Assessment of particulate matter (PM) in ambient air of different settings and its associated health risk in Haripur city, Pakistan / Avaliação de material particulado (MP) no ar ambiente de diferentes configurações e sua associação com o risco à saúde na cidade de Haripur, Paquistão

Particulate matter (PM) is a major air pollutant causing serious health problems. The aim of the present study was to find out concentration of PM in ambient air and its associated health risk in Haripur city, Pakistan. Twenty-three samples were taken at various educational institutes, hospitals, recreational areas and industries in Haripur city. Concentration of PM2.5 (µg/m3) and PM10 (µg/m3) was measured with Youngteng YT-HPC 3000A portable PM counter. The results revealed that values of both PM2.5 and PM10 were above the permissible limits (35 µg/m3 for PM2.5 and 150 µg/m3 for PM10) set by Environmental Protection Agency Pakistan (Pak-EPA) in all the educational institutes, hospitals, recreational areas and industries investigated. Furthermore, significant (p<0.05) variation was found in the concentration of both PM2.5 and PM10 in all the educational institutes, hospitals, recreational areas, and industries studied. The concentration of PM2.5 was positively correlated with the concentration of PM10 in all the sampling sites. Therefore, from 1-14 scale standard of health index, the values of PM2.5 and PM10 exhibited that the ambient air quality of Haripur city Pakistan is under high risk. If the regulatory authorities such as Environmental Protection Agency, Health Department and Local Government monitor PM pollution in different settings of Haripur city, then a decrease can be possible in the pollution level. The remedies that can be taken to overcome the problem of ambient air pollution such as PM are plantation of trees at the sites where there are higher levels of air pollutants and use of masks on personal protection basis along with implementation of pollution control system in industries of Hattar Industrial Estate Haripur city, Pakistan.

O material particulado (MP) é um importante poluente do ar que causa sérios problemas de saúde. O objetivo do presente estudo foi descobrir a concentração de MP no ar ambiente e sua associação com o risco à saúde na cidade de Haripur, Paquistão. Vinte e três amostras foram coletadas em várias instituições de ensino, hospitais, áreas recreativas e indústrias na cidade de Haripur. A concentração de MP2,5 (µg/m3) e MP10 (µg/m3) foi medida por meio do contador de MP portátil Youngteng YT-HPC 3000A. Os resultados revelaram que os valores de MP2,5 e MP10 estavam acima dos limites permitidos (35 µg/m3 para MP2,5 e 150 µg/m3 para MP10) estabelecidos pela Agência de Proteção Ambiental do Paquistão (Pak-EPA) em todas as instituições de ensino, hospitais, áreas recreativas e indústrias investigadas. Além disso, foi encontrada variação significativa (p < 0,05) na concentração de MP2,5 e MP10 em todos os locais estudados. A concentração de MP2,5 correlacionou-se positivamente com a concentração de MP10 em todos os locais de amostragem. Portanto, a partir da escala padrão 1-14 do índice de saúde, os valores de MP2,5 e MP10 mostraram que a qualidade do ar ambiente na cidade de Haripur, Paquistão, está sob alto risco. Se as autoridades reguladoras, como a Pak-EPA, o Departamento de Saúde e o governo local, monitorarem a poluição por MP em diferentes configurações da cidade de Haripur, pode ser que haja uma diminuição no nível de poluição. As medidas que podem ser tomadas para superar o problema da poluição do ar ambiente, como o MP, são o plantio de árvores nos locais onde há maiores níveis de poluentes atmosféricos, o uso de máscaras e a implantação de sistema de controle de poluição nas propriedades industriais de Hattar, na cidade Haripur, Paquistão.

