Doses Of Particulate Matter Research Articles

Size-resolved particulate matter inside selected fire stations and preliminary evaluation of the effectiveness of washing machines in reducing its concentrations

The study aimed to determine and compare the mass concentration and size distribution of particulate matter (PM) at two Polish fire stations, one equipped with a washing machine intended for the decontamination of uniforms (FSN) and the other not equipped with this type of device (FSC), to assess the effectiveness of washing machines in reducing PM concentrations inside fire stations and estimate PM doses inhaled by firefighters while performing activities in truck bays and changing rooms during one work shift. The average PM concentrations at the FSN were 18.2–28.9 µg/m3 and 27.5–37.3 µg/m3, while at FSC they were 27.4–37.9 µg/m3 and 24.6–32.8 µg/m3 in the truck bays and changing rooms, respectively. At each measurement point, most of the PM mass (65–75%) was accumulated as fine particles. The dominance of fine particles in the total mass of PM results in high values of PM deposition coefficients (0.59–0.61) in three sections of the respiratory tract at each monitoring site. This study initially indicates the effectiveness of washing machines in reducing the concentration of fine particles and demonstrates the necessity, as well as directions for further research in this area.

Seasonal variation in exposure to particulate matter among children attending different levels of education: Comparison of two dosimetry models

Exposure to particulate matter (PM) has been associated with several adverse health outcomes. Studies indicate that children may be exposed to much higher concentrations of PM at school than in other environments. There exists very little data on the deposited dose of PM while children attend classes. This study was carried out in a school located near an industrial complex in Portugal and attended by children aged 3–12 years. Indoor PM10, PM2.5 and PM1 were measured over two seasons in classrooms representing different school year groups. Particle deposition fractions in the respiratory tract, as well as the deposited doses, were calculated using the Multiple-Path Particle Dosimetry (MPPD) and the Exposure Dose Model (ExDoM2). Both models were implemented assuming an 8-h exposure scenario to represent the school day. In general, differences in PM concentrations were observed depending on room occupancy periods and season. The highest mean PM2.5 concentration was recorded in winter when the classroom was vacant (23.7 ± 20.5 μg m−3), while the highest mean PM10 level was observed in spring during school hours (61.7 ± 24.2 μg m−3). Regardless of the dosimetry model, the highest deposition of PM10 and PM2.5 was in the upper region, while the lowest was in the tracheobronchial (TB) region. The results indicate that deposited dose and deposition fraction in spring may be more harmful to pupils’ health than in winter. PM10 presented the highest doses, ranging from 54.2 to 128 μg and from 83.9 to 185 μg, according to MPPD and ExDoM2 estimates, respectively.

P30 Exposure to particulate matter induces structural and pigmentary changes to human skin

Abstract Introduction and aims The majority of the world’s population reside in places with high levels of air pollution. The impact of air pollution on human health has been extensively studied and demonstrates a significant correlation between particulate matter (PM) and risk of cardiovascular and respiratory diseases. However, little is known about the impact of air pollution on human skin health. Here, we develop an ex vivo skin model to investigate cutaneous changes induced by the topical application of PM. Methods PM (0, 0.5, 3, 6, 10, 20 and 40 μg mL−1) was topically applied to Genoskin® NativeSkin Access® (Genoskin, Salem, MA, USA) human ex vivo skin samples of White European ancestry (n = 3) for 8 days, with reapplication on day 4. Resultant samples were assessed using haematoxylin and eosin staining (for morphometric analyses), immunofluorescence for Ki67 and terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) (to determine cellular turnover), while pigmentary changes were analysed by colourimetry, Warthin–Starry (WS) staining and immunohistochemistry for the melanin markers tyrosinase (TYR), gp100 and c-kit. Results Morphological assessment revealed that epidermal thickness was significantly reduced following exposure to higher doses of PM (r = −0.9163, P < 0.01). In addition, there was reduced epidermal cell proliferation (Ki67) and increased apoptosis (TUNEL) at higher doses of PM. Exposure to PM resulted in a dose-dependent decrease in individual typology angle, which is indicative of skin colour becoming darker (r = −0.7895, P < 0.05). Furthermore, WS staining demonstrated significantly increased epidermal melanin (r = 0.9583, P < 0.01) and significantly increased expression of melanin markers TYR (P < 0.01), gp100 (P < 0.001) and c-kit (P < 0.01) in response to PM exposure. Conclusions This study confirms that PM induces pigmentary changes to ex vivo human skin by increasing epidermal melanin. Increased expression of c-kit in response to PM exposure suggests that increased pigmentation occurs owing to the upregulation of the microphthalmia-associated transcription factor signalling pathway. Further investigation of the mechanistic drivers of increased pigmentation is warranted.

