Urban Fine Particulate Matter Research Articles

Global spatial and temporal patterns of fine particulate concentrations and exposure risk assessment in the context of SDG indicator 11.6.2

Assessing the spatiotemporal patterns, exposure risks and sustainability of PM2.5 pollution from multi–scale spatial and temporal characteristics are relevant for achieving Goal 11.6.2 of the 2030 Agenda for Sustainable Development (assessing the effects of urban fine particulate matter pollution on public health). According to this study, methodological models combining trend analysis, spatial statistics, and population exposure risk assess the spatiotemporal patterns, exposure risks, and sustainability characteristics of PM2.5 pollution at global, continental, and national scales, and ultimately achieve SDG 11.6.2 Assessment framework at different spatial scales. The results indicate that: (1) The annual decline in global PM2.5 concentrations exhibited a rate of –0.023 µg/m3/yr, with more than 30 % of regions experiencing a decrease in PM2.5 concentrations of more than 0.1 µg/m3/yr, and showed significant spatial distribution differences. (2) The global population exposed to <10 µg/m3 continues to grow from 4.8 % in 2000 to 6.2 % in 2010 and further to 10.3 % in 2020 during the study period. By comparison, the population exposed to >70 µg/m3 shows a U–shaped change. Spatially, more than 60 % of the world’s regions are exposed to low risk (Low risk and Lower risk) and less than 30 % are exposed to high risk (Higher, High and Extremely high risk). Asia has the highest exposure (2.95), while Oceania has the lowest (0.11). (3) Inequalities in sustainable PM2.5 exposure risks between developed and developing countries will continually increase. The results of the study not only shed light on the present state of sustainable global air quality progress but also offer valuable insights and a blueprint for conducting similar multi–scale assessments in the coming times.

Evolution and chemical characteristics of organic aerosols during wintertime PM2.5 episodes in Shanghai, China: insights gained from online measurements of organic molecular markers

Abstract. Organic aerosol (OA) is a significant part of urban fine particulate matter (PM2.5), and a lack of detailed knowledge of their sources has increasingly hindered the improvement of air quality in China in recent years, as significant reductions have been achieved in inorganic ion constituents. In this study, a wide range of organic molecular markers in PM2.5 were monitored with a bi-hourly time resolution using a thermal desorption aerosol gas chromatograph system (TAG) in urban Shanghai in winter 2019. The molecular marker data have provided a unique source tracking ability in characterizing the evolution of organic aerosols during nine wintertime episodic events. Episodes primarily influenced by local air masses were characterized with higher proportions in PM2.5 and mass increments of both primary and secondary OA. Rapid increases in both the absolute mass concentration and relative proportion were observed for primary and secondary OA markers, indicative of vehicle emissions (e.g., alkanes, hopanes, and 2,3-dihydroxy-4-oxopentanoic acid) and cooking activities (e.g., saturated and unsaturated fatty acids and C9 acids). In comparison, episodes under significant influences of transported air mass were typically associated with a predominant PM2.5 contribution from secondary inorganic aerosols and enhanced OA contribution from biomass burning activities. The latter was evident from the tracer data (e.g., levoglucosan, aromatic polycarboxylic acids, and nitroaromatic compounds). Secondary OA markers associated with later-generation products of the hydrocarbon oxidation process, such as C3−5 dicarboxylic acids, were the most deficient during local episodes, while notably enhanced during the episodes under the influence of transported air masses, reflecting the different extent and pathways of atmospheric aging processing. The ability to distinguish the variations in the OA evolution during different types of episodes demonstrates the value of online organic molecular measurements for episodic analysis. The results indicate that control of local urban sources such as vehicular and cooking emissions would lessen severity of local episodes, while regional control of precursors for secondary inorganic aerosols and biomass burning activities would reduce PM2.5 episodes under synoptic conditions conducive for regional transport.

Polar Nitrated Aromatic Compounds in Urban Fine Particulate Matter: A Focus on Formation via an Aqueous-Phase Radical Mechanism.

