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The oxidative potential (OP) of airborne particulate matter (PM) is gaining increasing attention as a health-relevant metric to describe the capacity of PM to promote oxidative stress and cause adverse health effects. To date, most OP studies use filter-based approaches to sample PM and quantify OP, which have relatively poor time resolution (∼24 h) and underestimate the contribution of reactive components to OP due to the time delay between sample collection and analysis. To address this important limitation, we have developed a novel instrument which uses a direct-to-reagent sampling approach, providing robust, continuous, high time resolution (5 min) OP quantification, hence overcoming analytical limitations of filter-based techniques. In this study, we deployed this instrument in the Marylebone Road Air Quality Monitoring Station in London, UK, alongside a broad suite of high time resolution PM 2.5 composition measurements for three months continuous measurement during Summer 2023. High time resolution OP quantification reveals dynamic changes in volume-normalised (OP v ) and mass normalised (OP m ) OP evolving over ∼hourly timescales, observed at an average PM 2.5 mass concentration of 7.1 ± 4.2 µg m -3 , below the WHO interim 4 target of 10 µg m -3 . In addition, high time resolution data facilitates directional analysis, allowing us to determine the influence of wind speed and wind direction on OP, and the identification of PM 2.5 chemical components and sources which drive dynamic changes in OP; this includes traffic emissions, as well as emissions from the London Underground into the ambient airshed. These results demonstrate the capacity of high time resolution measurements to provide new insights into the temporal evolution of OP, as well as the composition and emission sources which drive OP, developing our understanding of the characteristics of PM 2.5 which may promote adverse health impacts., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Ltd.)

Background: There is increasing evidence that air pollution and noise may have detrimental psychological impacts, but there are few studies evaluating adolescents, ground-level ozone exposure, multi-exposure models, or metrics beyond outdoor residential exposure. This study aimed to address these gaps., Methods: Annual air pollution and traffic noise exposure at home and school were modelled for adolescents in the Greater London SCAMP cohort (N=7555). Indoor, outdoor and hybrid environments were modelled for air pollution. Cognitive and mental health measures were self-completed at two timepoints (baseline aged 11-12 and follow-up aged 13-15). Associations were modelled using multi-level multivariate linear or ordinal logistic regression., Results: This is the first study to investigate ground-level ozone exposure in relation to adolescent executive functioning, finding that a 1 interquartile range increase in outdoor ozone corresponded to -0.06 (p < 0.001) z-score between baseline and follow-up, 38 % less improvement than average (median development + 0.16). Exposure to nitrogen dioxide (NO 2 ), 24-hour traffic noise, and particulate matter < 10 µg/m 3 (PM 10 ) were also significantly associated with slower executive functioning development when adjusting for ozone. In two-pollutant models, particulate matter and ozone were associated with increased externalising problems. Daytime and evening noise were associated with higher anxiety symptoms, and 24-hour noise with worse speech-in-noise perception (auditory processing). Adjusting for air pollutants, 24-hour noise was also associated with higher anxiety symptoms and slower fluid intelligence development., Conclusions: Ozone's potentially detrimental effects on adolescent cognition have been overlooked in the literature. Our findings also suggest harmful impacts of other air pollutants and noise on mental health. Further research should attempt to replicate these findings and use mechanistic enquiry to enhance causal inference. Policy makers should carefully consider how to manage the public health impacts of ozone, as efforts to reduce other air pollutants such as NO 2 can increase ozone levels, as will the progression of climate change., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Exposure to ambient fine particulate matter (PM 2.5 ) has been associated with reduced human fecundity. However, the attributable burden has not been estimated for low- and middle-income countries (LMICs), where the exposure-response function between PM 2.5 and the infertility rate has been insufficiently studied., Objective: This study examined the associations between long-term exposure to PM 2.5 and human fecundity indicators, namely the expected time to pregnancy (TTP) and 12-month infertility rate (IR), and then estimated PM 2.5 -attributable burden of infertility in LMICs., Methods: We analyzed 164,593 eligible women from 100 Demographic and Health Surveys conducted in 49 LMICs between 1999 and 2021. We assessed PM 2.5 exposures during the 12 months before a pregnancy attempt using the global satellite-derived PM 2.5 estimates produced by Atmospheric Composition Analysis Group (ACAG). First, we created a series of pseudo-populations with balanced covariates, given different levels of PM 2.5 exposure, using a matching approach based on the generalized propensity score. For each pseudo-population, we used 2-stage generalized Gamma models to derive TTP or IR from the probability distribution of the questionnaire-based duration time for the pregnancy attempt before the interview. Second, we used spline regressions to generate nonlinear PM 2.5 exposure-response functions for each of the two fecundity indicators. Finally, we applied the exposure-response functions to estimate number of infertile couples attributable to PM 2.5 exposure in 118 LMICs., Results: Based on the Gamma models, each 10 µg/m 3 increment in PM 2.5 exposure was associated with a TTP increase by 1.7 % (95 % confidence interval [CI]: -2.3 %-6.0 %) and an IR increase by 2.3 % (95 %CI: 0.6 %-3.9 %). The nonlinear exposure-response function suggested a robust effect of an increased IR for high-concentration PM 2.5 exposure (>75 µg/m 3 ). Based on the PM 2.5 -IR function, across the 118 LMICs, the number of infertile couples attributable to PM 2.5 exposure exceeding 35 µg/m 3 (the first-stage interim target recommended by the World Health Organization global air quality guidelines) was 0.66 million (95 %CI: 0.061-1.43), accounting for 2.25 % (95 %CI: 0.20 %-4.84 %) of all couples affected by infertility. Among the 0.66 million, 66.5 % were within the top 10 % high-exposure infertile couples, mainly from South Asia, East Asia, and West Africa., Conclusion: PM 2.5 contributes significantly to human infertility in places with high levels of air pollution. PM 2.5 -pollution control is imperative to protect human fecundity in LMICs., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Particle size is a critical influencing factor in assessing human exposure risk as fine particles are generally more hazardous than larger coarse particles. However, how particle composition influences human health risk is only poorly understood as different studies have different utilised different definitions and as a consequence there is no consensus. Here, with a new methodology taking insights of each size fraction load (%GSF load ), metal bioaccessibility, we classify which specific particle size can reliably estimate the human exposure risk of lead and other metals. We then validate these by correlating the metals in each size fraction with those in human blood, hair, crop grain and different anthropogenic sources. Although increasing health risks are linked to metal concentration these increase as particle size decrease, the adjusted-risk for each size fraction differs when %GSF load is introduced to the risk assessment program. When using a single size fraction (250-50 µm, 50-5 µm, 5-1 µm, and < 1 µm) for comparison, the risk may be either over- or under-estimated. However, by considering bulk and adjusting the risk, it would be possible to obtain results that are closer to the real scenarios, which have been validated through human responses and evidence from crops. Fine particle size fractions (< 5 µm) bearing the mineral crystalline or aggregates (CaCO 3 , Fe 3 O 4 , Fe 2 O 3 , CaHPO 4 , Pb 5 (PO 4 ) 3 Cl) alter the accumulation, chemical speciation, and fate of metals in soil/dust/sediment from the different sources. Loaded lead in the size fraction of < 50 µm has a significantly higher positive association with the risk-receptor biomarkers (BLLs, Hair Pb, Corn Pb, and Crop Pb) than other size fractions (bulk and 50-250 µm). Thus, we conclude that the < 50 µm fraction would be likely to be recommended as a reliable fraction to include in a risk assessment program. This methodology acts as a valuable instrument for future research undertakings, highlighting the importance of choosing suitable size fractions and attaining improved accuracy in risk assessment results that can be effectively compared., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Lead is a toxic metal that can pose a huge threat to children's health. China has experienced rapid urbanization since the reform in 1978; however, there has been no examination of the potential influence of this urbanization on children's blood lead levels (BLLs). This study is the initial investigation to explore the correlation between urbanization and BLLs in Chinese children. Five windows of time are considered: pre-2000, 2001-2005, 2006-2010, 2011-2015 and 2016-2021. The results show that urbanization affected lead distribution in urban soil and agricultural soil during the above periods, especially in northern China. The higher non-carcinogenic risk of lead for children is consistent with the lead pollution in soil (3 < I geo  ≤ 4). Urban children's BLLs are slightly higher than those of rural children in 2001-2010, but rural children's BLLs in 2011-2021 are higher than those of urban children during China's urbanization. The areas of rural decline and the areas of urban growth increased across all the window periods. However, the BLLs decrease in all rural and urban areas during all window periods, especially in urban areas. Children's BLLs have a significantly negative correlation with urban areas (p < 0.01). Therefore, China's urbanization has a significant effect on the decrease in children's BLLs. The significance of this study is to provide a fresh perspective and innovative strategy for policymaking in order to reduce children's BLLs and prevent lead exposure. This can be achieved by transforming their external living environment from a rural lifestyle to an urban one, while also ensuring access to well education and maintaining a balanced nutrient intake., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: Environmental temperature is negatively associated with blood pressure (BP), and hypertension may exacerbate this association. The aim of this study is to investigate whether hypertensive individuals are more susceptible to acute BP increases following temperature decrease than non-hypertensive individuals., Methods: The study panel consisted of 126 hypertensive and 125 non-hypertensive (n = 251) elderly participants who completed 940 clinical visits during the winter of 2016 and summer of 2017 in Beijing, China. Personal-level environmental temperature (PET) was continuously monitored for each participant with a portable sensor platform. We associated systolic BP (SBP) and diastolic BP (DBP) with the average PET over 24 h before clinical visits using linear mixed-effects models and explored hourly lag patterns for the associations using distributed lag models., Results: We found that per 1 °C decrease in PET, hypertensive individuals showed an average (95 % confidence interval) increase of 0.96 (0.72, 1.19) and 0.28 (0.13, 0.42) mmHg for SBP and DBP, respectively; and non-hypertensive participants showed significantly smaller increases of 0.28 (0.03, 0.53) mmHg SBP and 0.14 (-0.01, 0.30) mmHg DBP. A lag pattern analysis showed that for hypertensive individuals, the increases in SBP and DBP were greatest following lag 1 h PET decrease and gradually attenuated up to lag 10 h exposure. No significant BP change was observed in non-hypertensive individuals associated with lag 1-24 h PET exposure. The enhanced increase in PET-associated BP in hypertensive participants (i.e., susceptibility) was more significant in winter than in summer., Conclusions: We found that a decrease in environmental temperature was associated with acute BP increases and these associations diminished over time, disappearing after approximately 10 hours. This implies that any intervention measures to prevent BP increases due to temperature drop should be implemented as soon as possible. Such timely interventions are particularly needed for hypertensive individuals especially during the cold season due to their increased susceptibility., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Stroke and dementia are the leading causes of neurological disease burden. Detrimental effects of air pollution on both conditions are increasingly recognised, while the impacts on the dynamic transitions have not yet been explored, and whether critical time intervals exist is unknown., Methods: This prospective study was conducted based on the UK Biobank. Annual average air pollution concentrations at baseline year 2010 estimated by land-use regression models were used as a proxy for long-term air pollution exposure. Associations between multiple air pollutants (PM 2.5 , PM 2.5-10 , and NO 2 ) indicated by air pollution score and the dynamic transitions of stroke and dementia were estimated, and the impacts during critical time intervals were explored. The date cutoff of this study was February 29, 2020., Findings: During a median follow-up of 10.9 years in 413,372 participants, 6484, 3813, and 376 participants developed incident stroke, dementia, and comorbidity of stroke and dementia. For the overall transition from stroke to comorbid dementia, the hazard ratio (HR) for each interquartile range (IQR) increase in air pollution score was 1.38 (95% CI, 1.15, 1.65), and the risks were limited to two time intervals (within 1 year and over 5 years after stroke). As for the transition from dementia to comorbid stroke, increased risk was only observed during 2-3 years after dementia., Interpretation: Our findings suggested that air pollution played an important role in the dynamic transition of stroke and dementia even at concentrations below the current criteria. The findings provided new evidence for alleviating the disease burden of neurological disorders related to air pollution during critical time intervals., Funding: The State Scholarship Fund of China Scholarship Council., Competing Interests: None reported., (© 2023 The Author(s).)