Alleviation of PM2.5-induced alveolar macrophage inflammation using extract of fermented Chenopodium formosanum Koidz sprouts via regulation of NF-κB pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Particulate matter 2.5 (PM2.5) is a dangerous airborne pollutant that has become a global issue due to its detrimental effect on macrophages. Chenopodium formosanum Koidz (Djulis), a native plant from Taiwan well known for its high antioxidant content and is frequently used in ethnomedicine, shows promise as a novel phytomedicine to combat against oxidative stress caused by PM2.5. However, the protective mechanism of Djulis against PM2.5 still remains unclear. AIM OF THE STUDY: This study aimed to characterize the deleterious effect of emerging PM2.5 contaminants on the alveolar macrophage cell of the respiratory system and explore the underlying mechanisms in the suppression of PM2.5-induced inflammation using the extract of fermented Djulis. METHODS AND MATERIALS: RNA sequencing, immunoblot, and ChIP assay approaches were used to gain insight into the deleterious effect of PM2.5 on the macrophage cell at the transcriptional and translational level; and to elucidate the contribution of fermented Djulis extract (FCS) as the remedy of PM-induced MH-S cell inflammation. UHPLC-ESI-MS/MS and LC-QQQ/MS were used to identify the bioactive compounds potentially contributing to phytomedicinal properties in the water fraction of FCS. Multiple ligands docking analysis was conducted to predict the in-silico interaction of Djulis metabolites and NF-κB. RESULTS: Here, we showed that PM2.5 exposure at 200 ppm accelerated the production of intracellular ROS and phosphorylated NF-κB (p-NFκB), and negatively affecting the alveolar macrophage cell viability. Treating the cells with water-extracted FCS can restore their viability to 76% while simultaneously suppressing the generation of ROS and p-NFκB up to 38%. These ameliorative effects can be attributed to the occurrence of bioactive compounds such as gluconic acid, uridine, pantothenic acid, L-pyroglutamic acid, L-(-)-malic acid, and acetyl-L-carnitine in the water-extracted FCS which potentially dock to the RELA subunit site and consequently inhibit NF-κB activity along with its downstream inflammation signaling cascade. CONCLUSION: This work demonstrated the hazardous effect of PM2.5 on alveolar macrophage and unveiled the potential of FCS as a therapeutic phytomedicine to alleviate PM-induced inflammation.

A comparative assessment of air pollutants of smog in wagah border and other sites in Lahore, Pakistan / Uma avaliação comparativa de poluentes do ar do smog na fronteira de wagah e outros sites em Lahore, Paquistão

Abstract Smog has become the fifth season of Pakistan especially in Lahore city. Increased level of air pollutants (primary and secondary) are thought to be responsible for the formation of smog in Lahore. Therefore, the current study was carried out for the evaluation of air pollutants (primary and secondary) of smog in Wagah border particularly and other sites (Jail road, Gulburg) Lahore. For this purpose, baseline data on winter smog from March to December on primary and secondary air pollutants and meteorological parameters was collected from Environmental Protection Department and Pakistan Meteorological Department respectively. Devices being used in both departments for analysis of parameters were also studied. Collected data was further statistically analyzed to determine the correlation of parameters with meteorological conditions and was subjected to air quality index. According to results, PM 10 and PM 2.5 were found very high above the NEQS. NOx concentrations were also high above the permissible limits whereas SO2 and O3 were found below the NEQS thus have no roles in smog formation. Air Quality Index (AQI) of pollutants was PM 2.5(86-227), PM 10 (46-332), NOx (26-110), O3 (19-84) and SO2 (10-95). AQI of PM 2.5 remained between moderate to very unhealthy levels. AQI of PM 10 remained between good to hazardous levels. AQI of NOx remained between good to unhealthy for sensitive groups' levels. AQI of O3 and SO2 remained between good to moderate levels. Pearson correlation showed that every pollutant has a different relation with different or same parameters in different areas. It is concluded from the present study that particulate matter was much more responsible for smog formation. Although NOx also played role in smog formation. So there is need to reduce sources of particulate matter and NOx specifically in order to reduce smog formation in Lahore.

Resumo Smog tornou-se a quinta estação do Paquistão, especialmente na cidade de Lahore. Acredita-se que o aumento do nível de poluentes atmosféricos (primários e secundários) seja responsável pela formação de poluição atmosférica em Lahore. Portanto, o presente estudo foi realizado para a avaliação dos poluentes atmosféricos (primários e secundários) do smog na fronteira de Wagah em particular e em outros locais (Jail road, Gulburg) Lahore. Para este propósito, os dados de referência sobre a poluição atmosférica de inverno de março a dezembro sobre poluentes atmosféricos primários e secundários e parâmetros meteorológicos foram coletados do Departamento de Proteção Ambiental e do Departamento Meteorológico do Paquistão, respectivamente. Dispositivos sendo usados ​​em ambos os departamentos para análise de parâmetros também foram estudados. Os dados coletados foram posteriormente analisados ​​estatisticamente para determinar a correlação dos parâmetros com as condições meteorológicas e foram submetidos ao índice de qualidade do ar. De acordo com os resultados, PM 10 e PM 2,5 foram encontrados muito acima do NEQS. As concentrações de NOx também estavam muito acima dos limites permitidos, enquanto SO2 e O3 foram encontrados abaixo do NEQS, portanto, não têm papéis na formação de smog. O índice de qualidade do ar (AQI) de poluentes foi PM 2,5 (86-227), PM 10 (46-332), NOx (26-110), O3 (19-84) e SO2 (10-95). O AQI de PM 2,5 permaneceu entre níveis moderados a muito prejudiciais à saúde. O AQI de PM 10 permaneceu entre níveis bons e perigosos. AQI de NOx permaneceu entre bom e não saudável para os níveis de grupos sensíveis. O AQI de O3 e SO2 permaneceu entre níveis bons a moderados. A correlação de Pearson mostrou que cada poluente tem uma relação diferente com parâmetros diferentes ou iguais em áreas diferentes. Conclui-se do presente estudo que o material particulado foi muito mais responsável pela formação de smog. Embora o NOx também tenha desempenhado um papel na formação do smog. Portanto, é necessário reduzir as fontes de partículas e NOx, especificamente para reduzir a formação de smog em Lahore.

