Capturing Exposure Disparities with Chemical Transport Models: Evaluating the Suitability of Downscaling Using Land Use Regression.

High resolution exposure surfaces are essential to capture disparities in exposure to traffic-related air pollution in urban areas. In this study, we develop an approach to downscale Chemical Transport Model (CTM) simulations to a hyperlocal level (∼100m) in the Greater Toronto Area (GTA) under three scenarios where emissions from cars, trucks and buses are zeroed out, thus capturing the burden of each transportation mode. This proposed approach statistically fuses CTMs with Land-Use Regression using machine learning techniques. With this proposed downscaling approach, changes in air pollutant concentrations under different scenarios are appropriately captured by downscaling factors that are trained to reflect the spatial distribution of emission reductions. Our validation analysis shows that high-resolution models resulted in better performance than coarse models when compared with observations at reference stations. We used this downscaling approach to assess disparities in exposure to nitrogen dioxide (NO2) for populations composed of renters, low-income households, recent immigrants, and visible minorities. Individuals in all four categories were disproportionately exposed to the burden of cars, trucks, and buses. We conducted this analysis at spatial resolutions of 12, 4, 1 km, and 100 m and observed that disparities were significantly underestimated when using coarse spatial resolutions. This reinforces the need for high-spatial resolution exposure surfaces for environmental justice analyses.

Integrated Benefits of Synergistically Reducing Air Pollutants and Carbon Dioxide in China.

China's advancements in addressing air pollution and reducing CO2 emissions offer valuable lessons for collaborative strategies to achieve diverse environmental objectives. Previous studies have assessed the mutual benefits of climate policies and air pollution control measures on one another, lacking an integrated assessment of the benefits of synergistic control attributed to refined measures. Here, we comprehensively used coupled emission inventory and response models to evaluate the integrated benefits and synergy degrees of various measures in reducing air pollutants and CO2 in China during 2013-2021. Results indicated that the implemented measures yielded integrated benefits value at 6.7 (2.4-12.6) trillion Chinese Yuan. The top five contributors, accounting for 55%, included promoting non-thermal power, implementing end-of-pipe control technologies in power plants and iron and steel industry, replacing residential scattered coal, and saving building energy. Measures demonstrating high synergies and integrated benefits per unit of reduction (e.g., green traffic promotion) yielded low benefits mainly due to their low application, which are expected to gain greater implementation and prioritization in the future. Our findings provide insights into the effectiveness and limitations of strategies aimed at joint control. By ranking these measures based on their benefits and synergy, we offer valuable guidance for policy development in China and other nations with similar needs.

Decreasing levels of atmospheric pollution and simultaneous reduced number of cardiovascular hospital admissions and operations with improved results. Analysis of the Italian National Registries.

BACKGROUND: The aim of our study was to determine a correlation between decrease of levels of atmospheric pollution (as determined by air levels of Particulate Matters with a diameter equal or less to 2.5 microns) and reduced number of hospital admissions and operations for patients with common cardiovascular diseases in Italy. METHODS: We correlated number of hospital admissions and cardiovascular operations and atmospheric levels of PM.2.5 from 2015 to 2019 in Italy. This time interval was chosen because the possibility to analyze data about other established cardiovascular risk factors as reported by the European Union Eurostat. RESULTS: A statistically significant decrease of hospital admissions for cardiovascular and pulmonary emergencies was registered in Italy from 2015 to 2019 (p<0.01). The number also of cardiovascular operations showed a trend towards reduction with improved 30-days results, without reaching a statistically significant correlation (p =0.10). In the period 2015-2019, there was a steady decrease of atmospheric levels of pM2.5, either in urban or rural areas (p<0.01). The decrease of atmospheric levels of PMs2.5 started in 2010 and continued with a steady trend until the year 2019. In the period 2015-2019 exposure of the Italian population to established risk factors for cardiovascular diseases showed a small increase. The number of admissions and operations for non- cardiovascular and non-pulmonary diseases remained unchanged in the period 2015-2019. CONCLUSIONS: The findings of our study underline the possibility that decrease of atmospheric pollution may determine almost immediate decrease of cardiovascular and pulmonary diseases.

Assessment of Indoor Particulate Matter and Teacher's Perceived Indoor Climate in Government Schools of Bilaspur District, Chhattisgarh, India: A Cross-Sectional Study.

