Short-term O3 Exposure Research Articles

Spatiotemporal assessment of health burden and economic losses attributable to short-term exposure to ground-level ozone during 2015\u20132018 in China

BackgroundGround-level ozone (O3) pollution is currently the one of the severe environmental problems in China. Although existing studies have quantified the O3-related health impact and economic loss, few have focused on the acute health effects of short-term exposure to O3 and have been limited to a single temporal and spatial dimension.MethodsBased on the O3 concentration obtained from ground monitoring networks in 334 Chinese cities in 2015–2018, this study used a two-stage exposure parameter weighted Log-linear exposure-response function to estimate the cause-specific mortality for short-term exposure to O3.ResultsThe value of statistical life (VSL) method that were used to calculate the economic loss at the city-level. Our results show that in China, the national all-cause mortality attributed to O3 was 0.27(95% CI: 0.14–0.55) to 0.39 (95% CI: 0.20–0.67) million across 2015–2018. The estimated economic loss caused by O3 was 387.76 (95% CI: 195.99–904.50) to 594.08 (95% CI: 303.34–1140.65) billion CNY, accounting for 0.52 to 0.69% of total reported GDP. Overall, the O3 attributed health and economic burden has begun to decline in China since 2017. However, highly polluted areas still face severe burden, and undeveloped areas suffer from high GDP losses.ConclusionsThere are substantial health impacts and economic losses related to short-term O3 exposure in China. The government should pay attention to the emerging ozone pollution, and continue to strengthen the intervention in traditional priority areas while solving the pollution problem in non-priority areas.

Association of ambient ozone with pneumonia hospital admissions in Hong Kong and Taipei: A tale of two Southeast Asian cities.

Ozone (O3) is a reactive oxidant exerting both inflammatory and oxidative damages to the respiratory system. With the ground-level O3 progressively increasing in the past decade, the reevaluation of the pneumonia hospitalization risk from exposure to O3 is of public health interest. We conducted an ecological time-series study to examine the city-specific association between short-term O3 exposure and pneumonia hospitalizations in Hong Kong and Taipei, respectively. We linked the daily pneumonia hospitalization count to air pollution concentrations and weather conditions according to the date of admission during 2010-2017. We applied a generalized additive distributed lag model to examine the association while adjusting for time-varying covariates. Stratified analysis by age group and the potential harvesting effect of O3 were evaluated. We observed the harvesting effects of O3 on pneumonia hospitalizations in children in both cities and adults in Taipei. The short-term effect of O3 lasted for around one week. An interquartile range (IQR) increment of daytime 8-hour mean concentration of O3 distributed over 0-6 lag days in Hong Kong (42.4μg/m3) was associated with a 7.04% (95% CI: 5.35-8.76%) increase in hospital admissions for elderly pneumonia, while the corresponding cumulative excess risk per IQR increment of O3 in Taipei (38.7μg/m3) was 3.41% (95% CI: 1.63-5.22%). Different O3 metrics, varying degrees of freedom for filtering the temporal trend, and three-pollutant models supported the robustness of the associations. We concluded that short-term O3 exposure was associated with pneumonia hospitalizations in the elderly population. Understanding the pneumonia hospitalization risk of O3 will help to inform public health policies in the planning of ozone control strategies and intervention measures to prevent ozone-related pneumonia in vulnerable elderly populations.

Elevated Tropospheric Ozone Concentration Alters Soil CO2 Emission: A Meta-Analysis

Elevated tropospheric ozone (O3) concentration may substantially influence the below-ground processes of terrestrial ecosystems. Nevertheless, a comprehensive and quantitative understanding of O3 impacts on soil CO2 emission remains elusive, making the future sources or sinks of soil C uncertain. In this study, 77 pairs of observations (i.e., elevated O3 concentration treatment versus control) extracted from 16 peer-reviewed studies were synthesized using meta-analysis. The results depicted that soil CO2 efflux was significantly reduced under short-term O3 exposure (≤1 year, p < 0.05), while it was increased under extended duration (>1 year, p < 0.05). Particularly, soil CO2 emission was stimulated in nonagricultural ecosystems, in the free-air CO2 enrichment (FACE) experiment, and in the soils of lower pH. The effect sizes of soil CO2 efflux were significantly positively correlated with experimental duration and were significantly negatively correlated with soil pH, respectively. The ozone effect on soil CO2 efflux would be enhanced at warm temperatures and high precipitation. The duration of O3 exposure was the fundamental factor in analyzing O3 impacts on soil CO2 emission.

Continuous increases of surface ozone and associated premature mortality growth in China during 2015-2019.

