Oxides of nitrogen (NO
) and volatile organic compounds (VOCs) released into the atmosphere can react in the presence of solar irradiation, leading to ozone formation in the troposphere. ...Historically, before clean air regulations were implemented to control NO
and VOCs, ozone concentrations were high enough to exert acute effects such as eye and nose irritation, respiratory disease emergencies, and lung function impairment. At or above current regulatory standards, day-to-day variations in ozone concentrations have been positively associated with asthma incidence and daily non-accidental mortality rate. Emerging evidence has shown that both short-term and long-term exposures to ozone, at concentrations below the current regulatory standards, were associated with increased mortality due to respiratory and cardiovascular diseases. The pathophysiology to support the epidemiologic associations between mortality and morbidity and ozone centers at the chemical and toxicological property of ozone as a strong oxidant, being able to induce oxidative damages to cells and the lining fluids of the airways, and immune-inflammatory responses within and beyond the lung. These new findings add substantially to the existing challenges in controlling ozone pollution. For example, in the United States in 2016, 90% of non-compliance to the national ambient air quality standards was due to ozone whereas only 10% was due to particulate matter and other regulated pollutants. Climate change, through creating atmospheric conditions favoring ozone formation, has been and will continue to increase ozone concentrations in many parts of world. Worldwide, ozone is responsible for several hundreds of thousands of premature deaths and tens of millions of asthma-related emergency room visits annually. To combat ozone pollution globally, more aggressive reductions in fossil fuel consumption are needed to cut NO
and VOCs as well as greenhouse gas emissions. Meanwhile, preventive and therapeutic strategies are needed to alleviate the detrimental effects of ozone especially in more susceptible individuals. Interventional trials in humans are needed to evaluate the efficacy of antioxidants and ozone-scavenging compounds that have shown promising results in animal studies.
Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), ...whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD. We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults.
In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers. Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases. All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study. Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park). Baseline measurements of participants were taken before the walk in the hospital laboratory. During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured.
Between October, 2012, and June, 2014, we screened 135 participants, of whom 40 healthy volunteers, 40 individuals with COPD, and 39 with ischaemic heart disease were recruited. Concentrations of black carbon, NO2, PM10, PM2.5, and ultrafine particles were higher on Oxford Street than in Hyde Park. Participants with COPD reported more cough (odds ratio OR 1·95, 95% CI 0·96–3·95; p<0·1), sputum (3·15, 1·39–7·13; p<0·05), shortness of breath (1·86, 0·97–3·57; p<0·1), and wheeze (4·00, 1·52–10·50; p<0·05) after walking down Oxford Street compared with Hyde Park. In all participants, irrespective of their disease status, walking in Hyde Park led to an increase in lung function (forced expiratory volume in the first second FEV1 and forced vital capacity FVC) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk. By contrast, these beneficial responses were attenuated after walking on Oxford Street. In participants with COPD, a reduction in FEV1 and FVC, and an increase in R5–20 were associated with an increase in during-walk exposure to NO2, ultrafine particles and PM2.5, and an increase in PWV and augmentation index with NO2 and ultrafine particles. In healthy volunteers, PWV and augmentation index were associated both with black carbon and ultrafine particles.
Short-term exposure to traffic pollution prevents the beneficial cardiopulmonary effects of walking in people with COPD, ischaemic heart disease, and those free from chronic cardiopulmonary diseases. Medication use might reduce the adverse effects of air pollution in individuals with ischaemic heart disease. Policies should aim to control ambient levels of air pollution along busy streets in view of these negative health effects.
British Heart Foundation.