Context: Indoor air pollution (IAP) affects the long-term health, cognitive growth, and academic performance of children. Since children spend most of their time at school, quantifying IAP in classrooms is an important parameter for air pollution. Aim: To assess the average particulate matter (PM) levels inside and outside of classrooms along with their associated factors and teacher's perceived indoor climate. Setting and Design: Cross-sectional survey in nine government-run schools. Methods and Material: PM2.5 and PM10 were measured inside the classroom and outdoors simultaneously during summers, using an Atmos monitor for two consecutive days, along with several school and classroom characteristics. Perception about indoor air quality was captured from teachers (n = 15) using a validated questionnaire. Statistical Analysis: Mean values of PM using mixed effect linear regression. Perceived indoor air quality is presented using percentages. Results: Mean indoor PM2.5 and PM10 was 52.5 µg/m3 and 65 µg/m3. Indoor and outdoor PM levels were highly correlated, but the indoor-outdoor ratio of PM concentrations was more than 1. Teachers were mostly bothered by dust, dirt, and noise in the schools. Conclusion: Indoor air quality was higher than World Health Organization (WHO) standards but within the national standards. Need further research to find the exact cause for higher indoor PM levels compared to outdoor PM levels.

Improved Z-number and fault tree analysis to predict the risk of air pollution due to ship boiler operation.

Ships present a significant source of air pollution, contributing to environmental degradation and posing health risks. Boilers are a significant part of the vessels in which the water is heated to evaporate and generate steam. The boilers emit pollutants such as hazardous air pollutants (HAPs), particle pollution, and volatile organic compounds (VOC). This paper conducts an extended risk analysis for air pollution due to boiler operation on ships. An improved Z-numbers theory and Fault Tree Analysis (FTA) are adopted to predict risk. Whilst improved Z-number theory is capable of handling uncertainties inherent in risk assessment, the FTA presents systematically the causal relationships among various factors contributing to the risk of air pollution on ships. The findings show that the failure probability of air pollution during ship boiler operation is 2.08E-05 and BE-12 is the most significant event. Results provide valuable data to maritime stakeholders in fostering environmentally sustainable practices.

Estimation of plant pollution removal capacity based on intensive air quality measurements.

This study investigated the role of present vegetation in improving air quality in Bucharest (Romania) by analyzing six years of air quality data (PM10 and NO2 ) from multiple monitoring stations. The target value for human health protection is regularly exceeded for PM10 and not for NO2 over time. Road traffic has substantially contributed (over 70%) to ambient PM10 and NO2 levels. The results showed high seasonal variations in pollutant concentrations, with a pronounced effect of vegetation in reducing PM10 and NO2 levels. Indeed, air quality improvements of 7% for PM10 and 25% for NO2 during the growing season were reported. By using Principal Component Analysis and pollution data subtraction methodology, we have disentangled the impact of vegetation on air pollution and observed distinct annual patterns, particularly higher differences in PM10 and NO2 concentrations during the warm season. Despite limitations such as a lack of full tree inventory for Bucharest and a limited number of monitoring stations, the study highlighted the efficiency of urban vegetation to mitigate air pollution.

Synergistic reduction of air pollutants and carbon dioxide emissions in Shanxi Province, China from 2013 to 2020.

Synergistic reduction of air pollutants and carbon dioxide (CO2) emissions is currently a key environmental policy in China, yet provincial-level studies remain scarce. To fill the gap, this study developed a coupled emission inventory from 2013 to 2020 in Shanxi, a coal-dependent province critical to China's energy security. This facilitated the investigation of emission trends, primary sources, synergistic effects, and spatial distribution. The results show that, while air pollutant emissions decreased significantly during the study period, CO2 emissions increased slightly. The main emitters of SO2, NOx, and CO2 were identified as power, heating, industrial boilers, and residential coal combustion. The iron and steel industry contributed significantly to PM2.5 emissions, coke production to VOCs, and vehicles to NOx and VOCs. NH3 emissions were mainly attributed to fertilizer use and livestock. Synergistic reductions were evident in coal-related sources, especially industrial boilers and residential coal combustion, underlining the importance of optimizing the energy structure. Anthropogenic emissions were concentrated in basins with poor dispersion conditions. Taiyuan, Yuncheng, and Linfen emerged as key areas for synergistic reduction efforts. This study provides important insights for environmental policy development in Shanxi and other coal-dependent regions.