Global population exposure to landscape fire air pollution from 2000 to 2019.

Wildfires are thought to be increasing in severity and frequency as a result of climate change1-5. Air pollution from landscape fires can negatively affect human health4-6, but human exposure to landscape fire-sourced (LFS) air pollution has not been well characterized at the global scale7-23. Here, we estimate global daily LFS outdoor fine particulate matter (PM2.5) and surface ozone concentrations at 0.25° × 0.25° resolution during the period 2000-2019 with the help of machine learning and chemical transport models. We found that overall population-weighted average LFS PM2.5 and ozone concentrations were 2.5 µg m-3 (6.1% of all-source PM2.5) and 3.2 µg m-3 (3.6% of all-source ozone), respectively, in 2010-2019, with a slight increase for PM2.5, but not for ozone, compared with 2000-2009. Central Africa, Southeast Asia, South America and Siberia experienced the highest LFS PM2.5 and ozone concentrations. The concentrations of LFS PM2.5 and ozone were about four times higher in low-income countries than in high-income countries. During the period 2010-2019, 2.18 billion people were exposed to at least 1 day of substantial LFS air pollution per year, with each person in the world having, on average, 9.9 days of exposure per year. These two metrics increased by 6.8% and 2.1%, respectively, compared with 2000-2009. Overall, we find that the global population is increasingly exposed to LFS air pollution, with socioeconomic disparities.

Prenatal ambient air pollution exposure and child weight trajectories from the 3rd trimester of pregnancy to 2 years of age: a cohort study.

BACKGROUND: Prenatal air pollution exposure may increase risk for childhood obesity. However, few studies have evaluated in utero growth measures and infant weight trajectories. This study will evaluate the associations of prenatal exposure to ambient air pollutants with weight trajectories from the 3rd trimester through age 2 years. METHODS: We studied 490 pregnant women who were recruited from the Maternal and Development Risks from Environmental and Social Stressors (MADRES) cohort, which comprises a low-income, primarily Hispanic population in Los Angeles, California. Nitrogen dioxide (NO2), particulate matter < 10 µm (PM10), particulate matter < 2.5 µm (PM2.5), and ozone (O3) concentrations during pregnancy were estimated from regulatory air monitoring stations. Fetal weight was estimated from maternal ultrasound records. Infant/child weight measurements were extracted from medical records or measured during follow-up visits. Piecewise spline models were used to assess the effect of air pollutants on weight, overall growth, and growth during each period. RESULTS: The mean (SD) prenatal exposure concentrations for NO2, PM2.5, PM10, and O3 were 16.4 (2.9) ppb, 12.0 (1.1) µg/m3, 28.5 (4.7) µg/m3, and 26.2 (2.9) ppb, respectively. Comparing an increase in prenatal average air pollutants from the 10th to the 90th percentile, the growth rate from the 3rd trimester to age 3 months was significantly increased (1.55% [95%CI 1.20%, 1.99%] for PM2.5 and 1.64% [95%CI 1.27%, 2.13%] for NO2), the growth rate from age 6 months to age 2 years was significantly decreased (0.90% [95%CI 0.82%, 1.00%] for NO2), and the attained weight at age 2 years was significantly lower (- 7.50% [95% CI - 13.57%, - 1.02%] for PM10 and - 7.00% [95% CI - 11.86%, - 1.88%] for NO2). CONCLUSIONS: Prenatal ambient air pollution was associated with variable changes in growth rate and attained weight from the 3rd trimester to age 2 years. These results suggest continued public health benefits of reducing ambient air pollution levels, particularly in marginalized populations.

The association between newborn cord blood steroids and ambient prenatal exposure to air pollution: findings from the ENVIRONAGE birth cohort.