CONTEXT Air pollution is a risk factor for cardiovascular diseases (CVD), but the underlying biological mechanisms are not well understood. OBJECTIVE To determine whether markers related to CVD ...pathophysiological pathways (biomarkers for systemic inflammation and thrombosis, heart rate, and blood pressure) are sensitive to changes in air pollution. DESIGN, SETTING, AND PARTICIPANTS Using a quasi-experimental opportunity offered by greatly restricted air pollution emissions during the Beijing Olympics, we measured pollutants daily and the outcomes listed below in 125 healthy young adults before, during, and after the 2008 Olympics (June 2-October 30). We used linear mixed-effects models to estimate the improvement in outcome levels during the Olympics and the anticipated reversal of outcome levels after pollution controls ended to determine whether changes in outcome levels were associated with changes in pollutant concentrations. MAIN OUTCOME MEASURES C-reactive protein (CRP), fibrinogen, von Willebrand factor, soluble CD40 ligand (sCD40L), soluble P-selectin (sCD62P) concentrations; white blood cell count (WBC); heart rate; and blood pressure. RESULTS Concentrations of particulate and gaseous pollutants decreased substantially (−13% to −60%) from the pre-Olympic period to the during-Olympic period. Using 2-sided tests conducted at the .003 level, we observed statistically significant improvements in sCD62P levels by −34.0% (95% CI, −38.4% to −29.2%; P < .001) from a pre-Olympic mean of 6.29 ng/mL to a during-Olympic mean of 4.16 ng/mL and von Willebrand factor by −13.1% (95% CI, −18.6% to −7.5%; P < .001) from 106.4% to 92.6%. After adjustments for multiple comparisons, changes in the other outcomes were not statistically significant. In the post-Olympic period when pollutant concentrations increased, most outcomes approximated pre-Olympic levels, but only sCD62P and systolic blood pressure were significantly worsened from the during-Olympic period. The fraction of above-detection-limit values for CRP (percentage ≥ 0.3 mg/L) was reduced from 55% in the pre-Olympic period to 46% in the during-Olympic period and reduced further to 36% in the post-Olympic period. Interquartile range increases in pollutant concentrations were consistently associated with statistically significant increases in fibrinogen, von Willebrand factor, heart rate, sCD62P, and sCD40L concentrations. CONCLUSIONS Changes in air pollution levels during the Beijing Olympics were associated with acute changes in biomarkers of inflammation and thrombosis and measures of cardiovascular physiology in healthy young persons. These findings are of uncertain clinical significance.
This paper reviews China’s achievements in energy efficiency improvements and air emissions reductions from the electric power sector during the 11th five-year plan (FYP) (2006–2010) and 12th FYP ...(2011–2015) periods, and discusses the remaining challenges and opportunities for policy formulation. Mandates for closure of small coal-fired power plants (CFPPs), and replacement with large ones, together with the promulgation of air emissions standards and the development of renewable energy projects, have resulted in an improvement of 15% in energy efficiency and a reduction of 91%, 89% and 96% in emission rates of SO2, NOx and PM from China’s electric power sector over the last decade. Compared to the United States, the Chinese electric power generation fleet is more energy efficient and has lower average emissions rates of SO2 and NOx. Despite these achievements, two characteristics of the current system pose serious challenges for China’s clean power development: a) two thirds of China’s power generation still rely on coal, and more CFPPs are being built and approved to be built; and b) high curtailment of renewable energy limits its benefits. We review the root causes of these challenges and highlight opportunities for enacting policies to address them.
•Last decade witnessed tremendous energy efficiency improvement and air emissions reduction.•Last decade’s efforts saved 230 Mt of coal and reduced 9.9 Mt, 9.0 Mt, 2.2 Mt of SO2, NOx, PM emissions.•Chinese power generators have better energy efficiency and environmental performance than in the U.S.•Large coal-fired power generation capacity and high curtailment of renewable are greatest challenges.•Economic, political and infrastructure barriers towards China’s clean power development are discussed.
It has been widely accepted that the induction of reactive oxygen species (ROS) is an important pathophysiologic pathway linking particulate matter (PM) exposure and adverse health effects. ROS can ...be either present on and/or within PM or generated in vivo by the interactions between PM and biological systems. Within the context of toxicology, PM oxidative potential (OP) is the capacity of PM to oxidize molecules in biological tissues or cells directly by oxidants that are present on and/or within PM and indirectly by the ROS generated via PM interactions with the biological system (e.g., fluids, cells, and tissues). In this review, we summarized the current PM OP measurement methods, current understanding of how PM physical characteristics and chemical compositions affect OP, and the epidemiological and toxicological evidence on whether PM OP is a better indicator than PM mass concentration for health effects. Among the two major types of OP measurement methods, cellular assays have been regarded to better reflect the actions of PM in a biological system than acellular assays. Recent epidemiological studies have associated short-term PM OP exposure with adverse cardiorespiratory health outcomes. Little is known about the health effects of long-term PM OP exposure and on the effect beyond the cardiovascular and respiratory systems. The existing evidence may be sufficient to suggest the use of PM OP as a more health-relevant exposure metric than conventional PM mass concentration, but critical methodologic issues must be resolved before this metric can be widely and accurately used.