Ambient ozone (O3) pollution has become a big issue in China. Recent studies have linked long- and short-term O3 exposure to several public health risks. In this study, we (1) characterize the long-term and short-term O3-attributed health metric in China from 2015 to 2019; (2) estimate the surface O3 trends; and (3) quantify the long-term and short-term health impacts (i.e. all-cause, cardiovascular and respiratory mortality) in 350 urban Chinese cities. In these 5-years, the national annual average of daily maximum 8h average (AVGDMA8) O3 concentrations and warm-season (April-September) 4th highest daily maximum 8h average (4DMA8) O3 concentrations increased from 74.0±15.5μg/m3 (mean±standard deviation) to 82.3±12.0μg/m3 and 167±37.0μg/m3 to 174±30.0μg/m3 respectively. During this period, the DMA8 O3 concentration increased by 1.9±3.3μg/m3/yr across China, with over 70% of the monitoring sites showing a positive upward trend and 19.4% with trends >5μg/m3/yr. The estimated long-term all-cause, cardiovascular and respiratory premature mortalities attributable to AVGDMA8 O3 exposure in 350 Chinese cities were 181,000 (95% CI: 91,500-352,000), 112,000 (95% CI: 38,100-214,000) and 33,800 (95% CI: 0-71,400) in 2019, showing increases of 52.5%, 52.9% and 54.6% respectively compared to 2015 levels. Similarly, short-term all-cause, cardiovascular and respiratory premature mortalities attributed to ambient 4DMA8 O3 exposure were 156,000 (95% CI: 85,300-227,000), 73,500 (95% CI: 27,500-119,000) and 28,600 (95% CI: 14,500-42,800) in 2019, increases of 19.6%, 19.8% and 21.2% respectively compared to 2015. The results of this study are important in ascertaining the effectiveness of recent emission control measures and to identify the areas that require urgent attention.

The effect of ambient ozone on glucose-homoeostasis: A prospective study of non-diabetic older adults in Beijing

ObjectiveTo investigate potential effects of short- and medium-term exposure to low levels of ozone (O3) on glucose-homeostasis in non-diabetic older adults. Methods166 non-diabetic, older participants in Beijing were deemed eligible to partake in this longitudinal population-based study. Observations were recorded on three separate occasions from November 2016 up until January 2018. Concentrations of outdoor O3 were monitored throughout the study period. Biomarkers indicative of glucose-homeostasis, including fasting blood glucose, insulin, HbAlc, glycated albumin percentage (glycated albumin/albumin), HOMA-IR and HOMA-B were measured at 3 sessions. A linear mixed effects model with random effects was adopted to quantify the effect of O3 across a comprehensive set of glucose-homeostasis markers. ResultsShort-term O3 exposure positively associated with increased fasting blood glucose, insulin, HOMA-IR and HOMA-B. The effect on glucose occurred at 3-, 5-, 6- and 7-days, although the largest effect manifested on 6-days (5.6%, 95% CI: 1.4, 9.9). Significant associations with both insulin and HOMA-IR were observed on the 3- and 4-days. For HOMA-B, positive associations were identified from 3- to 7-days with estimates ranging from 40.0% (95% CI: 2.3, 91.5) to 83.1% (95% CI: 25.3, 167.5). Stratification suggests that women may be more susceptible to short-term O3 exposure. There does not appear to be a significant association between O3 and glucose-homeostasis in medium-term exposures. ConclusionsIn this study, we found that O3 exposure is at least partially associated with type II diabetes in older adults with no prior history of this condition. O3 therefore appears to be a potential risk factor, which is a particular concern when we consider the rise in global concentrations. Evidence also suggests that women may be more susceptible to short-term O3 exposure although we are not quite sure why. Future research may look to investigate this phenomenon further.

The effect of ambient ozone on glucose-homoeostasis: A prospective study of non-diabetic older adults in Beijing

