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Chappell LC, Seed PT, Kelly FJ, et al. Am J Obstet Gynecol 2002;187:777-784. OBJECTIVE: We have previously reported a reduced incidence of preeclampsia in women who were at risk and [...]

Background: Evidence suggests that oxidative stress is a unifying feature underlying the toxic actions of particulate matter (PM). We have investigated whether individual plasma antioxidant concentrations (uric acid and vitamins C, A, and E) and 10 antioxidant genes modify the response to PM with respect to hospital admissions for chronic obstructive pulmonary disease (COPD) or asthma.Methods: Using a bidirectional, hospital-based, case-crossover study, 209 patients admitted for asthma or COPD to the Chelsea and Westminster Hospital (London), with 234 admissions, were recruited between May 2008 and July 2010. PM10 levels in the area of Kensington and Chelsea at the time of admission were compared with the levels 14 days before and 14 days after the event. Conditional logistic regression was used to estimate the effect of PM10 at several temporal lags, while controlling for confounders.Results: An increase in asthma/COPD admission rate was related to a 10 μg/m increase in PM10, with the highest effect noted 0-3 days before the exacerbation (for lag 0-3, odds ratio = 1.35 [95% confidence interval = 1.04-1.76]). Serum vitamin C modified the effect of PM10 on asthma/COPD exacerbations. A similar (although weaker) influence was observed for low levels of uric acid and vitamin E, whereas vitamin A showed no effect modification. GSTP1 (rs1695), SOD2 (rs4880), and Nrf2 (rs1806649) were associated with a trend toward an increased risk of hospital admissions during periods of high PM10 levels.Conclusions: Our study suggests that the concentration of antioxidants in patients' serum modifies the short-term effects of PM10 on asthma and COPD exacerbations. [ABSTRACT FROM AUTHOR]

Background: There is limited evidence on whether particulate matter (PM) can augment the progression of atherosclerosis; furthermore, the specific attributes of PM responsible for health effects are unclear. We developed models to predict exposure to PM <10 μm (PM10) and also to predict a measure of oxidative potential (the capacity of particles to induce oxidative damage). Our objectives were (1) to estimate the association between PM10 and carotid intima-media thickness, a measure of subclinical atherosclerosis, and (2) to compare this association with that of PM10 weighted by its oxidative potential (PM10*OP).Methods: Analysis was based on 2348 participants of the Whitehall II cohort of British civil servants who had intima-media thickness measured between 2003 and 2005 and lived in Greater London. Weekly PM10 and PM10*OP were predicted at each participant's residence. Primary exposure metrics were defined as PM10 and PM10*OP averaged over the year before scan. We estimated associations between exposure metrics and intima-media thickness using generalized linear regression models.Results: An interquartile range increase (5.2 μgm(-3)) in PM10 was associated with a 5.0% (95% confidence interval = 1.9% to 8.3%) increase in intima-media thickness after covariate adjustment. The association for an interquartile range change in PM10*OP (1.5 m(-3)) was weaker: 1.2% (0.2% to 2.2%).Conclusions: These findings support a relationship between PM exposure and atherosclerosis. PM weighted by this particular measure of oxidative potential was not more predictive of the extent of atherosclerosis than PM mass concentration. [ABSTRACT FROM AUTHOR]

Objective: It has been proposed that the redox activity of particles may represent a major determinant of their toxicity. We measured the in vitro ability of ambient fine particles [particulate matter with aerodynamic diameters

The lungs are continually exposed to relatively-high O(2) tensions, and as such, in comparison with other organs, they represent a unique tissue for the damaging effects of oxidant attack. At particular times during a lifetime this every day challenge may increase exponentially. The first oxidative insult occurs at birth, when cells are exposed to a sudden 5-fold increase in O(2) concentration. Thereafter, the human lung, from infancy through to old age, can be subjected to deleterious oxidative events as a consequence of inhaling environmental pollutants or irritants, succumbing to several pulmonary diseases (including infant and adult respiratory distress syndromes, asthma, chronic obstructive pulmonary disease, cystic fibrosis and cancer) and receiving treatment for these diseases. The present paper will review the concept that consumption of a healthy diet and the consequent ability to establish and then maintain adequate micronutrient antioxidant concentrations in the lung throughout life, and following various oxidative insults, could prevent or reduce the incidence of oxidant-mediated respiratory diseases. Furthermore, the rationale, practicalities and complexities of boosting the antioxidant pool of the respiratory-tract lining fluid in diseases in which oxidative stress is actively involved, by direct application to the lung v. dietary modification, in order to achieve a therapeutic effect will be discussed. [ABSTRACT FROM AUTHOR]

Air is one of our most important natural resources; however, it is also in the front line for receiving environmental pollution. Air quality decreased markedly following the industrial revolution, but it was not until the great London Smog in 1952 that air quality made it onto the political agenda. The introduction of the Clean Air Act in 1956 led to dramatic decreases in black smoke and SO2 concentrations over the next two decades, as domestic and industrial coal-burning activities ceased. However, as these improvements progressed, a new threat to public health was being released into the air in ever-increasing quantities. Rapid motorisation of society from the 1960s onwards has led to the increased release of atmospheric pollutants such as tiny particles (particulate matter of <10 microm in aerodynamic diameter) and oxides of N, and the generation of the secondary pollutant O3. These primary and secondary traffic-related pollutants have all proved to be major risks factors to public health. Recently, oxidative stress has been identified as a unifying feature underlying the toxic actions of these pollutants. Fortunately, the surface of the lung is covered with a thin layer of fluid containing a range of antioxidants that appear to provide the first line of defence against oxidant pollutants. As diet is the only source of antioxidant micronutrients, a plausible link now exists between the sensitivity to air pollution and the quality of the food eaten. However, many questions remain unanswered in relation to inter-individual sensitivity to ambient air pollution, and extent to which this sensitivity is modified by airway antioxidant defences. [ABSTRACT FROM AUTHOR]

Aims: To explore the effects in normal and asthmatic adults of exposure to 200 ppb sulphur dioxide (SO2) and 200 microg/m3 and 2000 microg/m3 aerosols of ammonium bisulphate (AB) and sulphuric acid (SA) (MMD 0.3 microm).Methods: Exposures were placebo controlled, for one hour at rest, double blind in random order. DeltaFEV1 was the primary outcome; secondary outcomes included symptoms, ventilation, exhaled nitric oxide (NO) concentrations, and nasal lavage fluid ascorbic (AA) and uric acid (UA) concentrations.Results: There were no significant changes in spirometry or symptoms with any exposure in either group. SO2 exposure was associated with an increased respiratory rate relative to air exposure in the asthmatic group (SO2: 958.9 breaths/hour; air: 906.8 breaths/hour) but the mean volume breathed did not differ significantly (SO2: 318.8 litres; air: 311.4 litres). AB exposures were associated with a significant rise in [NO] in the asthmatic (+1.51 ppb, and +1.39 ppb), but not in the normal group. Mean pre- and post-exposure [AA] tended to be higher in the normal than in the asthmatic group. Within each group, [AA] did not change significantly with any exposure. Post-exposure [UA] were greater than pre-exposure concentrations for all exposures, significantly so in the normal group for all exposures except SO2. There were no significant differences in the mean change in [UA] for any exposure relative to air.Conclusions: The pollutant exposure concentrations employed in this study were generally much greater than ambient. It is unlikely that short lived exposures at lower concentrations would show significant effects, but effects of longer term lower concentration exposures cannot be ruled out. [ABSTRACT FROM AUTHOR]

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.)