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BACKGROUND: Exposure to particulate matter (PM) emitted from vehicle exhaust might disrupt systemic function and elevate the risk of cardiovascular disease. In this study, we examined the changes of cardiometabolic biomarkers among vehicle inspectors exposed daily to PM0.25 and components. METHODS: This cross-sectional study was conducted at two vehicle inspection centers, Pulogadung and Ujung Menteng, located in East Jakarta, Indonesia. The exposed respondents were 43 workers from vehicle inspection centers, and the unexposed group consisted of 22 staff officers working in the same locations. Vehicle exhaust particulate matter was measured for eight hours using a Leland Legacy personal pump attached to a Sioutas Cascade Impactor. The used filters were 25 and 37-mm quartz filters. The particulate matter concentration was analyzed using a gravimetric method, whereas trace elements were analyzed using energy dispersive X-ray fluorescence. An EEL Smoke Stain Reflectometer analyzed black carbon. RESULTS: The personal exposure concentrations of PM0.25 were 10.4-fold higher than those in unexposed groups. Calcium and sulfur were the major components in the obtained dust, and their levels were 3.3- and 7.2-fold higher, respectively, in the exposed group. Based on an independent-samples t-test, high-density lipoprotein, triglyceride, HbA1c, total immunoglobulin E, high-sensitivity C-reactive protein, tumor necrosis factor-alpha, and nitric oxide levels were significantly different between the groups. CONCLUSIONS: In summary, it was suggested that PM0.25 exposure from vehicle exhaust might affect cardiometabolic biomarkers change.

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When the total ambient PM2.5 levels are several-fold higher than the recommended limit, it may be important to study the distributions of different sizes of particulate matter (PM). Here, we assess the distributions of various sizes of total PM2.5 for 12 months (on a monthly basis) in New Delhi, India. Importantly, we found that ultrafine particles (i.e., particles <0.5 µm) contribute significantly to total PM2.5. PM<0.25 were the most cytotoxic particles to human lung epithelial cells in all the 12 months. In addition, PM<0.25 were associated with significantly higher cytotoxicity per unit mass compared to other size fractions constituting PM2.5. For any given size of PM, the amount of reactive oxygen species (ROS) generated per unit mass is higher for the month of March as compared to that for the rest of the months in the year. The higher ROS generations for all sizes of PM collected in the month of March was not explained by differences in their metal content values. Our data suggests the lack of correlation between total PM2.5 levels and the highly cytotoxic PM<0.25. In summary, this work establishes the need for policy changes to routinely monitor PM<0.25 and the necessity to establish exposure limits for PM<0.25, especially when the total PM2.5 levels are breached.

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Gas cooking is an important source of airborne particulate matter (PM) indoors. Exposure to cooking-derived PM can lead to adverse human health impacts on non-smokers, especially in poorly-ventilated residential homes. Most of the previous studies on gas cooking emissions mainly focused on fine particles (PM2.5) with little information on their size-fractionation. Moreover, studies dealing with mitigation of indoor human exposure to cooking-derived PM are currently sparse. Therefore, a systematic study was conducted to investigate the characteristics of PM2.5 and size-fractionated PM derived from five commonly used cooking methods, namely, steaming, boiling, stir-frying, pan-frying and deep-frying in a poorly-ventilated domestic kitchen under controlled experimental conditions. Additionally, an indoor portable air cleaner was employed as a mitigation device to capture cooking-derived PM and improve indoor air quality (IAQ). Results revealed that the oil-based deep-frying cooking released the highest airborne particles which were about 170 folds higher compared to the baseline levels for PM2.5 mass concentrations. The use of the air cleaner showed a statistically significant (p < 0.05) reduction in the indoor PM2.5 levels. Moreover, PM<0.25 (particles with diameter ≤ 250 nm) showed a very high mass concentration (378.2 µg/m3) during deep-frying, raising human health concern. A substantial reduction (~60-85%) in PM<0.25 mass concentrations and their total respiratory deposition doses (RDD) in the human respiratory tract was observed while using the air cleaner during the five cooking methods. Furthermore, morphological characteristics and the relative abundance of trace elements in cooking-derived PM were also investigated. This study provides useful insights into the assessment and mitigation of indoor human exposure to cooking-derived PM.

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In this study, weekly samples of ambient PM0.25 (particulate matter with an aerodynamic diameter <0.25 µm) were collected in three contrasting locations, including central Los Angeles (USC), north Long Beach (NLB), and the Port of Long Beach (PRT), during June and July of 2017 to evaluate the chemical composition of ambient PM0.25 and identify the sources that contribute to the oxidative potential of ambient PM0.25 in these locations. Special focus was given in exploring the impact of emissions from the Ports of Los Angeles and Long Beach on the oxidative potential of ambient PM0.25 measured across these sites. The oxidative potential of the collected samples was quantified by means of an in vitro cell-based alveolar macrophage (AM) assay. We used multiple linear regression (MLR) analysis to link individual measured species, used as source markers, to the oxidative potential of the ambient PM0.25 across the monitoring sites. Results from the MLR analysis indicated that vehicular emissions and secondary organic aerosols (SOA) were the major contributors to the oxidative potential of ambient PM0.25 across the three sites, with corresponding contributions of 40 ±â€¯2% and 39 ±â€¯3%, respectively. Emissions of PM0.25 related to port activities, including emissions from ships, locomotives, and heavy-duty vehicles (HDVs) operating at the port, accounted for 16 ±â€¯3% of the overall oxidative potential of the ambient PM0.25 samples. The concentrations of the marker species at the three different sites suggested that the contributions of port-related emissions to the oxidative potential of PM0.25 decreased from the port area to central Los Angeles, underscoring the greater impact of these emissions on the PM0.25 toxicity in the communities near the Ports of Los Angeles and Long Beach, whereas we observed larger impact of SOA formation and vehicular emissions on the oxidative potential of ambient PM0.25 in the receptor sites located further inland.

