Cardiovascular Effects of Ozone Exposure in Human Volunteers

Gong, Henry; Wong, Richard G.; Sarma, Radha J.; Linn, William S.; Sullivan, Emmett D.; Shamoo, Deborah A.; Anderson, Karen R.; Prasad, Shankar B.

doi:10.1164/ajrccm.158.2.9709034

Cited by 66 publications

(24 citation statements)

References 33 publications

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“…In the effects seen in animal toxicology studies after human ozone exposure, as well, researchers have found a reduction in serum tocopherol (free radical scavenger), 35 an increase in the gradient of alveolar-to-arterial Po 2 potentially due to alveolar-arterial oxygen impairment, 36 and, most recently, changes in several proinflammatory cytokines in blood. 12 The lack of investigation of the association between ozone and OHCA may stem from practical considerations such as data limitations.…”

Section: Association Between Ozone and Ohcamentioning

confidence: 99%

A Case-Crossover Analysis of Out-of-Hospital Cardiac Arrest and Air Pollution

2013

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Background— Evidence of an association between the exposure to air pollution and overall cardiovascular morbidity and mortality is increasingly found in the literature. However, results from studies of the association between acute air pollution exposure and risk of out-of-hospital cardiac arrest (OHCA) are inconsistent for fine particulate matter, and, although pathophysiological evidence indicates a plausible link between OHCA and ozone, none has been reported. Approximately 300 000 persons in the United States experience an OHCA each year, of which >90% die. Understanding the association provides important information to protect public health. Methods and Results— The association between OHCA and air pollution concentrations hours and days before onset was assessed by using a time-stratified case-crossover design using 11 677 emergency medical service–logged OHCA events between 2004 and 2011 in Houston, Texas. Air pollution concentrations were obtained from an extensive area monitor network. An average increase of 6 µg/m 3 in fine particulate matter 2 days before onset was associated with an increased risk of OHCA (1.046; 95% confidence interval, 1.012–1.082). A 20-ppb ozone increase for the 8-hour average daily maximum was associated with an increased risk of OHCA on the day of the event (1.039; 95% confidence interval, 1.005–1.073). Each 20-ppb increase in ozone in the previous 1 to 3 hours was associated with an increased risk of OHCA (1.044; 95% confidence interval, 1.004–1.085). Relative risk estimates were higher for men, blacks, or those aged >65 years. Conclusions— The findings confirm the link between OHCA and fine particulate matter and introduce evidence of a similar link with ozone.

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Section: Association Between Ozone and Ohcamentioning

confidence: 99%

A Case-Crossover Analysis of Out-of-Hospital Cardiac Arrest and Air Pollution

2013

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“…86 Clearly, individual gases affect cardiovascular tissues differently. Ozone exposure impairs pulmonary gas exchange and increases myocardial work, 87 whereas SO 2 exposure reduces cardiac vagal control that could contribute to increased susceptibility to ventricular arrhythmias. 88 In contrast, acute cardiovascular effects of CO are mild and, at concentrations present in cigarette smoke, do not acutely affect cardiac function.…”

Section: Gaseous Copollutantsmentioning

confidence: 99%

Environmental Cardiology

Bhatnagar

2006

Circulation Research

367

129

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Abstract-Environmental factors are considered key determinants of cardiovascular disease. Although lifestyle choices such as smoking, diet, and exercise are viewed as major environmental influences, the contribution of pollutants and environmental chemicals is less clear. Accumulating evidence suggests that exposure to pollutants and chemicals could elevate the risk of cardiovascular disease. Many epidemiological studies report that exposure to fine particles present in ambient air is associated with an increase in cardiovascular mortality. Statistically significant relationships between particulate air pollution and ischemic heart disease, arrhythmias, and heart failure have been reported. Animal studies show that exposure to ambient air particles increases peripheral thrombosis and atherosclerotic lesion formation. Exposures to arsenic, lead, cadmium, pollutant gases, solvents, and pesticides have also been linked to increased incidence of cardiovascular disease. Mechanistically, these effects have been attributed to changes in the synthesis or reactivity of nitric oxide that may be caused by environmental oxidants or increased endogenous production of reactive oxygen species. Additional studies are urgently needed to: identify the contribution of individual pollutants to specific aspects of cardiovascular disease; establish causality; elucidate the underlying physiological and molecular mechanisms; estimate the relative susceptibility of diseased and healthy individuals and that of specific population groups; and determine whether pollutant exposure are risk correlates, that is, whether they influence major risk factors, such as hypertension, cholesterol, or diabetes, or whether they contribute to the absolute risk of heart disease. Collectively, these investigations could contribute to the emergent field of environmental cardiology.

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“…Foster et al 11 found a reduction in serum levels of the free radical scavenger ␣-tocopherol after ozone exposure, and Gong et al 12 observed an increase in alveolar-to-arterial PO 2 gradient that could be due to impaired alveolar-arterial oxygen transfer. Some animal toxicology studies have reported increased systolic blood pressure and heart rate, 13 which are thought to be related to a drop in core temperature in rats exposed to ozone.…”

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confidence: 99%

Controlled Exposure of Healthy Young Volunteers to Ozone Causes Cardiovascular Effects

et al. 2012

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Background— Recent epidemiology studies have reported associations between short-term ozone exposure and mortality. Such studies have previously reported associations between airborne particulate matter pollution and mortality, and support for a causal relationship has come from controlled-exposure studies that describe pathophysiological mechanisms by which particulate matter could induce acute mortality. In contrast, for ozone, almost no controlled-human-exposure studies have tested whether ozone exposure can modulate the cardiovascular system. Methods and Results— Twenty-three young healthy individuals were exposed in a randomized crossover fashion to clean air and to 0.3-ppm ozone for 2 hours while intermittently exercising. Blood was obtained immediately before exposure, immediately afterward, and the next morning. Continuous Holter monitoring began immediately before exposure and continued for 24 hours. Lung function was performed immediately before and immediately after exposure, and bronchoalveolar lavage was performed 24 hours after exposure. Immediately after ozone exposure, we observed a 98.9% increase in interleukin-8, a 21.4% decrease in plasminogen activator inhibitor-1, a 51.3% decrease in the high-frequency component of heart rate variability, and a 1.2% increase in QT duration. Changes in interleukin-1B and plasminogen activator inhibitor-1 were apparent 24 hours after exposure. In agreement with previous studies, we also observed ozone-induced drops in lung function and an increase in pulmonary inflammation. Conclusions— This controlled-human-exposure study shows that ozone can cause an increase in vascular markers of inflammation and changes in markers of fibrinolysis and markers that affect autonomic control of heart rate and repolarization. We believe that these findings provide biological plausibility for the epidemiology studies that associate ozone exposure with mortality. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01492517.

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Cardiovascular Effects of Ozone Exposure in Human Volunteers

Cited by 66 publications

References 33 publications

A Case-Crossover Analysis of Out-of-Hospital Cardiac Arrest and Air Pollution

A Case-Crossover Analysis of Out-of-Hospital Cardiac Arrest and Air Pollution

Environmental Cardiology

Controlled Exposure of Healthy Young Volunteers to Ozone Causes Cardiovascular Effects

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