Ambient Air Pollution and Apnea and Bradycardia in High-Risk Infants on Home Monitors

Peel, Jennifer L.; Klein, Mitchel; Flanders, W. Dana; Mulholland, James A.; Freed, Gary; Tolbert, Paige E.

doi:10.1289/ehp.1002739

Cited by 27 publications

(17 citation statements)

References 60 publications

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“…Panel and other epidemiological studies have shown associations between ozone levels and increases in blood pressure and heart rate (Cakmak et al, 2011), changes in the T wave of the ECG (Bhaskaran et al, 2011), increases in ischemic cardiovascular events (Bogdanov and Osterud), bradycardia in high risk infants (Peel et al, 2011), and ventricular tachycardia (Bartell et al, 2013). However, in panel and epidemiology studies where multiple ambient pollutants are involved, it is difficult to disentangle the effects of ozone from other pollutants including PM.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular effects of ozone in healthy subjects with and without deletion of glutathione-S-transferase M1

Frampton¹,

Pietropaoli²,

Dentler³

et al. 2015

Inhalation Toxicology

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Context Exposure to ozone has acute respiratory effects, but few human clinical studies have evaluated cardiovascular effects. Objective We hypothesized that ozone exposure alters pulmonary and systemic vascular function, and cardiac function, with more pronounced effects in subjects with impaired antioxidant defense from deletion of the glutathione S-transferase M1 gene (GSTM1 null). Methods 24 young, healthy never-smoker subjects (12 GSTM1 null) inhaled filtered air, 100 ppb ozone, and 200 ppb ozone for 3 hours, with intermittent exercise, in a double-blind, randomized, crossover fashion. Exposures were separated by at least 2 weeks. Vital signs, spirometry, arterial and venous blood nitrite levels, impedance cardiography, peripheral arterial tonometry, estimation of pulmonary capillary blood volume (Vc), and blood microparticles and platelet activation were measured at baseline and during 4 hours after each exposure. Results Ozone inhalation decreased lung function immediately after exposure (mean±SE change in FEV1, air: −0.03±0.04 L; 200 ppb ozone: −0.30±0.07 L; p<0.001). The immediate post-exposure increase in blood pressure, caused by the final 15-minute exercise period, was blunted by 200 ppb ozone exposure (mean±SE change for air: 16.7±2.6 mm Hg; 100 ppb ozone: 14.5±2.4 mm Hg; 200 ppb ozone: 8.5±2.5 mm Hg; p=0.02). We found no consistent effects of ozone on any other measure of cardiac or vascular function. All results were independent of the GSTM1 genotype. Conclusions We did not find convincing evidence for early acute adverse cardiovascular consequences of ozone exposure in young healthy adults. The ozone-associated blunting of the blood-pressure response to exercise is of unclear clinical significance.

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Section: Discussionmentioning

confidence: 99%

Cardiovascular effects of ozone in healthy subjects with and without deletion of glutathione-S-transferase M1

Frampton¹,

Pietropaoli²,

Dentler³

et al. 2015

Inhalation Toxicology

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“…These short-term average lags for gases seem to be most relevant for other health outcomes. [22][23][24] To investigate confounding by air pollutants, we conducted bivariate analyses using a subset of the data where we had both the relevant data for each pollutant as well as apparent temperature. We evaluated potential effect modification by the same pollutants by adding an interaction term with apparent temperature and each pollutant in separate models.…”

Section: Discussionmentioning

confidence: 99%

“…For all pollutants examined, an average of the same day and previous 2 days were used (lag02). These short‐term average lags for gases seem to be most relevant for other health outcomes . To investigate confounding by air pollutants, we conducted bivariate analyses using a subset of the data where we had both the relevant data for each pollutant as well as apparent temperature.…”