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Air traffic is rapidly growing, raising concerns about the air pollution in the surroundings of airports and its impact on public health. However, little is known about the impact of air pollution sources on air quality and health in the vicinity of airports. In this study, the sources and adverse health effects of airport-related particulate matter (PM) were investigated and compared to those of urban traffic emissions. Ambient PM0.25 were collected at the Los Angeles International Airport (LAX) and at a central Los Angeles site (USC campus), along with PM2.5 collected directly from turbine and diesel engines. The particle chemical composition, oxidative potential (OP) (ascorbic acid (AA), and electron spin resonance (ESR) assay) as well as their reactive oxygen species (ROS) activity, inflammatory potential (interleukin (IL) 6 and 8 and tumor necrosis factor (TNF)-α) and cytotoxicity on human bronchial epithelial (16HBE) cells were assessed. Chemical composition measurements confirmed that aircraft emissions were the major source to LAX PM0.25, while the sources of the USC samples were more complex, including traffic emissions, suspended road and soil dust, and secondary aerosols. The traffic-related transition metals (Fe and Cu) in LAX and USC samples mainly affected OP values of particles, while multiple factors such as composition, size distribution and internalized amount of particles contributed to the promotion of ROS generation in 16HBE cells during 4 h exposure. Internalized particles in cells might also play an important role in activating inflammatory responses during cell recovery period, with LAX particles being more potent. Our results demonstrated considerable toxicity of airport-related particles, even at low exposure concentrations, suggesting that airport emission as source of PM0.25 may also contribute to the adverse effects on public health attributable to PM. The potency of such particles is in the same range as those collected at a site in urban area impacted heavily by traffic emissions.

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Very fine particles (VFPs, PM0.25) are able to travel deeply into the respiratory tract and can produce adverse health effects, especially to children. Information on the VFPs in schools is generally lacking. We investigated the chemical compositions, sources and health risks of VFPs in a junior secondary school of Xi'an, China, during May 16th to 30th, 2012. The results showed that organic matter (37% and 39%), SO42- (13% and 11%) and geological material (20% and 24%) were the major components of VFPs both outdoors and indoors. The VFP species indoors, such as SO42- and elemental carbon, are mainly from outdoor origins, e.g. coal burning and traffic emissions. But particle resuspension by student activities, chalk dust and import from outdoors of soil dust also contributed to deteriorate air quality in the classroom. By contrast to outdoors, several indoor factors, like higher room temperature, limited volume and longer suspension time of classroom particles, can even lead to significant secondary pollutant production. Heavy metals (mainly from outside) bound to indoor VFPs are supposedly associated to non-cancer health risks, especially Pb through ingestion pathway and Mn through dermal contact. Outdoor VFPs may be associated to PAHs cancer health risks via inhalation way. This study confirms that both indoor and outdoor sources had contributions to indoor VFPs, and that VFPs health risk should be of higher concern in urban areas of Northwestern China.

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To investigate the relative impacts of emissions from Los Angeles International Airport (LAX), as well as the impacts of traffic emissions from freeways, on the oxidative potential of particulate matter (PM), PM0.25 were collected at two urban background locations in Los Angeles. Redox activity of the PM samples was measured by means of an in vitro alveolar macrophage assay that quantifies the formation of reactive oxygen species (ROS) in cells, and detailed chemical analyses were performed to determine the speciated chemical composition of collected PM. A molecular marker-based chemical mass balance (MM-CMB) model was applied to estimate the relative contributions from the following primary sources to the organic carbon (OC) component of PM: mobile sources (combined gasoline and diesel vehicles), wood smoke, vegetative detritus, road dust and ship emissions. A source profile of aircraft emissions was not included in the model; however its contribution was estimated from un-apportioned primary OC in the MM-CMB model ("other OC") after accounting for the contribution of secondary organic carbon (SOC) to OC. The contribution of mobile sources to OC was 82% and 28% at the central Los Angeles site (freeway emissions) and the LAX site, respectively. The estimated contribution of aircraft emissions to PM0.25 OC was 36% at the LAX site. ROS activity levels showed little spatial variability, with no statistically significant difference between the averages observed at LAX (24.75±4.01µgZymosan/m3) and central Los Angeles (27.77±2 0.32µgZymosan/m3), suggesting similar levels of inhalation exposure to redox active species of PM0.25. A multiple linear regression analysis indicated that the variability in ROS activity is best explained by the chemical markers of major identified sources: EC emitted by traffic, and sulfur, considered in our study as a potential tracer of aircraft emissions, with statistically significantly higher concentrations of sulfur at the LAX site (p<0.001).