Objective: To investigate potential effects of short- and medium-term exposure to low levels of ozone (O3) on glucose-homeostasis in non-diabetic older adults. Methods: 166 non-diabetic, older participants in Beijing were deemed eligible to partake in this longitudinal population-based study. Observations were recorded on three separate occasions from November 2016 up until January 2018. Concentrations of outdoor O3 were monitored throughout the study period. Biomarkers indicative of glucose-homeostasis, including fasting blood glucose, insulin, hemoglobin A1c (HbAlc), glycated albumin percentage, Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) and Homeostatic Model Assessment of Beta cell function (HOMA-B) were measured at 3 sessions. A linear mixed effects model with random effects was adopted to quantify the effect of O3 across a comprehensive set of glucose-homeostasis markers. Results: short-term O3 exposure positively associated with increased fasting blood glucose, insulin, HOMA-IR and HOMA-B. The effect on glucose occurred at 3-, 5-, 6- and 7-days, although the largest effect manifested on 6-days (5.6%, 95%CI: 1.4, 9.9). Significant associations with both insulin and HOMA-IR were observed on the 3- and 4-days, although the largest effect consistently occured on 4-days with estimations of 90.0% (95%CI: 19.0, 203.4) and 96.5% (95%CI: 14.9, 235.9), respectively. For HOMA-B, positive associations were identified from 3- to 7-days with estimates ranging from 40.0% (95%CI: 2.3, 91.5) to 83.1% (95%CI: 25.3, 167.5). Stratification suggests that women may be more susceptible to short-term O3 exposure with positive associations observed at 1-, 2-, 5-, 6-, and 7-days in both insulin and HOMA-IR. Conclusions: In this study, we found that O3 exposure is at least partially related to the onset of type II diabetes in older adults with no prior history of this condition. O3 therefore acts as a kind of catalyst for metabolic disorders, which is a particular concern when we consider the rise in global concentrations.

Investigating potential associations between O3 exposure and lipid profiles: A longitudinal study of older adults in Beijing

Background: Little information exists on the lipidemic effects of ozone exposure. Few studies have focused on the different patterns of the association among older adults population, and little attention has been given to comprehensive lipid indices when evaluating the effect of O3 exposure on the metabolism. Methods: We conducted a longitudinal study involving 201 older adults in Beijing, China between 2016-2018. A mixed regression model was applied with random effects to investigate the relationship between O3 and lipid profiles. Results: O3 exposure positively correlated with TC, LDL-C, CRI-I, CRI-II and AC at short-term and medium-term exposure periods. The largest increases in TC, LDL-C, CRI-I and CRI-II were found in the 28-days moving average indicating accumulative effects over prolonged exposure period. A 10μg/m3 increase of O3 at the 28-days moving average was associated with a significant increase of 3.9% (95% CI: 1.0, 6.9) in TC, 8.2% (95% CI: 4.2, 12.4) in LDL-C, 4.8% (95% CI: 1.1, 8.5) in CRI-I and 7.0% (95% CI: 2.7, 11.5) in CRI-II. Stratification by health status and characteristics revealed different patterns of lipid changes among older adults, lipid status, age, sex and BMI may modify the relationship between O3 exposure and lipid profiles. Conclusions: Our findings suggest that short-term and medium-term O3 exposure is associated with lipid profiles abnormalities among the older adults. Evidence also suggests there are patterns within population which differ according to both health status and demographic characteristics.

Associations of ozone exposure with urinary metabolites of arachidonic acid

BackgroundOzone (O3) exposure has been associated with biomarkers of platelet activation and oxidative stress. The metabolism of arachidonic acid (AA) plays an important role in platelet activation and oxidative stress. However, AA metabolic pathways have not been examined in relation to O3 and other air pollutants. MethodsEarly morning urine and fasting blood were longitudinally collected up to four times from 89 healthy adults (22–52 years old, 25 women) in Changsha City, China. We measured three urinary AA metabolites, namely 11-dehydro-Thromboxane B2 (11-dhTXB2) produced from the arachidonic cyclooxygenase pathway, 20-hydroxyeicosatetraenoic acid (20-HETE) from the CYPs pathway, and 8-isoprostane from the non-enzymatic pathway. Urinary malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) were measured as indicators of oxidative damage to lipids and DNA, respectively. We measured soluble P-selectin (sCD62p) concentrations in plasma as an indicator of platelet activation. Indoor and outdoor air pollutants were measured and combined with participants’ time-activity pattern to calculate personal exposure to O3, PM2.5, NO2, and SO2 averaged over 12-hour, 24-hour, 1-week, and 2-week periods prior to biospecimen collection, respectively. Linear mixed-effects models were used to examine the relationships of AA metabolites with air pollutant exposures, plasma sCD62p, and urinary MDA & 8-OHdG. ResultsWe found that a 10% increase in 12 h and 24 h O3 exposure were associated with increases in urinary11-dhTXB2 by 1.4% (95%, 0.1% to 2.6%) and 1.3% (0.05% to 2.5%), respectively. These associations remained robust after adjusting for co-pollutant exposures. No significant associations were observed between 11-dhTXB2 and other pollutants or between O3 exposures and other AA metabolites. All the three AA metabolites were significantly and positively associated with urinary MDA and 8-OHdG, whereas only urinary 11-dhTXB2 was significantly and positively associated with plasma sCD62p. ConclusionsA metabolite of AA from the cyclooxygenase pathway was positively associated with short-term O3 exposure, and with a plasma marker of platelet activation and two urinary markers of oxidative stress. The results suggest that O3 exposure may contribute to increased platelet activation and oxidative damages via altering the metabolism of AA.