Knowledge of whether prenatal exposure to ambient air pollution disrupts steroidogenesis is currently lacking. We investigated the association between prenatal ambient air pollution and highly accurate measurements of cord blood steroid hormones from the androgenic pathway.This study included 397 newborns born between the years 2010 and 2015 from the ENVIRONAGE cohort in Belgium of whom six cord blood steroid levels were measured: 17α-hydroxypregnenolone, 17α-hydroxyprogesterone, dehydroepiandrosterone, pregnenolone, androstenedione, and testosterone. Maternal ambient exposure to PM2.5 (particles with aerodynamic diameter ≤ 2.5 µm), NO2, and black carbon (BC) were estimated daily during the entire pregnancy using a high-resolution spatiotemporal model. The associations between the cord blood steroids and the air pollutants were tested and estimated by first fitting linear regression models and followed by fitting weekly prenatal exposures to distributed lag models (DLM). These analyses accounted for possible confounders, coexposures, and an interaction effect between sex and the exposure. We examined mixture effects and critical exposure windows of PM2.5, NO2 and BC on cord blood steroids via the Bayesian kernel machine regression distributed lag model (BKMR-DLM).An interquartile range (IQR) increment of 7.96 µg/m3 in PM2.5 exposure during pregnancy trimester 3 was associated with an increase of 23.01% (99% confidence interval: 3.26-46.54%) in cord blood levels of 17α-hydroxypregnenolone, and an IQR increment of 0.58 µg/m³ in BC exposure during trimester 1 was associated with a decrease of 11.00% (99% CI: -19.86 to -0.012%) in cord blood levels of androstenedione. For these two models, the DLM statistics identified sensitive gestational time windows for cord blood steroids and ambient air pollution exposures, in particular for 17α-hydroxypregnenolone and PM2.5 exposure during trimester 3 (weeks 28-36) and for androsterone and BC exposure during early pregnancy (weeks 2-13) as well as during mid-pregnancy (weeks 18-26). We identified interaction effects between pollutants, which has been suggested especially for NO2.Our results suggest that prenatal exposure to ambient air pollutants during pregnancy interferes with steroid levels in cord blood. Further studies should investigate potential early-life action mechanisms and possible later-in-life adverse effects of hormonal disturbances due to air pollution exposure.

Microplastics exposure and immunologic response

Objective: To assess the impact of microplastics (MPs) on human health. Data Source: The authors conducted a non-systematic review of articles published in English, Portuguese, French, and Spanish in the last decade in the following databases: PubMed, Google Scholar, EMBASE, and SciELO. The keywords used were: microplastics OR nanoplastics OR marine litter OR toxicology OR additives AND human health OR children OR adults. Data summary: MPs are a group of emerging contaminants that have attracted scientific interest and societal attention in the last decade due to their ubiquitous detection in all environments. Humans can primarily be exposed to MPs and nanoplastics via oral and inhalation routes, but dermal contact cannot be overlooked, especially in young children. The possible toxic effects of plastic particles are due to their potential toxicity, often combined with that of leachable additives and adsorbed contaminants. Conclusions: Unless the plastic value chain is transformed over the next two decades, the risks to species, marine ecosystems, climate, health, economy, and communities will be unmanageable. However, along with these risks are the unique opportunities to help transition to a more sustainable world (AU)

Integrated microbiome and multi-omics analysis reveal the molecular mechanisms of Eisenia fetida in response to biochar-derived dissolved and particulate matters.

At present, most ecotoxicological studies are still confined to focusing on the harmful effects of biochar itself on soil fauna. However, the potential ecotoxicity of different components separated from biochar to terrestrial invertebrates remains poorly understood. In this study, the dissolved matter (DM) and particulate matter (PM) were separated from biochar (BC) and then introduced into the soil-earthworm system to investigate the response mechanism of earthworms at the molecular level. The results showed that BC and DM exposure caused an increase in the abundance of Proteobacteria in the cast bacterial community, suggesting the dysbiosis of intestinal microbiota. It was also observed that the cast bacterial communities were more sensitive to DM exposure than PM exposure. Transcriptomic analysis showed that BC and DM exposure induced significant enrichment of functional pathways related to infectious and neuropathic diseases. Metabolomic profiling manifested that DM exposure caused metabolic dysfunction, antioxidant and detoxification abilities recession. Furthermore, significant differences in the responses of earthworms at transcriptomic and metabolic levels confirmed that DM exhibited greater ecotoxicity than PM. This study highlighted the significant contributions of dissolved matter to the ecotoxicity of biochar from the perspective of transcriptomic and metabolomic profiles.

The joint effect and hemodynamic mechanism of PA and PM2.5 exposure on cognitive function: A randomized controlled trial study.

