A comprehensive modelling approach has been developed to predict population exposure to the ambient air PM₂.₅ concentrations in different microenvironments in London. The modelling approach integrates air pollution dispersion and exposure assessment, including treatment of the locations and time activity of the population in three microenvironments, namely, residential, work and transport, based on national demographic information. The approach also includes differences between urban centre and suburban areas of London by taking account of the population movements and the infiltration of PM₂.₅ from outdoor to indoor. The approach is tested comprehensively by modelling ambient air concentrations of PM₂.₅ at street scale for the year 2008, including both regional and urban contributions. Model analysis of the exposure in the three microenvironments shows that most of the total exposure, 85%, occurred at home and work microenvironments and 15% in the transport microenvironment. However, the annual population weighted mean (PWM) concentrations of PM₂.₅ for London in transport microenvironments were almost twice as high (corresponding to 13–20 μg/m³) as those for home and work environments (7–12 μg/m³). Analysis has shown that the PWM PM₂.₅ concentrations in central London were almost 20% higher than in the surrounding suburban areas. Moreover, the population exposure in the central London per unit area was almost three times higher than that in suburban regions. The exposure resulting from all activities, including outdoor to indoor infiltration, was about 20% higher, when compared with the corresponding value obtained assuming inside home exposure for all times. The exposure assessment methodology used in this study predicted approximately over one quarter (−28%) lower population exposure, compared with using simply outdoor concentrations at residential locations. An important implication of this study is that for estimating population exposure, one needs to consider the population movements, and the infiltration of pollution from outdoors to indoors.

Both air pollution and dyslipidemias contributed to large number of deaths and disability-adjusted life lost years. Long-term air pollution exposure was related to changed blood lipids and risk of dyslipidemias. This study was designed to evaluate relationships between air pollutants, blood lipids and prevalence of dyslipidemias in a Chinese rural population exposed to high-level air pollution based on baseline data of The Henan Rural Cohort study. An amount of 39,057 participants from rural areas in China were included. The 3-year average exposure of air pollutants (PM2.5, PM10, NO2) was estimated by a spatiotemporal model. Logistic and linear regression models were employed to explore relationships between air pollutants, blood lipids (TC, TG, HDL-C and LDL-C) and prevalence of dyslipidemias. The three-year concentration of PM2.5, PM10 and NO2 was 72.8 ± 2.3 μg/m3, 131.5 ± 5.7 μg/m3and 39.1 ± 3.1 μg/m3, respectively. Overall, increased air pollution exposure was related to increased TC and LDL-C, while decreased TG and HDL-C. Each 1-μg/m3 increment of PM2.5 was related to 0.10% (0.07%–0.19%) increase in TC, 0.63% (0.50%–0.77%) increase in LDL-C, 2.93% (2.70%–3.16%) decrease in TG, 0.49% (0.38%–0.60%) decrease in HDL-C; and 5.7% (95%CI: 3.7%–7.6%), 4.0% (95%CI: 2.1%–6.0%) and 3.8% (95%CI: 2.5%–5.1%) increase in odds for hypercholesterolemia, hyperbetalipoproteinemia and hypoalphalipoproteinemia, respectively. Stronger associations were found in male and older participants. Findings suggest that air pollutants were associated with changed blood lipid levels and higher risk of dyslipidemias among rural population. Male and elder people should pay more attention to personal safety protection.

