Traffic-related air pollution and blood pressure in elderly subjects with coronary artery disease.

Ambient particulate matter (PM) air pollution has been associated with morbidity and mortality from cardiovascular diseases.1 Possible mechanisms behind these associations include autonomic dysfunction, oxidative stress and inflammation, and vasomotor dysfunction.2 Increased blood pressure (BP) or less vasodilatation was found in humans experimentally exposed to concentrated ambient PM2.5.3 One experimental study found the effects on BP were attributable to the organic carbon fraction of urban PM2.5, which suggests that fossil fuel combustion products may be causal.4 Organic components of particles, especially ultrafine particles (>0.1 μm in diameter), induce oxidative stress responses,5 and oxidative stress is a major mechanism underlying hypertension.6 Despite this experimental evidence, air pollutants have been inconsistently associated with BP in epidemiologic studies—some show positive associations7–15 and others inverse16–18 or no associations.19,20 In most studies, air-pollutant data came from regional air monitors situated far from subject locations, possibly leading to exposure error. Five of these studies collected home or personal air pollution data, but the number of BP measurements overall was small (n > 180) or was averaged.9,14,15,17,20 Only 2 studies have used ambulatory BP monitoring.8,14 One of these studies8 found positive associations of BP with ambient carbon monoxide (CO) in 46 young healthy nonsmoking vehicular traffic controllers. However, analyses were based on only three 24-hour averaged BP measurements across 3 seasons rather than real-time exposure-response relationships, which are among the potential strengths of ambulatory BP monitoring. The other study14 showed that systolic BP was higher by 7 mm Hg when 15 young healthy adults wore particle filter face-masks while walking for 2 hours on busy Beijing streets. None of these studies examined organic carbon, and none statistically evaluated confounding or effect modification by emotional stress or ambulatory physical activity. We addressed these gaps in methods by using ambulatory BP monitoring to assess acute effects of real-time changes in air pollution exposures, including organic carbon, and by simultaneously collecting ambulatory data on other important determinants of BP. Numerous studies have shown that BP assessment from ambulatory monitoring is more closely associated with end-organ damage than the isolated BP readings in clinics.21 Nevertheless, ambulatory BP needs to be clinically interpreted in reference to concurrent physical activity levels.22 Positive associations between ambulatory BP and activity are small, largely attributable to major changes in the level of activity,23 and show considerable between-individual variation.22 We tested the hypothesis that ambulatory BP would be positively associated with exposure to outdoor home air pollutants, especially combustion-derived pollutants in addition to PM2.5. This hypothesis is supported by the evidence that redox-active pollutant components impair vasomotor responses by inducing oxidative stress, systemic inflammation, and endothelial dysfunction.2 We recently reported associations of outdoor home PM with increased blood biomarkers of inflammation.24,25 We followed a cohort of 64 elderly individuals with a history of coronary artery disease, who might be expected to have increased susceptibility to the adverse cardiovascular effects of air pollutants.26 The design allowed us to test for the first time the responses of ambulatory BP to variations in acute (hourly) and long-term air-pollutant exposures (up to 9 days). Electronic diary data on time-location were used to assess the representativeness of outdoor home exposures and the effect of perceived exertion on the relation of BP to air pollution exposure.