The phytotoxic air-pollutant O3 enhances the emission of herbivore-induced volatile organic compounds (VOCs) and affects the susceptibility of black mustard plants to pest attack

Stress-induced changes to plant biochemistry and physiology can influence plant nutritional quality and subsequent interactions with herbivorous pests. However, the effects of stress combinations are unpredictable and differ to the effects of individual stressors. Here we studied the effects of exposure to the phytotoxic air-pollutant ozone (O3), feeding by larvae of the large cabbage white butterfly (Pieris brassicae), and a combination of the two stresses, on the emission of volatile organic compounds (VOCs) by black mustard plants (Brassica nigra) under field and laboratory conditions. Field-grown B. nigra plants were also measured for carbon-nitrogen (C–N) content, net photosynthetic activity (Pn), stomatal conductance (gs) and biomass. The effects of O3 on interactions between plants and a herbivorous pest were addressed by monitoring the abundance of wild diamondback moth larvae (Plutella xylostella) and feeding-damage to B. nigra plants in an O3-free air concentration enrichment (O3-FACE) field site. Herbivore-feeding induced the emission of VOCs that were not emitted by undamaged plants, both under field and laboratory conditions. The combination of O3 and herbivore-feeding stresses resulted in enhanced emission rates of several VOCs from field-grown plants. Short-term O3 exposure (of 10 days) and P. brassicae-feeding did not affect C–N content, but chronic O3 exposure (of 34 and 47 days) and P. brassicae-feeding exacerbated suppression of Pn. Ozone exposure also caused visible injury and decreased the plant biomass. Field-grown B. nigra under elevated O3 were infested with fewer P. xylostella larvae and received significantly less feeding damage. Our results suggest that plants growing in a moderately polluted environment may be of reduced quality and less attractive to foraging herbivores.

Associations of air pollution, obesity and cardiometabolic health in young adults: The Meta-AIR study

ObjectiveGrowing evidence indicates exposure to air pollution contributes to obesity and cardiometabolic disease risk in children and adults, however studies are lacking in young adulthood, an important transitional period in the life course. The aim of this study was to examine the associations of short- and long-term regional ambient and near-roadway air pollution (NRAP) exposures on adiposity and cardiometabolic health in young adults aged 17–22 years. MethodsFrom 2014 to 2018, a subset of participants (n = 158) were recruited from the Children's Health Study to participate in the Meta-AIR (Metabolic and Asthma Incidence Research) study to assess obesity (body composition and abdominal adiposity) and cardiometabolic health (fasting glucose, fasting insulin and lipid profiles) measures. Prior 1-month and 1-year average air pollution exposures were calculated from residential addresses. This included nitrogen dioxide (NO2), ozone (O3), particulate matter with aerodynamic diameter < 10 μm (PM10), particulate matter with aerodynamic diameter < 2.5 μm (PM2.5) and NRAP (freeway, non-freeway, and total nitrogen oxides (NOx)) exposures. Linear regression models examined associations of prior 1-month (short-term) and 1-year (long-term) air pollution exposures on obesity and cardiometabolic factors adjusting for covariates and past childhood air pollution exposures. ResultsIn the Meta-AIR study, we conducted a comprehensive analysis with short- and long-term regional ambient and NRAP exposures (in both single- and multi-pollutant models) and obesity- and cardiometabolic-related outcomes and found associations with a few outcomes. A 1 standard deviation (SD) change in long-term NO2 exposure was associated with a 11.3 mg/dL higher level of total cholesterol (p = 0.04) and 9.4 mg/dL higher level of low-density lipoproteins (LDL)-cholesterol (p = 0.04). Amongst obese participants, associations between long-term NO2 and total cholesterol and LDL-cholesterol were 4.5 and 9 times larger than the associations in non-obese participants (pinteraction = 0.008 and 0.03, respectively). Additionally, we observed a statistically significant association with increased short-term O3 exposure and higher triglyceride and very-low-density lipoprotein (VLDL) cholesterol levels (p = 0.04), lower high-density lipoprotein (HDL) cholesterol levels (p = 0.03), and higher hepatic fat levels (p = 0.02). Amongst glucose-related factors, long-term PM2.5 exposure was associated with higher levels of insulin area under the curve (p = 0.03). There were no other statistically significant associations with short- or long-term air pollutants and BMI, other measures of adiposity, and cardiometabolic outcomes. ConclusionHigher exposure to regional air pollutants, namely prior 1-year average NO2, was associated with higher fasting serum lipid measures. These associations were more pronounced in obese participants, suggesting obesity may exacerbate the effects of air pollution exposure on lipid levels in young adults. This study did not find any other associations between short- and long-term ambient and NRAP exposures across a range of other obesity and cardiometabolic indicators. Further studies in young adults are warranted as our study suggests potential deleterious associations of both short- and long-term air pollution exposures and lipid metabolism.