Polar nitrated aromatic compounds (pNACs) are key ambient brown carbon chromophores; however, their formation mechanisms, especially in the aqueous phase, remain unclear. We developed an advanced technique for pNACs and measured 1764 compounds in atmospheric fine particulate matter sampled in urban Beijing, China. Molecular formulas were derived for 433 compounds, of which 17 were confirmed using reference standards. Potential novel species with up to four aromatic rings and a maximum of five functional groups were found. Higher concentrations were detected in the heating season, with a median of 82.6 ng m-3 for Σ17pNACs. Non-negative matrix factorization analysis indicated that primary emissions particularly coal combustion were dominant in the heating season. While in the non-heating season, aqueous-phase nitration could generate abundant pNACs with the carboxyl group, which was confirmed by their significant association with the aerosol liquid water content. Aqueous-phase formation of 3- and 5-nitrosalicylic acids instead of their isomer of 4-hydroxy-3-nitrobenzoic acid suggests the existence of an intermediate where the intramolecular hydrogen bond favors kinetics-controlled NO2• nitration. This study provides not only a promising technique for the pNAC measurement but also evidence for their atmospheric aqueous-phase formation, facilitating further evaluation of pNACs' climatic effects.

Spatial-Temporal Characteristics and Influencing Factors of Particulate Matter: Geodetector Approach

In 2019, South Korea’s Framework Act on The Management of Disasters and Safety was revised to include respirable particulate matter as a social disaster. Urban air pollution, especially particulate matter pollution, has been a serious threat to socioeconomic development and public health. In order to address this problem, strong climate crisis response strategies and policies to improve urban air quality are necessary. Therefore, it is of great importance to assess the frequency of urban air pollution occurrence and its influencing factors. The objective of this study is to develop consistent methodologies for the construction of an index system and for assessing the influencing factors of urban particulate matter pollution based on population, social welfare, land use, environmental, transportation, and economic governance considerations. We applied the local indicators of spatial association and geographical detector methods, and 35 influencing factors were selected to assess their influence on urban air pollution occurrence in 229 cities and counties in South Korea. The results indicated the spatial pattern of the particulate matter concentration in these locations showed strong spatial correlation, and it was confirmed that there was a difference in distribution according to the season. As a result of the analysis of influencing factors, it was found that environment and land use characteristics were the main influencing factors for PM10 and PM2.5. The explanatory power between the two influencing factors of particulate matter was greater than that of a single influencing factor. In addition, most influencing factors resulted in both positive and negative effects on urban fine particulate matter pollution. The interaction relationship of all factors showed a strong action effect in the case of both PM10 and PM2.5, so it was confirmed that all influencing factors were interdependent. In particular, the findings proved that combining the two factors would have a more pronounced effect on particulate matter than when they were independent. We confirmed the significant results for the factors affecting particulate matter. This study offers suggestions on reducing urban air pollution occurrence that can be used to provide a basis and reference for the government to form policies on urban air pollution control in cities and counties.

LPS Response Is Impaired by Urban Fine Particulate Matter.

Fine particulate matter (PM2.5) is a complex mixture of components with diverse chemical and physical characteristics associated with increased respiratory and cardiovascular diseases mortality. Our study aimed to investigate the effects of exposure to concentrated PM2.5 on LPS-induced lung injury onset. BALB/c male mice were exposed to either filtered air or ambient fine PM2.5 in an ambient particle concentrator for 5 weeks. Then, an acute lung injury was induced with nebulized LPS. The animals were euthanized 24 h after the nebulization to either LPS or saline. Inflammatory cells and cytokines (IL-1β, IL-4, IL-5, IL-6, IL-10, IL-17, TNF) were assessed in the blood, bronchoalveolar lavage fluid (BALF), and lung tissue. In addition, lung morphology was assessed by stereological methods. Our results showed that the PM+LPS group showed histological evidence of injury, leukocytosis with increased neutrophils and macrophages, and a mixed inflammatory response profile, with increased KC, IL-6, IL-1β, IL-4, and IL-17. Our analysis shows that there is an interaction between the LPS nebulization and PM2.5 exposure, differently modulating the inflammatory response, with a distinct response pattern as compared to LPS or PM2.5 exposure alone. Further studies are required to explain the mechanism of immune modulation caused by PM2.5 exposure.