Characteristics of airborne particles in stone quarrying areas: Human exposure assessment and mitigation

This investigation aims to assess the levels of human exposure to airborne particulate matter (PM) in various locations of a natural stone quarry for the first time based on simultaneous measurements of both PM mass and number concentrations (PMC and PNC). A quarry located in Danang city, Vietnam, considered to be a “hotspot” of air pollution in the city, was selected for detailed investigations. Both PMC and PNC were found to be significantly higher (1.2–6.0 times) within the quarry compared to surrounding areas. Mechanical activities during mining, notably crushing, screening, hauling, and loading stones, contributed to increased emissions of PM in the coarser mode (1–10 μm) compared to the accumulation mode (0.1–1 μm) and thus increased deposition of PM1-10 in the human upper respiratory tract. In contrast, combustion activities, especially the diesel engine exhaust from various machines and vehicles used in the quarry, resulted in increased emissions of small particles in the accumulation mode that dominated the PNC and in their deposition in the lower respiratory tract. Simultaneous measurements of PNC and PMC revealed that the PM counts were strongly associated with PM deposition in the alveolar region (accounting for ≈ 76% of total PNC of particles less than 10 μm, N10), while the PM mass concentration was a better indicator of the deposition of PM in the head airway region (≈92% of total PMC of PM10). Overall, this study demonstrates the significance of measuring both PNC and PMC to assess PM exposure levels, regional respiratory doses, and potential health effects associated with human exposure to PM generated from stone quarrying activities. The novelty of this work is the integration of real-time mass and number concentrations of PM over the size range from 20 nm to 10 μm to provide insights into respiratory deposited doses of size-fractionated PM among quarry workers.

Calibration of DustTrak and Low-Cost Sensors and Their Application for Assessment of Inhalation Exposures to Traffic-Related PM2.5 and PM1 in Ho Chi Minh City

The in-traffic microenvironment can enhance personal exposure to fine particulate matter (PM). With this study, we aimed to calibrate a DustTrak instrument (DustTrak 8533 DRX Aerosol Monitor, TSI Incorporated, Shoreview, MN, USA) and low-cost sensors (AS-LUNG-P sensors) and then assess inhalation exposure to PM2.5 and PM1 for different commuters in central areas of Ho Chi Minh City (HCM). The DustTrak instrument and low-cost sensors were calibrated using a gravimetric method under side-by-side conditions. Relationships between the DustTrak signals and PM concentrations measured by the gravimetric method were identified using simple linear regression models for PM2.5 (R2 = 0.998, p-value < 0.05) and PM1 (R2 = 0.989, p-value < 0.05). Meanwhile, PM concentrations determined by the AS-LUNG-P sensors and the gravimetric method were correlated using two-segmented linear regressions. To obtain the corresponding two-segment regression equations, the response of the AS-LUNG-P sensors was compared with the corrected DustTrak data. The coefficient of variation (CV) evaluated for all sensors was smaller than 10%, indicating that the data were applicable for particle assessment. For inhalation exposure assessment, the results showed that commuters using open transport modes, such as bikes, motorbikes, and walking, were exposed to more PM than those using closed transport modes (e.g., cars). Specifically, the bicyclists had the highest inhaled doses of PM among the open transport groups. PM exposure levels in the morning were higher than in the afternoon. Additionally, exposure levels to PM concentrations rapidly increased when passing through intersections of major roads and moderately decreased when using surgical facemasks.

Simulating the impact of particulate matter exposure on health-related behaviour: A comparative study of stochastic modelling and personal monitoring data.

