Association of Ozone Exposure With Cardiorespiratory Pathophysiologic Mechanisms in Healthy Adults.
TL;DR: Short-term ozone exposure at levels not associated with lung function changes was associated with platelet activation and blood pressure increases, suggesting a possible mechanism by which ozone may affect cardiovascular health.
Abstract: Importance Exposure to ozone has been associated with cardiovascular mortality, but the underlying biological mechanisms are not yet understood. Objective To examine the association between ozone exposure and cardiopulmonary pathophysiologic mechanisms. Design, Setting, and Participants A longitudinal study involving 89 healthy adult participants living on a work campus in Changsha City, China, was conducted from December 1, 2014, to January 31, 2015. This unique quasiexperimental setting allowed for better characterization of air pollutant exposure effects because the participants spent most of their time in controlled indoor environments. Concentrations of indoor and outdoor ozone, along with the copollutants particulate matter, nitrogen dioxide, and sulfur dioxide, were monitored throughout the study period and then combined with time-activity information and filtration conditions of each residence and office to estimate 24-hour and 2-week combined indoor and outdoor mean exposure concentrations. Associations between each exposure measure and outcome measure were analyzed using single-pollutant and 2-pollutant linear mixed models controlling for ambient temperature, secondhand smoke exposure, and personal-level time-varying covariates. Main Outcomes and Measures Biomarkers indicative of inflammation and oxidative stress, arterial stiffness, blood pressure, thrombotic factors, and spirometry were measured at 4 sessions. Results Of the 89 participants, 25 (28%) were women and the mean (SD) age was 31.5 (7.6) years. The 24-hour ozone exposure concentrations ranged from 1.4 to 19.4 parts per billion (ppb), corresponding to outdoor concentrations ranging from 4.3 to 47.9 ppb. Within this range, in models controlling for a second copollutant and other potential confounders, a 10-ppb increase in 24-hour ozone was associated with mean increases of 36.3% (95% CI, 29.9%-43.0%) in the level of platelet activation marker soluble P-selectin, 2.8% (95% CI, 0.6%-5.1%) in diastolic blood pressure, 18.1% (95% CI, 4.5%-33.5%) in pulmonary inflammation markers fractional exhaled nitric oxide, and 31.0% (95% CI, 0.2%-71.1%) in exhaled breath condensate nitrite and nitrate as well as a −9.5% (95% CI, −17.7% to −1.4%) decrease in arterial stiffness marker augmentation index. A 10-ppb increase in 2-week ozone was associated with increases of 61.1% (95% CI, 37.8%-88.2%) in soluble P-selectin level and 126.2% (95% CI, 12.1%-356.2%) in exhaled breath condensate nitrite and nitrate level. Other measured biomarkers, including spirometry, showed no significant associations with either 24-hour ozone or 2-week ozone exposures. Conclusions and Relevance Short-term ozone exposure at levels not associated with lung function changes was associated with platelet activation and blood pressure increases, suggesting a possible mechanism by which ozone may affect cardiovascular health.
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TL;DR: 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.
Abstract: Oxides of nitrogen (NOx) 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 NOx 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 NOx 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.
280 citations
Cites background from "Association of Ozone Exposure With ..."
...found that an increase in 24-h or 2-week average exposure to ozone was associated with increased p-selectin (a soluble plasma marker of platelet activation), suggesting that ozone exposure increases the risk of thrombosis (21)....
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TL;DR: The human health benefits of increasing 21st-century CO2 reductions by 180 GtC are examined, an amount that would shift a ‘standard’ 2 °C scenario to 1.5°C or could achieve 2C without negative emissions, which is shown to result in approximately 150 million fewer premature deaths worldwide.
Abstract: Societal risks increase as Earth warms, and increase further for emissions trajectories accepting relatively high levels of near-term emissions while assuming future negative emissions will compensate, even if they lead to identical warming as trajectories with reduced near-term emissions
1
. Accelerating carbon dioxide (CO2) emissions reductions, including as a substitute for negative emissions, hence reduces long-term risks but requires dramatic near-term societal transformations
2
. A major barrier to emissions reductions is the difficulty of reconciling immediate, localized costs with global, long-term benefits3,4. However, 2 °C trajectories not relying on negative emissions or 1.5 °C trajectories require elimination of most fossil-fuel-related emissions. This generally reduces co-emissions that cause ambient air pollution, resulting in near-term, localized health benefits. We therefore examine the human health benefits of increasing 21st-century CO2 reductions by 180 GtC, an amount that would shift a ‘standard’ 2 °C scenario to 1.5 °C or could achieve 2 °C without negative emissions. The decreased air pollution leads to 153 ± 43 million fewer premature deaths worldwide, with ~40% occurring during the next 40 years, and minimal climate disbenefits. More than a million premature deaths would be prevented in many metropolitan areas in Asia and Africa, and >200,000 in individual urban areas on every inhabited continent except Australia. Emission mitigation is required to achieve global climate ambitions but can also offer local benefits. Reduction in air pollution because of low-carbon emission trajectories is shown to result in approximately 150 million fewer premature deaths worldwide.
