Size-fractionated particulate matters (SPMs) in a range of 9.0 to 0.43 μm, classified based on aerodynamic diameter (dₐₑ) as fine PMs (0.43 μm ≤ dₐₑ < 2.1 μm) and coarse PMs (2.1 μm ≤ dₐₑ < 9.0 μm) were collected by cascade impactors (7 fractions) during smoke haze (SH) and non-smoke haze (NSH) seasons in urban and rural areas of Chiang Mai, Thailand. Their polycyclic aromatic hydrocarbons (PAHs) compositions were determined for respiratory health risk assessment. During SH episode, concentrations of SPMs and PAHs in the rural area were approximately two times higher than in the urban area and about 62–68% of the SPMs were fine particles. Conversely, during NSH season the concentrations in the urban area were higher due to traffic emission. The finest particle sizes (0.65–0.43 μm) contained the highest PAHs concentrations among the other PM sizes. Benzo[b]fluoranthene was a main PAH component found during SH season suggesting biomass burning is a major pollutant source. High molecular weight (5–6 rings) PAHs with high carcinogenicity were likely to concentrate in fine particles. Distribution patterns of SPMs and PAHs during SH season were bimodal with the highest peak at a fine size range (0.65–0.43 μm) and a small peak at a coarse size range (5.8–4.7 μm). Respiratory health risk was estimated based on toxicity equivalent concentrations of PAHs bound-SPMs and inhalation cancer risk (ICR). Relatively high ICR values (1.14 × 10⁻⁴ (rural) and 6.80 × 10⁻⁵ (urban)) were found during SH season in both areas, in which fine particles played an important role. It revealed that high concentration of fine particles in ambient air is related to high respiratory health risk due to high content of carcinogenic substances.

Particulate matter with aerodynamic diameter not larger than 2.5 μm (PM₂.₅) escalated the risk of respiratory diseases. Mitochondrial dysfunction may play a pivotal role in PM₂.₅-induced airway injury. However, the potential effect of PM₂.₅ on mitochondrial permeability transition pore (mPTP)-related airway injury is still unknown. This study aimed to investigate the role of mPTP in PM₂.₅-induced mitochondrial dysfunction in airway epithelial cells in vitro. PM₂.₅ significantly reduced cell viability and caused apoptosis in BEAS-2B cells. We also found PM₂.₅ caused cellular and mitochondrial morphological alterations, evidenced by the disappearance of mitochondrial cristae, mitochondrial swelling, and the rupture of the outer mitochondrial membrane. PM₂.₅ induced mPTP opening via upregulation of voltage-dependent anion-selective channel (VDAC), leading to deprivation of mitochondrial membrane potential, increased mitochondrial reactive oxygen species (ROS) generation and intracellular calcium level. PM₂.₅ suppressed mitochondrial respiratory function by reducing basal and maximal respiration, and ATP production. The mPTP targeting compounds cyclosporin A [CsA; a potent inhibitor of cyclophilin D (CypD)] and VBIT-12 (a selective VDAC1 inhibitor) significantly inhibited PM₂.₅-induced mPTP opening and apoptosis, and preserved mitochondrial function by restoring mitochondrial membrane potential, reducing mitochondrial ROS generation and intracellular calcium content, and maintaining mitochondrial respiration function. Our data further demonstrated that PM₂.₅ caused reduction in nuclear expressions of PPARγ and PGC-1α, which were reversed in the presence of CsA. These findings suggest that mPTP might be a potential therapeutic target in the treatment of PM₂.₅-induced airway injury.

The health effects of potentially toxic elements (PTEs) in airborne particulate matter (PM) are strongly dependent on their size distribution and dissolution. This study examined PTEs within nine distinct sizes of PM in a Chinese megacity, with a focus on their deposited and dissolved bioaccessibility in the human pulmonary region. A Multiple Path Particle Dosimetry (MPPD) model was used to estimate the deposited bioaccessibility, and an in-vitro experiment with simulated lung fluid was conducted for dissolved bioaccessibility. During the non-heating season, the dissolved bioaccessible fraction (DBF) of As, Cd, Co, Cr, Mn, Pb and V were greater in fine PM (aerodynamics less than 2.1 μm) than in coarse PM (aerodynamics between 2.1 and 10 μm), and vice versa for Ni. With the increased demand of heating, the DBF of Pb and As decreased in fine particle sizes, probably due to the presence of oxide/silicate compounds from coal combustion. Inhalation health risks based on the bioaccessible concentrations of PTEs displayed the peaks in <0.43 μm and 2.1–3.3 μm particulate sizes. The non-cancer risk was at an acceptable level (95th percentiles of hazard index (HI) was 0.49), but the cancer risk exceeded the threshold value (95th percentiles of total incremental lifetime cancer risk (TCR) was 8.91 × 10⁻⁵). Based on the results of uncertainty analysis, except for the exposure frequency, the total concentrations and DBF of As and Cr in <0.43 μm particle size segment have a greater influence on the uncertainty of probabilistic risk.