Particulate air pollution is a continuing challenge in China, and its adverse effects on chronic obstructive pulmonary disease (COPD) have been widely reported. However, epidemiological evidence on the associations between size-fractionated particle number concentrations (PNCs) and COPD mortality is limited. In this study, we utilized a time-series approach to investigate the associations between PNCs of particles at 0.25–10 μm in diameter and COPD mortality in Shanghai, China. Quasi-Poisson regression generalized additive models were applied to evaluate these associations, with adjustment of time trend, day of week, holidays, temperature and relative humidity. Stratification analyses were performed by season and gender. There were a total of 3238 deaths due to COPD during the study period. We found that daily COPD deaths were significantly associated with PNCs of particles <0.5 μm, and the magnitude of associations increased with decreasing particle size. An interquartile range (IQR) increase in PNC₀.₂₅—₀.₂₈, PNC₀.₂₈—₀.₃, PNC₀.₃—₀.₃₅, PNC₀.₃₅—₀.₄, PNC₀.₄—₀.₄₅ and PNC₀.₄₅—₋₀.₅ was associated with increments of 7.51% (95%CI: 2.45%, 12.81%), 7.22% (95%CI: 2.16%, 12.53%), 6.95% (95%CI: 1.81%, 12.35%), 6.26% (95%CI: 1.25%, 11.52%), 5.24% (95%CI: 0.56%, 10.13%) and 4.15% (95%CI: 0.14%, 8.32%), respectively. The associations remained robustness after controlling for the mass concentrations of gaseous air pollutants. In stratification analyses, significant associations between PNCs and COPD mortality were observed in the cold seasons, and in males. Our results suggested that particles <0.5 μm in diameter might be most responsible for the adverse effects of particulate air pollution on COPD mortality, and COPD patients are more susceptible to PM air pollution in the cold seasons, especially for males.

The determination of the spatiotemporal patterns and driving factors of PM₂.₅ is of great interest to the atmospheric and climate science community, who aim to understand and better control the atmospheric linkage indicators. However, most previous studies have been conducted on pollution-sensitive cities, and there is a lack of large-scale and long-term systematic analyses. In this study, we investigated the spatiotemporal evolution of PM₂.₅ and its influencing factors by using an exploratory spatiotemporal data analysis (ESTDA) technique and spatial econometric model based on remote sensing imagery inversion data of the Yangtze River Economic Belt (YREB), China, between 2000 and 2016. The results showed that 1) the annual value of PM₂.₅ was in the range of 23.49–37.67 μg/m³ with an inverted U-shaped change trend, and the PM₂.₅ distribution presented distinct spatial heterogeneity; 2) there was a strong local spatial dependence and dynamic PM₂.₅ growth process, and the spatial agglomeration of PM₂.₅ exhibited higher path-dependence and spatial locking characteristics; and 3) the endogenous interaction effect of PM₂.₅ was significant, where each 1% increase in the neighbouring PM₂.₅ levels caused the local PM₂.₅ to increase by at least 0.4%. Natural and anthropogenic factors directly and indirectly influenced the PM₂.₅ levels. Our results provide spatial decision references for coordinated trans-regional air pollution governance as well as support for further studies which can inform sustainable development strategies in the YREB.

Exposure to air pollutants has been associated with respiratory and cardiovascular mortality, but the underlying molecular mechanisms remain inadequately understood. We aimed to examine molecular-level inflammatory and oxidative stress responses to personal air pollutant exposure. Fifty-three healthy adults aged 22–52 were measured three times for their blood inflammatory cytokines and urinary malondialdehyde (MDA, an oxidative stress biomarker) within 2 consecutive months. Pollutant concentrations monitored indoors and outdoors were combined with the time-activity data to calculate personal O₃, PM₂.₅, NO₂, and SO₂ exposures averaged over 12 h, 24 h, 1 week, and 2 weeks, respectively, prior to biospecimen collection. Inflammatory cytokines and MDA were associated with pollutant exposures using linear mixed-effects models controlling for various covariates. After adjusting for a co-pollutant, we found that concentrations of proinflammatory cytokines were significantly and negatively associated with 12-h O₃ exposures and significantly but positively associated with 2-week O₃ exposures. We also found significant and positive associations of proinflammatory cytokines with 12-h and 24-h NO₂ exposures, respectively. However, we did not find clear associations of PM₂.₅ and SO₂ exposure with proinflammatory cytokines and with MDA. The removal of an O₃-generating electrostatic precipitator in the mechanical ventilation systems of the offices and residences of the subjects was associated with significant decreases in IL-1β, IL-2, IL-6, IL-8, IL-17A, and TNF-α. These findings suggest that exposure to O₃ for different time durations may affect systemic inflammatory responses in different ways.