Section: Methodsmentioning

confidence: 99%

A Case‐Crossover Study of Temperature and Infant Mortality in California

Basu

Pearson

Sie

et al. 2015

Paediatric Perinatal Epid

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“…An increase in the maximum ozone level predicted increases in bradycardia and apnea in high-risk infants on home monitors. 12 Controlled human exposure to 1-hour exposures of diesel exhaust did not influence heart rhythm or variability in a UK study. 13 Increased spatial dispersion of myocardial repolarization, but not T-wave alternans, was seen after controlled human exposures to concentrated ambient particles, ozone, or a combination of the 2 exposures.…”

Section: Update 2010 To 2012: Cardiac Arrhythmia Arrhythmia Precursmentioning

confidence: 93%

New Insights Into Pollution and the Cardiovascular System

Gold

Mittleman

2013

Circulation

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Figure.Odds ratio of ischemic stroke onset for US Environmental Protection Agency categories (good and moderate) of mean ambient fine particulate matter air pollution (PM 2.5 ) levels in the 24 hours preceding stroke onset. Error bars indicate 95% confidence interval. Reproduced from Wellenius et al 5 with permission from the publisher. The increased risk was greatest within 12 to 14 hours of exposure. Update, 2010 to 2012: Cardiac Arrhythmia, Arrhythmia Precursors, and PollutionEvidence continues to be mixed for associations between pollution and documented cardiac arrhythmias or electrophysiological changes such as repolarization abnormalities that may increase the risk of arrhythmias. Even more so than studies of stroke, ascertainment of the timing of the onset of the outcome and the specific electrophysiological nature of the outcome can be challenging to ascertain without personal monitoring, which is absent in studies of administrative data sets, which often report null findings. 6 In their recent review, Link and Dockery 7 concluded that "the incremental risk of air pollution in triggering arrhythmias… is greatest for patients with underlying cardiac disease." A London study examined associations of 11 pollutants with activation of implanted cardioverter-defibrillators, finding mostly weak associations with the elevation of a number of secondary regional pollutants, the strongest of which was the nontraffic particle component sulfate. 8 Increases in premature ventricular counts, atrial fibrillation/flutter, and its precedent, P-wave complexity, were associated with increased PM 2.5 in the previous 1 to 2 hours in a Pennsylvania study of 105 middle-aged healthy nonsmokers with 24-hour ECG and personal particle monitoring.9,10 Ghio et al 11 presented a case report of new-onset atrial fibrillation that occurred 20 minutes into a controlled exposure to concentrated ambient particles and resolved within 2 hours with no sequella. In studies of vulnerable populations who have personal electrophysiological monitoring, ozone has also been considered a risk factor for arrhythmias. An increase in the maximum ozone level predicted increases in bradycardia and apnea in high-risk infants on home monitors. 12Controlled human exposure to 1-hour exposures of diesel exhaust did not influence heart rhythm or variability in a UK study.13 Increased spatial dispersion of myocardial repolarization, but not T-wave alternans, was seen after controlled human exposures to concentrated ambient particles, ozone, or a combination of the 2 exposures.14 Increases in long-term estimated residential PM 2.5 predicted increased odds of QT prolongation without overt ventricular abnormalities in the Multi-Ethnic Study of Atherosclerosis (MESA). 15 Two recent studies (the Table) also suggest acute effects of O 3 on repolarization abnormalities in sensitive subjects. 16,17 Update, 2010 to 2012: Cardiovascular Effects of the Coarse (PM 10-2.5 ) or Ultrafine (<0.1 μm) Fractions of PM 10 Findings on cardiovascular health effects of coarse or ultr...

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Ambient Air Pollution and Apnea and Bradycardia in High-Risk Infants on Home Monitors

Cited by 27 publications

References 60 publications

Cardiovascular effects of ozone in healthy subjects with and without deletion of glutathione-S-transferase M1

Cardiovascular effects of ozone in healthy subjects with and without deletion of glutathione-S-transferase M1

A Case‐Crossover Study of Temperature and Infant Mortality in California

New Insights Into Pollution and the Cardiovascular System

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