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Tropospheric ozone (O 3 ) is a key component of air pollution and an important anthropogenic greenhouse gas 1 . During the twentieth century, the proliferation of the internal combustion engine, rapid industrialization and land-use change led to a global-scale increase in O 3 concentrations 2 , 3 ; however, the magnitude of this increase is uncertain. Atmospheric chemistry models typically predict 4 – 7 an increase in the tropospheric O 3 burden of between 25 and 50 per cent since 1900, whereas direct measurements made in the late nineteenth century indicate that surface O 3 mixing ratios increased by up to 300 per cent 8 – 10 over that time period. However, the accuracy and diagnostic power of these measurements remains controversial 2 . Here we use a record of the clumped-isotope composition of molecular oxygen ( 18 O 18 O in O 2 ) trapped in polar firn and ice from 1590 to 2016 ad , as well as atmospheric chemistry model simulations, to constrain changes in tropospheric O 3 concentrations. We find that during the second half of the twentieth century, the proportion of 18 O 18 O in O 2 decreased by 0.03 ± 0.02 parts per thousand (95 per cent confidence interval) below its 1590–1958 ad mean, which implies that tropospheric O 3 increased by less than 40 per cent during that time. These results corroborate model predictions of global-scale increases in surface pollution and vegetative stress caused by increasing anthropogenic emissions of O 3 precursors 4 , 5 , 11 . We also estimate that the radiative forcing of tropospheric O 3 since 1850 ad is probably less than +0.4 watts per square metre, consistent with results from recent climate modelling studies 12 . Isotope data from polar firn and ice are used to constrain the increase in tropospheric ozone between 1850 and 2005 ad .

Background Childhood exposure to air pollution contributes to cardiovascular disease in adulthood. Immune and oxidative stress disturbances might mediate the effects of air pollution on the cardiovascular system, but the underlying mechanisms are poorly understood in adolescents. Therefore, we aimed to identify immune biomarkers linking air pollution exposure and blood pressure levels in adolescents. Methods We randomly recruited 100 adolescents (mean age, 16 years) from Fresno, California. Using central-site data, spatial-temporal modeling, and distance weighting exposures to the participant’s home, we estimated average pollutant levels [particulate matter (PM), polyaromatic hydrocarbons (PAH), ozone (O 3 ), carbon monoxide (CO) and nitrogen oxides (NO x )]. We collected blood samples and vital signs on health visits. Using proteomic platforms, we quantitated markers of inflammation, oxidative stress, coagulation, and endothelial function. Immune cellular characterization was performed via mass cytometry (CyTOF). We investigated associations between pollutant levels, cytokines, immune cell types, and blood pressure (BP) using partial least squares (PLS) and linear regression, while adjusting for important confounders. Results Using PLS, biomarkers explaining most of the variance in air pollution exposure included markers of oxidative stress (GDF-15 and myeloperoxidase), acute inflammation (C-reactive protein), hemostasis (ADAMTS, D-dimer) and immune cell types such as monocytes. Most of these biomarkers were independently associated with the air pollution levels in fully adjusted regression models. In CyTOF analyses, monocytes were enriched in participants with the highest versus the lowest PM 2.5 exposure. In both PLS and linear regression, diastolic BP was independently associated with PM 2.5 , NO, NO 2 , CO and PAH 456 pollution levels ( P  ≤ 0.009). Moreover, monocyte levels were independently related to both air pollution and diastolic BP levels ( P  ≤ 0.010). In in vitro cell assays, plasma of participants with high PM 2.5 exposure induced endothelial dysfunction as evaluated by eNOS and ICAM-1 expression and tube formation. Conclusions For the first time in adolescents, we found that ambient air pollution levels were associated with oxidative stress, acute inflammation, altered hemostasis, endothelial dysfunction, monocyte enrichment and diastolic blood pressure. Our findings provide new insights on pollution-related immunological and cardiovascular disturbances and advocate preventative measures of air pollution exposure.