It is enlightening to determine the discrepancies and potential reasons for the degree of impact from the COVID-19 control measures on air quality as well as the associated health and economic impacts. Analysis of air quality, socio-economic factors, and meteorological data from 447 cities in 46 countries indicated that the COVID-19 control measures had significant impacts on the PM₂.₅ (particulate matter with an aerodynamic diameter less than 2.5 μm) concentrations in 20 (reduced PM₂.₅ concentrations of −7.4–29.1 μg m⁻³) of the selected 46 countries. In these 20 countries, the robustly distinguished changes in the PM₂.₅ concentrations caused by the control measures differed between the developed (95% confidence interval (CI): −2.7–5.5 μg m⁻³) and developing countries (95% CI: 8.3–23.2 μg m⁻³). As a result, the COVID-19 lockdown reduced death and hospital admissions change from the decreased PM₂.₅ concentrations by 7909 and 82,025 cases in the 12 developing countries, and by 78 and 1214 cases in the eight developed countries. The COVID-19 lockdown reduced the economic cost from the PM₂.₅ related health burden by 54.0 million dollars in the 12 developing countries and by 8.3 million dollars in the eight developed countries. The disparity was related to the different chemical compositions of PM₂.₅. In particular, the concentrations of primary PM₂.₅ (e.g., BC) in cities of developing countries were 3–45 times higher than those in developed countries, so the mass concentration of PM₂.₅ was more sensitive to the reduced local emissions in developing countries during the COVID-19 control period. The mass fractions of secondary PM₂.₅ in developed countries were generally higher than those in developing countries. As a result, these countries were more sensitive to the secondary atmospheric processing that may have been enhanced due to reduced local emissions.

We quantify for the first time marine aerosol properties and their differences in the offshore and remote ocean in the mid-latitude South Asian waters, low-latitude South Asian waters, and equatorial waters of the Western Pacific Ocean, based on shipboard cruise observations conducted by the Western Pacific Ocean Scientific Observation Network in winter 2018, and further investigate the effects of long-range transport of continental aerosols on the marine environment. During the overall observation period, the average number concentration of particle matter which aerodynamic diameters<2.5 μm (PM₂.₅N) was 35.1 ± 87.4 cm⁻³ and the mass concentration (PM₂.₅M) was 12.3 ± 9.1 μg/m³. The PM₂.₅N and PM₂.₅M during the continental air mass transport period were 7.2 and 1.3 times higher than those during the non-transport period (109.2 ± 169.3 cm⁻³, 15.9 ± 14.9 μg/m³), respectively. Excluding transport period, the average PM₂.₅N and PM₂.₅M are reduced by 120% and 7%. Coarse mode particle number concentration (PM₂.₅–₁₀N) and mass concentration (PM₂.₅–₁₀M) are not significantly influenced by continental air masses (only a reduction of 7% and 2%). The variation of marine aerosol concentrations in different latitudes zones is greatly influenced by continental aerosol transport. The offshore PM₂.₅M/PM₁₀M was 30%, 21%, and 22% in the mid-latitude sea of South Asia, a low-latitude sea of South Asia, and the equatorial sea, respectively. In comparison, in the remote ocean, the distribution ratio of PM₂.₅M/PM₁₀M tended to be steady (22%–23%), and the background characteristics of marine aerosols were clearly represented. The aerosol concentration decreases with the increase of wind speed during the transport period, and the wind speed reflects the scavenging effect on aerosol. In the non-transport period, the wind speed at the sea surface promotes the generation of marine aerosols, and the impact in wind speed is strongest in the PM₂.₅–PM₅ particle size range.