Urban fine particulate matter causes cardiac hypertrophy through calcium-mediated mitochondrial bioenergetics dysfunction in mice hearts and human cardiomyocytes

In recent years, the cardiovascular toxicity of urban fine particulate matter (PM2.5) has sparked significant alarm. Mitochondria produce 90% of ATP and make up 30% of the volume of cardiomyocytes. Thus knowledge of myocardial mitochondrial dysfunction due to PM2.5 exposure is essential for further cardiotoxic effects. Here, the mechanism of PM2.5-induced cardiac hypertrophy through calcium overload and mitochondrial dysfunction was investigated in vivo and in vitro. Male and female BALB/c mice were given 1.28, 5.5, and 11 mg PM2.5/kg bodyweight weekly through oropharyngeal inhalation for four weeks and were assigned to low, medium, and high dose groups, respectively. PM2.5-induced myocardial edema and cardiac hypertrophy were detected in the high-dose group. Mitochondria were scattered and ruptured with abnormal ultrastructural morphology. In vitro experiments on human cardiomyocyte AC16 showed that exposure to PM2.5 for 24 h caused opened mitochondrial permeability transition pore --leading to excessive calcium production, decreased mitochondrial membrane potential, weakened mitochondrial respiratory metabolism capacity, and decreased ATP production. Nevertheless, the administration of calcium chelator ameliorated the mitochondrial damage in the PM2.5-treated group. Our in vivo and in vitro results confirmed that calcium overload under PM2.5 exposure triggered mTOR/AKT/GSK-3β activation, leading to mitochondrial bioenergetics dysfunction and cardiac hypertrophy.

Urban fine particulate air pollution exposure promotes atherosclerosis in apolipoprotein E-deficient mice by activating perivascular adipose tissue inflammation via the Wnt5a/Ror2 signaling pathway

Urban fine particulate matter (PM2.5) is a deleterious risk factor in the ambient air and is recognized to exacerbate atherosclerosis. Perivascular adipose tissue (PVAT) secretes a large number of inflammatory cytokines and plays a crucial role in the pathogenic microenvironment of atherogenesis. However, there is a lack of knowledge about the role of PVAT inflammation in the genesis of PM2.5-related atherosclerosis. The aim of this research was to probe the latent links between PM2.5 exposure and PVAT inflammation and further discovered the underlying mechanisms of PM2.5-triggered atherosclerosis pathogenesis. Apolipoprotein E-deficient (ApoE−/−) mice were exposed to real-world atmospheric PM2.5 or filtered clean air for three months, the Wnt5a inhibitor Box5 and the Ror2 inhibitor β-Arrestin2 were applied to verify the possible mechanisms. We noticed that the average daily PM2.5 mass concentration was 84.27 ± 28.84 μg/m3. PM2.5 inhalation might significantly expedite the deterioration of atherosclerosis, increase the protein and mRNA expressions of MCP-1, IL-6, TNF-α, Wnt5a, and Ror2 in PVAT tissues, upregulate the distributions of IL-6, TNF-α, MCP-1, and leptin in the histological sections of PVAT, promote lipid deposition in the aorta, elevate the plasma levels of leptin, MCP-1, IL-6, TNF-α, LDL-C, TC, and TG, however, decrease the plasma levels of adiponectin and HDL-C, downregulate the distribution of adiponectin. Nevertheless, these effects caused by PM2.5 exposure were dramatically diminished after the administration of Box5 or β-Arrestin2. This research illuminated that PVAT inflammation was involved in the PM2.5-induced atherosclerosis process, as well as lipid deposition, which was closely associated with the activation of the Wnt5a/Ror2 signaling pathway.