BackgroundMaternal exposure to fine particulate matter (PM2.5) was associated with pregnancy complications. However, we still lack comprehensive evidence regarding which specific chemical components of PM2.5 are more harmful for maternal and foetal health.ObjectiveWe focused on exposure over the first trimester (0–13 weeks of gestation), which includes the early placentation period, and investigated whether PM2.5 and its components were associated with placenta-mediated pregnancy complications (combined outcome of small for gestational age, preeclampsia, placental abruption, and stillbirth).MethodsFrom 2013 to 2015, we obtained information, from the Japan Perinatal Registry Network database, on 83,454 women who delivered singleton infants within 23 Tokyo wards (≈627 km2). Using daily filter sampling of PM2.5 at one monitoring location, we analysed carbon and ion components, and assigned the first trimester average of the respective pollutant concentrations to each woman.ResultsThe ORs of placenta-mediated pregnancy complications were 1.14 (95% CI = 1.08–1.22) per 0.51 μg/m3 (interquartile range) increase of organic carbon and 1.11 (1.03–1.18) per 0.06 μg/m3 increase of sodium. Organic carbon was also associated with four individual complications. There was no association between ozone and outcome.SignificanceThere were specific components of PM2.5 that have adverse effects on maternal and foetal health.

In the global COVID-19 epidemic, humans are faced with a new challenge. The concept of quarantine as a preventive measure has changed human activities in all aspects of life. This challenge has led to changes in the environment as well. The air quality index is one of the immediate concrete parameters. In this study, the actual potential of quarantine effects on the air quality index and related variables in Tehran, the capital of Iran, is assessed, where, first, the data on the pollutant reference concentration for all measuring stations in Tehran, from February 19 to April 19, from 2017 to 2020, are monitored and evaluated. This study investigated the hourly concentrations of six particulate matters (PM), including PM2.5, PM10, and air contaminants such as nitrogen dioxide (NO 2 ), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO). Changes in pollution rate during the study period can be due to reduced urban traffic, small industrial activities, and dust mites of urban and industrial origins. Although pollution has declined in most regions during the COVID-19 quarantine period, the PM2.5 rate has not decreased significantly, which might be of natural origins such as dust. Next, the air quality index for the stations is calculated, and then, the interpolation is made by evaluating the root mean square (RMS) of different models. The local and global Moran index indicates that the changes and the air quality index in the study area are clustered and have a high spatial autocorrelation. The results indicate that although the bad air quality is reduced due to quarantine, major changes are needed in urban management to provide favorable conditions. Contaminants can play a role in transmitting COVID-19 as a carrier of the virus. It is suggested that due to the rise in COVID-19 and temperature in Iran, in future studies, the effect of increased temperature on COVID-19 can be assessed.

The increasing emission of nitrogen oxides exerts large impacts on vegetation by raising surface ozone (O 3 ) concentrations and enhancing atmospheric nitrogen (N) deposition. We established a free-air O 3 concentration elevation and enhanced N deposition system (O 3 -N-FACE) in Beijing, China, to investigate long-term effects of elevated O 3 and N deposition on poplar plantation. Eight square plots with a side length of 16 m were randomly allocated to elevated O 3 (E-O 3 ) and ambient air (AA) treatments. Ozone generated by electric discharge in pure oxygen is mixed with clean and dry air, and released from small holes on the tubes installed above the plant canopy at a rate controlled to keep O 3 concentration in E-O 3 plots by 50% higher than that in AA plots. Each O 3 treatment plot consisted of four subplots with a factorial combination of 2 lines of poplar clones and 2 levels of N deposition rate. In enhanced N deposition subplots, we sprayed urea solution on the plantation floor at a rate of 60 kg ha −1 year −1 . We hereby present the system performances during the growing seasons of 2018 and 2019: the first 2 years of experiment. The mean daytime O 3 concentrations of E-O 3 plots were 38% and 31% higher than AA plots in 2018 and 2019, respectively. And, in 2019, the accumulated O 3 exposure over 40 ppb (AOT40) in E-O 3 plots was 70% higher than that in AA plots. The hourly mean O 3 concentrations in E-O 3 plots were within 20% of the target for 83% of time on average across the four E-O 3 plots. Within the E-O 3 plots, spatial distribution of the hourly O 3 concentration exhibited the maximum deviation at 24% in 2019. We concluded that performance of this system is better than other similar facilities for trees and suitable for a long-term experiment of enhanced O 3 and N.