Investigating potential associations between O3 exposure and lipid profiles: A longitudinal study of older adults in Beijing

BackgroundLittle information exists on the lipidemic effects of ozone exposure. Few studies have focused on the different patterns of the association among older adults population, and little attention has been given to comprehensive lipid indices when evaluating the effect of O3 exposure on the metabolism. MethodsWe conducted a longitudinal study involving 201 older adults in Beijing, China between 2016 and 2018. A mixed regression model was applied with random effects to investigate the relationship between O3 and lipid profiles. ResultsO3 exposure positively correlated with TC, LDL-C, CRI-I, CRI-II and AC at short-term and medium-term exposure periods. The largest increases in TC, LDL-C, CRI-I and CRI-II were found in the 28-days moving average indicating accumulative effects over prolonged exposure period. A 10 μg/m3 increase of O3 at the 28-days moving average was associated with a significant increase of 3.9% (95% CI: 1.0, 6.9) in TC, 8.2% (95% CI: 4.2, 12.4) in LDL-C, 4.8% (95% CI: 1.1, 8.5) in CRI-I and 7.0% (95% CI: 2.7, 11.5) in CRI-II. Stratification by health status and characteristics revealed different patterns of lipid changes among older adults, lipid status, age, sex and BMI may modify the relationship between O3 exposure and lipid profiles. ConclusionsOur findings suggest that short-term and medium-term O3 exposure is associated with lipid profiles abnormalities among the older adults. Evidence also suggests there are patterns within population which differ according to both health status and demographic characteristics.

Ozone and cardiac arrest: The role of previous hospitalizations

BackgroundSeveral studies have reported associations between exposure to particulate matter and incidence of out-of-hospital cardiac arrest (OHCA) and some have observed associations with ozone (O3). There are no studies investigating susceptibility based on previous disease history to short-term O3 exposure and the risk of OHCA. AimTo investigate the role of previous cardiovascular-related hospitalizations in modifying the associations between the risk of OHCA and short-term increase in O3 concentrations. MethodsA time-stratified case-crossover analysis of 11,923 OHCA registered in the Swedish Register for Cardiopulmonary Resuscitation from 2006 to 2014 was performed. Using personal identification numbers, OHCA were linked to all previous hospitalizations in Sweden since 1987 to create susceptible groups based on the principal diagnosis code at discharge. Susceptibility was based on hospitalization for i) acute myocardial infarction; ii) heart failure; iii) arrhythmias; iv) diabetes; v) hypertension; and vi) stroke. Moving 2 and 24-h averages for O3, PM2.5, PM10, and NO2 were constructed from hourly averages. ResultsA 10 μg/m3 higher 2-h average O3 concentration was associated with a 2% higher risk of OHCA (95% CI, 0% 3%). Associations were similar for 24-h average O3 and in individuals with or without hospitalizations for AMI, heart failure, diabetes, hypertension or stroke. Individuals with previous hospitalizations for arrhythmias had a lower risk of OHCA with higher O3. No associations were observed for other pollutants. ConclusionsShort-term exposure to O3 was associated with an elevated risk of OHCA, however, previous hospitalizations for cardiovascular diseases were not associated with additionally augmented risks.

Public health air pollution impacts of pathway options to meet the 2050 UK Climate Change Act target: a modelling study