Epidemiological and exposure studies concerning particulate matter (PM) often rely on data from sparse governmental stations. While low-cost personal monitors have some drawbacks, recent developments have shown that they can provide fairly accurate and fit-for-purpose data. Comparing a stochastic, i.e., agent-based model (ABM), with environmental, biometric and activity data, collected with personal monitors, could provide insight into how the two approaches assess PM exposure and dose. An ABM was constructed, simulating a PM exposure/dose assessment of 100 agents. Their actions were governed by inherent probabilities of performing an activity, based on population data. Each activity was associated with an intensity level, and a PM pollution level. The ABM results were compared with real-world results. Both approaches had comparable results, showing similar trends and a mean dose. Discrepancies were seen in the activities with the highest mean dose values. A stochastic model, based on population data, does not capture well some specifics of a local population. Combined, personal sensors could provide input for calibration, and an ABM approach can help offset a low number of participants. Implementing a function of agents influencing others transport choice, increased the importance of cycling/walking in the overall dose estimate. Activists, agents with an increased transport influence, did not play an important role at low PM levels. As concentrations rose, higher shares of activists (and their influence) caused the dose to increase. Simulating a person's PM exposure/dose in different scenarios and activities in a virtual environment provides researchers and policymakers with a valuable tool.

Size distribution and lung-deposition of ambient particulate matter oxidative potential: A contrast between dithiothreitol and ascorbic acid assays

Particulate matter (PM) inhaled into human lungs causes oxidative stress and adverse health effects through antioxidant depletion (oxidative potential, OP). However, there is limited knowledge regarding the association between the lung-deposited dose (LDD) of PM and OP in extrathoracic (ET), tracheobronchial (TB), and pulmonary (P) regions of human lungs. Dithiothreitol (DTT) and ascorbic acid (AA) assays were employed to measure the OP of PM size fractions to investigate OP distribution in human lungs and identify the chemical drivers. Quasi-ultrafine particles (quasi-UFP, ≤0.49 μm) exhibited high OP deposition in the TB and P regions, while coarse particles (CP, ≥3.0 μm) dominated in the ET region. A plot of extrinsic (per air volume) and intrinsic (per PM mass) OP versus LDD revealed that the OP for fine and coarse particles was greatest in the ET region, whereas the OP of quasi-UFP was greatest in alveoli. The study also demonstrated that extrinsic OP and PM doses are not strongly related. The decline in OP with increasing PM dose reveals the need for further investigation of the antagonistic effects of the chemical compositions. Overall, the results presented herein help address the gap in knowledge regarding the association between the OP and LDD of ambient particles in specific regions of human lungs.

Size-fractionated ambient particulate matter induce toxicity: Oxidative potential, cytotoxic effect and inflammatory potential

Present study highlighted the importance of examining the toxicological profile of size-segregated particulate matter (PM) bound metals (Fe, Mn, Ni, Pb, Zn, Cu, Cr, Co, Cd) at urban site of Pune city, India. The total aerosol mass was composed of 61.2% and 38% fine and coarse particles, respectively with maximum distribution observed in 4.7–2.1 μm size mode. Elemental size distributions indicated the prime association of Fe, Mn and Zn with coarse sized PM, while remaining metals were predominantly associated with fine PM. Seasonal mass and elemental distribution profile of size-resolved PM was characterized with maximum concentration found in winter season. Enrichment factor analysis revealed the contribution of anthropogenic emissions to Co and Ni in fine mode while less enriched metals, Fe and Mn were allied with crustal and natural sources. Oxidative potential of particles in terms of Dithiothreitol (DTT) loss was found to be maximum in the size range of 4.7–1.1 μm with dominant contribution of PM bound metals (Fe, Cu, Cr, Mn, Ni, Pb, and Zn). On exposure to PM samples, prominent enhancement in the expression of cytokines (especially TNFα) as compared to the control has confirmed their inflammatory nature. Incubation of A549 cells with PM suspension (75 mg/ml) caused pronounced reduction (p < 0.01) in cell viability with significant morphological changes, associated with cell death. Respiratory deposition doses of PM in head region were found to be more impacted by coarse sized particles while contribution of fine PM was dominant in alveolar and tracheobronchial region, signifying serious health risks to the exposed population. In addition to the basic knowledge of toxicity mechanisms associated with size fractionated PM, these results together with the analysis of correlation between PM bound metals and biological assays will be relevant to better characterize the potential health risks and possible future mitigation strategies.