Chemically and temporally resolved oxidative potential of urban fine particulate matter

Vehicle emissions are an important source of particulate matter (PM) in urban areas and have well-known adverse health effects on human health. Oxidative potential (OP) is used as a quantification metric for indexing PM toxicity. In this study, by using a liquid spot sampler (LSS) and the dithiothreitol (DTT) assay, the diurnal OP variation was assessed at a ground-level urban monitoring station. Besides, since the monitoring station was adjacent to the main road, the correlation between OP and traffic volume was also evaluated. PM components, including metals, water-soluble inorganic aerosols (WSIAs), black carbon (BC), and polycyclic aromatic hydrocarbons (PAHs), were also simultaneously monitored. The daytime and evening mean ± std volume-normalized OP (OPv) were 0.46 ± 0.27 and 0.48 ± 0.26 nmol/min/m3, and exhibited good correlations with PM1.0 and BC; however, these concentrations were only weakly correlated with mass-normalized OP (OPm). The mean ± std OPm was higher in the daytime (41.3 ± 13.8 pmol/min/μg) than in the evening (36.1 ± 11.5 pmol/min/μg). According to the PMF analysis, traffic emissions dominated the diurnal OP contribution. Organic matter and individual metals associated with non-exhaust traffic emissions, such as Mn, Fe, and Cu, contributed substantially to OP. Diurnal variations of PAH concentrations suggest that photochemical reactions could enhance OP, highlighting the importance of atmospheric aging on PM toxicity.

Identification of toxicity pathway of diesel particulate matter using AOP of PPARγ inactivation leading to pulmonary fibrosis

Diesel particulate matter (DPM), a major subset of urban fine particulate matter (PM2.5), raises huge concerns for human health and has therefore been classified as a group 1 carcinogen by the International Agency for Research on Cancer (IARC). However, as DPM is a complex mixture of various chemicals, understanding of DPM’s toxicity mechanism remains limited. As the major exposure route of DPM is through inhalation, we herein investigated its toxicity mechanism based on the Adverse Outcome Pathway (AOP) of pulmonary fibrosis, which we previously submitted to AOPWiki as AOP ID 206 (AOP206). We first screened whether individual chemicals in DPM have the potential to exert their toxicity through AOP206 by using the ToxCast database and deep learning models approach, then confirmed this by examining whether DPM as a mixture alters the expression of the molecular initiating event (MIE) and key events (KEs) of AOP206. For identifying the activeness of the component chemicals of DPM, we used 24 ToxCast assays potentially related to AOP206 and deep learning models based on these assays, which were identified and developed in our previous study. Of the 100 individual chemicals in DPM, 34 were active in PPARγ (MIE)-related assay, of which 17 were active in one or more KEs. To further identify whether individual chemicals in DPM are related to the MIE of AOP206, we performed molecular docking simulation on PPARγ for the chemicals showing activeness. Benzo[e]pyrene, benzo[a]pyrene and other related chemicals were the most likely to bind to PPARγ. In in vitro experiments, PPARγ activity increased with exposure of the DPM mixture, and the protein expression of PPARγ (MIE), and fibronectin (AO) also tended to be increased. Overall, we have demonstrated that AOP206 can be applied to identify the toxicity pathway of DPM. Further, we suggest that applying the AOP approach using ToxCast and deep learning models is useful for identifying potential toxicity pathways of chemical mixtures, such as DPM, by determining the activity of individual chemicals.

Tris(2,4-di-tert-butylphenyl)phosphate: An Unexpected Abundant Toxic Pollutant Found in PM2.5.

A novel pollutant, tris(2,4-di-tert-butylphenyl)phosphate (I168O), was identified in urban fine particulate matter (PM2.5) samples in a nontargeted screening based on mass spectrometry for the first time. I168O was detected in all samples collected from two typical cities far away from each other in China. The concentrations of I168O reached up to 851 (median: 153) ng/m3, indicating that it was a widespread and abundant pollutant in the air. The antioxidant Irgafos 168 [I168, tris(2,4-di-tert-butylphenyl)phosphite] popularly added in plastics was the most suspected source for the detected I168O. Simulation studies indicated that heating, UV radiation, and water contact might significantly (p < 0.05) transform I168 to I168O. In particular, I168O might be magnificently evaporated into the air at high temperatures. The outdoor inhalation exposure of I168O may exert substantial health risks.