Mitochondrial damage leading to oxidant stress may play an important role in the pathogenesis of airflow obstruction and emphysema. NLPR3 inflammasome can be activated by mitochondrial ROS (mtROS) ...and other stimuli. We examined the importance of mtROS and NLRP3 inflammasome and their interactions in multiple ozone-induced lung inflammation and emphysema.
C57/BL6 mice were exposed to ozone (2.5 ppm, 3 h) or filtered air twice a week over 6 weeks. MitoTEMPO (20 mg/kg), an inhibitor of mtROS, and VX765 (100 mg/kg), an inhibitor of caspase-1 activity, were administered by intraperitoneal or intragastric injection respectively 1 h prior to each ozone exposure for 6 weeks.
Ozone-exposed mice had increased bronchoalveolar lavage (BAL) total cells and levels of IL-1β, KC and IL-6, augmented lung tissue inflammation scores, enhanced oxidative stress with higher serum 8-OHdG concentrations, emphysema with greater mean linear intercept (Lm), airway remodeling with increased airway smooth muscle mass and airflow limitation as indicated by a reduction in the ratio of forced expiratory volume at 25 and 50 milliseconds to forced vital capacity (FEV
/FVC, FEV
/FVC). Both MitoTEMPO and VX765 reduced lung inflammation scores, cytokine levels, oxidative stress and increased mitochondrial fission proteins. VX765 also attenuated emphysema, airway remodeling and airflow limitation. MitoTEMPO inhibited the increased expression of mitochondrial complex II and IV and of NLPR3 while VX765 inhibited the expression and activity of NLRP3 and caspase-1 pathway in the lung.
Both mtROS and NLRP3 inflammasome play a role in ozone-induced lung inflammation while only NLRP3 is involved in ozone-induced emphysema.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
•Economic losses of indoor exposure to outdoor-infiltrated PM2.5 were evaluated.•The health/economic impacts of implementing daily indoor PM2.5 limits were assessed.•Enormous deaths and losses could ...be avoided by meeting suitable indoor PM2.5 limits.•The study provides quantitative evidence to support the completion of an IAQ policy.
Given a large fraction of people’s exposure to urban PM2.5 occur indoors, reducing indoor PM2.5 levels may offer a more feasible and immediate way to save substantial lives and economic losses attributable to PM2.5 exposure. We aimed to estimate the premature mortality and economic loss reductions associated with achieving the newly established Chinese indoor air guideline and a few hypothetical indoor PM2.5 guideline values. We used outdoor PM2.5 concentrations from 1497 monitoring sites in 339 Chinese cities in 2015, coupled with a steady-state mass balance model, to estimate indoor concentrations of outdoor-infiltrated PM2.5. Using province-specific time-activity patterns for urban residents, we estimated outdoor and indoor exposures to PM2.5 of outdoor origin. We then proceeded to use localized census-based concentration-response models and the value of statistical life estimates to calculate premature deaths and economic losses attributable to PM2.5 exposure across urban China. Finally, we estimated potentially avoidable mortality and corresponding economic losses by meeting the current 24-hour based guideline and various hypothetical indoor limits for PM2.5. In 2015 in urban areas of mainland China, the city-specific annual mean outdoor and indoor PM2.5 concentrations ranged 9–108 μg/m3 and 5–56 μg/m3, respectively. Indoor exposures contributed 62%–91% daily and 68%–83% annually to the total time-weighted exposures. The potential reductions in total deaths and economic losses for the scenario in which daily indoor concentrations met the current guideline of 75 μg/m3, 37.5 μg/m3, and 25 μg/m3 were 16.9 (95% CI: 0.7–62.1) thousand, 87.7 (95% CI: 9.7–197.7) thousand, and 165.5 (95% CI: 30.8–304.0) thousand, respectively. The corresponding reductions in economic losses were 5.7 (95% CI: 0.2–34.8) billion, 29.4 (95% CI: 2.4–109.6) billion, and 55.2 (95% CI: 7.7–168.0) billion US Dollars, respectively. Deaths and economic losses would be reduced exponentially within the range of 0–75 μg/m3 for hypothetical indoor PM2.5 limits. The findings demonstrate the effectiveness of reducing indoor concentrations of outdoor-originated PM2.5 in saving substantial lives and economic losses in China. The analysis provides quantitative evidence to support the implementation of an indoor air quality guideline or standard for PM2.5.