This study aimed to determine if short-term exposure to particulate matter (PM2.5) and ozone (O3) is associated with increased symptoms or lung function decline in fibrotic sarcoidosis. Sixteen patients with fibrotic sarcoidosis complicated by frequent exacerbations completed pulmonary function testing and questionnaires every three months for one year. We compared 7-, 10-, and 14-day average levels of PM2.5 and O3 estimated at patient residences to spirometry (forced expiratory volume in 1 s (FEV1), to forced vital capacity (FVC), episodes of FEV1 decline > 10%) and questionnaire outcomes (Leicester cough questionnaire (LCQ), Saint George Respiratory Questionnaire (SGRQ), and King’s Sarcoidosis Questionnaire (KSQ)) using generalized linear mixed effect models. PM2.5 level averaged over 14 days was associated with lower KSQ general health status (score change −6.60 per interquartile range (IQR) PM2.5 increase). PM2.5 level averaged over 10 and 14 days was associated with lower KSQ lung specific health status (score change −6.93 and −6.91, respectively). PM2.5 levels were not associated with FEV1, FVC, episodes of FEV1 decline > 10%, or respiratory symptoms measured by SGRQ or LCQ. Ozone exposure was not associated with any health outcomes. In this small cohort of patients with fibrotic sarcoidosis, PM2.5 exposure was associated with increased severity of respiratory and quality of life symptoms.

Background Epidemiological studies have shown that as ambient air pollution (AP) increases the risk of cardiovascular mortality also increases. The mechanisms of this effect may be linked to alterations in autonomic nervous system function. We wished to examine the effects of industrial AP on heart rate variability (HRV), a measure of subtle changes in heart rate and rhythm representing autonomic input to the heart. Methods Sixty healthy adults were randomized to spend five consecutive 8-h days outdoors in one of two locations: (1) adjacent to a steel plant in the Bayview neighbourhood in Sault Ste Marie Ontario or (2) at a College campus, several kilometers from the plant. Following a 9–16 day washout period, participants spent five consecutive days at the other site. Ambient AP levels and ambulatory electrocardiogram recordings were collected daily. HRV analysis was undertaken on a segment of the ambulatory ECG recording during a 15 min rest period, near the end of the 8-h on-site day. Standard HRV parameters from both time and frequency domains were measured. Ambient AP was measured with fixed site monitors at both sites. Statistical analysis was completed using mixed-effects models. Results Compared to the College site, HRV was statistically significantly reduced at the Bayview site by 13% (95%CI 3.6,19.2) for the standard deviation of normal to normal, 8% (95%CI 0.1, 4.9) for the percent normal to normal intervals differing by more than 50 ms, and 15% (95%CI 74.9, 571.2) for low frequency power. Levels of carbon monoxide, sulphur dioxide, nitrogen dioxide, and fine and ultrafine particulates were slightly, but statistically significantly, elevated at Bayview when compared to College. Interquartile range changes in individual air pollutants were significantly associated with reductions in HRV measured on the same day. The patterns of effect showed a high degree of consistency, with nearly all pollutants significantly inversely associated with at least one measure of HRV. Conclusions The significant associations between AP and changes in HRV suggest that ambient AP near a steel plant may impact autonomic nervous system control of the heart.