Background: Diesel exhaust (DE) induces neutrophilia and lymphocytosis in experimentally exposed humans. These responses occur in parallel to nuclear migration of NF-κB and c-Jun, activation of mitogen activated protein kinases and increased production of inflammatory mediators. There remains uncertainty regarding the impact of DE on endogenous antioxidant and xenobiotic defences, mediated by nuclear factor erythroid 2-related factor 2 (Nrf2) and the aryl hydrocarbon receptor (AhR) respectively, and the extent to which cellular antioxidant adaptations protect against the adverse effects of DE., Methods: Using immunohistochemistry we investigated the nuclear localization of Nrf2 and AhR in the epithelium of endobronchial mucosal biopsies from healthy subjects six-hours post exposure to DE (PM 10 , 300 µg/m 3 ) versus post-filtered air in a randomized double blind study, as a marker of activation. Cytoplasmic expression of cytochrome P450s, family 1, subfamily A, polypeptide 1 (CYP1A1) and subfamily B, Polypeptide 1 (CYP1B1) were examined to confirm AhR activation; with the expression of aldo-keto reductases (AKR1A1, AKR1C1 and AKR1C3), epoxide hydrolase and NAD(P)H dehydrogenase quinone 1 (NQO1) also quantified. Inflammatory and oxidative stress markers were examined to contextualize the responses observed., Results: DE exposure caused an influx of neutrophils to the bronchial airway surface (p = 0.013), as well as increased bronchial submucosal neutrophil (p < 0.001), lymphocyte (p = 0.007) and mast cell (p = 0.002) numbers. In addition, DE exposure enhanced the nuclear translocation of the AhR and increased the CYP1A1 expression in the bronchial epithelium (p = 0.001 and p = 0.028, respectively). Nuclear translocation of AhR was also increased in the submucosal leukocytes (p < 0.001). Epithelial nuclear AhR expression was negatively associated with bronchial submucosal CD3 numbers post DE (r = -0.706, p = 0.002). In contrast, DE did not increase nuclear translocation of Nrf2 and was associated with decreased NQO1 in bronchial epithelial cells (p = 0.02), without affecting CYP1B1, aldo-keto reductases, or epoxide hydrolase protein expression., Conclusion: These in vivo human data confirm earlier cell and animal-based observations of the induction of the AhR and CYP1A1 by diesel exhaust. The induction of phase I xenobiotic response occurred in the absence of the induction of antioxidant or phase II xenobiotic defences at the investigated time point 6 h post-exposures. This suggests DE-associated compounds, such as polycyclic aromatic hydrocarbons (PAHs), may induce acute inflammation and alter detoxification enzymes without concomitant protective cellular adaptations in human airways., (© 2023. The Author(s).)

Biomedical research is a significant contributor to the global carbon footprint. Practices are available that could make a difference; however, there are significant obstacles ahead, including a lack of specialist expertise in sustainable research practices., Competing Interests: The author has declared that no competing interests exist., (Copyright: © 2023 Frank J Kelly. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Background: In 2021, WHO suggested new target concentration limits for long-term exposure to ambient ozone. However, the harmful effects of ozone on vulnerable children have not been sufficiently studied. We aimed to evaluate the association between long-term ozone exposure and mortality in children younger than 5 years (hereafter denoted under-5 mortality) in low-income and middle-income countries (LMICs) and to estimate this mortality burden for 97 LMICs., Methods: By combining information from 128 Demographic and Health Surveys, we evaluated the association between the survival status of more than 1·2 million children younger than 5 years from 2457 sampling strata in 55 LMICs and the average peak-season ozone concentration during the life course, using a fixed-effects Cox model. A non-linear exposure-response function was developed by integrating the marginal effects of within-strata variation in exposure. We extrapolated the function obtained from the 55 LMICs to estimate the under-5 mortality burden attributable to ozone exposure in 97 LMICs, in which more than 95% of global deaths in this age group occur., Findings: The fixed-effects model showed a robust association between ozone and under-5 mortality. According to the fully adjusted linear model, an increment of 10 ppb in the life-course average peak-season ozone concentration was associated with a 6·4% (95% CI 2·4-10·7) increase in the risk of under-5 mortality. The non-linear exposure-response function showed a sublinear curvature with a threshold, suggesting that the effect of ozone exposure was non-significant at concentrations lower than the first-stage interim target (100 μg/m 3 ) recommended by WHO. Using this function, we estimate that, in 2010, long-term ozone exposure contributed to 153 361 (95% CI 17 077-276 768; 2·3% [0·3-4·1]) deaths of children younger than 5 years in 97 LMICs, which is equivalent to 56·8% of all ozone-related deaths in adults (269 785) in these countries. From 2003 to 2017, the ozone-related under-5 mortality burden decreased in most of the 97 LMICs., Interpretation: Long-term exposure to ozone concentrations higher than the WHO first-stage interim target is a risk factor for under-5 mortality, and ozone exposure contributes substantially to mortality in this age group in LMICs. Increased efforts should be made to control ambient ozone pollution as this will lead to positive health benefits., Funding: Ministry of Science and Technology of the People's Republic of China and China National Natural Science Foundation., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2023 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: Prenatal exposure to air pollution is associated with adverse neurologic consequences in childhood. However, the relationship between in utero exposure to air pollution and neonatal brain development is unclear., Methods: We modelled maternal exposure to nitrogen dioxide (NO 2 ) and particulate matter (PM 2.5 and PM 10 ) at postcode level between date of conception to date of birth and studied the effect of prenatal air pollution exposure on neonatal brain morphology in 469 (207 male) healthy neonates, with gestational age of ≥36 weeks. Infants underwent MR neuroimaging at 3 Tesla at 41.29 (36.71-45.14) weeks post-menstrual age (PMA) as part of the developing human connectome project (dHCP). Single pollutant linear regression and canonical correlation analysis (CCA) were performed to assess the relationship between air pollution and brain morphology, adjusting for confounders and correcting for false discovery rate., Results: Higher exposure to PM 10 and lower exposure to NO 2 was strongly canonically correlated to a larger relative ventricular volume, and moderately associated with larger relative size of the cerebellum. Modest associations were detected with higher exposure to PM 10 and lower exposure to NO 2 and smaller relative cortical grey matter and amygdala and hippocampus, and larger relaive brainstem and extracerebral CSF volume. No associations were found with white matter or deep grey nuclei volume., Conclusions: Our findings show that prenatal exposure to air pollution is associated with altered brain morphometry in the neonatal period, albeit with opposing results for NO 2 and PM 10 . This finding provides further evidence that reducing levels of maternal exposure to particulate matter during pregnancy should be a public health priority and highlights the importance of understanding the impacts of air pollution on this critical development window., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier Ltd.)

