Air Pollution and Respiratory Infection: An Emerging and Troubling Association.
700 - 701
Am J Respir Crit Care Med
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Evidence that inhalation of combustion-derived material increases vulnerability to airway infection dates back to at least the 1952 London smog, in which coal smoke was temporarily trapped over the city. The subsequent landmark paper published a year later in the Lancet by Logan (1) reported that, during the smog, deaths from pneumonia increased threefold, with the very young and the elderly particularly at risk. Notifications for pneumonia also increased 1.4-fold during the smog event itself, and 2.4- to 2.7-fold in the subsequent 2 weeks compared with the corresponding weekly average during 1947–1951. Indeed, Bell and colleagues (2) recently estimated that pneumonia was a significant cause of the 12,000 excess deaths resulting from acute and persisting effects of exposure to the 1952 London smog. Since then, the types of combustion sources associated with increased risk for pneumonia have expanded. For example, in Vietnam, a population-based survey found a 1.5-fold (95% confidence interval [CI], 1.25-fold to 1.92-fold) increased risk for pneumonia in young children exposed to environmental tobacco smoke, with 28% of childhood pneumonia attributable to environmental tobacco smoke (3); more recently, a meta-analysis of 10 European birth cohorts found a 1.3-fold (95% CI, 1.02-fold to 1.65-fold) increase in risk for pneumonia in young children with long-term exposure to traffic-related nitrogen dioxide (per 10 μg/m3 NO2), and 1.8-fold (95% CI, 1.0-fold to 3.09-fold) increase for particulate matter less than 10 microns in aerodynamic diameter (per 10 μg/m3 PM10) (4).