BACKGROUND: While PM2.5 has been shown to impair cognitive function, physical activity (PA) is known to enhance it. Nonetheless, considering the increased inhalation of PM2.5 during exercise, the potential of PA to counteract the detrimental effects of PM2.5, along with the underlying hemodynamic mechanisms, remains uncertain. METHODS: We conducted a double-blinded, randomized controlled trial among healthy young adults in Beijing, China. Ninety-three participants were randomly allocated to groups experiencing different intensities of PA interventions, and either subjected to purified or unpurified air conditions. Cognitive function was measured by the Color-Word Matching Stroop task, and the hemodynamic response was measured using functional near-infrared spectroscopy during participants performed the Stroop task both before and after the intervention. Linear mixed-effect models were used to estimate the impact of PA and PM2.5 on cognitive function and hemodynamic response. RESULTS: The reaction time for congruent and incongruent Stroop tasks improved by - 80.714 (95% CI: -136.733, -24.695) and - 105.843 (95% CI: -188.6, -23.085) milliseconds after high-intensity interval training (HIIT) intervention. PM2.5 and HIIT had interaction effects on cognition, such that every 1 µg/m3 increase in PM2.5 attenuated the benefits of HIIT on reaction time by 2.231 (95% CI: 0.523, 3.938) and 3.305 (95% CI: 0.791, 5.819) milliseconds for congruent and incongruent Stroop tasks. Moreover, we divided participants into high and low PM2.5 exposure groups based on average PM2.5 concentration (32.980 µg/m3), and found that HIIT intervention in high PM2.5 concentration led to 69.897 (95% CI: 9.317, 130.476) and 99.269 (95% CI: 10.054, 188.485) milliseconds increased in the reaction time of congruent and incongruent Stroop, compared with the control group among low PM2.5. Furthermore, we found a significant interaction effects of PM2.5 and moderate-intensity continuous training (MICT) on the middle frontal gyrus (MFG) and dorsolateral superior frontal gyrus (DLPFC). PM2.5 and HIIT had a significant interaction effect on the DLPFC. CONCLUSIONS: HIIT improved cognitive function, but the cognitive benefits of HIIT were attenuated or even reversed under high PM2.5 exposure. The activation of the DLPFC and MFG could serve as hemodynamic mechanisms to explain the joint effect of PA and PM2.5.

Associations between exposure to ambient particulate matter and advanced liver fibrosis in Chinese MAFLD patients.

BACKGROUND & AIMS: Liver fibrosis is an important feature in patients with metabolic dysfunction-associated fatty liver disease (MAFLD). This study aimed to explore the association between long-term ambient particulate matter (PM) exposure and advanced liver fibrosis (ALF) in MAFLD participants. METHODS: A cross-sectional study of 23170 adults recruited from 33 provinces of China from 2010 to 2020. ALF was detected using the nonalcoholic fatty liver disease fibrosis score (NFS). The annual average levels of particulate matter with aerodynamic diameters of ≤ 1 µm (PM1), ≤ 2.5 µm (PM2.5) and ≤ 10 µm (PM10) were calculated using validated spatiotemporal models. Generalized additive models were applied to analyze the association between PM and ALF in patients with MAFLD. RESULTS: One-year exposure to higher levels of all PM was found to increase the risk of ALF, with odds ratios (ORs) of 1.10 (95% CI 1.06-1.14), 1.05 (1.03-1.07), and 1.03(1.02-1.04) for each 10 µg/m3 increase in PM1, PM2.5 and PM10, respectively. With the dissection of the impact of PM1 in PM2.5, PM2.5 in PM10 and PM1 in PM10, we found that PM2.5 had a stronger impact on ALF (both Pinteraction＜0.05) in comparison with PM1 and PM10. CONCLUSIONS: Long-term exposure to PM is associated with ALF in patients with MAFLD, with PM2.5 playing a dominant role.

Criteria air pollutants and diabetes mortality classified by different subtypes and complications: A nationwide, case-crossover study.

The associations between air pollution and diabetes mortality of different subtypes and complications were largely unclear. We performed an individual-level, time-stratified case-crossover study among over 0.9 million diabetes deaths from all administrative regions of Chinese mainland during 2013-2019. Daily concentrations of fine particles (PM2.5), coarse particles (PM2.5-10), nitrogen dioxide (NO2) and ozone (O3) were obtained for each decedent using high-resolution prediction models. Conditional logistic regression models were utilized to analyze the data. Each interquartile range increment in PM2.5, PM2.5-10, NO2 and O3 concentrations on lag 0-2 d increased the risks of overall diabetes mortality by 2.81 %, 1.92 %, 3.96 % and 2.15 %, respectively. Type 2 diabetes had stronger associations with air pollution than type 1 diabetes. Air pollutants were associated with diabetic ketoacidosis and diabetic nephropathy, but not other complications. The exposure-response curves were approximately linear with a plateau at higher concentrations of PM2.5, PM2.5-10, and NO2, while the associations for O3 appear to be statistically significant beyond 60 µg/m3. This nationwide study reinforces the evidence of higher risks of acute diabetic events following short-term air pollution exposure. We identified differential effects of air pollutants on various subtypes and complications of diabetes, which require further mechanistic investigations.