Importance: Air pollution is increasingly recognized as an important environmental risk factor for mental health. However, epidemiologic evidence on long-term exposure to low levels of air pollutants with incident depression and anxiety is still very limited., Objectives: To investigate the association of long-term joint exposure to multiple air pollutants with incident depression and anxiety., Design, Setting, and Participants: This prospective, population-based cohort study used data from the UK Biobank. The participants were recruited between March 13, 2006, and October 1, 2010, and included individuals who had never been diagnosed with depression or anxiety at baseline and had full information on exposure and covariates. Data were analyzed from May 1 to October 10, 2022., Exposures: Annual mean air pollution concentrations of particulate matter (PM) with aerodynamic diameter of 2.5 μm or less (PM2.5) and PM with aerodynamic diameter between 2.5 μm and 10 μm (PM2.5-10). Nitrogen dioxide (NO2) and nitric oxide (NO) were estimated for each participant's residential address using the land use regression model, and joint exposure to air pollution reflected by air pollution score was calculated by principal components analysis., Main Outcomes and Measures: Incidence of diagnosed depression (F32-F33) and anxiety (F40-F48) were ascertained with International Statistical Classification of Diseases and Related Health Problems, Tenth Revision codes., Results: During a median (IQR) follow-up of 10.9 (10.1-11.6) years, among 389 185 participants (mean [SD] age, 56.7 [8.1] years, 205 855 female individuals [52.9%]), a total of 13 131 and 15 835 patients were diagnosed with depression and anxiety, respectively. The median (IQR) concentration of pollutants was as follows: PM2.5, 9.9 (9.3-10.6) μg/m3; PM2.5-10, 6.1 (5.8-6.6) μg/m3; NO2, 26.0 (21.3-31.1) μg/m3; and NO, 15.9 (11.6-20.6) μg/m3. Long-term estimated exposure to multiple air pollutants was associated with increased risk of depression and anxiety, and the exposure-response curves were nonlinear, with steeper slopes at lower concentrations and plateauing trends at higher exposure. The hazard ratios (HRs) and 95% CIs for depression and anxiety were 1.16 (95% CI, 1.09-1.23; P < .001) and 1.11 (95% CI, 1.05-1.17; P < .001) in the highest quartile compared with the lowest quartile of air pollution score, respectively. Similar trends were shown for PM2.5, NO2, and NO. Subgroup analysis showed the association between PM2.5 and anxiety tended to be higher in male individuals than in female individuals (quartile 4: male individuals, 1.18; 95% CI, 1.08-1.29; female individuals, 1.07; 95% CI, 1.00-1.14; P = .009)., Conclusions and Relevance: Study results suggest that estimates of long-term exposure to multiple air pollutants was associated with increased risk of depression and anxiety. The nonlinear associations may have important implications for policy making in air pollution control. Reductions in joint exposure to multiple air pollutants may alleviate the disease burden of depression and anxiety.

Longitudinal evidence on the association between air pollution and blood pressure (BP) in adolescence is scarce. We explored this association in an ethnically diverse cohort of schoolchildren. Sex-stratified, linear random-effects modelling was used to examine how modelled residential exposure to annual average nitrogen dioxide (NO2), particulate matter (PM2.5, PM10) and ozone (O3), measures in μg/m3, associated with blood pressure. Estimates were based on 3,284 adolescents; 80% from ethnic minority groups, recruited from 51 schools, and followed up from 11-13 to 14-16 years old. Ethnic minorities were exposed to higher modelled annual average concentrations of pollution at residential postcode level than their White UK peers. A two-pollutant model (NO2 & PM2.5), adjusted for ethnicity, age, anthropometry, and pubertal status, highlighted associations with systolic, but not diastolic BP. A μg/m3 increase in NO2 was associated with a 0.30 mmHg (95% CI 0.18 to 0.40) decrease in systolic BP for girls and 0.19 mmHg (95% CI 0.07 to 0.31) decrease in systolic BP for boys. In contrast, a 1 μg/m3 increase in PM2.5 was associated with 1.34 mmHg (95% CI 0.85 to 1.82) increase in systolic BP for girls and 0.57 mmHg (95% CI 0.04 to 1.03) increase in systolic BP for boys. Associations did not vary by ethnicity, body size or socio-economic advantage. Associations were robust to adjustments for noise levels and lung function at 11-13 years. In summary, higher ambient levels of NO2 were associated with lower and PM2.5 with higher systolic BP across adolescence, with stronger associations for girls., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2023 Karamanos et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

We systematically reviewed the association of ambient air pollution with blood pressure (BP) as a primary outcome in adolescents (10-19 years). Five databases (Ovid Medline, Ovid Embase, Web of Science, The Cochrane Library, and LILACS) were searched for relevant articles published up to August 2022. Meta-analyses were conducted using STATA v17 (Protocol - OSF Registries https://doi.org/10.17605/OSF.IO/96G5Q). Eight studies (5 cohort, 3 cross-sectional) with approximately 15,000 adolescents were included. Data from 6 studies were suitable for inclusion in the meta-analyses. In sub-group analyses, non-significant positive associations were observed for cohort studies assessing long-term exposure to PM 10 , PM 2.5 , and NO 2 on systolic and diastolic BP. At age 12 years old (3702 adolescents), we found significant positive associations for long-term exposure to PM 2.5 (β=5.33 (1.56, 9.09) mmHg) and PM 10 (β=2.47 (0.10, 4.85) mmHg) on diastolic BP. Significant positive associations were observed (3,592 adolescents) for long-term exposure to PM 10 (β=0.34 (0.19, 0.50) mmHg) and NO 2 on diastolic BP (β=0.40 (0.09, 0.71) mmHg), and PM 10 on systolic BP (β=0.48 (0.19, 0.77) mmHg). The overall quality of evidence analysed was graded as "low/very low." Insufficient data for short-term exposures to PM 2 . 5 , PM 10 , NO 2 , CO on BP led to their exclusion from the meta-analysis. Inconsistent associations were reported for gender-stratified results. The evidence, though of low-quality and limited, indicated that ambient air pollution was positively associated with adolescent BP. Future studies need improved measures of air pollutant exposures, consideration of gender and socio-economic circumstances on the observed pollution effects, as well as adjustment for other potential confounding factors., (Copyright © 2022. Published by Elsevier Inc.)