Dietary intake is one of the major exposure pathways of polycyclic aromatic hydrocarbons (PAHs), especially in Chinese people because foods are often prepared with grilling and/or frying that would ...produce high levels of PAHs. In this paper, we assessed daily dietary intakes (DDI) of PAHs, using a “duplicate plate method”, among 100 Chinese urban residents. The DDI of benzo(a)pyrene ranged from 0.06 µg per day to 13.5 µg per day with a median of 0.69 µg per day, varying largely across subjects. The median Incremental Lifetime Cancer Risk (ILCR) attributable to PAH dietary intake was 6.65 × 10−5 (4.41 × 10−5 to 1.02 × 10−4 as inter-quartile range). The contribution of several high-PAH containing foods like barbecued, smoked or deep-fried meats to the overall DDIs was about 13%. The use of raw foods may underestimate dietary intake of PAHs and associated exposure risk considerably. Results from foods sampled in different seasons suggested that seasonal variability within an individual may contribute notably to overall variability measured in a population and more future studies with longer-term investigation on food ingestion and pollutant exposure are needed. The study indicates that measuring actually consumed foods is more appropriate for dietary intake exposure assessment, and intra-individual variance should be taken into account during study design and data analysis.
•Duplicated plate method to estimate dietary intake exposure of priority PAHs.•Serious ingestion exposure risk associated with cooked food intake among Chinese residents.•Use of raw foods underestimates dietary intake dose and consequent exposure risk.•Within-subject variation contributes notably to the overall variation in dietary intake.•Risk due to dietary PAH intake is comparable to that from the inhalation exposure.
ABSTRACT
Epidemiologic evidence suggests that air pollution is a risk factor for childhood obesity. Limited experimental data have shown that early‐life exposure to ambient particles either increases ...susceptibility to diet‐induced weight gain in adulthood or increases insulin resistance, adiposity, and inflammation. However, no data have directly supported a link between air pollution and non‐diet‐induced weight increases. In a rodent model, we found that breathing Beijing's highly polluted air resulted in weight gain and cardiorespiratory and metabolic dysfunction. Compared to those exposed to filtered air, pregnant rats exposed to unfiltered Beijing air were significantly heavier at the end of pregnancy. At 8 wk old, the offspring prenatally and postnatally exposed to unfiltered air were significantly heavier than those exposed to filtered air. In both rat dams and their offspring, after continuous exposure to unfiltered air we observed pronounced histologic evidence for both perivascular and peribronchial inflammation in the lungs, increased tissue and systemic oxidative stress, dyslipidemia, and an enhanced proinflammatory status of epididymal fat. Results suggest that TLR2/4‐dependent inflammatory activation and lipid oxidation in the lung can spill over systemically, leading to metabolic dysfunction and weight gain.—Wei, Y., Zhang, J., Li, Z., Gow, A., Chung, K. F., Hu, M., Sun, Z., Zeng, L., Zhu, T., Jia, G., Li, X., Duarte, M., Tang, X. Chronic exposure to air pollution particles increases the risk of obesity and metabolic syndrome: findings from a natural experiment in Beijing. FASEB J. 30, 2115–2122 (2016). www.fasebj.org
Negative ion air purifiers (NIAPs), as a less costly alternative to the HEPA filtration, have been increasingly deployed in China and potentially elsewhere. While reducing indoor concentrations of ...fine particulate matter (PM2.5), NIAPs generate massive amounts of negative ions that may be of health concern. We performed week‐long interventions with NIAPs in the dormitories of 56 healthy college students living in Beijing. In a randomized order, each student underwent a true and a sham NIAP session. Cardiorespiratory outcomes were measured before and after each session. The use of true NIAPs reduced indoor PM2.5 concentrations significantly, while notably increased negative ion levels. Increases in PM2.5 and negative ion (NI) exposure were independently associated with increased urinary concentration of malondialdehyde, a biomarker of systemic oxidative stress, resulting in a null net effect of NIAP on malondialdehyde. Likewise, no significant net effects of NIAPs were observed for other outcomes indicative of lung function, vascular tone, arterial stiffness, and inflammation. Our findings suggest that negative ions, possibly along with their reaction products with the room air constituents, adversely affect health. The downsides do not support the use of NIAPs as a health‐based mitigation strategy to reduce PM2.5 exposure, especially in residences with PM2.5 concentrations that are not extremely high.
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