Air pollutants, genetic susceptibility and the risk of schizophrenia: large prospective study.

BACKGROUND: Evidence linking air pollutants and the risk of schizophrenia remains limited and inconsistent, and no studies have investigated the joint effect of air pollutant exposure and genetic factors on schizophrenia risk. AIMS: To investigate how exposure to air pollution affects schizophrenia risk and the potential effect modification of genetic susceptibility. METHOD: Our study was conducted using data on 485 288 participants from the UK Biobank. Cox proportional hazards models were used to estimate the schizophrenia risk as a function of long-term air pollution exposure presented as a time-varying variable. We also derived the schizophrenia polygenic risk score (PRS) utilising data provided by the UK Biobank, and investigated the modification effect of genetic susceptibility. RESULTS: During a median follow-up period of 11.9 years, 417 individuals developed schizophrenia (mean age 55.57 years, s.d. = 8.68; 45.6% female). Significant correlations were observed between long-term exposure to four air pollutants (PM2.5; PM10; nitrogen oxides, NOx; nitrogen dioxide, NO2) and the schizophrenia risk in each genetic risk group. Interactions between genetic factors and the pollutants NO2 and NOx had an effect on schizophrenia events. Compared with those with low PRS and low air pollution, participants with high PRS and high air pollution had the highest risk of incident schizophrenia (PM2.5: hazard ratio = 6.25 (95% CI 5.03-7.76); PM10: hazard ratio = 7.38 (95% CI 5.86-9.29); NO2: hazard ratio = 6.31 (95% CI 5.02-7.93); NOx: hazard ratio = 6.62 (95% CI 5.24-8.37)). CONCLUSIONS: Long-term exposure to air pollutants was positively related to the schizophrenia risk. Furthermore, high genetic susceptibility could increase the effect of NO2 and NOx on schizophrenia risk.

Air pollution, viral spread and health outcomes evidence from strikes in France.

To evidence the impact of air pollution on the health of urban populations, several studies use natural experiments that shift commuting from public transport to cars (or vice-versa). However, as public transport use declines, reduced interpersonal contact may lead to slower virus spread and thus lower respiratory morbidity. Using a difference-in-differences strategy, we show that respiratory hospitalisations are both positively affected by air pollution and negatively affected by viral spread following partial unavailability of public transport due to strikes in the ten most populated French cities during the period 2010-2015. Our results are in line with studies in other countries that have found a significant increase in urgent respiratory hospitalisations following a public transport strike, most likely due to car pollution, but we also find a detectable interaction with viral spread, which should not be overlooked when interpreting these studies.

Prenatal and early-life air pollutant exposure and epigenetic aging acceleration.

BACKGROUND: This study investigated the association of prenatal and early childhood exposure to air pollution with epigenetic age acceleration (EAA) at six years of age using the Environment and Development of Children Cohort (EDC Cohort) MATERIALS & METHODS: Air pollution, including particulate matter [< 2.5 µm (PM2.5) and < 10 µm (PM10) in an aerodynamic diameter], nitrogen dioxide (NO2), ozone (O3), carbon monoxide (CO), and sulfur dioxide (SO2) were estimated based on the residential address for two periods: 1) during the whole pregnancy, and 2) for one year before the follow-up in children at six years of age. The methylation levels in whole blood at six years of age were measured, and the methylation clocks, including Horvath's clock, Horvath's skin and blood clock, PedBE, and Wu's clock, were estimated. Multivariate linear regression models were constructed to analyze the association between EAA and air pollutants. RESULTS: A total of 76 children in EDC cohort were enrolled in this study. During the whole pregnancy, interquartile range (IQR) increases in exposure to PM2.5 (4.56 µg/m3) and CO (0.156 ppm) were associated with 0.406 years and 0.799 years of EAA (Horvath's clock), respectively. An IQR increase in PM2.5 (4.76 µg/m3) for one year before the child was six years of age was associated with 0.509 years of EAA (Horvath's clock) and 0.289 years of EAA (Wu's clock). PM10 (4.30 µg/m3) and O3 (0.003 ppm) exposure in the period were also associated with EAA in Horvath's clock (0.280 years) and EAA in Horvath's skin and blood clock (0.163 years), respectively. CONCLUSION: We found that prenatal and childhood exposure to ambient air pollutants is associated with EAA among children. The results suggest that air pollution could induce excess biological aging even in prenatal and early life.