In vitro genomic damage induced by urban fine particulate matter on human lymphocytes

Urban air pollution represents a global problem, since everyday many mutagenic and carcinogens compounds are emitted into the atmosphere, with consequent adverse health effects on humans and biota. Specifically, particulate matter air pollution was associated with increased risks in human mortality and morbidity. In this paper, we analyse the genomic effects on human lymphocytes of different concentrations of annual Turin PM2.5 extract by an in vitro micronuclei assay. Samplings were collected from an urban meteorological-chemical station positioned in Turin (Italy), one of the most polluted cities in Europe. PM2.5 sampled on filters was used for organic extraction in monthly pools and successively aggregated to produce a mixture representative for a full year PM2.5 collection. Lymphocytes were exposed to four concentrations of PM2.5: 5, 10, 15 and 20 μg/mL and micronuclei, nucleoplasmic bridges and nuclear buds were scored. With respect to controls, PM2.5 significantly increased the frequencies of all analysed biomarkers at all tested concentrations, whereas the CBPI index was significantly reduced only at the concentration of 20 μg/mL. Such in vitro effects can both to stimulate local authorities to adopt efficient measures for air pollution mitigation and to improve human monitoring to detect early precancer lesions.

Influence of Inorganic Gases on Formation and Chemical Composition of Monoaromatic Hydrocarbons Secondary Organic Aerosol

Abstract SO2, NOx and NH3 are common low molecular weight inorganic gases in the atmosphere that can affect the formation and chemical composition of secondary organic aerosols (SOA) through photochemical reaction processes. SOA formed from photooxidation of volatile organic compounds (VOCs) released by motor vehicle exhaust, such as monoaromatic hydrocarbons, are an important component of urban fine particulate matter, which has a significant impact on climate change, human health and atmospheric visibility. However, previous studies focused on photooxidation of biogenic volatile organic compounds, and relatively few on the reaction of anthropogenic monoaromatic hydrocarbons with high content in the atmosphere with inorganic gases such as SO2, NOx and NH3. In this paper, the photochemical mechanism and five kinds of common chemical composition of the laboratory simulation of SOA formation from OH• radical initiating oxidation of monoaromatic hydrocarbons were summarized, and the effects of SO2, NOx and NH3 on the formation and chemical composition of monoaromatic hydrocarbons SOA by homogeneous and heterogeneous chemical reactions were also discussed. It is helpful to deeply understand the formation mechanism and chemical composition of SOA and atmospheric brown carbon under the conditions of complex atmospheric pollution, and has certain reference significance for the prevention, control and treatment of air pollution in China at present.

The effect and mechanism of urban fine particulate matter (PM2.5) on horizontal transfer of plasmid-mediated antimicrobial resistance genes

Fine particulate matter (PM2.5) and antimicrobial resistance are two major threats to public health worldwide. Current air pollution studies rely heavily on the assessment of PM2.5 chemistry and toxicity. However, whether and how PM2.5 affects the proliferation and transfer of antimicrobial resistance genes (ARGs) in various environments has remained unanswered. This study investigated the effects and potential mechanisms of urban PM2.5 on the horizontal transfer of ARGs between opportunistic Escherichia coli (E. coli) strains. The results showed that urban PM2.5 samples collected from Xi'an (XA), Shanghai (SH), and Shijiazhuang (SJZ) in China induced location- and concentration-dependent promotion of conjugative transfer frequencies compared to the control group. The relevant mechanisms were also explored, including the formation of intracellular reactive oxygen species (ROS) and the subsequent induction of oxidative stress, SOS response, changes in membrane permeability, and alternations in mRNA expression of genes involved in horizontal transfer. This study highlights the effect of PM2.5 on promoting the horizontal transfer of ARGs and elucidates the mechanism of the antimicrobial-resistance risks posed by urban PM2.5. These findings are of great value in understanding the transmission of antimicrobial resistance in various environments and provide valuable information for re-evaluating air quality assessment practices.

