Table 2.
Study population | Design | Main findings | Comments | Reference |
---|---|---|---|---|
Sixty mild to moderate asthmatic adults in London | Exposure during 2 hr walking in OS or HP, pre/postexposure physiologic measurements: median PM2.5 concentration, 28 (OS) vs. 11 μg/m3 (HP); median EC, 7.5 vs. 1.3 μg/m3; median UFP, 63,700 vs. 18,300 particles/cm3 | Asymptomatic decrease in lung function and increase in inflammation after walking in OS compared with HP; changes most consistently associated with EC and UFP; per 1-μg/m3 significant increase in EC decrement in lung function of ~ 1% decrement in lung function and ~ 2% increase in exhaled NO (inflammation) | OS has diesel traffic only | McCreanor et al. 2007 |
Subjects (n = 691) with MI in Augsburg | Case–crossover study comparing the frequency of participation in traffic in the hours before the MI and a control period (24–72 hr before MI) | RR = 2.92 for participation in traffic in the hour before the MI; increased risk found for all transport means (car, bicycle, public transport) | May be stressors other than air pollution | Peters et al. 2004 |
Nine healthy young U.S. policemen | Physiologic measurements before and after 8-hr work shift; average in-vehicle PM2.5, 24 μg/m3 | Significant increases of heart rate variability, ectopic beats, blood inflammatory and coagulation markers, and red blood cell volume; per 10-μg/m3 PM2.5 effect on C-reactive protein, +32%; neutrophils, +6%; von Willebrand factor, +12%; and ectopic beats, +20%. | Riediker et al. 2004 | |
Twelve healthy young subjects | Physiologic measurements before and after 1-hr cycling trip from city center to university in Utrecht | Statistically nonsignificant 1–3% decrements in lung function per 105/m soot concentration and a 15% increase in exhaled NO per 38,000 particles/cm3 | Strak et al. 2010 |
Abbreviations: EC, elemental carbon; HP, Hyde Park; MI, myocardial infarction; NO, nitric oxide; OS, Oxford Street; RR, relative risk; UFP, ultrafine particle count.