Impact of PM2.5 exposure in old age and its interactive effect with smoking on incidence of diabetes.

PURPOSE: To determine the impact of PM2.5 exposure in old age and its interactive effect with smoking on incident diabetes. METHODS: A total of 2766 participants aged ≥60 years in China were interviewed at baseline for disease risk factors in 2001-03 and were then followed up for 10 years to document incident diabetes. They were assessed for daily PM2.5 exposure in 2005. Multivariate Cox regression models were used to examine the association of PM2.5 exposure with incident diabetes and interactive effect between PM2.5 and smoking on incident diabetes. RESULTS: During the cohort follow-up, 176 participants developed diabetes. The incidence of diabetes increased with PM2.5 exposure; the multiple-adjusted hazard ratio (HR) of diabetes was 2.27 (95 % CI 1.36-3.77) in participants with PM2.5 at ≥62.0 µg/m3 compared to those with <62.0 µg/m3. There was a significant interaction effect of PM2.5 with smoking on increased risk of diabetes. The adjusted HR for participants exposed to PM2.5 levels ≥62.0 µg/m3 who smoked was 4.39 (95 % CI 1.72-11.21), while for non-smokers it was 1.65 (95 % CI 0.88-3.09), compared to those with <62.0 µg/m3. CONCLUSIONS: Exposure to PM2.5 in old age was associated with an increased incidence of diabetes and smoking enhanced the impact of PM2.5 on diabetic risk. These findings underscore the urgent need for air quality improvement measures and smoking cessation programs to mitigate the risk of diabetes in aging populations.

Association between exposure to air pollution and arterial stiffness in participants with and without atherosclerotic cardiovascular disease.

AIMS: To assess the association of air pollution exposure at different time scales with arterial stiffness in participants with and without atherosclerotic cardiovascular disease (ASCVD). METHODS: We measured participants' arterial stiffness with brachial-ankle pulse wave velocity (baPWV) from October 2016 to January 2020. Concentrations of air pollutants including fine particles < 2.5 µm aerodynamic diameter (PM2.5), inhalable particles < 10 µm aerodynamic diameter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) measured by fixed ambient air monitoring stations were collected for short- (7-day) and long-term (365-day) exposure assessment. We used generalized estimating equations (GEEs) to analyze and further explored the modification effects between ASCVD and air pollutants. RESULTS: Seven hundred sixty-five participants were finally included and four hunderd sixty (60.1%) participants had a history of ASCVD. Based on the partial regression coefficients (ß) and 95% confidence intervals (95% CI) calculated from GEEs using linear regression, each 10 µg/m3 increase in long-term exposure to PM2.5 and PM10 was associated with 31.85 cm/s (95% CI, 17.97 to 45.73) and 35.93 cm/s (95% CI, 21.01 to 50.84) increase in baPWV. There was no association between short-term exposure to air pollution and arterial stiffness. Although no significant interaction effect was observed between air pollution and ASCVD, baPWV showed a greater increment in the subgroup without ASCVD. CONCLUSION: Long-term exposure to air pollution is closely associated with higher arterial stiffness in participants with and without ASCVD. Reducing air pollution exposure is essential in the primary and secondary prevention of ASCVD.

Ambient air pollution and survival in childhood cancer: A nationwide survival analysis.