Evidence of the mitigated urban particulate matter island (UPI) effect in China during 2000–2015

Urban fine particulate matter (PM2.5) pollution has been the subject of great concern, due to its remarkable adverse effects on public health. However, quantitative investigations of the spatial concentration trends from urban to background areas are still lacking. The urban particulate matter island (UPI) effect, referring to the phenomenon that higher particle concentrations in urban areas are gradually attenuated to background areas, is found and investigated in this study. UPI intensity (UPII) and its footprint (UPIFP) are defined to quantify the magnitude and extent of UPI, respectively. Based on observations from 338 Chinese prefectures for 2000–2015, we confirm the existence of the UPI effect, and further reveal its spatiotemporal patterns. We find that: 1) 84% (283/338) of the cities in China in various city levels and climatic zones showed the UPI phenomenon during 2000–2015, and this phenomenon is closely related to the land-use/cover patterns between the urban area and surrounding areas; 2) different spatial patterns of UPI effect are apparent, with high UPII values and small UPIFP values in Beijing-Tianjin-Hebei, moderate UPII values and large UPIFP values in northern China, the Pearl River Delta and the Yangtze River Delta, and high UPII and UPIFP values in the Western Taiwan Straits region; 3) UPI mitigation can be observed nationwide, with significant decreasing trends for both UPII and UPIFP, benefiting from the increase in urban green spaces and the built-up proportion differences between urban and suburban areas during urbanization. Additionally, it is indicated that more urban residents and faster urban expansion correspond to a steeper decline of UPII in China during 2000–2015. The existence and characteristics of the UPI effect in China will allow new insight and understanding of urban pollution patterns, and will provide scientific evidence for urban planning and pollution control.

Diurnal variation in the proinflammatory activity of urban fine particulate matter (PM 2.5) by in vitro assays.

Background: Ambient particulate matter (PM) smaller than 2.5 µm in diameter (PM 2.5) undergoes diurnal changes in chemical composition due to photochemical oxidation. In this study we examine the relationships between oxidative activity and inflammatory responses associated with these diurnal chemical changes. Because secondary PM contains a higher fraction of oxidized PM species, we hypothesized that PM 2.5 collected during afternoon hours would induce a greater inflammatory response than primary, morning PM 2.5. Methods: Time-integrated aqueous slurry samples of ambient PM 2.5 were collected using a direct aerosol-into-liquid collection system during defined morning and afternoon time periods. PM 2.5 samples were collected for 5 weeks in the late summer (August-September) of 2016 at a central Los Angeles site. Morning samples, largely consisting of fresh primary traffic emissions (primary PM), were collected from 6-9am (am-PM 2.5), and afternoon samples were collected from 12-4pm (pm-PM 2.5), when PM composition is dominated by products of photochemical oxidation (secondary PM). The two diurnally phased PM 2.5 slurries (am- and pm-PM 2.5) were characterized for chemical composition and BV-2 microglia were assayed in vitro for oxidative and inflammatory gene responses. Results: Contrary to expectations, the am-PM 2.5 slurry had more proinflammatory activity than the pm-PM 2.5 slurry as revealed by nitric oxide (NO) induction, as well as the upregulation of proinflammatory cytokines IL-1β, IL-6, and CCL2 (MCP-1), as assessed by messenger RNA production. Conclusions: The diurnal differences observed in this study may be in part attributed to the greater content of transition metals and water-insoluble organic carbon (WIOC) of am-PM 2.5 (primary PM) vs. pm-PM 2.5 (secondary PM), as these two classes of compounds can increase PM 2.5 toxicity.

Pro-inflammatory effects of extracted urban fine particulate matter on human bronchial epithelial cells BEAS-2B.