BackgroundThe UK’sClimate Change Act 2008(CCA; Great Britain.Climate Change Act 2008. Chapter 27. London: The Stationery Office; 2008) requires a reduction of 80% in carbon dioxide-equivalent emissions by 2050 on a 1990 base. This project quantified the impact of air pollution on health from four scenarios involving particulate matter of ≤ 2.5 µm (PM2.5), nitrogen dioxide (NO2) and ozone (O3). Two scenarios met the CCA target: one with limited nuclear power build (nuclear replacement option; NRPO) and one with no policy constraint on nuclear (low greenhouse gas). Another scenario envisaged no further climate actions beyond those already agreed (‘baseline’) and the fourth kept 2011 concentrations constant to 2050 (‘2011’).MethodsThe UK Integrated MARKAL–EFOM System (UKTM) energy system model was used to develop the scenarios and produce projections of fuel use; these were used to produce air pollutant emission inventories for Great Britain (GB) for each scenario. The inventories were then used to run the Community Multiscale Air Quality model ‘air pollution model’ to generate air pollutant concentration maps across GB, which then, combined with relationships between concentrations and health outcomes, were used to calculate the impact on health from the air pollution emitted in each scenario. This is a significant improvement on previous health impact studies of climate policies, which have relied on emissions changes. Inequalities in exposure in different socioeconomic groups were also calculated, as was the economic impact of the pollution emissions.ResultsConcentrations of NO2declined significantly because of a high degree of electrification of the GB road transport fleet, although the NRPO scenario shows large increases in oxides of nitrogen emissions from combined heat and power (CHP) sources. Concentrations of PM2.5show a modest decrease by 2050, which would have been larger if it had not been for a significant increase in biomass (wood burning) use in the two CCA scenarios peaking in 2035. The metric quantifying long-term exposure to O3is projected to decrease, while the important short-term O3exposure metric increases. Large projected increases in future GB vehicle kilometres lead to increased non-exhaust PM2.5and particulate matter of ≤ 10 µm emissions. The two scenarios which achieve the CCA target resulted in more life-years lost from long-term exposures to PM2.5than in the baseline scenario. This is an opportunity lost and arises largely from the increase in biomass use, which is projected to peak in 2035. Reduced long-term exposures to NO2lead to many more life-years saved in the ‘CCA-compliant’ scenarios, but the association used may overestimate the effects of NO2itself. The more deprived populations are estimated currently to be exposed to higher concentrations than those less deprived, the contrast being largest for NO2. Despite reductions in concentrations in 2050, the most socioeconomically deprived are still exposed to higher concentrations than the less deprived.LimitationsModelling of the atmosphere is always uncertain; we have shown the model to be acceptable through comparison with observations. The necessary complexity of the modelling system has meant that only a small number of scenarios were run.ConclusionsWe have established a system which can be used to explore a wider range of climate policy scenarios, including more European and global scenarios as well as local measures. Future work could explore wood burning in more detail, in terms of the sectors in which it might be burned and the spatial distribution of this across the UK. Further analyses of options for CHP could also be explored. Non-exhaust emissions from road transport are an important source of particles and emission factors are uncertain. Further research on this area coupled with our modelling would be a valuable area of research.FundingThe National Institute for Health Research Public Health Research programme.

Ambient ozone and asthma hospital admissions in Texas: a time-series analysis

BackgroundMany studies have evaluated associations between asthma emergency department (ED) visits, hospital admissions (HAs), and ambient ozone (O3) across the US, but not in Texas. We investigated the relationship between O3 and asthma HAs, and the potential impacts of outdoor pollen, respiratory infection HAs, and the start of the school year in Texas.MethodsWe obtained daily time-series data on asthma HAs and ambient O3 concentrations for Dallas, Houston, and Austin, Texas for the years 2003–2011. Relative risks (RRs) and 95% confidence intervals (CIs) of asthma HAs per 10-ppb increase in 8-h maximum O3 concentrations were estimated from Poisson generalized additive models and adjusted for temporal trends, meteorological factors, pollen, respiratory infection HAs, day of the week, and public holidays. We conducted a number of sensitivity analyses to assess model specification.ResultsWe observed weak associations between total asthma HAs and O3 at lags of 1 day (RR10 ppb = 1.012, 95% CI: 1.004–1.021), 2 days (RR10 ppb = 1.011, 95% CI: 1.002–1.019), and 0–3 days (RR10 ppb = 1.017, 95% CI: 1.005–1.030). The associations were primarily observed in children aged 5–14 years (e.g., for O3 at lag 0–3 days, RR10 ppb = 1.037, 95% CI: 1.011–1.064), and null in individuals 15 years or older. The effect estimates did not change significantly with adjustment for pollen and respiratory infections, but they attenuated considerably and lost statistical significance when August and September data were excluded. A significant interaction between time around the start of the school year and O3 at lag 2 day was observed, with the associations with pediatric asthma HAs stronger in August and September (RR10 ppb = 1.040, 95% CI: 1.012–1.069) than in the rest of the year (October–July) (RR10 ppb = 1.006, 95% CI: 0.986–1.026).ConclusionsWe observed small but statistically significant positive associations between total and pediatric asthma HAs and short-term O3 exposure in Texas, especially in August and September. Further research is needed to determine how the start of school could modify the observed association between O3 and pediatric asthma HAs.

