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Background Traffic-related air pollution may contribute to cardiovascular morbidity. In urban areas, exposures during physical activity are of interest owing to increased breathing rates and close proximity to vehicle emissions. Methods We conducted a cross-over study among 53 healthy non-smoking women in Montreal, Canada during the summer of 2013. Women were exposed to traffic pollutants for 2-hours on three separate occasions during cycling on high and low-traffic routes as well as indoors. Personal air pollution exposures (PM 2.5 , ultrafine particles (UFP), black carbon, NO 2 , and O 3 ) were evaluated along each route and linear mixed-effects models with random subject intercepts were used to estimate the impact of air pollutants on acute changes in blood pressure, heart rate variability, and micro-vascular function in the hours immediately following exposure. Single and multi-pollutant models were examined and potential effect modification by mean regional air pollution concentrations (PM 2.5 , NO 2 , and O 3 ) was explored for the 24-hour and 5-day periods preceding exposure. Results In total, 143 exposure routes were completed. Each interquartile increase (10,850/cm 3 ) in UFP exposure was associated with a 4.91% (95% CI: -9.31, -0.512) decrease in reactive hyperemia index (a measure of micro-vascular function) and each 24 ppb increase in O 3 exposure corresponded to a 2.49% (95% CI: 0.141, 4.84) increase in systolic blood pressure and a 3.26% (95% CI: 0.0117, 6.51) increase in diastolic blood pressure 3-hours after exposure. Personal exposure to PM 2.5 was associated with decreases in HRV measures reflecting parasympathetic modulation of the heart and regional PM 2.5 concentrations modified these relationships (p < 0.05). In particular, stronger inverse associations were observed when regional PM 2.5 was higher on the days prior to the study period. Regional PM 2.5 also modified the impact of personal O 3 on the standard deviation of normal to normal intervals (SDNN) (p < 0.05): a significant inverse relationship was observed when regional PM 2.5 was low prior to study periods and a significant positive relationship was observed when regional PM 2.5 was high. Conclusion Exposure to traffic pollution may contribute to acute changes in blood pressure, autonomic and micro-vascular function in women. Regional air pollution concentrations may modify the impact of these exposures on autonomic function.

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.

Background Exposures to ambient particulate matter (PM) are associated with increased morbidity and mortality. PM 2.5 (<2.5 μm) and ozone exposures have been shown to associate with carotid intima media thickness in humans. Animal studies support a causal relationship between air pollution and atherosclerosis and identified adverse PM effects on HDL functionality. We aimed to determine whether brief exposures to PM 2.5 and/or ozone could induce effects on HDL anti-oxidant and anti-inflammatory capacity in humans. Methods Subjects were exposed to fine concentrated ambient fine particles (CAP) with PM 2.5 targeted at 150 μg/m 3 , ozone targeted at 240 μg/m 3 (120 ppb) , PM 2.5 plus ozone targeted at similar concentrations, and filtered air (FA) for 2 h, on 4 different occasions, at least two weeks apart, in a randomized, crossover study. Blood was obtained before exposures (baseline), 1 h after and 20 h after exposures. Plasma HDL anti-oxidant/anti-inflammatory capacity and paraoxonase activity were determined. HDL anti-oxidant/anti-inflammatory capacity was assessed by a cell-free fluorescent assay and expressed in units of a HDL oxidant index (HOI). Changes in HOI (ΔHOI) were calculated as the difference in HOI from baseline to 1 h after or 20 h after exposures. Results There was a trend towards bigger ΔHOI between PM 2.5 and FA 1 h after exposures ( p  = 0.18) but not 20 h after. This trend became significant ( p  <0.05) when baseline HOI was lower (<1.5 or <2.0), indicating decreased HDL anti-oxidant/anti-inflammatory capacity shortly after the exposures. There were no significant effects of ozone alone or in combination with PM 2.5 on the change in HOI at both time points. The change in HOI due to PM 2.5 showed a positive trend with particle mass concentration ( p  = 0.078) and significantly associated with the slope of systolic blood pressure during exposures ( p  = 0.005). Conclusions Brief exposures to concentrated PM 2.5 elicited swift effects on HDL anti-oxidant/anti-inflammatory functionality, which could indicate a potential mechanism for how particulate air pollution induces harmful cardiovascular effects.