Short-term and repeated exposure to particulate matter sizes from Imperial Valley, California to induce inflammation and asthmatic-like symptoms in mice.

Imperial Valley, California has become increasingly hot, dry, and polluted over the past decade. Particulate matter (PM) levels are amongst the highest in this State, associated with significantly higher asthma prevalence among children in the region compared to national and state averages. The present study was performed to test the hypothesis that Imperial Valley PM by size and chemical composition might possess allergenic properties following introduction into murine lungs without prior sensitization to a known allergen with size fraction as a determining factor. In acute exposure experiments, BALB/c male mice were administered a single 50-µl oropharyngeal aspiration of nanopure water (H2O; control) or a stock 1 µg/µl PM solution. In sub-acute exposure experiments, male and female mice were treated with a total of six 16.6-µl intranasal instillations of H2O or stock PM solution over the course of 14 days. In all experiments, pulmonary function tests were performed 24 hr after the final instillation followed by necropsies for the collection of biological samples. Inflammatory responses measured via cellularity in histopathological tissue sections as well as significant, marked influxes of eosinophils and lymphocytes were noted in the bronchoalveolar lavage fluid in mice administered PM compared to control. Allergic responses, including airway hyperresponsiveness and significantly increased expression of IL-1ß, were found in male mice exposed to either PM2.5 or ultrafine (PMUF). A combination of all three size fractions of PM from Imperial Valley initiated atopic and asthmatic-like symptoms in the lungs of mice in the absence of additional allergen or preexisting condition.

Identification of differentially expressed genes and pathways in BEAS-2B cells upon long-term exposure to particulate matter (PM2.5) from biomass combustion using bioinformatics analysis.

BACKGROUND: Long-term exposure to PM2.5 from burning domestic substances has been linked to an increased risk of lung disease, but the underlying mechanisms are unclear. This study is to explore the hub genes and pathways involved in PM2.5 toxicity in human bronchial epithelial BEAS-2B cells. METHODS: The GSE158954 dataset is downloaded from the GEO database. Differentially expressed genes (DEGs) were screened using the limma package in RStudio (version 4.2.1). In addition, DEGs analysis was performed by Gene Ontology (GO) functional analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. A protein-protein interaction (PPI) network was constructed, MCODE plug-in and the cytoHubba plug-in in Cytoscape software was used to identify the hub genes. Finally, CytoHubba and DEGs were used to integrate the hub genes, and preliminary validation was performed by comparing the toxicology genomics database (CTD). Differential immune cell infiltration was investigated using the CIBERSORT algorithm. RESULTS: A total of 135 DEGs were identified, of which 57 were up-regulated and 78 were down-regulated. Functional enrichment analyses in the GO and KEGG indicated the potential involvement of DEGs was mainly enriched in the regulation of endopeptidase activity and influenza A. Gene Set Enrichment Analysis revealed that Chemical Carcinogenesis - DNA adducts were remarkably enriched in PM2.5 groups. 53 nodes and 198 edges composed the PPI network. Besides, 5 direct-acting genes were filtered at the intersection of cytohubba plug-in, MCODE plug-in and CTD database. There is a decreasing trend of dendritic cells resting after BEAS-2B cells long-term exposure to PM2.5. CONCLUSIONS: The identified DEGs, modules, pathways, and hub genes provide clues and shed light on the potential molecular mechanisms of BEAS-2B cells upon long-term exposure to PM2.5.

On thresholds for controlling negative particle (PM2.5) readings in air quality reporting.

Ambient PM2.5 (particles less than 2.5 µm in diameter) is monitored in many countries including Australia. Occasionally PM2.5 instruments may report negative measurements, although in realty the ambient air can never contain negative amounts of particles. Some negative readings are caused by instrument faults or procedural errors, thus can be simply invalidated from air quality reporting. There are occasions, however, when negative readings occur due to other factors including technological or procedural limitations. Treatment of such negative data requires consideration of factors such as measurement uncertainty, instrument noise and risk for significant bias in air quality reporting. There is very limited documentation on handling negative PM2.5 data in the literature. This paper demonstrates how a threshold is determined for controlling negative hourly PM2.5 readings in the New South Wales (NSW) air quality data system. The investigation involved a review of thresholds used in different data systems and an assessment of instrument measurement uncertainties, zero air test data and impacts on key reporting statistics when applying different thresholds to historical datasets. The results show that a threshold of -10.0 µg/m3 appears optimal for controlling negative PM2.5 data in public reporting. This choice is consistent with the measurement uncertainty estimates and the zero air test data statistics calculated for the NSW Air Quality Monitoring Network, and is expected not to have significant impacts on key compliance reporting statistics such as data availability and annual average pollution levels. The analysis can be useful for air quality monitoring in other Australian jurisdictions or wider context.