Ozone and PM2.5 in the air pollution mixture differentially impact cardiopulmonary pathophysiologic mechanisms

Introduction: The relative contributions of ozone (O3) and PM2.5 in air pollution mixtures to cardiopulmonary outcomes remain poorly understood. This study examines whether and how O3 and PM2.5 may differentially impact mechanisms of cardiopulmonary pathophysiology. Methods: Exposures to each pollutant were manipulated for 89 office workers living together on a work campus in China with various combinations of an O3-generating electrostatic precipitator (ESP) and a high efficiency particulate air (HEPA) filter. Subjects were measured for biomarkers of cardiopulmonary pathophysiology at four time points each separated by 2-3 week intervals. Results: Mean 24-hour exposure concentrations during the study were 37 ± 1.5 µg/m3 for PM2.5 and 6.4 ± 0.2 ppb for O3, and they were significantly negatively correlated. Contrary to previous literature showing these biomarkers all being associated with PM2.5 exposure, this study shows that lung inflammation (fractional exhaled nitric oxide and exhaled breath condensate (EBC) nitrite and nitrate), systolic and diastolic blood pressure, and platelet activation (soluble P-selectin (sP-sel)) were tightly associated with short-term and chronic O3 exposure. In contrast, pulmonary oxidative stress (EBC malondialdehyde), arterial stiffness (augmentation index), and endothelial cell dysfunction (von Willebrand factor (VWF)) were significantly associated with chronic PM2.5 exposure. For example, an interquartile range (IQR) increase in 24-hour O3 exposure concentration (4.1 ppb) and 2-week mean ambient O3 (11.0 ppb) was significantly associated with a 12.5% and 27.4% increase in sP-sel, respectively. An IQR increase in 2-week mean ambient PM2.5 (41.4 µg/m3) was associated with a significant 11.2% increase in VWF. Conclusions: These findings have provided insights into biological mechanisms by which O3 and PM2.5 can differentially enhance cardiopulmonary disease risk.

Is daily exposure to ozone associated with respiratory morbidity and lung function in a representative sample of schoolchildren? Results from a panel study in Greece.

Previous time series or panel studies of asthmatics have reported respiratory health effects following short-term exposure to ozone (O3). We followed 186 children aged 10 years old in Athens and Thessaloniki, Greece for 5 weeks during the academic year 2013-2014 and recorded daily their respiratory symptoms, absenteeism and peak expiratory flow (PEF). We applied mixed models controlling for various possible confounders to investigate the daily associations between O3 exposure - derived from weekly personal and fixed school site measurements calibrated using daily values of the fixed monitoring site nearest to the child's school location - and PEF, presence of any symptom, cough and stuffy nose, as well as absenteeism. We tested the robustness of our findings to varying modeling assumptions and confounders and investigated effect modification patterns by medication use, time spent outdoors and prevalence of asthma. A 10 μg/m3 increase in O3 personal exposure was associated with increased odds of any symptom (odds ratio (OR): 1.19, 95% confidence interval (CI): 0.98, 1.44), largely attributed to the increase in the odds of stuffy nose (OR: 1.23, 95% CI: 1.00, 1.51). PEF and absenteeism were not related to O3 exposure. Our results were robust to several sensitivity analyses. Effects were modified by medication use as presence of symptoms but also decreases in PEF were mainly reported among non-users, while our effect estimates were not driven by the asthmatic subgroup of children. Our findings indicate that short-term O3 exposure may be associated with respiratory symptoms extending previously reported results for asthmatics to the general population.

Short-term Exposure to Ozone and Mortality in Subjects With and Without Previous Cardiovascular Disease.

Exposure to ground level ozone (O3) is a public health problem associated with a range of risks across population subgroups. Our aim was to investigate the role of previous cardiovascular diseases (CVDs) in mortality related to short-term O3 exposure. Deaths between 1990 and 2010 in Stockholm County were matched with previous hospitalizations in Swedish registries. An urban background monitoring station provided hourly values of air quality data, from which we calculated 8-hour running averages and daily 8-hour maximum. We analyzed associations between daily O3 concentrations and mortality among persons with and without previous CVD hospitalization with a generalized additive model adjusted for time trend, influenza, and weather. We also performed two-pollutant models. There were 302,283 nontrauma-related deaths, out of which 196,916 had previous CVD hospitalization. The mean concentration of daily maximum 8-hour O3 was 62.9 μg/m. An average 10 μg/m increase in the same and preceding day was associated with an increased mortality of 1.72% (95% confidence interval: 0.44%, 3.02%) in those with prior admission for acute myocardial infarction (AMI), which was more than three times higher than for those with no previous AMI (0.50, 95% confidence interval: 0.10%, 0.89%, P value for interaction 0.098). The association between O3 and mortality remained essentially unchanged in two-pollutant models with NO2, NOx, and PM10. Our study indicates that short-term exposure to O3 is associated with increased mortality in those with a previous hospitalization for AMI.