BACKGROUND: Particulate matter consisting of fine particles measuring 2.5 microns or less in diameter (PM2.5), a component of air pollution, has been linked to adverse health outcomes. The objective of this study was to assess the association between ambient PM2.5 exposure and survival in children with cancer in the United States. METHODS: Individuals aged birth to 19 years who were diagnosed with cancer between January 1, 2004, and December 31, 2019, were selected from the National Cancer Database. The association between the annual PM2.5 level at the patient's zip code of residence at the time of diagnosis and overall survival was evaluated using time-varying Cox proportional hazards models (crude and adjusted for diagnosis year and age). To address concerns that exposure to air pollution is correlated with other social determinants of health, the authors tested the association between PM2.5 levels and survival among sociodemographic subgroups. RESULTS: Of the 172,550 patients included, 27,456 (15.9%) resided in areas with annual PM2.5 concentrations above the US Environmental Protection Agency (EPA) annual PM2.5 standard of 12 µg/m3. Residing in these high-pollution areas was associated with worse overall survival (adjusted hazard ratio [aHR], 1.06; 95% confidence interval [CI], 1.012-1.10). Similarly, when PM2.5 was evaluated as a linear measure, each unit increase in PM2.5 exposure was associated with worse survival (aHR, 1.011; CI, 1.005-1.017). Exposure to PM2.5 at levels above the EPA standards was also significantly associated with worse overall survival among sociodemographic subgroups. CONCLUSIONS: Exposure to PM2.5 was significantly associated with worse overall survival among children with cancer, even at levels below EPA air quality standards. These results underscore the importance of setting appropriate air quality standards to protect the health of this sensitive population. PLAIN LANGUAGE SUMMARY: The authors investigated how living in areas with high air pollution (defined as particulate matter consisting of fine particles measuring 2.5 microns or less in diameter; PM2.5) affects the overall survival of children with cancer in the United States. The results indicated that children living in areas with higher PM2.5 levels, and even at levels below prior and current US Environmental Protection Agency standards, had lower survival rates than children living in areas with lower levels of PM2.5. This finding emphasizes the need for stricter air quality standards to better protect children, particularly those with serious health conditions like childhood cancer.

Short-term air pollution and greenness exposures on oxidative stress in urban and peri-urban residents in Beijing: A part of AIRLESS study.

BACKGROUND: Exposure to air pollution has been associated with increased risks of cardiopulmonary diseases, cancer, and mortality, whereas residing near green spaces may reduce the risks. However, limited research explores their combined effect on oxidative stress. METHODS: A total of 251 participants with multi-time measurements were included in the longitudinal-designed study. Personal gaseous air pollutants (CO, NO, NO2, and O3,) and particulate pollution (PM1, PM2.5, and PM10) were measured and followed in two 7-day windows while ambient exposure levels and urine samples were collected simultaneously. Participants' Normalized Difference Vegetation Index (NDVI) was estimated and used to represent greenness exposure. Urinary oxidative stress biomarkers include free malondialdehyde (MDA), total MDA, and 8-hydroxydeoxyguanosine (8-OHdG). Linear mixed-effects models were used to independently and jointly estimate the associations of greenness and air pollution with oxidative stress biomarkers. RESULTS: We found consistent positive associations of personal ozone (O3) exposure with 8-OHdG percent changes, and this association was modified by gender and outdoor activity frequency. Consistent positive associations of personal lag 2-day carbon monoxide (CO) exposure with the percent changes of the three oxidative stress biomarkers were significant. We additionally observed that individuals who lived in greener areas had lower levels of urinary-free and total MDA. Participants in the highest NDVI tertile had 0.38 and 0.46 lower free and total MDA levels, [95 % CI: (-0.70, -0.05) and (-0.78, -0.13)], compared to the lowest NDVI tertile. There was also evidence indicating the modification effects by area, education, and outdoor activity frequency on associations between NDVI exposure and creatinine adjusted free MDA (all Pfor interaction < 0.05). Additional greenness modification effects on personal O3 exposure with urinary 8-OHdG was observed. CONCLUSION: Our study provides biological evidence of the modification effect of the built environment on the impact of air pollution.

Reflections of stress: Ozone damage in broadleaf saplings can be identified from hyperspectral leaf reflectance.

Tropospheric ozone (O3) causes widespread damage to vegetation; however, monitoring of O3 induced damage is often reliant on manual leaf inspection. Reflectance spectroscopy of vegetation can identify and detect unique spectral signatures of different abiotic and biotic stressors. In this study, we tested the use of hyperspectral leaf reflectance to detect O3 stress in alder, beech, birch, crab apple, and oak saplings exposed to five long-term O3 regimes (ranging from daily target maxima of 30 ppb O3 to 110 ppb). Hyperspectral reflectance varied significantly between O3 treatments, both in whole spectra analysis and when simplified to representative components. O3 damage had a multivariate impact on leaf reflectance, underpinned by changes in pigment balance, water content and structural composition. Vegetation indices derived from reflectance which characterised the visible green peak were able to differentiate between O3 treatments. Iterative normalised difference spectral indices across the hyperspectral wavelength range were correlated to visual damage scores to identify significant wavelengths for O3 damage detection. We propose a new Ozone Damage Index (OzDI), which characterises the reflectance peak in the shortwave infrared region and outperformed existing vegetation indices in terms of correlation to O3 treatment. These results demonstrate the potential application of hyperspectral reflectance as a high throughput method of O3 damage detection in a range of common broadleaf. species.