Genotoxic effects of particulate matter on larvae of a common and widespread butterfly along an urbanization gradient

Biodiversity is currently declining worldwide. Several threats have been identified such as habitat loss and climate change. It is unknown if and how air pollution can work in addition or in synergy to these threats, contributing to the decline of current species and/or local extinction. Few studies have investigated the effects of particulate matter (PM), the main component of air pollution, on insects, and no studies have investigated its genotoxic effects through Micronucleus assay. Butterflies play an important role in the environment, as herbivores during larval stages, and as pollinators as adults. The aim of this study was to evaluate the genotoxic effects of PM10 from different sites along a gradient of population urbanization, on a common cabbage butterfly species (Pieris brassicae). PM10 was collected from April to September in an urban (Turin, Italy), a suburban (Druento, Italy) and a mountain site (Ceresole Reale, Italy) with different urbanization levels. P. brassicae larvae (n = 218) were reared in the laboratory under controlled conditions (26 °C, L:D 15:9) on cabbage plants (average 9.2 days), and they were exposed to PM10 organic extracts (20 and 40 m3/mL) or dimethyl sulfoxide (controls) through vaporization. After exposure, larvae were dissected and cells were used for the Micronucleus (MN) assay. Results showed that all PM extracts induced significant DNA damage in exposed larvae compared to controls, and that increasing the PM dose (from 20 to 40 m3/mL) increased genotoxic effects. However, we did not detect any significant differences between sites with different urbanization levels. In conclusion, PM at different concentrations induced genotoxic effects on larvae of a common butterfly species. More alarmingly, PM could work in addition to and/or in synergy with other compounds (e.g. pesticides) and, especially on species already threatened by other factors (e.g. fragmentation), thus affecting the vitality of populations, leading to local extinctions.

Urban particulate air pollution linked to dyslipidemia by modification innate immune cells

Air particulate matter (PM) is an essential risk factor for lipid metabolism disorders. However, the underlying mechanism remains unclear. In this cross-sectional study, 216 healthcare workers were recruited to estimate the associations among the daily exposure dose (DED) of air PM, innate immune cells, and plasma lipid levels. All participants were divided into two groups according to the air particulate combined DED (DED-PMC). The peripheral white blood cell counts, lymphocyte counts, and monocyte counts and percentages were higher in the higher-exposure group (HEG) than in the lower-exposure group (LEG), whereas the percentage of natural-killer cells was lower in the HEG than in the LEG. The plasma concentrations of the total cholesterol, triglycerides, LDL-C, and apolipoprotein B were higher in the HEG than in the LEG, whereas the HDL-C and apolipoprotein A1 were lower in the HEG than in the LEG. A dose-effect analysis indicated that when the DED of the air PM increased, there were increased peripheral monocyte counts and percentages, a decreased NK cell percentage, elevated plasma concentrations of total cholesterol, triglycerides, LDL-C, and apolipoprotein B, and reduced plasma levels of HDL-C and apolipoprotein A1. In addition, the modification of the innate immune cells was accompanied by alterations in the plasma lipid levels in a dose-dependent manner. Mediation effect analysis suggested innate immune cells were the potential mediators for the associations among air PM exposure on abnormal lipid metabolism. These results indicated that chronic exposure to air PM may disturb lipid metabolism by altering the distribution of innate immune cells in the peripheral blood, ultimately advancing cardiovascular disease risk.