Daytime and Phenological Characteristics of O3 and CO2 Fluxes of Winter Wheat Canopy Under Short-Term O3 Exposure

To analyze the daytime and phenological variations of canopy O3 and CO2 uptake of winter wheat, the canopy fluxes of wheat plants were measured using a chamber system with four different O3 levels (0, 40, 80, and 120 nmol mol−1) being applied. During the daytime (7:30–18:00 hours), canopy fluxes usually peaked around noon in early growing stages, while a generally decreasing trend from morning to afternoon was observed in the later stages. O3 and CO2 fluxes were positively and negatively correlated with O3 concentration, respectively. Significant differences were observed in O3 fluxes but CO2 fluxes among O3 treatments. Photosynthetically active radiation (PAR) and vapor pressure deficit (VPD) could affect canopy gas uptake in opposite ways. On the phenological timescale, both O3 and CO2 fluxes followed the variation of leaf area index (LAI) with the maximum occurring simultaneously at the booting stage. The daytime mean fluxes varied from −10.6 to −17.2 nmol m−2 s−1 for O3 and from −5.9 to −19.6 μmol m−2 s−1 for CO2. Quantitatively important O3 deposition (−3.1∼−11.6 nmol m−2 s−1) was also observed at night with the ratios being about 40∼70 % relative to the daytime O3 fluxes for most measuring days, which indicates a significant contribution from non-stomatal components to canopy O3 removal. This study confirms that environmental variables and plant phenology are important factors in regulating canopy O3 and CO2 uptake. O3 exposure (≤120 nmol mol−1) could not significantly affect the CO2 uptake of wheat canopy in a short time (ca. 10 min).

Inhaled ozone (O3)-induces changes in serum metabolomic and liver transcriptomic profiles in rats

Air pollution has been linked to increased incidence of diabetes. Recently, we showed that ozone (O3) induces glucose intolerance, and increases serum leptin and epinephrine in Brown Norway rats. In this study, we hypothesized that O3 exposure will cause systemic changes in metabolic homeostasis and that serum metabolomic and liver transcriptomic profiling will provide mechanistic insights. In the first experiment, male Wistar Kyoto (WKY) rats were exposed to filtered air (FA) or O3 at 0.25, 0.50, or 1.0ppm, 6h/day for two days to establish concentration-related effects on glucose tolerance and lung injury. In a second experiment, rats were exposed to FA or 1.0ppm O3, 6h/day for either one or two consecutive days, and systemic metabolic responses were determined immediately after or 18h post-exposure. O3 increased serum glucose and leptin on day 1. Glucose intolerance persisted through two days of exposure but reversed 18h-post second exposure. O3 increased circulating metabolites of glycolysis, long-chain free fatty acids, branched-chain amino acids and cholesterol, while 1,5-anhydroglucitol, bile acids and metabolites of TCA cycle were decreased, indicating impaired glycemic control, proteolysis and lipolysis. Liver gene expression increased for markers of glycolysis, TCA cycle and gluconeogenesis, and decreased for markers of steroid and fat biosynthesis. Genes involved in apoptosis and mitochondrial function were also impacted by O3. In conclusion, short-term O3 exposure induces global metabolic derangement involving glucose, lipid, and amino acid metabolism, typical of a stress–response. It remains to be examined if these alterations contribute to insulin resistance upon chronic exposure.

Gene expression in snapbeans exposed to ozone and protected by ethylenediurea

Ethylenediurea (EDU) is the most common chemical used to prevent ozone (O3) injury on vegetation. Despite considerable research, its mode of action remains elusive and gene expression has not been studied. Transcripts of major antioxidant enzymes (catalase, glutathione reductase, glutathione peroxidase) were measured for the first time in a model plant (Phaseolus vulgaris cv S156) after short-term O3 exposure (0 or 90 ppb, 5 h/d, 4 days) and a single spray with EDU (0 or 300 ppm). Visible, physiological and biochemical parameters were assessed as indices of O3-induced stress. In O3-exposed EDU-protected plants, levels of transcript, enzyme activity, H2O2 accumulation, gas exchange and foliar visible injury were similar to those in control plants. These results suggest that EDU may halt the O3-induced ROS generation within 24 h from the exposure, and thus the downstream cascade mechanisms leading to increased H2O2 production, impaired gas exchange, and occurrence of leaf lesions.