Source Attribution of Health Burdens From Ambient PM2.5, O3, and NO2 Exposure for Assessment of South Korean National Emission Control Scenarios by 2050.

We quantify anthropogenic sources of health burdens associated with ambient air pollution exposure in South Korea and forecast future health burdens using domestic emission control scenarios by 2050 provided by the United Nations Environment Programme (UNEP). Our health burden estimation framework uses GEOS-Chem simulations, satellite-derived NO2, and ground-based observations of PM2.5, O3, and NO2. We estimate 19,000, 3,300, and 8,500 premature deaths owing to long-term exposure to PM2.5, O3, and NO2, respectively, and 23,000 NO2-associated childhood asthma incidences in 2016. Next, we calculate anthropogenic emission contributions to these four health burdens from each species and grid cell using adjoint sensitivity analysis. Domestic sources account for 56%, 38%, 87%, and 88% of marginal emission contributions to the PM2.5-, O3-, and NO2-associated premature deaths and the NO2-associated childhood asthma incidences, respectively. We project health burdens to 2050 using UNEP domestic emission scenarios (Baseline and Mitigation) and population forecasts from Statistics Korea. Because of population aging alone, there are 41,000, 10,000, and 20,000 more premature deaths associated with PM2.5, O3, and NO2 exposure, respectively, and 9,000 fewer childhood asthma incidences associated with NO2. The Mitigation scenario doubles the NO2-associated health benefits over the Baseline scenario, preventing 24,000 premature deaths and 13,000 childhood asthma incidences by 2050. It also slightly reduces PM2.5- and O3-associated premature deaths by 9.9% and 7.0%, unlike the Baseline scenario where these pollutants increase. Furthermore, we examine foreign emission impacts from nine SSP/RCP-based scenarios, highlighting the need for international cooperation to reduce PM2.5 and O3 pollution.

Volatile organic compounds and mortality from ischemic heart disease: A case-cohort study.

Background: Volatile organic compounds (VOCs) are major components of air pollution and tobacco smoke, two known risk factors for cardiovascular diseases. VOCs are ubiquitous in the environment and originate from a wide range of sources, including the burning of biomass, fossil fuels, and consumer products. Direct evidence for associations between specific VOCs and ischemic heart disease (IHD) mortality in the general population is scarce. Methods: In a case-cohort study (stratified by age groups, sex, residence, and tobacco smoking), nested within the population-based Golestan cohort study (n = 50,045, 40-75 years, 58% women, enrollment: 2004-2008) in northeastern Iran, we measured urinary concentrations of 20 smoking-related VOC biomarkers using ultra high-performance liquid chromatography coupled with electrospray ionization tandem mass spectrometry. We calculated hazard ratio (HR) and 95% confidence interval (CI) for their associations with IHD mortality during follow-up to 2018, using Cox regression models adjusted for age, ethnicity, education, marital status, body mass index, physical activity, wealth, and urinary cotinine. Results: There were 575 non-cases from random subcohort and 601 participants who died from IHD, mean (standard deviation) age, 58.2 (9.3) years, with a median of 8.4 years follow-up. Significant associations [3rd vs. 1st tertile, HR (95% CI), P for trend] were observed between biomarkers of acrylamide [1.68(1.05,2.69), 0.025], acrylonitrile [2.06(1.14,3.72), 0.058], acrolein [1.98(1.30,3.01), 0.003 and 2.44(1.43,4.18), 0.002], styrene/ethylbenzene [1.83(1.19,2.84), 0.007 and 1.44(1.01,2.07), 0.046], dimethylformamide/methylisocyanate [2.15(1.33,3.50), 0.001], and 1,3butadiene [2.35(1.52,3.63),<0.001] and IHD mortality. These associations were independent of tobacco smoking, and they were only present in the non-smoking subgroup. Conclusion: Our findings provide direct evidence for associations between exposure to several VOCs with widespread household and commercial use and IHD mortality many years after these exposures. These results highlight the importance of VOC exposure in the general population as a risk factor for cardiovascular diseases and underline the importance of bio-monitoring non-tobacco VOC exposure.

