Electrocardiographic ST-Segment Depression and Exposure to Traffic‐Related Aerosols in Elderly Subjects with Coronary Artery Disease

BackgroundAir pollutants have not been associated with ambulatory electrocardiographic evidence of ST-segment depression ≥ 1 mm (probable cardiac ischemia). We previously found that markers of primary (combustion-related) organic aerosols and gases were positively associated with circulating biomarkers of inflammation and ambulatory blood pressure in the present cohort panel study of elderly subjects with coronary artery disease.ObjectivesWe specifically aimed to evaluate whether exposure markers of primary organic aerosols and ultrafine particles were more strongly associated with ST-segment depression of ≥ 1 mm than were secondary organic aerosols or PM2.5 (particulate matter with aerodynamic diameter ≤ 2.5 µm) mass.MethodsWe evaluated relations of air pollutants to ambulatory electrocardiographic evidence of cardiac ischemia over 10 days in 38 subjects without ST depression on baseline electrocardiographs. Exposures were measured outdoors in retirement communities in the Los Angeles basin, including daily size-fractionated particle mass and hourly markers of primary and secondary organic aerosols and gases. Generalized estimating equations were used to estimate odds of hourly ST-segment depression (≥ 1 mm) from hourly air pollution exposures and to estimate relative rates of daily counts of ST-segment depression from daily average exposures, controlling for potential confounders.ResultsWe found significant positive associations of hourly ST-segment depression with markers of combustion-related aerosols and gases averaged 1-hr through 3-4 days, but not secondary (photochemically aged) organic aerosols or ozone. The odds ratio per interquartile increase in 2-day average primary organic carbon (5.2 µg/m3) was 15.4 (95% confidence interval, 3.5-68.2). Daily counts of ST-segment depression were consistently associated with primary combustion markers and 2-day average quasi-ultrafine particles < 0.25 µm.ConclusionsResults suggest that exposure to quasi-ultrafine particles and combustion-related pollutants (predominantly from traffic) increase the risk of myocardial ischemia, coherent with our previous findings for systemic inflammation and blood pressure

Personal and Ambient Air Pollution is Associated with Increased Exhaled Nitric Oxide in Children with Asthma

BACKGROUND: Research has shown associations between pediatric asthma outcomes and airborne particulate matter (PM). The importance of particle components remains to be determined. METHODS: We followed a panel of 45 schoolchildren with persistent asthma living in Southern California. Subjects were monitored over 10 days with offline fractional exhaled nitric oxide (Fe(NO)), a biomarker of airway inflammation. Personal active sampler exposures included continuous particulate matter < 2.5 μm in aerodynamic diameter (PM(2.5)), 24-hr PM(2.5) elemental and organic carbon (EC, OC), and 24-hr nitrogen dioxide. Ambient exposures included PM(2.5), PM(2.5) EC and OC, and NO(2). Data were analyzed with mixed models controlling for personal temperature, humidity and 10-day period. RESULTS: The strongest positive associations were between Fe(NO) and 2-day average pollutant concentrations. Per interquartile range pollutant increase, these were: for 24 μg/m(3) personal PM(2.5), 1.1 ppb Fe(NO) [95% confidence interval (CI), 0.1–1.9]; for 0.6 μg/m(3) personal EC, 0.7 ppb Fe(NO) (95% CI, 0.3–1.1); for 17 ppb personal NO(2), 1.6 ppb Fe(NO) (95% CI, 0.4–2.8). Larger associations were found for ambient EC and smaller associations for ambient NO(2). Ambient PM(2.5) and personal and ambient OC were significant only in subjects taking inhaled corticosteroids (ICS) alone. Subjects taking both ICS and antileukotrienes showed no significant associations. Distributed lag models showed personal PM(2.5) in the preceding 5 hr was associated with Fe(NO). In two-pollutant models, the most robust associations were for personal and ambient EC and NO(2), and for personal but not ambient PM(2.5). CONCLUSION: PM associations with airway inflammation in asthmatics may be missed using ambient particle mass, which may not sufficiently represent causal pollutant components from fossil fuel combustion

Personal endotoxin exposure in a panel study of school children with asthma

<p>Abstract</p> <p>Background</p> <p>Endotoxin exposure has been associated with asthma exacerbations and increased asthma prevalence. However, there is little data regarding personal exposure to endotoxin in children at risk, or the relation of personal endotoxin exposure to residential or ambient airborne endotoxin. The relation between personal endotoxin and personal air pollution exposures is also unknown.</p> <p>Methods</p> <p>We characterized personal endotoxin exposures in 45 school children with asthma ages 9-18 years using 376 repeated measurements from a PM_2.5active personal exposure monitor. We also assayed endotoxin in PM_2.5samples collected from ambient regional sites (N = 97 days) and from a subset of 12 indoor and outdoor subject home sites (N = 109 and 111 days, respectively) in Riverside and Whittier, California. Endotoxin was measured using the Limulus Amoebocyte Lysate kinetic chromogenic assay. At the same time, we measured personal, home and ambient exposure to PM_2.5mass, elemental carbon (EC), and organic carbon (OC). To assess exposure relations we used both rank correlations and mixed linear regression models, adjusted for personal temperature and relative humidity.</p> <p>Results</p> <p>We found small positive correlations of personal endotoxin with personal PM_2.5EC and OC, but not personal PM_2.5mass or stationary site air pollutant measurements. Outdoor home, indoor home and ambient endotoxin were moderately to strongly correlated with each other. However, in mixed models, personal endotoxin was not associated with indoor home or outdoor home endotoxin, but was associated with ambient endotoxin. Dog and cat ownership were significantly associated with increased personal but not indoor endotoxin.</p> <p>Conclusions</p> <p>Daily fixed site measurements of endotoxin in the home environment may not predict daily personal exposure, although a larger sample size may be needed to assess this. This conclusion is relevant to short-term exposures involved in the acute exacerbation of asthma.</p