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Concentrations of ambient PM2.5 (particulate matter <2.5 microm in aerodynamic diameter) were associated with increased mortality in two prospective cohort studies. In this paper, I assess whether the weight of the evidence supports a causal association. I assumed the study population in each city to have the same exposure; therefore, these are ecologic studies because exposure is at the group level. Health outcome and confounding data are at the individual level. Ambient PM concentrations are inadequate surrogates for personal exposure because they are at the group level and comprise only a small proportion of personal exposure, they change over time, and they constitute only a small proportion of a life span. The strength of association and exposure-response relationships cannot be determined because the ecologic group-level risks of PM2.5 are overestimated 150- to 300-fold based on an analogy with individual-level exposure to inhaled cigarette smoke. Risk estimates may also be high because of confounding from factors such as physical activity and lung function. The evidence is not coherent because the stronger associations are expected to be with morbidity, but instead are with mortality. For example, PM2.5 was associated with mortality but not with measurable reductions in lung function. Biological plausibility is lacking because lifetime exposure of rats to combustion products at concentrations two to three orders of magnitude higher than air pollution levels cause lung overloading but no consistent reduction in survival. Criteria for quantitative risk assessment are not met so the data are not useful for setting air quality standards. The weight of evidence suggests there is no substantive basis for concluding that a cause-effect relationship exists between long-term ambient PM2.5 and increased mortality.ImagesFigure 1Figure 2Figure 3Figure 4Figure 5

The relationship between crystalline silica and lung cancer has been the subject of many recent publications, conferences, and regulatory considerations. An influential, international body has determined that there was sufficient evidence to conclude that quartz and cristobalite are carcinogenic in humans. The present authors believe that the results of these studies are inconsistent and, when positive, only weakly positive. Other, methodologically strong, negative studies have not been considered, and several studies viewed as providing evidence supporting the carcinogenicity of silica have significant methodological weaknesses. Silica is not directly genotoxic and is a pulmonary carcinogen only in the rat, a species that seems to be inappropriate for assessing particulate carcinogenesis in humans. Data on humans demonstrate a lack of association between lung cancer and exposure to crystalline silica. Exposure-response relationships have generally not been found. Studies in which silicotic patients were not identified from compensation registries and in which enumeration was complete did not support a causal association between silicosis and lung cancer, which further argues against the carcinogenicity of crystalline silica.