Ambient aerosol fine particulate matter (PM2.5) is associated with male reproductive toxicity in experiments and may have adverse effects in the female. However, studies evaluating the protective effects and precise mechanisms of aspirin, Vitamin C, Vitamin E, or ozone against toxic effects of PM2.5are sparse. This study was conducted to investigate the possible protective effects and mechanisms of aspirin, Vitamin C, Vitamin E, or ozone on fertility in female mice treated with PM2.5. Eighty-four ICR mice were divided into six groups: control group, PM2.5group, PM2.5 + aspirin group, PM2.5 + Vitamin C group, PM2.5 + Vitamin E group, and PM2.5 + ozone group. PM2.5was given by intratracheal instillation every 2 days for 3 weeks. Aspirin, Vitamin C, and Vitamin E were given once a day by oral gavage for 3 weeks, and ozone was administered by intraperitoneal injection once a day for 3 weeks. The levels of anti-Müllerian hormone (AMH), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were measured using enzyme-linked immunosorbent assay. Western blotting analysis was used to analyze the expressions of Bcl-2, Bax, and caspase-3 in ovaries. Changes in histological structure were examined by light microscope and electron microscopy was used to detect ultramicrostructure. The results demonstrated that PM2.5 decreased AMH levels (P < 0.001); however, aspirin (P < 0.001), Vitamin C (P < 0.001), Vitamin E (P = 0.001), and ozone (P = 0.002) alleviated the decrease. Changes of IL-6, TNF-α, 8-OHdG, Bax/Bcl-2, and caspase-3 in PM2.5group were increased compared to control group (P < 0.001), while in PM2.5 + aspirin, PM2.5 + Vitamin C, PM2.5 + Vitamin E, and PM2.5 + ozone groups, they were statistically decreased compared to PM2.5group (P < 0.001 or P< 0.05). PM2.5cause the damage of ovaries, and aspirin, Vitamin C, Vitamin E, and ozone antagonizes the damage. The protective mechanism is probably due to its ability to blunt the inflammatory and oxidative stress caused by PM2.5, which subsequently suppressing the expression of apoptotic regulatory protein and reducing the incidence of ovary apoptosis.

Background: Human controlled-exposure studies have assessed the impact of ambient fine paniculate matter on cardiac autonomic function measured by heart rate variability (HRV), but whether these effects are modified by concomitant ozone exposure remains unknown. Objective: In this study we assessed the impact of O₃ and paniculate matter exposure on HRV in humans. Methods: In a crossover design, 50 subjects (19-48 years of age) were randomized to 2-hr controlled exposures to filtered air (FA), concentrated ambient particles (CAPs), O₃, or combined CAPs and ozone (CAPs + O₃). The primary end point was change in HRV between the start and end of exposure. Secondary analyses included blood pressure (BP) responses, and effect modification by asthmatic status. RESULTS: Achieved mean CAPs and O₃ exposure concentrations were 121.6 ± 48.0 ¼g/m³ and 113.9 ± 6.6 ppb, respectively. In a categorical analysis, exposure had no consistent effect on HRV indices. However, the dose-response relationship between CAPs mass concentration and HRV indices seemed to vary depending on the presence of O₃. This heterogeneity was statistically significant for the low-frequency component of HRV (p = 0.02) and approached significance for the high-frequency component and time-domain measures of HRV. Exposure to CAPs + O₃ increased diastolic BP by 2.0 mmHg (SE , 1.2; p = 0.02). No other statistically significant changes in BP were observed. Asthmatic status did not modify these effects. Conclusion: The potentiation by O₃ of CAPs effects on diastolic BP and possibly HRV is of small magnitude in young adults. Further studies are needed to assess potential effects in more vulnerable populations.

The potential effects of combinations of dilute whole diesel exhaust (DE) and ozone (O 3 ), each a common component of ambient airborne pollutant mixtures, on lung function were examined. Healthy young human volunteers were exposed for 2 hr to pollutants while exercising (~50 L/min) intermittently on two consecutive days. Day 1 exposures were either to filtered air, DE (300 μg/m 3 ), O 3 (0.300 ppm), or the combination of both pollutants. On Day 2 all exposures were to O 3 (0.300 ppm), and Day 3 served as a followup observation day. Lung function was assessed by spirometry just prior to, immediately after, and up to 4 hr post-exposure on each exposure day. Functional pulmonary responses to the pollutants were also characterized based on stratification by glutathione S-transferase mu 1 (GSTM1) genotype. On Day 1, exposure to air or DE did not change FEV1 or FVC in the subject population (n = 15). The co-exposure to O 3 and DE decreased FEV1 (17.6%) to a greater extent than O 3 alone (9.9%). To test for synergistic exposure effects, i.e., in a greater than additive fashion, FEV1 changes post individual O 3 and DE exposures were summed together and compared to the combined DE and O 3 exposure; the p value was 0.057. On Day 2, subjects who received DE exposure on Day 1 had a larger FEV1 decrement (14.7%) immediately after the O 3 exposure than the individuals' matched response following a Day 1 air exposure (10.9%). GSTM1 genotype did not affect the magnitude of lung function changes in a significant fashion. These data suggest that altered respiratory responses to the combination of O 3 and DE exposure can be observed showing a greater than additive manner. In addition, O 3 -induced lung function decrements are greater with a prior exposure to DE compared to a prior exposure to filtered air. Based on the joint occurrence of these pollutants in the ambient environment, the potential exists for interactions in more than an additive fashion affecting lung physiological processes.

Background: We recently reported that antioxidant supplementation with vitamins C and E mitigated ozone related decline in forced expiratory flow (FEF25–75) in 158 asthmatic children in an area with high ozone exposure in Mexico City. Methods: A study was undertaken to determine whether deletion of glutathione S-transferase M1 (GSTM1 null genotype), a gene involved in response to oxidative stress, influences ozone related decline in FEF25–75 and the benefit of antioxidant supplementation. Results:GSTM1 null children receiving placebo had significant ozone related decrements in FEF25–75 (percentage change per 50 ppb of ozone 2.9 (95% CI −5.2 to −0.6), p = 0.01); GSTM1 positive children did not. Conversely, the effect of antioxidants was stronger in children with the GSTM1 null genotype. Conclusions: Asthmatic children with a genetic deficiency of GSTM1 may be more susceptible to the deleterious effects of ozone on the small airways and might derive greater benefit from antioxidant supplementation.