Leaf fitness and stress response after the application of contaminated soil dust particulate matter

In this study, we observed the effect of the application of soil dust enriched with risk elements (Cd, Pb, As and Zn) to leaf surfaces of lettuce (Lactuca sativa var. capitata) while it was grown under hydroponic conditions. This study aimed to determine how low soil dust particulate matter (PM) doses affected the activity of or damaged the photosynthetic apparatus and how the uptake of risk elements was associated with both epigenetic changes (5-methylcytosine content, i.e., 5mC) and stress metabolism. During the study, we obtained many results pertaining to risk element contents and biochemical (total phenolic content (TPC), malondialdehyde (MDA) content and the amount of free amino acids (AAs)) and physiological (photosynthesis parameters: net photosynthetic rate, transpiration rate, intercellular CO2 concentration, stomatal conductance, instantaneous water-use efficiency, maximum quantum yield of PSII, chlorophyll and carotenoid contents, and leaf water potential (WP)) plant features. The results showed an increase in MDA and 5mC. However, the transpiration rate, WP and free AAs decreased. In conclusion, contamination by very low doses of soil dust PM had no direct or significant effect on plant fitness, as shown by the TPC and 5mC content, which indicates that plants can overcome the oxidative stress caused by the accumulation of risk elements. From the above, we propose the use of epigenetic changes as biomarkers of potential changes in the activation of plant metabolism under stress caused by environmental pollution.

Commuter exposures to in-transit PM in an urban city dominated by motorcycle: A case study in Vietnam

Exposure to in-transit particulate matter (PM) has negatively affected human health but is barely reported in an urban area dominated by motorcycles. This study aimed to investigate the personal exposure and inhaled dose of PM for commuting modes in Ho Chi Minh City (HCMC), Vietnam. To do this, we conducted simultaneously sampled trips between on motorcycle without and with facemasks, car, and bus. Measurements were performed using portable PM monitors across representing routes in HCMC. In total, we conducted 1086 km in length of paired mode trips. The result shows that motorcyclist was exposed to the highest PM concentrations followed by bus and car commuters. A facemask worn by a motorcyclist while riding was consistent in reducing the in-transit PM exposures (e.g., ∼33–43% lower in PM2.5), and surgical facemask had higher PM removal efficiency than that of cloth facemask (p < 0.01). Ratios (I/O) for PM1 ranged from 0.31 for car/motorcycle to 0.77 for motorcycle-cloth facemask/motorcycle, and PM10 tend to have the lowest ratios. However, bus/motorcycle ratios show the opposite trend with the highest ratio obtained for PM10 due to the effect of a stop-and-go pattern during bus trips. Compared to ambient PM2.5 concentration, in-transit PM2.5 concentration on motorcycle has a good correlation with those measured at the urban station. In conclusion, our work suggests that motorcycle should be urgently restricted in megacities (like HCMC) to protect human health. Policy makers should also pay attention to in-transit PM exposure in public transport mode for future urban transport planning.

Associations between lung-deposited dose of particulate matter and culture-positive pulmonary tuberculosis pleurisy.

Epidemiological studies identified the relationship between air pollution and pulmonary tuberculosis. Effects of lung-deposited dose of particulate matter (PM) on culture-positive pulmonary tuberculosis remain unclear. This study investigates the association between lung-deposited dose of PM and pulmonary tuberculosis pleurisy. A case-control study of subjects undergoing pleural effusion drainage of pulmonary tuberculosis (case) and chronic heart failure (control) was conducted. Metals and biomarkers were quantified in the pleural effusion. The air pollution exposure was measured and PM deposition in the head, tracheobronchial, alveolar region, and total lung region was estimated by Multiple-path Particle Dosimetry (MPPD) Model. We performed multiple logistic regression to examine the associations of these factors with the risk of tuberculosis. We observed that 1-μg/m3 increase in PM10 was associated with 1.226-fold increased crude odds ratio (OR) of tuberculosis (95% confidence interval (CI): 1.023-1.469, p<0.05), 1-μg/m3 increase in PM2.5-10 was associated with 1.482-fold increased crude OR of tuberculosis (95% CI: 1.048-2.097, p < 0.05), 1-ppb increase in NO2 was associated with 1.218-fold increased crude OR of tuberculosis (95% CI: 1.025-1.447, p < 0.05), and 1-ppb increase in O3 was associated with 0.735-fold decreased crude OR of tuberculosis (95% CI: 0.542 0.995). We observed 1-μg/m3 increase in PM deposition in head and nasal region was associated with 1.699-fold increased crude OR of tuberculosis (95% CI: 1.065-2.711, p < 0.05), 1-μg/m3 increase in PM deposition in tracheobronchial region was associated with 1.592-fold increased crude OR of tuberculosis (95% CI: 1.095-2.313, p < 0.05), 1-μg/m3 increase in PM deposition in alveolar region was associated with 3.981-fold increased crude OR of tuberculosis (95% CI: 1.280-12.386, p < 0.05), and 1-μg/m3 increase in PM deposition in total lung was associated with 1.511-fold increased crude OR of tuberculosis (95% CI: 1.050-2.173, p < 0.05). The results indicate that particle deposition in alveolar region could cause higher risk of pulmonary tuberculosis pleurisy than deposition in other lung regions.