118 citations
University of London1, Oeschger Centre for Climate Change Research2, University of Bern3, Fudan University4, Monash University5, Shanghai Jiao Tong University6, Queensland University of Technology7, Anhui Medical University8, Health Canada9, University of Ottawa10, Academy of Sciences of the Czech Republic11, Czech University of Life Sciences Prague12, University of Tartu13, Potsdam Institute for Climate Impact Research14, Pablo de Olavide University15, National and Kapodistrian University of Athens16, King's College London17, University of Tokyo18, University of Tsukuba19, Nagasaki University20, Instituto Nacional de Saúde Dr. Ricardo Jorge21, University of Porto22, Emory University23, Council for Scientific and Industrial Research24, University of Pretoria25, North-West University26, Seoul National University27, University of Valencia28, Umeå University29, Swiss Tropical and Public Health Institute30, University of Basel31, National Taiwan University32, Harvard University33, Yale University34
TL;DR: Results suggest that ozone related mortality could be potentially reduced under stricter air quality standards, and have relevance for the implementation of efficient clean air interventions and mitigation strategies designed within national and international climate policies.
Abstract: OBJECTIVE: To assess short term mortality risks and excess mortality associated with exposure to ozone in several cities worldwide.DESIGN: Two stage time series analysis.SETTING: 406 cities in 20 c ...
114 citations
TL;DR: It is found that long-term exposure to O3 is associated with increased risk for multiple causes of mortality, suggesting that establishment of annual and/or seasonal federal O3 standard(s) are needed to more adequately protect public health from ambient O3 exposures.
Abstract: Rationale: Many studies have linked short-term exposure to ozone (O3) with morbidity and mortality, but epidemiologic evidence of associations between long-term O3 exposure and mortality is more li...
95 citations
Cites background from "Association of Ozone Exposure With ..."
...A study of 89 healthy adults in China found that short-term ozone exposure was associated with platelet activation and increased blood pressure (36)....
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TL;DR: This study estimates adult mortalities attributed to PM2.5 across urban China in 2015 and the corresponding mortalities that might be avoided by meeting the yearly averaged indoor PM 2.5 threshold in the newly established Assessment Standard for Healthy Building (ASHB) and seven other potential thresholds.
Abstract: This study estimates adult mortalities attributed to PM2.5 across urban China in 2015 and the corresponding mortalities that might be avoided by meeting the yearly averaged indoor PM2.5 threshold i...
82 citations
References
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TL;DR: In this paper, it was shown that a simple FDR controlling procedure for independent test statistics can also control the false discovery rate when test statistics have positive regression dependency on each of the test statistics corresponding to the true null hypotheses.
Abstract: Benjamini and Hochberg suggest that the false discovery rate may be the appropriate error rate to control in many applied multiple testing problems. A simple procedure was given there as an FDR controlling procedure for independent test statistics and was shown to be much more powerful than comparable procedures which control the traditional familywise error rate. We prove that this same procedure also controls the false discovery rate when the test statistics have positive regression dependency on each of the test statistics corresponding to the true null hypotheses. This condition for positive dependency is general enough to cover many problems of practical interest, including the comparisons of many treatments with a single control, multivariate normal test statistics with positive correlation matrix and multivariate $t$. Furthermore, the test statistics may be discrete, and the tested hypotheses composite without posing special difficulties. For all other forms of dependency, a simple conservative modification of the procedure controls the false discovery rate. Thus the range of problems for which a procedure with proven FDR control can be offered is greatly increased.
9,335 citations
TL;DR: Fine particulate and sulfur oxide--related pollution were associated with all-cause, lung cancer, and cardiopulmonary mortality and long-term exposure to combustion-related fine particulate air pollution is an important environmental risk factor for cardiopULmonary and lung cancer mortality.
Abstract: ContextAssociations have been found between day-to-day particulate air pollution
and increased risk of various adverse health outcomes, including cardiopulmonary
mortality. However, studies of health effects of long-term particulate air
pollution have been less conclusive.ObjectiveTo assess the relationship between long-term exposure to fine particulate
air pollution and all-cause, lung cancer, and cardiopulmonary mortality.Design, Setting, and ParticipantsVital status and cause of death data were collected by the American
Cancer Society as part of the Cancer Prevention II study, an ongoing prospective
mortality study, which enrolled approximately 1.2 million adults in 1982.