Background: Fine particulate matter (PM 2.5 ) produced by landscape fires is thought to be more toxic than that from non-fire sources. However, the effects of "fire-sourced" PM 2.5 on acute respiratory infection (ARI) are unknown., Methods: We combined Demographic and Health Survey (DHS) data from 48 countries with gridded global estimates of PM 2.5 concentrations from 2003 to 2014. The proportions of fire-sourced PM 2.5 were assessed by a chemical transport model using a variety of PM 2.5 source data. We tested for associations between ARI and short-term exposure to fire- and "non-fire-sourced" PM 2.5 using a bidirectional case-crossover analysis. The robustness and homogeneity of the associations were examined by sensitivity analyses. We also established a nonlinear exposure-response relationship between fire- and non-fire-sourced PM 2.5 and ARI using a two-dimensional spline function., Results: The study included 36,432 children under 5 years who reported ARI symptoms. Each 1 µg/m 3 increment of fire-sourced PM 2.5 was associated with a 3.2 % (95 % confidence interval [CI] 0.2, 6.2) increment in the risk of ARI. This effect was comparable to that of each ∼5 µg/m 3 increment in PM 2.5 from non-fire sources (3.1 %; 95 % CI 2.4, 3.7). The association between ARI and total PM 2.5 concentration was significantly mediated by the proportion of fire-sourced particles. Nonlinear analysis showed that the risk of ARI was increased by both fire- and non-fire-sourced PM 2.5 , but especially by the former., Conclusions: PM 2.5 produced by landscape fire was more strongly associated to ARI among children under 5 years than that from non-fire sources., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: Air pollution epidemiology has primarily relied on measurements from fixed outdoor air quality monitoring stations to derive population-scale exposure. Characterisation of individual time-activity-location patterns is critical for accurate estimations of personal exposure and dose because pollutant concentrations and inhalation rates vary significantly by location and activity., Methods: We developed and evaluated an automated model to classify major exposure-related microenvironments (home, work, other static, in-transit) and separated them into indoor and outdoor locations, sleeping activity and five modes of transport (walking, cycling, car, bus, metro/train) with multidisciplinary methods from the fields of movement ecology and artificial intelligence. As input parameters, we used GPS coordinates, accelerometry, and noise, collected at 1 min intervals with a validated Personal Air quality Monitor (PAM) carried by 35 volunteers for one week each. The model classifications were then evaluated against manual time-activity logs kept by participants., Results: Overall, the model performed reliably in classifying home, work, and other indoor microenvironments (F1-score>0.70) but only moderately well for sleeping and visits to outdoor microenvironments (F1-score=0.57 and 0.3 respectively). Random forest approaches performed very well in classifying modes of transport (F1-score>0.91). We found that the performance of the automated methods significantly surpassed those of manual logs., Conclusions: Automated models for time-activity classification can markedly improve exposure metrics. Such models can be developed in many programming languages, and if well formulated can have general applicability in large-scale health studies, providing a comprehensive picture of environmental health risks during daily life with readily gathered parameters from smartphone technologies., (© 2022. The Author(s).)

Limited number of projects have attempted to partition and quantify indoor- and outdoor-generated PM 2.5 (PM 2.5 ig and PM 2.5 og ) where strong indoor sources (e.g., solid fuel, tobacco smoke, or kerosene) exist. This study aimed to apply and refine a previous recursive model used to derive infiltration efficiency (F inf ) to additionally partition pollution concentrations into indoor and outdoor origins within residences challenged by elevated ambient and indoor combustion-related sources. During the winter of 2016 and summer of 2017 we collected residential measurements in 72 homes in urban and peri-urban Beijing, 12 of which had additional paired residential outdoor measurements during the summer season. Local ambient measurements were collected throughout. We then compared the calculated PM 2.5 ig and using (i) outdoor and (ii) ambient measurements as model inputs. The results from outdoor and ambient measurements were not significantly different, which suggests that ambient measurements can be used as a model input for pollution origin partitioning when paired outdoor measurements are not available. From the results calculated using ambient measurements, the mean percentage contribution of indoor-generated PM 2.5 was 19 % (σ = 22 %), and 7 % (11 %) of the total indoor PM 2.5 for peri-urban and urban homes respectively during the winter; and 18 % (18 %) and 6 % (10 %) of the total indoor PM 2.5 during the summer. Partitioning pollution into PM 2.5 ig and PM 2.5 og is important to allow investigation of distinct associations between health outcomes and particulate mixes, often with different physiochemical composition and toxicity. It will also inform targeted interventions that impact indoor and outdoor sources of pollution (e.g., domestic fuel switching vs. power generation), which are typically radically different in design and implementation., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

Microplastics (MPs) in freshwater environments have been recognized as one of the important sources of plastic contamination in marine ecosystems. Reducing the amount and spatial distribution of MPs reaching the sea through accumulation behind dams remains unclear. In this study we analyzed the spatial distribution of sediment and surface water MPs in the Aras Dam and from nineteen upstream and downstream locations of the Dam in the Aras River. The MPs abundance ranged from 32 to 528 items/kg dry weight (mean 217.8 ± 132.6) and 1 to 43 items/m 3 (mean 12.8 ± 10.5) in the sediment and surface water stations, respectively. MPs abundance in surface waters collected within the Dam reservoir was significantly higher than those found either upstream or downstream (P < 0.05). For sediments, reservoir MPs concentration was generally higher than upstream and downstream, although their differences were not significant. High MPs concentration was observed in the vicinity of urban areas. Moreover, MPs abundance was positively correlated with total organic carbon (TOC) and clay content (P < 0.01). GAM analysis revealed that clay is the most important variable with lowest Akaike information criterion (AIC) and explained 61.3 % of deviance (R-sq.(adj) = 0.344) in MPs abundance. MP particles ranged from 0.1 to 5 mm in size and were dominated by fibers (53.5 %), black color (24 %) and PE polymer (36.6 %). Our results highlight the high MPs distribution in the Aras River and demonstrate that they accumulate in the surface waters behind the Dam. Consequently, the fate and effects of MPs in international rivers is one of the most politicized issues between countries with a common boundary and therefore needs joint management policies that help mitigate this insidious problem., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Background: Due to the adverse health effects of air pollution, researchers have advocated for personal exposure measurements whereby individuals carry portable monitors in order to better characterise and understand the sources of people's pollution exposure., Objectives: The aim of this systematic review is to assess the differences in the magnitude and sources of personal PM 2.5 exposures experienced between countries at contrasting levels of income., Methods: This review summarised studies that measured participants personal exposure by carrying a PM 2.5 monitor throughout their typical day. Personal PM 2.5 exposures were summarised to indicate the distribution of exposures measured within each country income category (based on low (LIC), lower-middle (LMIC), upper-middle (UMIC), and high (HIC) income countries) and between different groups (i.e. gender, age, urban or rural residents)., Results: From the 2259 search results, there were 140 studies that met our criteria. Overall, personal PM 2.5 exposures in HICs were lower compared to other countries, with UMICs exposures being slightly lower than exposures measured in LMICs or LICs. 34% of measured groups in HICs reported below the ambient World Health Organisation 24-h PM 2.5 guideline of 15 μg/m 3 , compared to only 1% of UMICs and 0% of LMICs and LICs. There was no difference between rural and urban participant exposures in HICs, but there were noticeably higher exposures recorded in rural areas compared to urban areas in non-HICs, due to significant household sources of PM 2.5 in rural locations. In HICs, studies reported that secondhand smoke, ambient pollution infiltrating indoors, and traffic emissions were the dominant contributors to personal exposures. While, in non-HICs, household cooking and heating with biomass and coal were reported as the most important sources., Conclusion: This review revealed a growing literature of personal PM 2.5 exposure studies, which highlighted a large variability in exposures recorded and severe inequalities in geographical and social population subgroups., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

Implementation of regulatory standards has reduced exhaust emissions of particulate matter from road traffic substantially in the developed world. However, nonexhaust particle emissions arising from the wear of brakes, tires, and the road surface, together with the resuspension of road dust, are unregulated and exceed exhaust emissions in many jurisdictions. While knowledge of the sources of nonexhaust particles is fairly good, source-specific measurements of airborne concentrations are few, and studies of the toxicology and epidemiology do not give a clear picture of the health risk posed. This paper reviews the current state of knowledge, with a strong focus on health-related research, highlighting areas where further research is an essential prerequisite for developing focused policy responses to nonexhaust particles.

