Letter by Brook Regarding Article, “Residential Exposure to Traffic Is Associated With Coronary Atherosclerosis”
To the Editor:
I congratulate Hoffmann and colleagues for demonstrating that residence proximity to traffic is associated with coronary calcium.1 Indeed, animal studies provide plausibility for a cause-and-effect relationship between particulate matter (PM) and atherosclerosis. However, the minor proatherosclerotic effect (≈7% greater calcium score) in their study cannot explain the magnitude of cardiovascular morbidity observed in epidemiological studies.
The authors highlight that longer-term cohort studies (hazard ratio, 1.76)2 observe larger heath risks than shorter-term time series (relative risk, ≈1.0) per 10-μg/m3 increase in PM and suggest a biological explanation. However, this discrepancy is not likely explained by independent health effects of long-term exposure occurring incrementally to the numerous detrimental effects after (sub)acute exposures. One would have to implausibly posit that PM produces a 76-fold–greater risk of cardiovascular death after 6 years than over weeks of exposure as a result of the modest atherosclerotic lesion growth observed in their study in response to the relatively low particle concentrations (orders of magnitude smaller than passive tobacco smoke).
Paradoxically, case-crossover studies show that myocardial infarction risk is raised by an even greater magnitude than cohort analyses after only 1 hour of traffic/pollution exposure (odds ratio, 2.73).3 These temporal discrepancies are likely explained largely by differences in designs, statistics, outcomes, populations, and pollution characteristics among studies and not by biology. Moreover, the evidence suggests that most cardiovascular morbidity is due to biological actions of PM occurring fairly rapidly (hours to weeks) and mostly in at-risk individuals. Simply extending exposure-lag durations of time series to several weeks yields health risks similar to cohort studies. Reducing air pollution, analogous to passive tobacco smoke, largely mitigates the associated cardiovascular risk within only months.4 In support of this possibility, a recent study showed that myocardial infarctions were triggered by PM solely among patients with preexisting significant (≥70% obstructive) coronary atherosclerosis.5
Although I do not question the importance and veracity of the authors’ findings, this small degree of enhanced atherosclerosis is not likely a major biological pathway explaining the larger cardiovascular morbidity observed among cohort studies. It is most probable that PM acts principally as a “triggering factor” instigating acute events, which may nonetheless advance mortality even by years in individuals who could have otherwise avoided exposure at vulnerable times. I believe this to be of fundamental importance because the National Ambient Air Quality Standards should begin to focus also on very brief elevations in PM (peak hourly levels), beyond the trend of long-term annual averages (which may actually serve to mask biologically important short-term high-pollution episodes).
Hoffmann B, Moebus S, Möhlenkamp, Stang A, Lehmann N, Dragano N, Schmermund A, Memmesheimer M, Mann K, Erbel R, Jöckel K-H. Residential exposure to traffic is associated with coronary atherosclerosis. Circulation. 2007; 116: 489–496.
Pope CA III, Muhlestein JB, May TH, Renlund DG, Anderson JL, Horne BD. Ischemic heart disease events triggered by short-term exposure to fine particulate air pollution. Circulation. 2006; 114: 2443–2448.