PM 2.5 and Mortality in Long-Term Prospective Cohort Studies: Cause-Effect or Statistical Associations?

Concentrations of ambient PM2.5 (particulate matter c2.5 pm in aerodynamic diameter) were associated with increased mortality in two prospective cohort studies.In this paper, 1 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 arc at the individual level.Ambient PM concentrations are inadequate surrogates for personal exposue because they are at the group lev and comprise only a small proportion of personal xposre, they change over time, and they con- stitute only a small proportion of a lif span.The strength ofassociation and eposure-response relationships cannot be deter ed because the ecologic group-level risk of PM2.5 are overesti- mated 150-to 300-fold based on an analogy with individual-levd 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 stroger asocations are expected to be with morbidity, but instead are with mortality.For exmple, PM,, wa ted 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 hee orders of tude higher than air poliution levels cause lung overloading but no consistent reduction in survival.Criteria for quantitative risk assessment are not met so the data are not use- fil for setting air quality standards.The weight of evidence suggt there is no substantive basis for concluding that a cause-effect relationship exists between long-term ambient PM2.5 and increased mortality.