Background: Empirical evidence suggests a strong link between exposure to air pollution and heart failure incidence, hospitalizations, and mortality, but the biological basis of this remains unclear. We sought to determine the relationship between differential air pollution levels and changes in cardiac structure and function in patients with dilated cardiomyopathy., Methods and Results: We undertook a prospective longitudinal observational cohort study of patients in England with dilated cardiomyopathy (enrollment 2009-2015, n = 716, 66% male, 85% Caucasian) and conducted cross sectional analysis at the time of study enrollment. Annual average air pollution exposure estimates for nitrogen dioxide (NO 2 ) and particulate matter with diameter of 2.5 µm or less (PM 2.5 ) at enrolment were assigned to each residential postcode (on average 12 households). The relationship between air pollution and cardiac morphology was assessed using linear regression modelling. Greater ambient exposure to NO 2 was associated with higher indexed left ventricular (LV) mass (4.3 g/m 2 increase per interquartile range increase in NO 2 , 95% confidence interval 1.9-7.0 g/m 2 ) and lower LV ejection fraction (-1.5% decrease per interquartile range increase in NO 2 , 95% confidence interval -2.7% to -0.2%), independent of age, sex, socioeconomic status, and clinical covariates. The associations were robust to adjustment for smoking status and geographical clustering by postcode area. The effect of air pollution on LV mass was greatest in women. These effects were specific to NO 2 exposure., Conclusions: Exposure to air pollution is associated with raised LV mass and lower LV ejection fraction, with the strongest effect in women. Although epidemiological associations between air pollution and heart failure have been established and supported by preclinical studies, our findings provide novel empirical evidence of cardiac remodeling and exposure to air pollution with important clinical and public health implications., Competing Interests: Declaration of Interests DJP declares consultancy fees from ApoPharma; research support from Bayer, ApoPharma, and Siemens; speakers fees from ApoPharma and Bayer. JW declares consultancy fees from MyoKardia and research support from MyoKardia. The remaining authors have no conflicts of interest., (Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.)

We report on the concentration ranges and combustion source-related emission profiles of organic and inorganic species released during 34 major industrial fires in the UK. These episodic events tend to be acute in nature and demand a rapid public health risk assessment to indicate the likely impact on exposed populations. The objective of this paper is to improve our understanding of the nature, composition and potential health impacts of emissions from major incident fires and so support the risk assessment process. Real world monitoring data was obtained from portable Fourier Transform Infrared (FTIR) monitoring (Gasmet DX-4030/40) carried out as part of the UK's Air Quality in Major Incidents service. The measured substances include carbon monoxide, sulphur dioxide, nitrogen dioxide, ammonia, hydrogen chloride, hydrogen bromide, hydrogen fluoride, hydrogen cyanide, formaldehyde, 1,3-butadiene, benzene, toluene, xylenes, ethyl benzene, acrolein, phosgene, arsine, phosphine and methyl isocyanate. We evaluate the reported concentrations against Acute Exposure Guideline Values (AEGLs) and Emergency Response Planning Guidelines (ERPGs), as well as against UK, EU and WHO short-term ambient guideline values. Most exceedances of AEGL or ERPG guideline values were at levels likely only to cause discomfort to exposed populations (hydrogen cyanide, hydrogen chloride, hydrogen fluoride and formaldehyde), though for several substances the exceedances could have potentially given rise to more serious health effects (acrolein, phosphine, phosgene and methyl isocyanate). In the latter cases, the observed high concentrations are likely to be due to cross-interference from other substances that absorb in the mid-range of the infrared spectrum, particularly when the ground level plume is very concentrated., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Traffic is one of the major contributors to PM2.5 in cities worldwide. Quantifying the role of traffic is an important step towards understanding the impact of transport policies on the possibilities to achieve cleaner air and accompanying health benefits. With the aim of estimating potential health benefits of eliminating traffic emissions, we carried out a meta-analysis using the World Health Organisation (WHO) database of source apportionment studies of PM2.5 concentrations. Specifically, we used a Bayesian meta-regression approach, modelling both overall and traffic-related (tailpipe and non-tailpipe) concentrations simultaneously. We obtained the distributions of expected PM2.5 concentrations (posterior densities) of different types for 117 cities worldwide. Using the non-linear Integrated Exposure Response (IER) function of PM2.5, we estimated percent reduction in different disease endpoints for a scenario with complete removal of traffic emissions. We found that eliminating traffic emissions results in achieving the WHO-recommended concentration of PM2.5 only for a handful of cities that already have low concentrations of pollution. The percentage reduction in premature mortality due to cardiovascular and respiratory diseases increases up to a point (30-40 ug/m3), and above this concentration, it flattens off. For diabetes-related mortality, the percentage reduction in mortality decreases with increasing concentrations-a trend that is opposite to other outcomes. For cities with high concentrations of pollution, the results highlight the need for multi-sectoral strategies to reduce pollution. The IER functions of PM2.5 result in diminishing returns of health benefits at high concentrations, and in case of diabetes, there are even negative returns. The results show the significant effect of the shape of IER functions on health benefits. Overall, despite the diminishing results, a significant burden of deaths can be prevented by policies that aim to reduce traffic emissions even at high concentrations of pollution., Competing Interests: The authors have declared that no competing interests exist.

This study examines for the first time the characteristics and human exposure of microplastics (MPs) in settled indoor dust in schools. An average of 195 MPs·g -1 of dust were detected in settled indoor composite dust samples from 28 schools in Shiraz. White-transparent microfibres with lengths 500-1000 μm were the most abundant type of MP found among the samples examined. Polyethylene terephthalate and polypropylene MPs were dominant across all types of MP found including microfibres. MPs had generally smooth morphology with sharp or regular edges which could have been released to the environment as primary MPs. Among all sampling sites, higher concentrations of MPs were found in the south and centre of the city. These were areas affected by high population density, high traffic load and high presence of industrial units and workshops. Principal Component Analysis (PCA) showed a positive strong correlation between sampling sites and MP physical characteristics. The PCA plots revealed that MP sheets and fragments were prevalent in sites in the North of Shiraz, whereas microfibres were mainly associated with sites in the South. The levels of MPs in the South of Shiraz were greater than in the rest of the country and the wind direction and topography were found to be important factors affecting the MP distribution observed. Compared to other population groups, elementary school students had relatively high exposure risk to MPs. This study reveals that microfibres are widespread in Shiraz' schools and pose a high exposure risk to MPs for young students., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 Elsevier B.V. All rights reserved.)

The use of plastics is common across all aspects of human life owing to its durable and versatile nature. The generation and utilization of plastics are directly related to the anthropogenic activities. The extensive use of plastics and adoption of inappropriate waste-management frameworks has resulted in their release into the environment, where they may persist. Different environmental factors, such as, photochemical, thermo-oxidation, and biological degradation, can lead to the degradation of plastics into micro- (MPs) and nano-plastics (NPs). The behaviour and concentration of MPs in the terrestrial environment can depend on their size, density, and local atmospheric conditions. Microplastics and nanoplastics may enter the food web, carrying various organic pollutants, which bio-accumulate at different trophic levels, prompting organism health concerns. Microplastics being airborne identifies as new exposure route. Dietary and airborne exposure to MPs has led researchers to stress the importance of evaluating their toxicological potential. The primary goal of this paper is to explore the environmental fate of MPs from sources to sink in the terrestrial environment, as well as detail their potential impacts on human health. Additionally, this review article focuses on the presence of airborne microplastics, detailed sample pre-processing methods, and outlines analytical methods for their characterization., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Background . Increasing evidence from human studies has revealed the adverse impact of ambient fine particles (PM 2.5 ) on health outcomes related to metabolic disorders and distant organs. Whether exposure to ambient PM 2.5 leads to kidney impairment remains unclear. The rapid air quality improvement driven by the clean air actions in China since 2013 provides an opportunity for a quasiexperiment to investigate the beneficial effect of PM 2.5 reduction on kidney function. Methods . Based on two repeated nationwide surveys of the same population of 5115 adults in 2011 and 2015, we conducted a difference-in-difference study. Variations in long-term exposure to ambient PM 2.5 were associated with changes in kidney function biomarkers, including estimated glomerular filtration rate by serum creatinine (GFR scr ) or cystatin C (GFR cys ), blood urea nitrogen (BUN), and uric acid (UA). Results . For a 10  μ g/m 3 reduction in PM 2.5 , a significant improvement was observed for multiple kidney functional biomarkers, including GFR scr , BUN and UA, with a change of 0.42 (95% confidence interval [CI]: 0.06, 0.78) mL/min/1.73m 2 , -0.38 (-0.64, -0.12) mg/dL, and -0.06 (-0.12, -0.00) mg/dL, respectively. A lower socioeconomic status, indicated by rural residence or low educational level, enhanced the adverse effect of PM 2.5 on kidney function. Conclusions . These results support a significant nephrotoxicity of PM 2.5 based on multiple serum biomarkers and indicate a beneficial effect of improved air quality on kidney function., Competing Interests: The authors declare that they have no conflicts of interest.