Background Fraction of exhaled nitric oxide (FENO) is a promising non-invasive index of airway inflammation that may be used to assess respiratory effects of air pollution. We evaluated FENO as a measure of airway inflammation after controlled exposure to diesel exhaust or ozone. Methods Healthy volunteers were exposed to either diesel exhaust (particle concentration 300 μg/m 3 ) and filtered air for one hour, or ozone (300 ppb) and filtered air for 75 minutes. FENO was measured in duplicate at expiratory flow rates of 10, 50, 100 and 270 mL/s before, 6 and 24 hours after each exposure. Results Exposure to diesel exhaust increased FENO at 6 hours compared with air at expiratory flow rates of 10 mL/s (p = 0.01) and at 50 mL/s (p = 0.011), but FENO did not differ significantly at higher flow rates. Increases in FENO following diesel exhaust were attenuated at 24 hours. Ozone did not affect FENO at any flow rate or time point. Conclusions Exposure to diesel exhaust, but not ozone, increased FENO concentrations in healthy subjects. Differences in the induction of airway inflammation may explain divergent responses to diesel exhaust and ozone, with implications for the use of FENO as an index of exposure to air pollution.

Acute exposure to air pollution has been linked to myocardial infarction, but its effect on heart failure is uncertain. We did a systematic review and meta-analysis to assess the association between air pollution and acute decompensated heart failure including hospitalisation and heart failure mortality. Five databases were searched for studies investigating the association between daily increases in gaseous (carbon monoxide, sulphur dioxide, nitrogen dioxide, ozone) and particulate (diameter <2·5 μm [PM2·5] or <10 μm [PM10]) air pollutants, and heart failure hospitalisations or heart failure mortality. We used a random-effects model to derive overall risk estimates per pollutant. Of 1146 identified articles, 195 were reviewed in-depth with 35 satisfying inclusion criteria. Heart failure hospitalisation or death was associated with increases in carbon monoxide (3·52% per 1 part per million; 95% CI 2·52–4·54), sulphur dioxide (2·36% per 10 parts per billion; 1·35–3·38), and nitrogen dioxide (1·70% per 10 parts per billion; 1·25–2·16), but not ozone (0·46% per 10 parts per billion; −0·10 to 1·02) concentrations. Increases in particulate matter concentration were associated with heart failure hospitalisation or death (PM2·5 2·12% per 10 μg/m3, 95% CI 1·42–2·82; PM10 1·63% per 10 μg/m3, 95% CI 1·20–2·07). Strongest associations were seen on the day of exposure, with more persistent effects for PM2·5. In the USA, we estimate that a mean reduction in PM2·5 of 3·9 μg/m3 would prevent 7978 heart failure hospitalisations and save a third of a billion US dollars a year. Air pollution has a close temporal association with heart failure hospitalisation and heart failure mortality. Although more studies from developing nations are required, air pollution is a pervasive public health issue with major cardiovascular and health economic consequences, and it should remain a key target for global health policy. British Heart Foundation.

The damage and injury that ground level ozone (O 3 ) causes vegetation has become increasingly evident over the past half century with a large body of observational and experimental evidence demonstrating a variety of effects at ambient concentrations on crop, forest and grassland species and ecosystems. This paper explores the use of experimental data to develop exposure-response relationships for use in risk assessment studies. These studies have typically identified the USA mid-West, much of Europe, the Indo Gangetic Plain in South Asia and the Eastern coastal region of China as global regions where O 3 is likely to threaten food supply and other ecosystems. Global risk assessment modelling estimates yield losses of staple crops between 3 to 16% causing economic losses of between US$14 to 26 billion in the year 2000. Changes in anthropogenic emissions of O 3 precursors in recent decades have modified O 3 concentration profiles (peaks versus background O 3 ) and global distributions with the Northern Hemisphere seeing increases in O 3 levels of between 1 and 5 ppb/decade since the 1950s and the emergence of Asia as the region with the highest O 3 concentrations. In the future, O 3 mitigation could focus on methane (CH 4 ) and nitrogen oxide (NOx) emissions; these will differentially influence global and local/regional O 3 concentrations and influence daily and seasonal profiles. The consequent effects on vegetation will in part depend on how these changes in O 3 profile alter the exceedance of detoxification thresholds for plant damage. Adaptation options may play an important role in enhancing food supply while mitigation strategies are being implemented. An improved understanding of the mechanisms by which O 3 affects plants, and how this might influence detoxification thresholds and interactions with other environmental variables such as water stress and nutrients, would help develop O 3 deposition and impact models to support the development of crop, land-surface exchange and ultimately earth system models for holistic assessments of global change. This article is part of a discussion meeting issue ‘Air quality, past present and future’.