Smoke from plastic waste incineration in an open air travels worldwide and is a major source of air pollution particulate matter (PM) that is very withstand to degradation and hazard to human health. Suspension of smoke aerosol components in water occurs during rains and fire extinguishing. Here, water-suspended plastic smoke aerosol (WPS) preparations suitable for biotesting were synthesized. It has been revealed using dynamic light scattering that WPS contained major nano-sized (∼30 nm) PM fraction, and this result was confirmed by electron microscopy. Optical absorption of WPS was in the UV region and an increase in λₑₓ led to a red-shift in fluorescence emission with a corresponding decrease in fluorescence intensity. WPS was analyzed in neurotoxicity studies in vitro using presynaptic rat cortex nerve terminals (synaptosomes). Generation of spontaneous reactive oxygen species (ROS) detected using fluorescent dye 2′,7-dichlorofluorescein in nerve terminals was decreased by WPS (10–50 μg/ml) in a dose-dependent manner. WPS also reduced the H₂O₂-evoked ROS production in synaptosomes, thereby influencing cellular oxidative processes and this effect was similar to that for carbon nanodots. WPS (0.1 mg/ml) decreased the synaptosomal membrane potential and synaptic vesicle acidification in fluorimetric experiments. WPS (1.0 mg/ml) attenuated the synaptosomal transporter-mediated uptake of excitatory and inhibitory neurotransmitters, L-[¹⁴C]glutamate and [³H]GABA, respectively. This can lead to an excessive increase in the glutamate concentration in the synaptic cleft and neurotoxicity via over activation of ionotropic glutamate receptors. Therefore, WPS was neurotoxic and provoked presynaptic malfunction through changes of oxidative activity, reduction of the membrane potential, synaptic vesicle acidification, and transporter-mediated uptake of excitatory and inhibitory neurotransmitters in nerve terminals. In summary, synthesis and emission to the environment of ultrafine PM occur during combustion of plastics, thereby polluting air and water resources, and possibly triggering development of neuropathologies.

Microbiota associated with airborne particulate matter (PM) is an important indicator of indoor pollution as they can be pathogenic and cause serious health threats to the exposed occupants. Present study aimed to investigate the level of culturable microbes associated with PM and their toxicological characterization in urban and rural houses of Pune city. Highest concentration of bacterial aerosols observed to be associated with PM₁₀ size fraction in urban site (2136 ± 285 CFU/m³) whereas maximum fungal concentration has been measured in rural houses (1521 ± 302 CFU/m³). Predominantly found bacterial species were Bacillus sp., S. aureus, and Pseudomonas aeruginosa and fungal species were Aspergillus sp., Cladosporium sp., and Penicillium sp. in both urban and rural residential premises. Concentration of endotoxin measured using the kinetic Limulus Amebocyte Lysate assay exhibited that the level of endotoxin in both urban and rural sites are associated with household characteristics and the activities performed in indoor as well as outdoor. Cell free DTT assay confirmed the ability of these airborne microbes to induce the production of reactive oxygen species (ROS) varying along with the types of microorganisms. On exposure of A549 cells to airborne microbes, a significant decrease in cell viability was observed in terms of both necrosis and apoptosis pathway. Elevated production of nitric oxide (NO) and proinflammatory cytokines in epithelial cells and macrophages clearly suggest the inflammatory nature of these airborne microbes. Results derived from the present study demonstrated that the indoor air of urban and rural houses of Pune is contaminated in terms of microbial load. Therefore, attention should be paid to control the factors favoring the microbial growth in order to safeguard the health of exposed inhabitants.