Remarkable perturbations in the stratospheric abundances of chlorine species and ozone were observed over Southern Hemisphere mid-latitudes following the 2020 Australian wildfires 1 , 2 . These changes in atmospheric chemical composition suggest that wildfire aerosols affect stratospheric chlorine and ozone depletion chemistry. Here we propose that wildfire aerosol containing a mixture of oxidized organics and sulfate 3 – 7 increases hydrochloric acid solubility 8 – 11 and associated heterogeneous reaction rates, activating reactive chlorine species and enhancing ozone loss rates at relatively warm stratospheric temperatures. We test our hypothesis by comparing atmospheric observations to model simulations that include the proposed mechanism. Modelled changes in 2020 hydrochloric acid, chlorine nitrate and hypochlorous acid abundances are in good agreement with observations 1 , 2 . Our results indicate that wildfire aerosol chemistry, although not accounting for the record duration of the 2020 Antarctic ozone hole, does yield an increase in its area and a 3–5% depletion of southern mid-latitude total column ozone. These findings increase concern 2 , 12 , 13 that more frequent and intense wildfires could delay ozone recovery in a warming world. Comparison of model simulations with atmospheric observations from the Southern Hemisphere mid-latitudes following the 2020 Australian wildfires shows that the wildfire aerosol composition promotes stratospheric chlorine and ozone depletion chemistry.

Objective We examined the association of outdoor air pollution and meteorological parameters with primary care visits (PCVs) at night due to asthma attack. Setting A case-crossover study was conducted in a primary care clinic in Himeji City, Japan. Participants Participants were 1447 children aged 0–14 years who visited the clinic with an asthma attack from April 2010 until March 2013. Exposure Daily concentrations of air pollutants and meteorological parameters were measured. Primary outcome PCVs at night due to asthma attack. A conditional logistic regression model was used to estimate ORs of PCVs per unit increment of air pollutants or meteorological parameters (the per-unit increments of particulate matter with an aerodynamic diameter ≤2.5 µm (PM2.5) and ozone were 10 μg/m3 and 10 ppb, respectively). Analyses took into consideration the effects of seasonality. Results We noted an association between PCVs and daily ozone levels on the day before a PCV (OR=1.17; 95% CI 1.01 to 1.35; p=0.04), as well as between PCVs and 3-day mean ozone levels before a PCV (OR=1.29; 95% CI 1.00 to 1.46; p=0.04), from April until June. We also observed an association between PCVs and daily PM2.5 levels on the day before a PCV from December until March (OR=1.16; 95% CI 1.01 to 1.33; p=0.05). Meteorological parameters, such as hours of sunshine from September until November, atmospheric pressure from April until June, and temperature from April until August, were also found to be associated with PCVs. Conclusions The findings in the present study supported an association between ozone and PCVs and suggest that certain meteorological items may be associated with PCVs.

SignificanceDrastic air pollution control in China since 2013 has achieved sharp decreases in fine particulate matter (PM2.5), but ozone pollution has not improved. After removing the effect of meteorological variability, we find that surface ozone has increased in megacity clusters of China, notably Beijing and Shanghai. The increasing trend cannot be simply explained by changes in anthropogenic precursor [NOx and volatile organic compound (VOC)] emissions, particularly in North China Plain (NCP). The most important cause of the increasing ozone in NCP appears to be the decrease in PM2.5, slowing down the sink of hydroperoxy radicals and thus speeding up ozone production. Decreasing ozone in the future will require a combination of NOx and VOC emission controls to overcome the effect of decreasing PM2.5. Observations of surface ozone available from ∼1,000 sites across China for the past 5 years (2013–2017) show severe summertime pollution and regionally variable trends. We resolve the effect of meteorological variability on the ozone trends by using a multiple linear regression model. The residual of this regression shows increasing ozone trends of 1–3 ppbv a−1 in megacity clusters of eastern China that we attribute to changes in anthropogenic emissions. By contrast, ozone decreased in some areas of southern China. Anthropogenic NOx emissions in China are estimated to have decreased by 21% during 2013–2017, whereas volatile organic compounds (VOCs) emissions changed little. Decreasing NOx would increase ozone under the VOC-limited conditions thought to prevail in urban China while decreasing ozone under rural NOx-limited conditions. However, simulations with the Goddard Earth Observing System Chemical Transport Model (GEOS-Chem) indicate that a more important factor for ozone trends in the North China Plain is the ∼40% decrease of fine particulate matter (PM2.5) over the 2013–2017 period, slowing down the aerosol sink of hydroperoxy (HO2) radicals and thus stimulating ozone production.