PM exposure contributes to the pathogenesis of many diseases including several types of cancer, as well as pulmonary, cardiovascular and neurodegenerative diseases. Also exposure to NO2 has been related to increased cardiovascular mortality. In search of an early diagnostic biomarker for improved air pollution-associated health risk assessment, recent human studies have shown that certain circulating miRNAs are altered upon exposure to traffic-related air pollutants. Here, we present for the first time a global analysis of the circulating miRNA genome in an experimental cross-over study of a human population exposed to traffic-related air pollution. By utilizing next-generation sequencing technology and detailed real-time exposure measurements we identified 54 circulating miRNAs to be dose- and pollutant species-dependently associated with PM10, PM2.5, black carbon, ultrafine particles and NO2 already after 2 h of exposure. Bioinformatics analysis suggests that these circulating miRNAs actually reflect the adverse consequences of traffic pollution-induced toxicity in target tissues including the lung, heart, kidney and brain. This study shows the strong potential of circulating miRNAs as novel biomarkers for environmental health risk assessment.

Divergent Electrocardiographic Responses to Whole and Particle-Free Diesel Exhaust Inhalation in Spontaneously Hypertensive Rats

Diesel exhaust (DE) is a major contributor to traffic-related fine particulate matter (PM)(2.5). Although inroads have been made in understanding the mechanisms of PM-related health effects, DE's complex mixture of PM, gases, and volatile organics makes it difficult to determine how the constituents contribute to DE's effects. We hypothesized that exposure to particle-filtered DE (fDE; gases alone) will elicit less cardiac effects than whole DE (wDE; particles plus gases). In addition, we hypothesized that spontaneously hypertensive (SH) rats will be more sensitive to the electrocardiographic effects of DE exposure than Wistar Kyoto rats (WKY; background strain with normal blood pressure). SH and WKY rats, implanted with telemeters to monitor electrocardiogram and heart rate (HR), were exposed once for 4 h to 150 μg/m(3) or 500 μg/m(3) of wDE (gases plus PM) or fDE (gases alone) DE, or filtered air. Exposure to fDE, but not wDE, caused immediate electrocardiographic alterations in cardiac repolarization (ST depression) and atrioventricular conduction block (PR prolongation) as well as bradycardia in SH rats. Exposure to wDE, but not fDE, caused postexposure ST depression and increased sensitivity to the pulmonary C fiber agonist capsaicin in SH rats. The only notable effect of DE exposure in WKY rats was a decrease in HR. Taken together, hypertension may predispose to the potential cardiac effects of DE and components of DE may have divergent effects with some eliciting immediate irritant effects (e.g., gases), whereas others (e.g., PM) trigger delayed effects potentially via separate mechanisms.

Occupational exposure to organic dust increases lung cancer risk in the general population

BackgroundOrganic dust is a complex mixture of particulate matter from microbial, plant or animal origin. Occupations with exposure to animal products have been associated with an increased lung cancer risk,...

Cardiac effects of carbon monoxide and ambient particles in a rat model of myocardial infarction.

Ambient air pollution is a complex mixture of particulate matter (PM) and gaseous pollutants such as carbon monoxide (CO). The effect of exposure to CO, alone or in combination with ambient PM, on arrhythmia incidence is unclear. To evaluate these effects, left-ventricular myocardial infarction was induced in Sprague-Dawley rats by thermocoagulation. Diazepam-sedated rats were exposed (1 h) to either filtered air (n = 40), CO (35 ppm, n = 19), concentrated air particles (CAPs, median concentration = 350.5 microg/m(3), n = 53), or CAPs and CO (CAPs median concentration = 318.2 microg/m(3), n = 23), 12-18 h after surgery. Each exposure was immediately preceded and followed by a 1 h exposure to filtered air (pre-exposure and post-exposure periods, respectively). The CO target dose of 35 ppm is related to the 1 h U.S. National Ambient Air Quality Standard. Surface electrocardiograms were recorded and heart rate and arrhythmia incidence were quantified. CO exposure reduced ventricular premature beat (VPB) frequency by 60.4% (p = 0.012) during the exposure period compared to controls. This effect was modified by both infarct type and the number of pre-exposure VPBs, and was not mediated through changes in heart rate. Overall, CAPs exposure increased VPB frequency during the exposure period, but this effect did not reach statistical significance. This effect was modified by the number of pre-exposure VPBs. Overall, neither CAPs nor CO had any effect on heart rate, but CAPs increased heart rate in specific subgroups. No significant interactions were observed between the effects of CO and CAPs. In this animal model, the responses to CO and CAPs are distinctly different.