Comments on "PM(2.5) mortality in long-term prospective cohort studies: cause-effect or statistical association?".

Most models of how science works propose that competition between ideas contributes to the advancement of knowledge. Criticism of scientific work plays a part in facilitating such competition by exposing the strengths and weaknesses of rival explanations , encouraging debate, and suggesting alternatives. Nevertheless, not all criticism has equal value to the scientific process. In a review of epidemiologic studies on fine particles and mortality that appeared recently in EHP, Gamble (1) charged that the two major studies on this topic (2,3) may have been compromised by bias, yet he offered no serious effort to evaluate the alleged errors with the same standards of rigor demanded of the original studies. For example, in Gamble's (1) claim that the study findings are compromised by the ecologic fallacy, he failed to address two important issues. First, the major prospective studies of fine particles and mortality are not classical ecologic designs because only air pollution exposures are measured on the aggregate level; the outcome and potential confounders are based on individual level measurements. Thus the biases stemming from the ecologic fallacy do not apply to these studies. Instead, these should be viewed as individual level studies in which exposure is measured with error (4). The calculations in Gamble's Table 2 (1) are erroneously portrayed as demonstrating the ecologic fallacy. Instead they appear to present strong evidence of a supralinear dose-response relationship between particles and mortality. This type of dose response would be expected if there existed a subset with much greater susceptibility, e.g., a bimodal distrubution of susceptibility. Second, the inference that the U.S. Environmental Protection Agency (EPA) and others have drawn from the studies' results is logically consistent with evidence based on exposure measured at the group level. The correct inference is that individuals living in communities with high air pollution levels have a higher risk of dying than people living in communities with low pollution levels and, therefore, that lowering community-wide air pollution levels should reduce community mortality rates. Such a policy is a logical and efficient means of minimizing the health impact of a widespread exposure (5). Even when the criticism focuses on specific factors that might explain the results of the studies, it does not consistently address the potential magnitude and direction of alleged biases. For example, Gamble (1) conduded that lung function is a probable confounder of the observed relative risk for PM2.5 because the average lung function …