Pontardawe in South Wales, United Kingdom (UK), consistently has the highest concentrations of nickel (Ni) in PM 10 in the UK and repeatedly breaches the 20 ng m -3 annual mean EU target value. Several local industries use Ni in their processes. To assist policy makers and regulators in quantifying the relative Ni contributions of these industries and developing appropriate emission reduction approaches, the hourly concentrations of 23 elements were measured using X-ray fluorescence alongside meteorological variables and black carbon during a four-week campaign in November-December 2015. Concentrations of Ni ranged between 0 and 2480 ng m -3 as hourly means. Positive Matrix Factorization (PMF) was used to identify sources contributing to measured elements. Cluster analysis of bivariate polar plots of those factors containing Ni in their profile was further used to quantify the industrial processes contributing to ambient PM 10 concentrations. Two sources were identified to contribute to Ni concentrations, stainless-steel (which contributed to 10% of the Ni burden) and the Ni refinery (contributing 90%). From the stainless-steel process, melting activities were responsible for 66% of the stainless-steel factor contribution., (Copyright © 2021. Published by Elsevier Ltd.)

Desertification and climate change indicate a future expansion of the global area of dry land and an increase in the risk of drought. Humans may therefore be at an ever-increasing risk of frequent exposure to, and resultant adverse health effects of desert sand dust. This review appraises a total of 52 experimental studies that have sought to identify mechanisms and intermediate endpoints underlying epidemiological evidence of an impact of desert dust on cardiovascular and respiratory health. Toxicological studies, in main using doses that reflect or at least approach real world exposures during a dust event, have demonstrated that virgin sand dust particles and dust storm particles sampled at remote locations away from the source induce inflammatory lung injury and aggravate allergen-induced nasal and pulmonary eosinophilia. Effects are orchestrated by cytokines, chemokines and antigen-specific immunoglobulin potentially via toll-like receptor/myeloid differentiation factor signaling pathways. Findings suggest that in addition to involvement of adhered chemical and biological pollutants, mineralogical components may also be implicated in the pathogenesis of human respiratory disorders during a dust event. Whilst comparisons with urban particulate matter less than 2.5 μm in diameter (PM 2.5 ) suggest that allergic inflammatory responses are greater for microbial element-rich dust- PM 2.5 , aerosols generated during dust events appear to have a lower oxidative potential compared to combustion-generated PM 2.5 sampled during non-dust periods. In vitro findings suggest that the significant amounts of suspended desert dust during storm periods may provide a platform to intermix with chemicals on its surfaces, thereby increasing the bioreactivity of PM 2.5 during dust storm episodes, and that mineral dust surface reactions are an unrecognized source of toxic organic chemicals in the atmosphere, enhancing toxicity of aerosols in urban environments. In summary, the experimental research on desert dust on respiratory endpoints go some way in clarifying the mechanistic effects of atmospheric desert dust on the upper and lower human respiratory system. In doing so, they provide support for biological plausibility of epidemiological associations between this particulate air pollutant and events including exacerbation of asthma, hospitalization for respiratory infections and seasonal allergic rhinitis., (Crown Copyright © 2021. Published by Elsevier Ltd. All rights reserved.)

Background: The evidence on the association between ultrafine (UFP) particles and mortality is still inconsistent. Moreover, health effects of specific UFP sources have not been explored. We assessed the impact of UFP sources on daily mortality in Barcelona, Helsinki, London, and Zurich., Methods: UFP sources were previously identified and quantified for the four cities: daily contributions of photonucleation, two traffic sources (fresh traffic and urban, with size mode around 30 nm and 70 nm, respectively), and secondary aerosols were obtained from data from an urban background station. Different periods were investigated in each city: Barcelona 2013-2016, Helsinki 2009-2016, London 2010-2016, and Zurich 2011-2014. The associations between total particle number concentrations (PNC) and UFP sources and daily (natural, cardiovascular [CVD], and respiratory) mortality were investigated using city-specific generalized linear models (GLM) with quasi-Poisson regression., Results: We found inconsistent results across cities, sources, and lags for associations with natural, CVD, and respiratory mortality. Increased risk was observed for total PNC and natural mortality in Helsinki (lag 2; 1.3% [0.07%, 2.5%]), CVD mortality in Barcelona (lag 1; 3.7% [0.17%, 7.4%]) and Zurich (lag 0; 3.8% [0.31%, 7.4%]), and respiratory mortality in London (lag 3; 2.6% [0.84%, 4.45%]) and Zurich (lag 1; 9.4% [1.0%, 17.9%]). A similar pattern of associations between health outcomes and total PNC was followed by the fresh traffic source, for which we also found the same associations and lags as for total PNC. The urban source (mostly aged traffic) was associated with respiratory mortality in Zurich (lag 1; 12.5% [1.7%, 24.2%]) and London (lag 3; 2.4% [0.90%, 4.0%]) while the secondary source was associated with respiratory mortality in Zurich (lag 1: 12.0% [0.63%, 24.5%]) and Helsinki (4.7% [0.11%, 9.5%]). Reduced risk for the photonucleation source was observed for respiratory mortality in Barcelona (lag 2, -8.6% [-14.5%, -2.4%]) and for CVD mortality in Helsinki, as this source is present only in clean atmospheres (lag 1, -1.48 [-2.75, -0.21])., Conclusions: We found inconsistent results across cities, sources and lags for associations with natural, CVD, and respiratory mortality., (Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: The prevalence of landscape fires has increased, particularly in low-income and middle-income countries (LMICs). We aimed to assess the impact of exposure to landscape fire smoke (LFS) on the health of children., Methods: We conducted a sibling-matched case-control study and selected 552 155 children (aged <18 years) from Demographic and Health Surveys in 55 LMICs from 2000 to 2014. Each deceased child was matched with their sibling(s). The exposure indicators were fire-sourced PM 2·5 and dry-matter emissions. We associated these exposure indicators with child mortality using conditional regressions, and derived an exposure-response function using a non-linear model. Based on the association, we quantified the global burden of fire-attributable child deaths in LMICs from 2000 to 2014., Findings: Each 1 μg/m 3 increment of fire-sourced PM 2·5 was associated with a 2·31% (95% CI 1·50-3·13) increased risk of child mortality. The association was robust to different models. The exposure-response function was superlinear and suggested per-unit exposure to larger fires was more toxic. Based on our non-linear exposure-response function, we estimated that between 2000 and 2014, the five countries with the largest number of child deaths associated with fire-sourced PM 2·5 were Nigeria (164 000 [126 000 to 209 000] annual deaths), Democratic Republic of the Congo (126 000 [95% CI 114 000 to 139 000] annual deaths), India (65 900 [-22 200 to 147 000] annual deaths), Uganda (30 200 [24 500 to 36 300] annual deaths), and Indonesia (28 900 [19 100 to 38 400])., Interpretation: Exposure to landscape fire smoke contributes substantially to the global burden of child mortality., Funding: National Natural Science Foundation of China, Ministry of Science and Technology of China, Peking University, UK National Institute for Health Research Health Protection Research Unit, Leverhulme Center for Wildfires, Environment and Society, and National Environment Research Council National Capability funding to National Centre for Earth Observation and Energy Foundation., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2021 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Previous studies have investigated the effects of air pollution on chronic obstructive pulmonary disease (COPD) patients using either fixed-site measurements or a limited number of personal measurements, usually for one pollutant and a short time period. These limitations may introduce bias and distort the epidemiological associations as they do not account for all the potential sources or the temporal variability of pollution.We used detailed information on individuals' exposure to various pollutants measured at fine spatiotemporal scale to obtain more reliable effect estimates. A panel of 115 patients was followed up for an average continuous period of 128 days carrying a personal monitor specifically designed for this project that measured temperature, nitrogen dioxide (NO 2 ), ozone (O 3 ), nitric oxide (NO), carbon monoxide (CO), and particulate matter with aerodynamic diameter <2.5 and <10 μm at 1-min time resolution. Each patient recorded daily information on respiratory symptoms and measured peak expiratory flow (PEF). A pulmonologist combined related data to define a binary variable denoting an "exacerbation". The exposure-response associations were assessed with mixed effects models.We found that gaseous pollutants were associated with a deterioration in patients' health. We observed an increase of 16.4% (95% CI 8.6-24.6%), 9.4% (95% CI 5.4-13.6%) and 7.6% (95% CI 3.0-12.4%) in the odds of exacerbation for an interquartile range increase in NO 2 , NO and CO, respectively. Similar results were obtained for cough and sputum. O 3 was found to have adverse associations with PEF and breathlessness. No association was observed between particulate matter and any outcome.Our findings suggest that, when considering total personal exposure to air pollutants, mainly the gaseous pollutants affect COPD patients' health., Competing Interests: Conflict of interest: D. Evangelopoulos has nothing to disclose. Conflict of interest: L. Chatzidiakou has nothing to disclose. Conflict of interest: H. Walton has nothing to disclose. Conflict of interest: K. Katsouyanni has nothing to disclose. Conflict of interest: F.J. Kelly has nothing to disclose. Conflict of interest: J.K. Quint reports grants from the Medical Research Council (MRC), during the conduct of the study; grants from Asthma UK, Chiesi, MRC and The Health Foundation, grants and personal fees from AstraZeneca, Boehringer Ingelheim and Bayer, outside the submitted work. Conflict of interest: R.L. Jones has nothing to disclose. Conflict of interest: B. Barratt has nothing to disclose., (Copyright ©ERS 2021.)