Prostaglandin E2 and phagocytosis of inhaled particulate matter by airway macrophages in cystic fibrosis

BackgroundExposure to particulate matter (PM) air pollution is associated with adverse health outcomes in children with cystic fibrosis (CF). Airway macrophages (AM) phagocytose and retain inhaled PM in vivo, and the area of carbon in AM reflects both inhaled PM dose and phagocytic function. Since airway prostaglandin-E2 (PGE2) is increased in CF, and PGE2 suppresses AM phagocytosis, we sought evidence for PGE2-mediated suppression of AM phagocytosis of inhaled carbonaceous PM in CF. MethodsAfter informed consent, urine was obtained from 20 controls and 24 CF children. In the subgroup of older children, at least one induced sputum was done in 20 controls and 19 CF children. Urinary tetranor PGEM, the major metabolite of PGE2, and sputum PGE2 were measured by mass spectrometry. The area of carbon in AM was determined by image analysis. Exposure to PM was assessed by modelling and personal monitoring. The effect of either PGE2 or CF sputum supernatant on phagocytosis of diesel exhaust particle (DEP) by AM was assessed in vitro. Data were analysed by t-test. ResultsBoth urinary tetranor PGEM (P<0.05), and sputum PGE2 (P<0.05) were increased in CF . Despite no difference in PM exposure between groups, the area of phagocytosed carbon by AM was decreased in children with CF (P<0.01). PGE2 suppressed phagocytosis of DEP by AM from both controls and CF (P<0.0001). CF sputum supernatant suppressed phagocytosis of DEP by AM (P<0.0001) in a PGE2-dependent manner. ConclusionIncreased PGE2 in the CF airway suppresses phagocytosis of inhaled PM by AM.

Oxidative stress-induced inflammation in susceptible airways by anthropogenic aerosol.

Ambient air pollution is one of the leading five health risks worldwide. One of the most harmful air pollutants is particulate matter (PM), which has different physical characteristics (particle size and number, surface area and morphology) and a highly complex and variable chemical composition. Our goal was first to comparatively assess the effects of exposure to PM regarding cytotoxicity, release of pro-inflammatory mediators and gene expression in human bronchial epithelia (HBE) reflecting normal and compromised health status. Second, we aimed at evaluating the impact of various PM components from anthropogenic and biogenic sources on the cellular responses. Air-liquid interface (ALI) cultures of fully differentiated HBE derived from normal and cystic fibrosis (CF) donor lungs were exposed at the apical cell surface to water-soluble PM filter extracts for 4 h. The particle dose deposited on cells was 0.9–2.5 and 8.8–25.4 μg per cm2 of cell culture area for low and high PM doses, respectively. Both normal and CF HBE show a clear dose-response relationship with increasing cytotoxicity at higher PM concentrations. The concurrently enhanced release of pro-inflammatory mediators at higher PM exposure levels links cytotoxicity to inflammatory processes. Further, the PM exposure deregulates genes involved in oxidative stress and inflammatory pathways leading to an imbalance of the antioxidant system. Moreover, we identify compromised defense against PM in CF epithelia promoting exacerbation and aggravation of disease. We also demonstrate that the adverse health outcome induced by PM exposure in normal and particularly in susceptible bronchial epithelia is magnified by anthropogenic PM components. Thus, including health-relevant PM components in regulatory guidelines will result in substantial human health benefits and improve protection of the vulnerable population.

