Author Affiliation: Sunlight, Nutrition, and Health Research Center, San Francisco, California.
The recent article by Weuve and colleagues1 provides additional evidence that particulate air pollution contributes to cognitive decline. The mechanisms suggested to explain the observed association are generally consistent with an additional characteristic of a major component of PM2.5 (particulate matter ≤2.5 μm in aerodynamic diameter), black carbon, namely adsorption of polycyclic aromatic hydrocarbons (PAHs). The role of PAHs in cancer and reproductive and cardiovascular disease was reviewed by Lewtas.2 One PAH, benzo[a]pyrene, has been shown to cause neuronal death in a mouse through a combination of increase in reactive oxygen species, nitric oxide, and proinflammatory cytokines.3 Smoking is a risk factor for cognitive decline,4 and both particulates and PAHs are important emissions from smoking tobacco.
An ecological study of cancer mortality rates in the United States used an index of air pollution for acid deposition.5 There are 3 primary sources of black carbon particulates: coal-fired combustion, diesel combustion, and wood combustion. That index had the highest values in the Northeast and was considered to be associated primarily with coal-fired power plants. That index was correlated with respiratory, digestive tract, urogenital, female organ, blood, and skin cancer. There was no indication that automobiles using gasoline such as in southern California were associated with increased risk of cancer.
Thus, it would be interesting to know if the data by Weuve and colleagues1 showed any evidence of a geographical variation, as well as whether any information on black carbon and PAH exposure could be obtained to extend the study.
Correspondence: Dr Grant, Sunlight, Nutrition, and Health Research Center, PO Box 641603, San Francisco, CA 94164-1603 (email@example.com).
Financial Disclosure: None reported.
Grant WB. Polycyclic Aromatic Hydrocarbons, Particulate Air Pollution, and Cognitive Decline. Arch Intern Med. 2012;172(13):1045-1046. doi:10.1001/archinternmed.2012.1698