We present a global atlas of 4,728 metagenomic samples from mass-transit systems in 60 cities over 3 years, representing the first systematic, worldwide catalog of the urban microbial ecosystem. This atlas provides an annotated, geospatial profile of microbial strains, functional characteristics, antimicrobial resistance (AMR) markers, and genetic elements, including 10,928 viruses, 1,302 bacteria, 2 archaea, and 838,532 CRISPR arrays not found in reference databases. We identified 4,246 known species of urban microorganisms and a consistent set of 31 species found in 97% of samples that were distinct from human commensal organisms. Profiles of AMR genes varied widely in type and density across cities. Cities showed distinct microbial taxonomic signatures that were driven by climate and geographic differences. These results constitute a high-resolution global metagenomic atlas that enables discovery of organisms and genes, highlights potential public health and forensic applications, and provides a culture-independent view of AMR burden in cities., Competing Interests: Declaration of interests C.E.M. is co-founder of Biotia and Onegevity Health. D.B. is co-founder and CSO of Poppy Health Inc. The other authors declare they have no competing interests that impacted this study., (Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.)

Evidence to advocate for cleaner air for people with asthma is not in short supply. We know that air pollution is associated with the development and worsening of the condition and that mitigating interventions can improve respiratory outcomes. We have clear targets, particularly traffic emissions, especially in urban areas, and plenty of potentially effective actions. Road traffic must be reduced, and what remains should be cleaner and greener. Urban green spaces, safe cycle networks and wider pavements will promote active travel and leisure time exercise. Healthcare professionals must ensure people are aware of their air quality, its impact on asthma and the appropriate behaviour to safeguard health. What remains are realistic policies and effective measures, based on the correct scientific evidence, to be taken forth with political courage and investment so that air pollution no longer contributes to the development or worsening of respiratory ill health.

Background: The public transit is a built environment with high occupant density across the globe, and identifying factors shaping public transit air microbiomes will help design strategies to minimize the transmission of pathogens. However, the majority of microbiome works dedicated to the public transit air are limited to amplicon sequencing, and our knowledge regarding the functional potentials and the repertoire of resistance genes (i.e. resistome) is limited. Furthermore, current air microbiome investigations on public transit systems are focused on single cities, and a multi-city assessment of the public transit air microbiome will allow a greater understanding of whether and how broad environmental, building, and anthropogenic factors shape the public transit air microbiome in an international scale. Therefore, in this study, the public transit air microbiomes and resistomes of six cities across three continents (Denver, Hong Kong, London, New York City, Oslo, Stockholm) were characterized., Results: City was the sole factor associated with public transit air microbiome differences, with diverse taxa identified as drivers for geography-associated functional potentials, concomitant with geographical differences in species- and strain-level inferred growth profiles. Related bacterial strains differed among cities in genes encoding resistance, transposase, and other functions. Sourcetracking estimated that human skin, soil, and wastewater were major presumptive resistome sources of public transit air, and adjacent public transit surfaces may also be considered presumptive sources. Large proportions of detected resistance genes were co-located with mobile genetic elements including plasmids. Biosynthetic gene clusters and city-unique coding sequences were found in the metagenome-assembled genomes., Conclusions: Overall, geographical specificity transcends multiple aspects of the public transit air microbiome, and future efforts on a global scale are warranted to increase our understanding of factors shaping the microbiome of this unique built environment.

The current study is the intented to investigate the intensity of pollution, source characterization, oxidative potential, and human health risks of fourteen potentially toxic elements in the street dust of the Middle East oldest oil refinery zone. Thirty five street dust samples were collected from various regions in Abadan and Khorramshahr cities. The mean concentration of As, Mo, Cu, Pb, Hg, Zn, Cd, and Sb in Abadan street dust were 5.55, 3.39, 83.68, 49.82, 4493.54, 281.24, 1.15,and 1.17, while in Khorramshahr As, Mo, Cu, Pb, Hg, Zn, Cd, and Sb were.14, 2.58, 74.35, 56.50, 0.74, 214.26, 0.62, and 1.18, respectively. The concentration of these elements in both cities is higher than the local background values. Potential ecological risk index and pollution load index at all stations of both cities are greater than 1, indicating a high pollution load in the study area. Calculated enrichment factor showed high enrichment of Hg, Sb, Cd, Mo, Cu, Pb, and Zn in both areas. Of particular concern is the enrichment factor for mercury which proved to be 3370.54 ppb in the vicinity of the petrochemical unit in Abadan city (EF > 40). The results of positive matrix factorization receptor model together with geochemical maps and multivariate statistics indicated that industrial activities (especially petrochemical industries) are responsible for Hg, Cu, and Zn pollution, while exhaust emissions are responsible for Mo, Pb, Cd, and Sb, and natural sources for Al, Cr, Mn, Fe, Co, and Ni. The percentage of OP AA in the region ranged from 15.1 to 26.4 and OP GSH ranged from 9.5 to 24.4. The percentage of OP TOTAL /μg (OP AA /μg + OP GSH /μg) values varied between 0.6 and 1. The health risk evaluation models indicated that specific attention should be paid to Hg, Cd, Pb, and Zn and that the higher oxidative potential of street dust recovered from polluted locations is also a matter of concern in Abadan and Khorramshahr Cities., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Crown Copyright © 2020. Published by Elsevier Ltd. All rights reserved.)

This study investigates the mineralogy, micro-morphology, chemical characteristics and oxidation toxicity of respirable dusts generated in underground coal mines. The active sampling was applied to collect airborne particulates with aerodynamic diameter <4 µm (PM 4 ) at depth greater than 500 m from earth surface. The average mass concentration of PM 4 was extremely higher than recommended values. QXRD and FESEM-EDS analyses were applied to study the micro-mineralogy and micro-morphology of respirable dusts. The chemical analysis by ICP-MS revealed an enrichment of V, Cr, Cu, Zn, As, Ag, Cd and Sb in respirable dust compared with the background environment and world coals. The EPA's health risk model showed that the health risk posed by Cr and Co in all workplaces exceeded the acceptable risk value for human health. The synthetic respiratory tract lining fluid (RTLF) model was utilized to achieve a novel insight into the toxicity of respirable coal dust. The result showed an overall depletion of lung surface antioxidants with the decreasing trend of ascorbic acid > reduced glutathione >> urate, implying low- to medium level of oxidative stress. The result of this study can be applied globally by decision-makers to decrease hazardous exposure of mine workers to respirable dust., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Measurement of ambient fine particulate matter (PM 2.5 ) is often used as a proxy of personal exposure in epidemiological studies. However, the difference between personal and ambient exposure, and whether it biases the estimates of health effects remain unknown. Based on an epidemiological study (AIRLESS) and simultaneously launched intensive monitoring campaigns (APHH), we quantified and compared the personal and ambient exposure to PM 2.5 and the related health impact among residents in Beijing, China. In total, 123 urban and 128 peri-urban non-smoking participants were recruited from two well-established cohorts in Beijing. During winter 2016 and summer 2017, each participant was instructed to carry a validated personal air monitor (PAM) to measure PM 2.5 concentration at high spatiotemporal resolution for seven consecutive days in each season. Multiple inflammatory biomarkers were measured, including exhaled NO, blood monocytes counts and C-reactive protein. Linear mixed-effect models were used for the associations between exposure and health outcomes with adjustment for confounders. The average level of daily personal exposure to PM 2.5 was consistently lower than using corresponding ambient concentration, and the difference is greater during the winter. The personal to ambient (P/A) ratio of exposure to PM 2.5 exhibited an exponentially declining trend, and showed larger variations when ambient PM 2.5 levels < 25 μg m -3 . Personal exposure to PM 2.5 was significantly associated with the increase in respiratory and systemic inflammatory biomarkers; however, the associations were weaker or became insignificant when ambient concentrations were used. Exposure to ambient PM 2.5 might not be a good proxy to estimate the health effect of exposure to personal PM 2.5 .

