The present investigation examined the impact of highways on the global dispersion patterns of metallic elements present in dust and snow. A total of 18 mixed snow samples were collected from both sides of the Moscow-Tambo-Astrakhan Caspian Highway by the end of the winter season. The analysis of the samples indicated the presence of 35 distinct chemical elements, where Al, Ba, Ca, Fe, K, Mg, Na, and Zn were identified as the primary contaminants. The primary area of pollution on the windward side originating from the road spans a distance of 20-40 meters, while on the leeward side, it extends to 10 meters. The data presented suggests that the metals found in highways exhibited variability in terms of their solubility in water and concentration. Our findings demonstrate that the predominant wind directions affect the dispersion of pollutants. Furthermore, it was observed that the region with a higher concentration of metal on the side of the road facing the wind had a thickness that was 2-3 times less than that of the opposite side. It is advisable to conduct a subsequent inquiry within the ensuing five years to obtain dependable data regarding the extent of metal pollution.

Traffic contributes to fine particulate matter (PM₂.₅) in the atmosphere through engine exhaust emissions and road dust generation. However, the evolution of traffic related PM₂.₅ emission over recent years remains unclear, especially when various efforts to reduce emission e.g., aftertreatment technologies and high emission standards from China IV to China V, have been implemented. In this study, hourly elemental carbon (EC), a marker of primary engine exhaust emissions, and trace element of calcium (Ca), a marker of road dust, were measured at a nearby highway sampling site in Shanghai from 2016 to 2019. A random forest-based machine learning algorithm was applied to decouple the influences of meteorological variables on the measured EC and Ca, revealing the deweathered trend in exhaust emissions and road dust. After meteorological normalization, we showed that non-exhaust emissions, i.e., road dust from traffic, increased their fractional contribution to PM₂.₅ over recent years. In particular, road dust was found to be more important, as revealed by the deweathered trend of Ca fraction in PM₂.₅, increasing at 6.1% year⁻¹, more than twice that of EC (2.9% year⁻¹). This study suggests that while various efforts have been successful in reducing vehicular exhaust emissions, road dust will not abate at a similar rate. The results of this study provide insights into the trend of traffic-related emissions over recent years based on high temporal resolution monitoring data, with important implications for policymaking.

Particulate matter from wood burning emissions (Cwₒₒd) was quantified at five locations in the United Kingdom (UK), comprising three rural and two urban sites between 2009 and 2021. The aethalometer method was used. Mean winter Cwₒₒd concentrations ranged from 0.26 μg m⁻³ (in rural Scotland) to 1.30 μg m⁻³ (London), which represented on average 4% (in rural environments) and 5% (urban) of PM₁₀ concentrations; and 8% of PM₂.₅. Concentrations were greatest in the evenings in winter months, with larger evening concentrations in the weekends at the urban sites. Random-forest (RF) machine learning regression models were used to reconstruct Cwₒₒd concentrations using both meteorological and temporal explanatory variables at each site. The partial dependency plots indicated that temperature and wind speed were the meteorological variables explaining the greatest variability in Cwₒₒd, with larger concentrations during cold and calm conditions. Peaks of Cwₒₒd concentrations took place during and after events that are celebrated with bonfires. These were Guy Fawkes events in the urban areas and on New Year's Day at the rural sites; the later probably related to long-range transport. Time series were built using the RF. Having removed weather influences, long-term trends of Cwₒₒd were estimated using the Theil Sen method. Trends for 2015–2021 were downward at three of the locations (London, Glasgow and rural Scotland), with rates ranging from −5.5% year⁻¹ to −2.5% year⁻¹. The replacement of old fireplaces with lower emission wood stoves might explain the decrease in Cwₒₒd especially at the urban sites The two rural sites in England observed positive trends for the same period but this was not statistically significant.

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.

Plastic pollution has become one of the most pressing environmental issues. Recycling is a potential means of reducing plastic pollution in the environment. However, plastic fragments are still likely released to the aquatic environment during mechanical recycling processes. Here, we examined the plastic inputs and effluent outputs of three mechanical recycling facilities in Vietnam dealing with electronic, bottle, and household plastic waste, and we found that large quantities of microplastics (plastics <5 mm in length) are generated and released to the aquatic environment during mechanical recycling without proper treatment. Comparisons with literature data for microplastics in wastewater treatment plant effluents and surface water indicated that mechanical recycling of plastic waste is likely a major point source of microplastics pollution. Although there is a mismatch between the size of the microplastics examined in the present study and the predicted no-effect concentration reported, it is still possible that microplastics generated at facilities pose risks to the aquatic environment because there might be many plastic particulates smaller than 315 μm, as suggested by our obtained size distributions. With mechanical recycling likely to increase as we move to a circular plastics economy, greater microplastics emissions can be expected. It is therefore an urgent need to fully understand not only the scale of microplastic generation and release from plastic mechanical recycling but also the environmental risk posed by microplastics in the aquatic environment.