Several studies have reported an association between residential surrounding particulate matter with an aerodynamic diameter ≤2.5 μm (PM₂.₅) and coronary heart disease (CHD). However, the underlying biological mechanism remains unclear. To fill this research gap, this study enrolled a residentially stable sample of 942 patients with CHD and 1723 controls. PM₂.₅ concentration was obtained from satellite-based annual global PM₂.₅ estimates for the period 1998–2019. MicroRNA microarray and pathway analysis of target genes was performed to elucidate the potential biological mechanism by which PM₂.₅ increases CHD risk. The results showed that individuals exposed to high PM₂.₅ concentrations had higher risks of CHD than those exposed to low PM₂.₅ concentrations (odds ratio = 1.22, 95% confidence interval: 1.00, 1.47 per 10 μg/m³ increase in PM₂.₅). Systolic blood pressure mediated 6.6% of the association between PM₂.₅ and CHD. PM₂.₅ and miR-4726-5p had an interaction effect on CHD development. Bioinformatic analysis demonstrated that miR-4726-5p may affect the occurrence of CHD by regulating the function of RhoA. Therefore, individuals in areas with high PM₂.₅ exposure and relative miR-4726-5p expression have a higher risk of CHD than their counterparts because of the interaction effect of PM₂.₅ and miR-4726-5p on blood pressure.

Airborne bacteria may absorb the substance from the atmospheric particles and play a role in biogeochemical cycling. However, these studies focused on a few culturable bacteria and the samples were usually collected from one site. The metabolic potential of a majority of airborne bacteria on a regional scale and their driving factors remain unknown. In this study, we collected particulates with aerodynamic diameter ≤2.5 μm (PM₂.₅) from 8 cities that represent different regions across China and analyzed the samples via high-throughput sequencing of 16S rRNA genes, quantitative polymerase chain reaction (qPCR) analysis, and functional database prediction. Based on the FAPROTAX database, 326 (80.69%), 191 (47.28%) and 45 (11.14%) bacterial genera are possible to conduct the pathways of carbon, nitrogen, and sulfur cycles, respectively. The pathway analysis indicated that airborne bacteria may lead to the decrease in organic carbon while the increase in ammonium and sulfate in PM₂.₅ samples, all of which are the important components of PM₂.₅. Among the 19 environmental factors studied including air pollutants, meteorological factors, and geographical conditions, PM₂.₅ concentration manifested the strongest correlations with the functional genes for the transformation of ammonium and sulfate. Moreover, the PM₂.₅ concentration rather than the sampling site will drive the distribution of functional genera. Thus, a bi-directional relationship between PM₂.₅ and bacterial metabolism is suggested. Our findings shed light on the potential bacterial pathway for the biogeochemical cycling in the atmosphere and the important role of PM₂.₅, offering a new perspective for atmospheric ecology and pollution control.

PM₂.₅ (particulate matter having aerodynamic diameter ≤2.5 μm) samples were collected during wintertime from two polluted urban sites (Allahabad and Kanpur) in the central Indo-Gangetic Plain (IGP) to comprehend the sources and atmospheric transformations of light-absorbing water-soluble organic aerosol (WSOA). The aqueous extract of each filter was atomized and analyzed in a high-resolution time-of-flight aerosol mass spectrometer (HR-ToF-AMS). Water-soluble organic carbon (WSOC) and WSOA concentrations at Kanpur were ∼1.2 and ∼1.5 times higher than that at Allahabad. The fractions of WSOC and secondary organic carbon (SOC) to total organic carbon (OC) were also significantly higher ∼53% and 38%, respectively at Kanpur compared to Allahabad. This indicates a higher abundance of oxidized WSOA at Kanpur. The absorption coefficient (bₐbₛ₋₃₆₅) of light-absorbing WSOA measured at 365 nm was 46.5 ± 15.5 Mm⁻¹ and 73.2 ± 21.6 Mm⁻¹ in Allahabad and Kanpur, respectively, indicating the dominance of more light-absorbing fractions in WSOC at Kanpur. The absorption properties such as mass absorption efficiency (MAE₃₆₅) and imaginary component of refractive index (kₐbₛ₋₃₆₅) at 365 nm at Kanpur were also comparatively higher than Allahabad. The absorption forcing efficiency (Abs SFE; indicates warming effect) of WSOA at Kanpur was ∼1.4 times higher than Allahabad. Enhancement in light absorption capacity was observed with the increase in f44/f43 (fraction of m/z 44 (f44) to 43 (f43) in organic mass spectra) and O/C (oxygen to carbon) ratio of WSOA at Kanpur while no such trend was observed for the Allahabad site. Moreover, the correlation between carbon fractions and light absorption properties suggested the influence of low-volatile organic compounds (OC3 + OC4 fraction obtained from thermal/optical carbon analyzer) in increasing the light absorption capacity of WSOA in Kanpur.