Estimation of premature death attributed to short- and long-term PM2.5 exposure in Thailand.

Particulate matter with a diameter of less than 2.5 microns (PM2.5) has been identified as a global health concern in recent decades. Indeed, PM2.5 exposure causes detrimental health problems in the general population. Estimating the short- and long-term health impacts of PM2.5 exposure should help to shape public health policy concerning air pollution. Hence, this study sought to estimate the rate of premature death attributable to PM2.5 exposure among the Thai population if the PM2.5 concentration met the applied counterfactual factor. The PM2.5 concentration, population numbers, and numbers of health incidences were collected from secondary data sources in 2019. A health impact analysis was performed using AirQ+ software to estimate the incidences of premature deaths attributable to PM2.5 exposure. More specifically, the analysis provided the estimated proportion of attributable cases and the rate of premature death per 100,000 population aged ≥ 30 years. The annual average PM2.5 concentration in Thailand was found to be 24.15 µg per cubic meter (µg/m3) in 2019, while the natural mortality rate was around 1,107 per 100,000 population nationwide. With regard to short-term PM2.5 exposure, it was determined that 8 premature deaths per 100,000 population could be prevented if the PM2.5 concentration met the World Health Organization (WHO) short-term gold standard of 15 µg/m3. Moreover, 159 premature deaths per 100,000 population could be avoided if the PM2.5 concentration met the WHO's long-term gold standard of 5 µg/m3. This estimation of premature deaths due to the short- and long-term impacts of PM2.5 exposure can support policymakers and stakeholders in creating a roadmap to combating the adverse impacts of PM2.5 exposure and protect the health of the Thai population.

The origin of suspended particulate matter in the Great Barrier Reef.

River run-off has long been regarded as the largest source of organic-rich suspended particulate matter (SPM) in the Great Barrier Reef (GBR), contributing to high turbidity, pollutant exposure and increasing vulnerability of coral reef to climate change. However, the terrestrial versus marine origin of the SPM in the GBR is uncertain. Here we provide multiple lines of evidence (13C NMR, isotopic and genetic fingerprints) to unravel that a considerable proportion of the terrestrially-derived SPM is degraded in the riverine and estuarine mixing zones before it is transported further offshore. The fingerprints of SPM in the marine environment were completely different from those of terrestrial origin but more consistent with that formed by marine phytoplankton. This result indicates that the SPM in the GBR may not have terrestrial origin but produced locally in the marine environment, which has significant implications on developing better-targeted management practices for improving water quality in the GBR.

A review on potential approach for in silico toxicity analysis of respirable fraction of ambient particulate matter.

Epidemiological and toxicological studies have shown the adverse effect of ambient particulate matter (PM) on respiratory and cardiovascular systems inside the human body. Various cellular and acellular assays in literature use indicators like ROS generation, cell inflammation, mutagenicity, etc., to assess PM toxicity and associated health effects. The presence of toxic compounds in respirable PM needs detailed studies for proper understanding of absorption, distribution, metabolism, and excretion mechanisms inside the body as it is difficult to accurately imitate or simulate these mechanisms in lab or animal models. The leaching kinetics of the lung fluid, PM composition, retention time, body temperature, etc., are hard to mimic in an artificial experimental setup. Moreover, the PM size fraction also plays an important role. For example, the ultrafine particles may directly enter systemic circulations while coarser PM10 may be trapped and deposited in the tracheo-bronchial region. Hence, interpretation of these results in toxicity models should be done judiciously. Computational models predicting PM toxicity are rare in the literature. The variable composition of PM and lack of proper understanding for their synergistic role inside the body are prime reasons behind it. This review explores different possibilities of in silico modeling and suggests possible approaches for the risk assessment of PM particles. The toxicity testing approach for engineered nanomaterials, drugs, food industries, etc., have also been investigated for application in computing PM toxicity.

New concentration-response functions for seven morbidity endpoints associated with short-term PM2.5 exposure and their implications for health impact assessment.

