Mittleman, Murray A.; Verrier, Richard L.
From Beth Israel Medical Center, Boston, MA.
Correspondence: Murray A. Mittleman, Beth Israel Deaconess Medical Center, One Autumn Street, Kennedy Building, 5th Floor, Boston MA 02215. E-mail: firstname.lastname@example.org.
In this issue of Epidemiology two studies from opposite sides of the Atlantic Ocean underscore the global interest in the potential adverse cardiovascular effects of fine particulate matter and gaseous air pollutants.1,2 They corroborate and extend recurring findings that the small-mass air pollutants derived from combustion sources appear to exert a transient influence on autonomic function and on risk for acute cardiovascular events.3–7
The article by Holguín and coworkers from Mexico City describes the results of a longitudinal examination of nursing home residents who underwent 5-minute electrocardiographic monitoring sessions every other day for a 3-month period.1 The study is notable for its extensive exposure assessment and activity diaries. The investigators found that higher levels of particulate air pollution were associated with lower levels of the high-frequency component of heart rate variability (HRV). They also show data suggesting that the association between particles and HRV might be more prominent in elderly patients with hypertension. It is well known that reduced HRV in the setting of myocardial infarction is associated with greater risk of cardiac death, presumably attributable to loss of the cardioprotective effect of vagus nerve activity, which can help maintain cardiac electrical stability. However, the clinical significance of minor, transient changes in HRV, as observed in this study, is uncertain.
D’Ippoliti and coworkers described the results of a case-crossover study of the effects of air pollution on acute myocardial infarction among residents of Rome between 1995 and 1997.2 They found that higher levels of particles and NO2 were associated with transient increases in the rate of hospitalization for acute myocardial infarction. This investigation had several important strengths, including a relatively large number of cases and a well-defined control-sampling scheme. However, the study was limited by its reliance on administrative records, incomplete information on the time of symptom onset, and absence of direct measures of particulate matter.
Well-conducted studies evaluating the effects of air pollution are of great importance. It is not yet certain that air pollution has cardiovascular effects, and those effects that have been reported are typically quite small on a relative scale. Still, if these effects are true and causal, then a potentially large number of excess cases might be triggered by exposures, which affect entire populations. Development of a full understanding of the effects of particulate and gaseous pollutants on cardiovascular health will require a multidisciplinary approach with a unique and important role to be played by epidemiologists. To make rapid progress, either in identifying a causal association or in debunking an illusory one, environmental and cardiovascular epidemiologists must unite with experts in exposure assessment, cardiovascular biology, and cardiologists to design and conduct novel studies. It is also important that investigators maintain a healthy skepticism and use a rigorous refutationist outlook in designing and interpreting the results of these studies. Furthermore, we must guard against the specter of publication bias, both on the part of investigators, who might be motivated to pursue “interesting” findings and to downplay or ignore null results, and on the part of journal editors, who must seriously weigh the cost of devoting valuable space to publishing null results.
These two studies make valuable contributions to the growing literature on the potential cardiovascular effects of air pollution. Clearly, the stakes are high as regulatory bodies turn to the scientific community for information that might impact policy decisions with the potential to affect cardiovascular disease morbidity and mortality. The public health consequences of incorrectly identifying the causal effects of air pollution on cardiovascular health are great. If a causal association exists but is not detected and the exposure is not reduced, the potential burden of excess cardiovascular morbidity and mortality is likely to be immense. On the other hand, the opportunity cost of implementing policies to limit exposures, if in fact they are not deleterious to the public health, might exclude the implementation of other potentially beneficial public health programs.
1.Holguín F, Téllez-Rojo MM, Hernández M, et al. Air pollution and heart rate variability among the elderly in Mexico City. Epidemiology
2.D’Ippoliti D, Forastiere F, Ancona C, et al. Air pollution and myocardial infarction in Rome: a case-crossover analysis. Epidemiology
3.Pope CA III, Verrier RL, Lovett EG, et al. Heart rate variability associated with particulate air pollution. Am Heart J
4.Gold DR, Litonjua A, Schwartz J, et al. Ambient pollution and heart rate variability. Circulation
5.Peters A, Dockery DW, Muller JE, et al. Increased particulate air pollution and the triggering of myocardial infarction. Circulation
6.Pope CA, Burnett RT, Thun MJ, et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA
7.Dockery DW. Epidemiologic evidence of cardiovascular effects of particulate air pollution. Environ Health Perspect
. 2001;109(suppl 4):483–486.
© 2003 Lippincott Williams & Wilkins, Inc.