Atmospheric particulate matter (PM) constitutes the major part of urban air pollution and is a heterogeneous mixture of solid and liquid particles of different origin, size, and chemistry. Human exposure to PM in urban areas poses considerable and significant adverse effects on the respiratory system and human health in general. Major contributors to PM content are combustion-related sources such as diesel vehicles, household, and industrial heating. PM is composed of thousands of different high molecular weight organic compounds, including poly-aromatic hydrocarbons (PAHs). The aim of this study was to clarify the cytotoxic effects of the extract of actual urban PM1 with high benzo[a]pyrene (BaP) content collected in Eastern European mid-sized city during winter heating season on human bronchial epithelial cells (BEAS-2B). Decreased cell viability, alteration of cell layer integrity, increased apoptosis, and oxidative stress were observed during the 3-day exposure to the PM extract. In addition, following PM exposure pro-inflammatory cytokine expression was upregulated at gene and protein levels. Morphology and motility changes, i.e., decreased cells' ability to cover scratch area, were also documented. We report here that the extract of urban PM1 may induce bronchial epithelium changes and render it pro-inflammatory and compromised within 3days.

Diurnal variation in the proinflammatory activity of urban fine particulate matter (PM 2.5) by in vitro assays

Background: Ambient particulate matter (PM) smaller than 2.5 µm in diameter (PM 2.5) undergoes diurnal changes in chemical composition due to photochemical oxidation. In this study we examine the relationships between oxidative activity and inflammatory responses associated with these diurnal chemical changes. Because secondary PM contains a higher fraction of oxidized PM species, we hypothesized that PM 2.5 collected during afternoon hours would induce a greater inflammatory response than primary, morning PM 2.5. Methods: Time-integrated aqueous slurry samples of ambient PM 2.5 were collected using a direct aerosol-into-liquid collection system during defined morning and afternoon time periods. PM 2.5 samples were collected for 5 weeks in the late summer (August-September) of 2016 at a central Los Angeles site. Morning samples, largely consisting of fresh primary traffic emissions (primary PM), were collected from 6-9am (am-PM 2.5), and afternoon samples were collected from 12-4pm (pm-PM 2.5), when PM composition is dominated by products of photochemical oxidation (secondary PM). The two diurnally phased PM 2.5 slurries (am- and pm-PM 2.5) were characterized for chemical composition and BV-2 microglia were assayed in vitro for oxidative and inflammatory gene responses. Results: Contrary to expectations, the am-PM 2.5 slurry had more proinflammatory activity than the pm-PM 2.5 slurry as revealed by nitric oxide (NO) induction, as well as the upregulation of proinflammatory cytokines IL-1β, IL-6, and CCL2 (MCP-1), as assessed by messenger RNA production. Conclusions: The diurnal differences observed in this study may be in part attributed to the greater content of transition metals and water-insoluble organic carbon (WIOC) of am-PM 2.5 (primary PM) vs. pm-PM 2.5 (secondary PM), as these two classes of compounds can increase PM 2.5 toxicity.

Diurnal variation in the proinflammatory activity of urban fine particulate matter (PM2.5) by in vitro assays

Background: Ambient particulate matter (PM) smaller than 2.5 µm in diameter (PM2.5) undergoes diurnal changes in chemical composition due to photochemical oxidation. In this study we examine the relationships between oxidative activity and inflammatory responses associated with these diurnal chemical changes. Because secondary PM contains a higher fraction of oxidized PM species, we hypothesized that PM2.5 collected during afternoon hours would induce a greater inflammatory response than primary, morning PM2.5. Methods: Time-integrated aqueous slurry samples of ambient PM2.5 were collected using a direct aerosol-into-liquid collection system during defined morning and afternoon time periods. PM2.5 samples were collected for 5 weeks in the late summer (August-September) of 2016 at a central Los Angeles site. Morning samples, largely consisting of fresh primary traffic emissions (primary PM), were collected from 6-9am (am-PM2.5), and afternoon samples were collected from 12-4pm (pm-PM2.5), when PM composition is dominated by products of photochemical oxidation (secondary PM). The two diurnally phased PM2.5 slurries (am- and pm-PM2.5) were characterized for chemical composition and BV-2 microglia were assayed in vitro for oxidative and inflammatory gene responses. Results: Contrary to expectations, the am-PM2.5 slurry had more proinflammatory activity than the pm-PM2.5 slurry as revealed by nitric oxide (NO) induction, as well as the upregulation of proinflammatory cytokines IL-1β, IL-6, and CCL2 (MCP-1), as assessed by messenger RNA production. Conclusions: The diurnal differences observed in this study may be in part attributed to the greater content of transition metals and water-insoluble organic carbon (WIOC) of am-PM2.5 (primary PM) vs. pm-PM2.5 (secondary PM), as these two classes of compounds can increase PM2.5 toxicity.