Approximately 3 billion people world-wide are exposed to air pollution from biomass burning. Herein, particulate matter (PM) emitted from artisanal cashew nut roasting, an important economic activity worldwide, was investigated. This study focused on: i) chemical characterization of polycyclic aromatic hydrocarbons (PAHs) and oxygenated (oxy-) PAHs; ii) intracellular levels of reactive oxygen species (ROS); iii) genotoxic effects and time- and dose-dependent activation of DNA damage signaling, and iv) differential expression of genes involved in xenobiotic metabolism, inflammation, cell cycle arrest and DNA repair, using A549 lung cells. Among the PAHs, chrysene, benzo[a]pyrene (B[a]P), benzo[b]fluoranthene, and benz[a]anthracene showed the highest concentrations (7.8–10 ng/m³), while benzanthrone and 9,10-anthraquinone were the most abundant oxy-PAHs. Testing of PM extracts was based on B[a]P equivalent doses (B[a]Pₑq). IC₅₀ values for viability were 5.7 and 3.0 nM B[a]Pₑq at 24 h and 48 h, respectively. At these low doses, we observed a time- and dose-dependent increase in intracellular levels of ROS, genotoxicity (DNA strand breaks) and DNA damage signaling (phosphorylation of the protein checkpoint kinase 1 – Chk1). In comparison, effects of B[a]P alone was observed at micromolar range. To our knowledge, no previous study has demonstrated an activation of pChk1, a biomarker used to estimate the carcinogenic potency of PAHs in vitro, in lung cells exposed to cashew nut roasting extracts. Sustained induction of expression of several important stress response mediators of xenobiotic metabolism (CYP1A1, CYP1B1), ROS and pro-inflammatory response (IL-8, TNF-α, IL-2, COX2), and DNA damage response (CDKN1A and DDB2) was also identified. In conclusion, our data show high potency of cashew nut roasting PM to induce cellular stress including genotoxicity, and more potently when compared to B[a]P alone. Our study provides new data that will help elucidate the toxic effects of low-levels of PAH mixtures from air PM generated by cashew nut roasting.

To investigate chemical characteristics, abatement mechanisms and regional transport of atmospheric pollutants during the COVID-19 outbreak control period in the Yangtze River Delta (YRD) region, China, the measurements of air pollutants including fine particulate matter (PM₂.₅) and volatile organic compounds (VOCs) on non-control period (NCP, 24 December 2019–23 January 2020) and control period (CP, 24 January–23 February 2020) were analyzed at the urban Pudong Supersite (PD) and the regional Dianshan Lake Supersite (DSL). Due to the stricter outbreak control, the levels of PM₂.₅ and VOCs, and the occurrence frequencies of haze-fog episodes decreased substantially from NCP to CP, with average reduction rates of 31.6%, 38.9% and 35.1% at PD, and 34.5%, 50.7% and 37.9% at DSL, respectively. The major source for PM₂.₅ was secondary sulfate & nitrate in both periods, and the emission control of primary sources such as coal burning and vehicle exhaust decreased the levels of precursors gas sulfur dioxide and nitrogen oxide, which highly contributed to the abatement of PM₂.₅ from NCP to CP. The higher levels of ozone at both PD and DSL on CP might be due to the weak nitrogen monoxide titration, low relative humidity and high visibility compared with NCP. Vehicle exhaust and fugitive emission from petrochemical industry were the major contributors of ambient VOCs and their decreasing activities mainly accounted for VOCs abatement. Moreover, the high frequency of haze-fog events was closely impacted by medium-scale regional transport within Anhui and Jiangsu provinces. Therefore, the decreasing regional transported air pollutants coincided with the emission control of local sources to cause the abatement of haze-fog events in YRD region on CP. This study could improve the understanding of the change of atmospheric pollutants during the outbreak control period, and provide scientific base for haze-fog pollution control in YRD region, China.

Human exposure to particulate matter (PM) originating from air pollution is inevitable since more and more population is present in large cities that are characterized by poor air quality. The impact on human health is evident and we need to intensify research regarding this problem to get molecular insight into versatile effects of chronic exposure to PM inducing organism responses and initiating the development of selected disorders. Herein, the impact of standard PM representing urban pollution on the structure and function of human serum albumin (HSA) was evaluated by the application of various analytical techniques. HSA was selected due to its high likeliness of being exposed to PM because of the abundance of this protein in blood. The studies were focused mainly on the inorganic residue of PM resulting from removing organic components by a low-temperature plasma. To mimic physiological conditions, dialysis technique was used to simulate the release of nanoparticles and ions from PM to aqueous environment under, which in turn may interact with biomolecules inside the living system. Capture of metals from the bulk suspension was found for many metals like Al, Fe, Zn and Pb in quantities of more than 1 mol of metal ions per mole of HSA. No significant structural changes of the protein upon dialysis with PM were observed, however, an increase in the thermal stabilization of the HSA structure was observed. Moreover, the interaction of HSA dialyzed in the presence of PM with selected drugs (warfarin, aspirin) was negatively affected, indicating a lower affinity of drugs towards the protein, even though only small conformational changes of the PM exposed protein were observed. Our findings point to a possible interference of air pollutants with the drugs taken by patients living in highly polluted areas.