The adverse effects of fine atmospheric particulate matter with aerodynamic diameters of ≤2.5 μm (PM₂.₅) are closely associated with particulate chemicals. In this study, PM₂.₅ samples were collected from highway and industry sites in Hangzhou, China, during the autumn and winter, and their cytotoxicity and pulmonary toxicity and endocrine-disrupting potential (EDP) were evaluated in vitro and in vivo; the particulate polycyclic aromatic hydrocarbons (PAHs), phthalate esters (PAEs), and heavy metals were then characterized. The toxicological results suggested that the PM₂.₅ from highway site induced higher cytotoxicity (cell viability inhibition, intracellular oxidative stress, and cell membrane injury) and pulmonary toxicity (inflammatory response (IR) and oxidative stress (OS)) than the samples from industry site, while the PM₂.₅ from industry site exhibited higher EDP (estrogenic and anti-androgenic activity). The cytotoxicity and pulmonary toxicity of PM₂.₅ in the winter were higher than those in the autumn, while no seasonal difference in the endocrine-disrupting potential was observed (p > 0.05). The Pearson correlation analysis between the biological effects and particulate chemicals revealed that the PM₂.₅-induced inflammatory response and oxidative stress were closely associated with the particulate PAHs and heavy metals (Pearson correlation coefficients: rIR, PAHₛ = 0.822–0.988, rIR, ₕₑₐᵥy ₘₑₜₐₗₛ = 0.895–0.971, rOS, PAHₛ = 0.843–0.986, and rOS, ₕₑₐᵥy ₘₑₜₐₗₛ = 0.887–0.933), while particulate di (2-ethylhexyl)phthalate (DEHP) substantially contributed to the EDP of PM₂.₅ (rEDP, DEHP = 0.981). This study indicated that the toxicity and EDP of PM₂.₅ could vary with the surrounding environment and season, which was closely associated with the variations of particulate chemicals. Further studies are needed to clarify the associations between the harmful effects of PM₂.₅ and other contributing factors.

The presence of urban greenspace may lead to reduced personal exposure to air pollution via several mechanisms, for example, increased dispersion of airborne particulates; however, there is a lack of real-time evidence across different urban contexts. Study participants were 79 adolescents with asthma who lived in Delhi, India and were recruited to the Delhi Air Pollution and Health Effects (DAPHNE) study. Participants were monitored continuously for exposure to PM₂.₅ (particulate matter with an aerodynamic diameter of less than 2.5 μm) for 48 h. We isolated normal day-to-day walking journeys (n = 199) from the personal monitoring dataset and assessed the relationship between greenspace and personal PM₂.₅ using different spatial scales of the mean Normalised Difference Vegetation Index (NDVI), mean tree cover (TC), and proportion of surrounding green land use (GLU) and parks or forests (PF). The journeys had a mean duration of 12.7 (range 5, 53) min and mean PM₂.₅ personal exposure of 133.9 (standard deviation = 114.8) μg/m³. The within-trip analysis showed weak inverse associations between greenspace markers and PM₂.₅ concentrations only in the spring/summer/monsoon season, with statistically significant associations for TC at the 25 and 50 m buffers in adjusted models. Between-trip analysis also indicated inverse associations for NDVI and TC, but suggested positive associations for GLU and PF in the spring/summer/monsoon season; no overall patterns of association were evident in the autumn/winter season. Associations between greenspace and personal PM₂.₅ during walking trips in Delhi varied across metrics, spatial scales, and season, but were most consistent for TC. These mixed findings may partly relate to journeys being dominated by walking along roads and small effects on PM₂.₅ of small pockets of greenspace. Larger areas of greenspace may, however, give rise to observable spatial effects on PM₂.₅, which vary by season.