Background: The role of antioxidant status on microvascular blood flow and glomerular filtration (eGFR) in patients with type 2 diabetes and hypertension whose risk of progressive renal disease varies by ethnicity is unknown., Methods: Adult, non-Caucasian (n = 101) and Caucasian (n = 69) patients with type 2 diabetes, hypertension and/or microalbuminuria and an eGFR > 45 mL/min/1.73 m 2 were randomised to receive 400 IU vitamin E and/or 20 μg selenium daily or matching placebo. eGFR (CKD-EPI) was measured at baseline, 3,6 and 12 months and renal blood flow by contrast-enhanced ultrasonography in a sub-group (n = 9) at baseline and 3 months by assessing the area under the time intensity curve (TIC). Circulating glutathione peroxidase 3 (GPx-3) activity was measured as a biomarker of oxidative defence status., Results: The time to change in eGFR was shortest with combined vitamin E and selenium than usual care (5.6 [4.0-7.0] vs 8.9 [6.8-10.9 months]; p = 0.006). Area under the TIC was reduced compared to baseline (38.52 [22.41-90.49] vs 123 [86.98-367.03]dB.s; P ≤ 0.05 and 347 [175.88-654.92] vs 928.03 [448.45-1683]dB.s; P ≤ 0.05, respectively] at 3 months suggesting an increase in rate of perfusion. The proportional change in eGFR at 12 months was greater in the group whose GPx-3 activity was above, compared with those below the cohort median (360 U/L) in the non-Caucasian and the Caucasian groups (19.1(12.5-25.7] % vs 6.5[-3.5 to 16.5] % and 12.8 [0.7 to 24] % vs 0.2 [-6.1 to 6.5] %)., Conclusion: In these patients with type 2 diabetes and early CKD, antioxidant treatment derepresses renal blood flow and a rise in eGFR correlated directly with GPx-3 activity., Significance: Diabetes mellitus is the world's leading cause of end-stage renal disease which has a predilection for black and minor ethnic groups compared with Caucasians. The differences in risk despite the benefits of conventional care may be related to oxidative stress. We found that glomerular filtration and renal blood flow is suppressed when renal function is preserved in high-risk patients with type 2 diabetes. Conventional care supplemented with selenium - the co-factor for glutathione peroxidase-3 (GPx-3) - improves renal perfusion and increase glomerular filtration according to host antioxidant defence determined by GPx-3 activity. Circulating GPx-3 activity warrants further investigation as a novel biomarker of reversible haemodynamic changes in early diabetic kidney disease to better enable targeting of renoprotective strategies., (Copyright © 2020. Published by Elsevier Inc.)

Background: Air pollution epidemiology has primarily relied on fixed outdoor air quality monitoring networks and static populations., Methods: Taking advantage of recent advancements in sensor technologies and computational techniques, this paper presents a novel methodological approach that improves dose estimations of multiple air pollutants in large-scale health studies. We show the results of an intensive field campaign that measured personal exposures to gaseous pollutants and particulate matter of a health panel of 251 participants residing in urban and peri-urban Beijing with 60 personal air quality monitors (PAMs). Outdoor air pollution measurements were collected in monitoring stations close to the participants' residential addresses. Based on parameters collected with the PAMs, we developed an advanced computational model that automatically classified time-activity-location patterns of each individual during daily life at high spatial and temporal resolution., Results: Applying this methodological approach in two established cohorts, we found substantial differences between doses estimated from outdoor and personal air quality measurements. The PAM measurements also significantly reduced the correlation between pollutant species often observed in static outdoor measurements, reducing confounding effects., Conclusions: Future work will utilise these improved dose estimations to investigate the underlying mechanisms of air pollution on cardio-pulmonary health outcomes using detailed medical biomarkers in a way that has not been possible before.

Objectives: More than 90% of the global population live in areas exceeding the PM 2.5 air quality guidelines (AQGs). We provide an overview of the ambient PM 2.5 -related burden of disease (BoD) studies along with scenario analysis in the framework of the WHO AQG update on the estimated reduction in the BoD if AQGs were achieved globally., Methods: We reviewed the literature for large-scale studies for the BoD attributed to ambient PM 2.5 . Moreover, we used the latest WHO statistics to calculate the BoD at current levels and the scenarios of aligning with interim targets and AQG levels., Results: The most recent BoD studies (2010 onwards) share a similar methodology, but there are differences in the input data which affect the estimates for attributable deaths (2.9-8.9 million deaths annually). Moreover, we found that if AQGs were achieved, the estimated BoD would be reduced by up to 50% in total deaths worldwide., Conclusions: Understanding the BoD across countries, especially in those that do not align with the AQGs, is essential in order to inform actions to reduce air pollution globally.

Epidemiological research has taught us a great deal about the health effects of airborne particulate matter (PM), particularly cardiorespiratory effects of combustion-related particles. This has been matched by toxicological research to define underlying mechanistic pathways. To keep abreast of the substantial challenges that air pollution continues to throw at us requires yet more strides to be achieved. For example, being aware of the most toxic components/sources and having a definitive idea of the range of associated disease outcomes. This review discusses approaches designed to close some of these knowledge gaps. These include a focus on particles arising from non-exhaust PM at the roadside and microplastics-both of which are becoming more relevant in the light of a shift in PM composition in response to global pressure to reduce combustion emissions. The application of hypothesis-free approaches in both mechanistic studies and epidemiology in unveiling unexpected relationships and generating novel insights is also discussed. Previous work, strengthening the evidence for both the adverse effects and benefits of intervention tell us that the sooner we act to close knowledge gaps, increase awareness and develop creative solutions, the sooner we can reduce the public health burden attributable to these complex and insidious environmental pollutants. This article is part of a discussion meeting issue 'Air quality, past present and future'.

Microplastics have been observed in indoor and outdoor air. This raises concern for human exposure, especially should they occur in small enough sizes, which if inhaled, reach the central airway and distal lung. As yet, methods for their detection have not spectroscopically verified the chemical composition of microplastics in this size-range. One proposed method is an automated spectroscopic technique, Raman spectral imaging; however, this generates large and complex data sets. This study aims to optimize Raman spectral imaging for the identification of microplastics (≥2 μm) in ambient particulate matter, using different chemometric techniques. We show that Raman spectral images analyzed using chemometric statistical approaches are appropriate for the identification of both virgin and environmental microplastics ≥2 μm in size. On the basis of the sensitivity, we recommend using the developed Pearson's correlation and agglomerative hierarchical cluster analysis for the identification of microplastics in spectral data sets. Finally, we show their applicability by identifying airborne microplastics >4.7 μm in an outdoor particulate matter sample obtained at an urban sampling site in London, United Kingdom. This semiquantitative method will enable the procurement of exposure concentrations of airborne microplastics guiding future toxicological assessments.

Since air pollutants are difficult and expensive to control, a strong scientific underpinning to policies is needed to guide mitigation aimed at reducing the current burden on public health. Much of the evidence concerning hazard identification and risk quantification related to air pollution comes from epidemiological studies. This must be reinforced with mechanistic confirmation to infer causality. In this review we focus on data generated from four contrasting sources of particulate air pollution that result in high population exposures and thus where there remains an unmet need to protect health: urban air pollution in developing megacities, household biomass combustion, wildfires and desert dust storms. Taking each in turn, appropriate measures to protect populations will involve advocating smart cities and addressing economic and behavioural barriers to sustained adoption of clean stoves and fuels. Like all natural hazards, wildfires and dust storms are a feature of the landscape that cannot be removed. However, many efforts from emission containment (land/fire management practices), exposure avoidance and identifying susceptible populations can be taken to prepare for air pollution episodes and ensure people are out of harm's way when conditions are life-threatening. Communities residing in areas affected by unhealthy concentrations of any airborne particles will benefit from optimum communication via public awareness campaigns, designed to empower people to modify behaviour in a way that improves their health as well as the quality of the air they breathe., (© The Author(s) 2020. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)