A peer-reviewed open access journal published by the National Institute of Environmental Health Sciences

Background Wildfire smoke is known to exacerbate respiratory conditions; however, evidence for cardiovascular and cerebrovascular events has been inconsistent, despite biological plausibility. Methods and Results A population‐based epidemiologic analysis was conducted for daily cardiovascular and cerebrovascular emergency department (ED) visits and wildfire smoke exposure in 2015 among adults in 8 California air basins. A quasi‐Poisson regression model was used for zip code‐level counts of ED visits, adjusting for heat index, day of week, seasonality, and population. Satellite‐imaged smoke plumes were classified as light, medium, or dense based on model‐estimated concentrations of fine particulate matter. Relative risk was determined for smoky days for lag days 0 to 4. Rates of ED visits by age‐ and sex‐stratified groups were also examined. Rates of all‐cause cardiovascular ED visits were elevated across all lags, with the greatest increase on dense smoke days and among those aged ≥65 years at lag 0 (relative risk 1.15, 95% confidence interval [1.09, 1.22]). All‐cause cerebrovascular visits were associated with smoke, especially among those 65 years and older, (1.22 [1.00, 1.49], dense smoke, lag 1). Respiratory conditions were also increased, as anticipated (1.18 [1.08, 1.28], adults >65 years, dense smoke, lag 1). No association was found for the control condition, acute appendicitis. Elevated risks for individual diagnoses included myocardial infarction, ischemic heart disease, heart failure, dysrhythmia, pulmonary embolism, ischemic stroke, and transient ischemic attack. Conclusions Analysis of an extensive wildfire season found smoke exposure to be associated with cardiovascular and cerebrovascular ED visits for all adults, particularly for those over aged 65 years.

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.

Rationale: Exposure to ozone causes a decrease in spirometric lung function and an increase in airway inflammation in healthy young adults at concentrations as low as 0.08 ppm, close to the National Ambient Air Quality Standard for ground level ozone. Objectives: To test whether airway effects occur below the current ozone standard and if they are more pronounced in potentially susceptible individuals, such as those deficient in the antioxidant gene glutathione S-transferase mu 1 (GSTM1). Methods: Pulmonary function and subjective symptoms were measured in 59 healthy young adults (19–35 yr) immediately before and after exposure to 0.0 (clean air, CA) and 0.06 ppm ozone for 6.6 hours in a chamber while undergoing intermittent moderate exercise. The polymorphonuclear neutrophil (PMN) influx was measured in 24 subjects 16 to 18 hours postexposure. Measurements and Main Results: Subjects experienced a significantly greater (P = 0.008) change in FEV1 (± SE) immediately after exposure to 0.06 ppm ozone compared with CA (−1.71 ± 0.50% vs. −0.002 ± 0.46%). The decrement in FVC was also greater (P = 0.02) after ozone versus CA (−2.32 ± 0.41% vs. −1.13 ± 0.34%). Similarly, changes in %PMN were greater after ozone (54.0 ± 4.6%) than CA (38.3 ± 3.7%) exposure (P < 0.001). Symptom scores were not different between ozone versus CA. There were no significant differences in changes in FEV1, FVC, and %PMN between subjects with GSTM1-positive and GSTM1-null genotypes. Conclusions: Exposure of healthy young adults to 0.06 ppm ozone for 6.6 hours causes a significant decrement of FEV1 and an increase in neutrophilic inflammation in the airways. GSTM1 genotype alone appears to have no significant role in modifying the effects.