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.

Fine particulate matter (PM₂.₅) has been associated with risk of oral and respiratory diseases. However, the biological mechanisms of adverse oral and respiratory health response to PM₂.₅ fluctuation have not been well characterized. This study aims to explore the relationships of PM₂.₅ with airway inflammation, salivary biomarkers and buccal mucosa microbiota. We performed a panel study among 40 college students involving 4 follow-ups from August to October 2021 in Hefei, Anhui Province, China. Health outcomes included fractional exhaled nitric oxide (FeNO), salivary biomarkers [C-reactive protein (CRP), cortisol, lysozyme and alpha-amylase] and buccal mucosa microbial diversity. Linear mixed-effect models were applied to explore the cumulative impacts of PM₂.₅ on health indicators. PM₂.₅ was positively correlated with FeNO, CRP, cortisol and alpha-amylase, while negatively with lysozyme. Per 10-μg/m³ increase in PM₂.₅ was linked to maximum increments in FeNO of 10.71% (95%CI: 2.01%, 19.41%) at lag 0–24 h, in CRP of 7.10% (95%CI: 5.39%, 8.81%) at lag 0–24 h, in cortisol of 1.25% (95%CI: 0.44%, 2.07%) at lag 0–48 h, and in alpha-amylase of 2.12% (95%CI: 0.53%, 3.71%) at lag 0–24 h, while associated with maximum decrement in lysozyme of 0.53% (95%CI: 0.12%, 0.95%) at lag 0–72 h. Increased PM₂.₅ was linked to reduction in the richness and evenness of buccal microbe and o_Bacillales and o_Bacteroidales were identified as differential microbes after PM₂.₅ inhalation. Bio-information analysis indicated that immunity system pathway was the most important enriched abundant process altered by PM₂.₅ exposure. In summary, short-term PM₂.₅ exposure may impair oral and respiratory health by inducing inflammatory and stress responses, weakening immune function and altering buccal mucosa microbial diversity.

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.

Recently, increasing attention has been paid to antibiotic resistance genes (ARGs) in urban stormwater runoff. However, there were little data on the diversity and distribution of ARGs associated with road sediments transported in runoff. The investigation of ARGs diversity showed that sulfonamide resistance genes (sul2 and sul3) occupied 61.7%–82.3% of total ARGs in runoff. The analysis of ARGs distribution in particulate matter (PM) implied that both tetQ and trbC existed mainly in PM with size of 150–300 μm, but other ARGs and mobile genetic elements (MGEs) were dominant in PM with size <75 μm. The discussion of potential hosts indicated that target genes (ermF, blaOXA1/blaOXA30, ermC, qnrA, sul2, tnpA-01, intI2, tetW, intI1, sul3, trbC) had the strongest subordinate relationship with Proteobacteria at phylum level and Enterobacter at genus level. The effect evaluation of ARGs distribution suggested that 13 kinds of ARGs were positively correlated with Pr/PS and Zeta potential, resulting in the more ARGs in PM with smaller size (<75 μm).

The consequence of the lockdowns implemented to address the COVID-19 pandemic on human health damage due to air pollution and other environmental issues must be better understood. This paper analyses the effect of reducing energy demand on the evolution of environmental impacts during the occurrence of 2020-lockdown periods in Italy, with a specific focus on life expectancy. An energy metabolism analysis is conducted based on the life cycle assessment (LCA) of all monthly energy consumptions, by sector, category and province area in Italy between January 2015 to December 2020. Results show a general decrease (by ∼5% on average) of the LCA midpoint impact categories (global warming, stratospheric ozone depletion, fine particulate matter formation, etc.) over the entire year 2020 when compared to past years. These avoided impacts, mainly due to reductions in fossil energy consumptions, are meaningful during the first lockdown phase between March and May 2020 (by ∼21% on average). Regarding the LCA endpoint damage on human health, ∼66 Disability Adjusted Life Years (DALYs) per 100,000 inhabitants are estimated to be saved. The analysis shows that the magnitude of the officially recorded casualties is substantially larger than the estimated gains in human lives due to the environmental impact reductions. Future research could therefore investigate the complex cause-effect relationships between the deaths occurred in 2020 imputed to COVID-19 disease and co-factors other than the SARS-CoV-2 virus.