Diurnal variation in the proinflammatory activity of urban fine particulate matter (PM 2.5) by in vitro assays.

Background: Ambient particulate matter (PM) smaller than 2.5 µm in diameter (PM 2.5) undergoes diurnal changes in chemical composition due to photochemical oxidation. In this study we examine the relationships between oxidative activity and inflammatory responses associated with these diurnal chemical changes. Because secondary PM contains a higher fraction of oxidized PM species, we hypothesized that PM 2.5 collected during afternoon hours would induce a greater inflammatory response than primary, morning PM 2.5. Methods: Time-integrated aqueous slurry samples of ambient PM 2.5 were collected using a direct aerosol-into-liquid collection system during defined morning and afternoon time periods. PM 2.5 samples were collected for 5 weeks in the late summer (August-September) of 2016 at a central Los Angeles site. Morning samples, largely consisting of fresh primary traffic emissions (primary PM), were collected from 6-9am (am-PM 2.5), and afternoon samples were collected from 12-4pm (pm-PM 2.5), when PM composition is dominated by products of photochemical oxidation (secondary PM). The two diurnally phased PM 2.5 slurries (am- and pm-PM 2.5) were characterized for chemical composition and BV-2 microglia were assayed in vitro for oxidative and inflammatory gene responses. Results: Contrary to expectations, the am-PM 2.5 slurry had more proinflammatory activity than the pm-PM 2.5 slurry as revealed by nitric oxide (NO) induction, as well as the upregulation of proinflammatory cytokines IL-1β, IL-6, and CCL2 (MCP-1), as assessed by messenger RNA production. Conclusions: The diurnal differences observed in this study may be in part attributed to the greater content of transition metals and water-insoluble organic carbon (WIOC) of am-PM 2.5 (primary PM) vs. pm-PM 2.5 (secondary PM), as these two classes of compounds can increase PM 2.5 toxicity.

Urban fine particulate matter (PM2.5) exposure destroys blood–testis barrier (BTB) integrity through excessive ROS-mediated autophagy

Context: Blood–testis barrier (BTB), constituted by tight junctions (TJs), adherens junctions and gap junctions, is important for spermatogenesis. PM2.5 is known to impair testicular functions and reproduction. However, its effects on BTB and the underlying mechanisms remain obscure.Objective: To investigate the roles of autophagy in BTB toxicity induced by PM2.5.Materials and methods: Sprague–Dawley rats were developmentally exposed to normal saline (NS) or PM2.5 with the doses of 9 mg/kg b.w. and 24 mg/kg b.w. via intratracheal instillation for seven weeks. Success rate of mating, sperm quality, testicular morphology, expressions of BTB junction proteins and autophagy-related proteins were detected. In addition, expressions of oxidative stress markers were also analyzed.Results: Our results demonstrated that developmental PM2.5 exposure induced noticeable decreased fertility, significantly reduced sperm count, increased sperm abnormality rate and severe testicular damage in histomorphology. The expressions of TJ (such as ZO-1 and occludin), gap junction (such as connexin43) were down-regulated significantly after PM2.5 treatment. Intriguingly, PM2.5 simultaneously increased the number of autophagosomes and the levels of autophagy marker LC3-II and p62, suggesting that the accumulated autophagosomes resulted from impaired autophagy degradation. Moreover, the expressions of HO-1 levels remarkably increased and expression levels of Gpx and SOD were significantly decreased after PM2.5 exposure. Vitamins E and C could alleviate the PM2.5-induced oxidative stress, reverse the autophagy defect and restore the BTB impairment.Conclusions: Taken together, the results suggest that PM2.5 exposure destroys BTB integrity through excessive ROS-mediated autophagy. Our finding could contribute to a better understanding of PM2.5-induced male reproductive toxicity.