Particulate matter exposure at a densely populated urban traffic intersection and crosswalk.

Exposure to elevated particulate matter (PM) pollution is of great concern to both the general public and air quality management agencies. At urban traffic intersections, for example, pedestrians are often at a higher risk of exposure to near-source PM pollution from traffic while waiting on the roadside or while walking in the crosswalk. This study offers an in-depth investigation of pedestrian exposure to PM pollution at an urban traffic intersection. Fixed-site measurements near an urban intersection were conducted to examine the variations in particles of various sizes through traffic signal cycles. This process aids in the identification of major PM dispersion patterns on the roadside. In addition, mobile measurements of pedestrian exposure to PM were conducted across six time intervals that correspond to different segments of a pedestrian's journey when passing through the intersection. Measurement results are used to estimate and compare the cumulative deposited doses of PM by size categories and journey segments for pedestrians at an intersection. Furthermore, comparisons of pedestrian exposure to PM on a sunny day and a cloudy day were analyzed. The results indicate the importance of reducing PM pollution at intersections and provide policymakers with a foundation for possible measures to reduce pedestrian PM exposure at urban traffic intersections.

Urban air PM modifies differently immune defense responses against bacterial and viral infections in vitro

Epidemiological evidence has shown the association between exposure to ambient fine particulate matter (PM) and increased susceptibility to bacterial and viral respiratory infections. However, to date, the underlying mechanisms of immunomodulatory effects of PM remain unclear. Our objective was to explore how exposure to relatively low doses of urban air PM alters innate responses to bacterial and viral stimuli in vitro. We used secondary alveolar epithelial cell line along with monocyte-derived macrophages to replicate innate lung barrier in vitro. Co-cultured cells were first exposed for 24 h to PM2.5-1 (particle aerodynamic diameter between 1 and 2.5 μm) and subsequently for an additional 24 h to lipopolysaccharide (TLR4), polyinosinic-polycytidylic acid (TLR3), and synthetic single-stranded RNA oligoribonucleotides (TLR7/8) to mimic bacterial or viral stimulation. Toxicological endpoints included pro-inflammatory cytokines (IL-8, IL-6, and TNF-α), cellular metabolic activity, and cell cycle phase distribution. We show that cells exposed to PM2.5-1 produced higher levels of pro-inflammatory cytokines following stimulation with bacterial TLR4 ligand than cells exposed to PM2.5-1 or bacterial ligand alone. On the contrary, PM2.5-1 exposure reduced pro-inflammatory responses to viral ligands TLR3 and TLR7/8. Cell cycle analysis indicated that viral ligands induced cell cycle arrest at the G2-M phase. In PM-primed co-cultures, however, they failed to induce the G2-M phase arrest. Contrarily, bacterial stimulation caused a slight increase in cells in the sub-G1 phase but in PM2.5-1 primed co-cultures the effect of bacterial stimulation was masked by PM2.5-1. These findings indicate that PM2.5-1 may alter responses of immune defense differently against bacterial and viral infections. Further studies are required to explain the mechanism of immune modulation caused by PM in altering the susceptibility to respiratory infections.

Size distribution and lung-deposited doses of particulate matter from household exposure to biomass smoke.

Exposure to high concentrations of particulate matter (PM) is associated with a number of adverse health effects. However, it is unclear which aspects of PM are most hazardous, and a better understanding of particle sizes and personal exposure is needed. We characterized particle size distribution (PSD) from biomass-related pollution and assessed total and regional lung-deposited doses using multiple-path deposition modeling. Gravimetric measurements of kitchen and personal PM2.5 (<2.5µm in size) exposures were collected in 180 households in rural Puno, Peru. Direct-reading measurements of number concentrations were collected in a subset of 20 kitchens for particles 0.3-25µm, and the continuous PSD was derived using a nonlinear least-squares method. Mean daily PM2.5 kitchen concentration and personal exposure was 1205±942µg/m3 and 115±167µg/m3 , respectively, and the mean mass concentration consisted of a primary accumulation mode at 0.21µm and a secondary coarse mode at 3.17µm. Mean daily lung-deposited surface area (LDSA) and LDSA during cooking were 1009.6±1469.8 µm2 /cm3 and 10,552.5±8261.6 µm2 /cm3 , respectively. This study presents unique data regarding lung deposition of biomass smoke that could serve as a reference for future studies and provides a novel, more biologically relevant metric for exposure-response analysis compared to traditional size-based metrics.