The Impact of Air Pollution on Neurological and Psychiatric Health.

Air pollution is a critical global issue with extensive implications beyond respiratory health, significantly affecting neurological and psychiatric disorders. Emerging evidence establishes a link between exposure to fine particulate matter (PM < 2.5 µm), sulfur dioxide (SO2), and nitrogen dioxide (NO2) and heightened risks of dementia, Alzheimer's disease, schizophrenia, ADHD, stroke, Parkinson's disease, and multiple sclerosis. Mechanistic pathways include neuroinflammation, oxidative stress, microglial activation, cerebrovascular dysfunction, and blood-brain barrier disruption. Epidemiological studies indicate increased susceptibility among urban residents, particularly men, middle-aged individuals, and married persons, to the mental health impacts of air pollution. Additionally, socioeconomic factors, such as GDP per capita, access to health resources, green spaces, and sports facilities, modulate these health outcomes. Addressing this public health challenge necessitates stricter industrial emission controls, sustainable agricultural practices, promotion of cleaner energy sources, and incorporation of pollution exposure history into clinical assessments. Enhanced public awareness and interdisciplinary research are vital for mitigating the detrimental effects of air pollution on neurological and psychiatric health, ultimately striving for a cleaner and healthier environment for future generations.

Long-term spatiotemporal variation of benzo[a]pyrene in Japan: Significant decrease in ambient concentrations, human exposure, and health risk.

Although Benzo[a]pyrene (BaP) is considered carcinogenic to humans, the health effects of exposure to ambient levels have not been sufficiently investigated. This study estimated the long-term spatiotemporal variation of BaP in Japan over nearly two decades at a fine spatial resolution of 1 km. This study aimed to obtain an accurate spatiotemporal distribution of BaP that can be used in epidemiological studies on the health effects of ambient BaP exposure. The annual BaP concentrations were estimated using an ensemble machine learning approach using various predictors, including the concentrations and emission intensities of the criteria air pollutants, and meteorological, land use, and traffic-related variables. The model performance, evaluated by location-based cross-validation, exhibited satisfactory accuracy (R2 of 0.693). Densely populated areas showed higher BaP levels and greater temporal reduction, whereas BaP levels remained higher in some industrial areas. The population-weighted BaP in 2018 was 0.12 ng m-3, a decrease of approximately 70% from its 2000 value of 0.44 ng m-3, which was also reflected in the estimated excess number of lung cancer incidences. Accordingly, the proportion of BaP exposure below 0.12 ng m-3, which is the BaP concentration associated with an excess lifetime cancer risk of 10-5, reached 67% in 2018. Our estimates can be used in epidemiological studies to assess the health effects of BaP exposure at ambient concentrations.

Aqueous PM2.5 promotes lipid accumulation, classical macrophage polarisation and heat shock response.

Fine particulate matter (PM2.5) is an air pollutant that enhances susceptibility to cardiovascular diseases. Macrophages are the first immune cells to encounter the inhaled particles and orchestrate an inflammatory response. Given their role in atherosclerosis development, we investigated whether aqueous PM2.5 could elicit atherogenic effects by polarising macrophages to a pro-oxidative and pro-inflammatory phenotype and enhancing foam cell formation. The RAW264.7 macrophage cell line was exposed to PM2.5 for 48 h, with PBS as the control. Aqueous PM2.5 induced apoptosis and reduced cell proliferation. In surviving cells, we observed morphological, phagocytic, oxidative, and inflammatory features (i.e. enhanced iNOS, Integrin-1ß, IL-6 expression), indicative of classical macrophage activation. We also detected an increase in total and surface HSP70 levels, suggesting macrophage activation. Further, exposure of high-cholesterol diet-fed mice to PM2.5 resulted in aortic wall enlargement, indicating vascular lesions. Macrophages exposed to PM2.5 and non-modified low-density lipoprotein (LDL) showed exacerbated lipid accumulation. Given the non-oxidised LDL used and the evidence linking inflammation to disrupted cholesterol negative feedback, we hypothesise that PM2.5-induced inflammation in macrophages enhances their susceptibility to transforming into foam cells. Finally, our results indicate that exposure to aqueous PM2.5 promotes classical macrophage activation, marked by increased HSP70 expression and that it potentially contributes to atherosclerosis.