BACKGROUND: Morbidity burdens from ambient air pollution are associated with market and non-market costs and are therefore important for policymaking. The estimation of morbidity burdens is based on concentration-response functions (CRFs). Most existing CRFs for short-term exposures to PM2.5 assume a fixed risk estimate as a log-linear function over an extrapolated exposure range, based on evidence primarily from Europe and North America. OBJECTIVES: We revisit these CRFs by performing a systematic review for seven morbidity endpoints previously assessed by the World Health Organization, including data from all available regions. These endpoints include all cardiovascular hospital admission, all respiratory hospital admission, asthma hospital admission and emergency room visit, along with the outcomes that stem from morbidity, such as lost work days, respiratory restricted activity days, and child bronchitis symptom days. METHODS: We estimate CRFs for each endpoint, using both a log-linear model and a nonlinear model that includes additional parameters to better fit evidence from high-exposure regions. We quantify uncertainties associated with these CRFs through randomization and Monte Carlo simulations. RESULTS: The CRFs in this study show reduced model uncertainty compared with previous CRFs in all endpoints. The nonlinear CRFs produce more than doubled global estimates on average, depending on the endpoint. Overall, we assess that our CRFs can be used to provide policy analysis of air pollution impacts at the global scale. It is however important to note that improvement of CRFs requires observations over a wide range of conditions, and current available literature is still limited. DISCUSSION: The higher estimates produced by the nonlinear CRFs indicates the possibility of a large underestimation in current assessments of the morbidity impacts attributable to air pollution. Further studies should be pursued to better constrain the CRFs studied here, and to better characterize the causal relationship between exposures to PM2.5 and morbidity outcomes.

Geochemical characteristics and socioeconomic associations of carbonaceous aerosols in coal-fueled cities with significant seasonal pollution pattern.

Carbonaceous aerosols, comprising organic carbon (OC) and elemental carbon (EC), are critical component of fine particulate matter (PM2.5), with diverse impacts on air quality and human health. This study investigated the concentrations and seasonal patterns of carbonaceous species in PM2.5 during both the heating season (January 2021) and non-heating season (July 2021) in three coal-fueled cities in northern China, as well as the differences in carbonaceous aerosols and their associations with socioeconomic parameters in cities situated on either side of the "Hu Line" in China. The results showed that, owing to intensified coal combustion and unfavorable meteorological conditions, levels of OC, EC, and OC/EC ratios were higher in winter compared to summer. Moreover, the presence of dust (DU) and light pollution (LP) days resulted in elevated OC levels but decreased EC levels. The Char-EC/Soot-EC ratios were highest during LP, followed by CL and DU. A source apportionment analysis demonstrated that coal burning, vehicle exhaust, road dust, and biomass burning were the primary contributors to carbonaceous aerosols, as confirmed by diagnostic ratios, Char-EC/Soot-EC ratios, and PCA analysis. Furthermore, our study found that carbonaceous aerosols concentrations and source apportionment primarily varied with diurnal and seasonal trends and different pollution types. Additionally, at the national scale, population density and urban green space exhibited a positive correlation with OC/EC ratios (p < 0.05), while energy consumption per unit of GDP showed a negative correlation (p < 0.05). The observation that OC/EC ratios were lower in coal-fueled cities than in economy-based cities suggests a more severe pollution scenario. These findings highlight the importance of comprehending of the seasonal variation and chemical characteristics of carbonaceous aerosol for understanding air pollution sources and characteristics, which is essential for both air quality management and human health.

Systems toxicology of complex wood combustion aerosol reveals gaseous carbonyl compounds as critical constituents.

Epidemiological studies identified air pollution as one of the prime causes for human morbidity and mortality, due to harmful effects mainly on the cardiovascular and respiratory systems. Damage to the lung leads to several severe diseases such as fibrosis, chronic obstructive pulmonary disease and cancer. Noxious environmental aerosols are comprised of a gas and particulate phase representing highly complex chemical mixtures composed of myriads of compounds. Although some critical pollutants, foremost particulate matter (PM), could be linked to adverse health effects, a comprehensive understanding of relevant biological mechanisms and detrimental aerosol constituents is still lacking. Here, we employed a systems toxicology approach focusing on wood combustion, an important source for air pollution, and demonstrate a key role of the gas phase, specifically carbonyls, in driving adverse effects. Transcriptional profiling and biochemical analysis of human lung cells exposed at the air-liquid-interface determined DNA damage and stress response, as well as perturbation of cellular metabolism, as major key events. Connectivity mapping revealed a high similarity of gene expression signatures induced by wood smoke and agents prompting DNA-protein crosslinks (DPCs). Indeed, various gaseous aldehydes were detected in wood smoke, which promote DPCs, initiate similar genomic responses and are responsible for DNA damage provoked by wood smoke. Hence, systems toxicology enables the discovery of critical constituents of complex mixtures i.e. aerosols and highlights the role of carbonyls on top of particulate matter as an important health hazard.