Mitochondrial alterations triggered by repeated exposure to fine (PM2.5-0.18) and quasi-ultrafine (PM0.18) fractions of ambient particulate matter

Nowadays ambient particulate matter (PM) levels still regularly exceed the guideline values established by World Health Organization in most urban areas. Numerous experimental studies have already demonstrated the airway toxicity of the fine fraction of PM (FP), mainly triggered by oxidative stress-induced airway inflammation. However, only few studies have actually paid close attention to the ultrafine fraction of PM (UFP), which is likely to be more easily internalized in cells and more biologically reactive. Mitochondria are major endogenous sources of reactive oxygen species (ROS) through oxidative metabolism, and coordinate many critical cellular signaling processes. Mitochondria have been often studied in the context of PM toxicity and generally associated with apoptosis activation. However, little is known about the underlying adaptation mechanisms that could occur following exposure at sub-apoptotic doses of ambient PM. Here, normal human bronchial epithelial BEAS-2B cells were acutely or repeatedly exposed to relatively low doses (5 µg.cm−2) of FP (PM2.5-0.18) or quasi-UFP (Q-UFP; PM0.18) to better access the critical changes in mitochondrial morphology, functions, and dynamics. No significant cytotoxicity nor increase of apoptotic events were reported for any exposure. Mitochondrial membrane potential (ΔΨm) and intracellular ATP content were also not significantly impaired. After cell exposure to sub-apoptotic doses of FP and notably Q-UFP, oxidative phosphorylation was increased as well as mitochondrial mass, resulting in increased production of mitochondrial superoxide anion. Given this oxidative boost, the NRF2-ARE signaling pathway was significantly activated. However, mitochondrial dynamic alterations in favor of accentuated fission process were observed, in particular after Q-UFP vs FP, and repeated vs acute exposure. Taken together, these results supported mitochondrial quality control and metabolism dysfunction as an early lung underlying mechanism of toxicity, thereby leading to accumulation of defective mitochondria and enhanced endogenous ROS generation. Therefore, these features might play a key role in maintaining PM-induced oxidative stress and inflammation within lung cells, which could dramatically contribute to the exacerbation of inflammatory chronic lung diseases. The prospective findings of this work could also offer new insights into the physiopathology of lung toxicity, arguably initiate and/or exacerbate by acutely and rather repeated exposure to ambient FP and mostly Q-UFP.

Pathogenic Role of Air Pollution Particulate Matter in Cardiometabolic Disease: Evidence from Mice and Humans.

Significance: Air pollution is a considerable global threat to human health that dramatically increases the risk for cardiovascular pathologies, such as atherosclerosis, myocardial infarction, and stroke. An estimated 4.2 million cases of premature deaths worldwide are attributable to outdoor air pollution. Among multiple other components, airborne particulate matter (PM) has been identified as the major bioactive constituent in polluted air. While PM-related illness was historically thought to be confined to diseases of the respiratory system, overwhelming clinical and experimental data have now established that acute and chronic exposure to PM causes a systemic inflammatory and oxidative stress response that promotes cardiovascular disease. Recent Advances: A large body of evidence has identified an impairment of redox metabolism and the generation of oxidatively modified lipids and proteins in the lung as initial tissue response to PM. In addition, the pathogenicity of PM is mediated by an inflammatory response that involves PM uptake by tissue-resident immune cells, the activation of proinflammatory pathways in various cell types and organs, and the release of proinflammatory cytokines as locally produced tissue response signals that have the ability to affect organ function in a remote manner. Critical Issues: In the present review, we summarize and discuss the functional participation of PM in cardiovascular pathologies and its risk factors with an emphasis on how oxidative stress, inflammation, and immunity interact and synergize as a response to PM. Future Directions: The impact of PM constituents, doses, and novel anti-inflammatory therapies against PM-related illness is also discussed.