Participants completed a questionnaire detailing individual risk factor data
(age, sex, race, weight, height, smoking history, education, marital status,
diet, alcohol consumption, and occupational exposures). The risk factor data
for approximately 500 000 adults were linked with air pollution data
for metropolitan areas throughout the United States and combined with vital
status and cause of death data through December 31, 1998.Main Outcome MeasureAll-cause, lung cancer, and cardiopulmonary mortality.ResultsFine particulate and sulfur oxide–related pollution were associated
with all-cause, lung cancer, and cardiopulmonary mortality. Each 10-µg/m3 elevation in fine particulate air pollution was associated with approximately
a 4%, 6%, and 8% increased risk of all-cause, cardiopulmonary, and lung cancer
mortality, respectively. Measures of coarse particle fraction and total suspended
particles were not consistently associated with mortality.ConclusionLong-term exposure to combustion-related fine particulate air pollution
is an important environmental risk factor for cardiopulmonary and lung cancer
mortality.
7,803 citations
TL;DR: This paper summarizes the proceedings of several meetings of the European Network for Non-invasive Investigation of Large Arteries and is aimed at providing an updated and practical overview of the most relevant methodological aspects and clinical applications in this area.
Abstract: In recent years, great emphasis has been placed on the role of arterial stiffness in the development of cardiovascular diseases. Indeed, the assessment of arterial stiffness is increasingly used in the clinical assessment of patients. Although several papers have previously addressed the methodological issues concerning the various indices of arterial stiffness currently available, and their clinical applications, clinicians and researchers still report difficulties in selecting the most appropriate methodology for their specific use. This paper summarizes the proceedings of several meetings of the European Network for Non-invasive Investigation of Large Arteries and is aimed at providing an updated and practical overview of the most relevant methodological aspects and clinical applications in this area.
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Journal Article•
TL;DR: In this paper, the authors summarized the proceedings of several meetings of the European Network for Non-invasive Investigation of Large Arteries and aimed at providing an updated and practical overview of the most relevant methodological aspects and clinical applications in this area.
Abstract: In recent years, great emphasis has been placed on the role of arterial stiffness in the development of cardiovascular diseases. Indeed, the assessment of arterial stiffness is increasingly used in the clinical assessment of patients. Although several papers have previously addressed the methodological issues concerning the various indices of arterial stiffness currently available, and their clinical applications, clinicians and researchers still report difficulties in selecting the most appropriate methodology for their specific use. This paper summarizes the proceedings of several meetings of the European Network for Non-invasive Investigation of Large Arteries and is aimed at providing an updated and practical overview of the most relevant methodological aspects and clinical applications in this area.
4,410 citations
TL;DR: The addition of CRP to standard cholesterol evaluation may provide a simple and inexpensive method to improve global risk prediction and compliance with preventive approaches.
Abstract: In an attempt to improve global cardiovascular risk prediction, considerable interest has focused on C-reactive protein (CRP), a marker of inflammation that has been shown in multiple prospective epidemiological studies to predict incident myocardial infarction, stroke, peripheral arterial disease, and sudden cardiac death. CRP levels have also been shown to predict risk of both recurrent ischemia and death among those with stable and unstable angina, those undergoing percutaneous angioplasty, and those presenting to emergency rooms with acute coronary syndromes. These highly consistent clinical data are supported by abundant laboratory and experimental evidence that demonstrate that atherothrombosis, in addition to being a disease of lipid accumulation, also represents a chronic inflammatory process. In terms of clinical application, CRP seems to be a stronger predictor of cardiovascular events than LDL cholesterol, and it adds prognostic information at all levels of calculated Framingham Risk and at all levels of the metabolic syndrome. Using widely available high-sensitivity assays, CRP levels of 3 mg/L correspond to low-, moderate-, and high-risk groups for future cardiovascular events. Individuals with LDL cholesterol below 130 mg/dL who have CRP levels >3 mg/L represent a high-risk group often missed in clinical practice. The addition of CRP to standard cholesterol evaluation may thus provide a simple and inexpensive method to improve global risk prediction and compliance with preventive approaches.
Composed of five 23 kDa subunits, C-reactive protein (CRP) is an hepatically derived pentraxin that plays a key role in the innate immune response. CRP has a long plasma half-life and is now understood to be a mediator as well as a marker of atherothrombotic disease. To date, over a dozen prospective epidemiological studies carried out among individuals with no prior history of cardiovascular disease demonstrate that a single, non-fasting measure of CRP is a strong predictor …
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