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Environ Health Perspect. 2003 Jul;111(9):1209-14.

Toxicologic and epidemiologic clues from the characterization of the 1952 London smog fine particulate matter in archival autopsy lung tissues.

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Department of Pathology, State University of New York Upstate Medical University, Syracuse, New York, USA.


Exposure to atmospheric fine particulate matter (PM), even at low ambient concentrations, has clearly been linked to increases in mortality and morbidity. A 10- micro g m(-3) increase in PM10 (PM < 10 micro m) has been found to produce a 0.5% increase in daily mortality. The mechanism of action is a source of debate, although recent attention has focused on the cardiac effects of PM exposures. Likewise, several possible etiologic agents have been implicated, including ultrafine PM (PM <or= 100 nm), metals, and the acid components, yet the responsible constituent remains undetermined. During the catastrophic PM exposure episode in London in December 1952, some 4,000 excess deaths occurred at the height of the event. The extreme mortality during that episode and the preservation of archival autopsy tissues allow us the unique opportunity to report on the form and composition of December 1952 London PM in situ in tissues from persons known to have died from the smog exposure. Because absolute increases in mortality with current levels of PM in Western Europe and North America are low, analogous tissues are unlikely to be contemporaneously available. Taking a lung compartment (airway, airspace, interstitium, and lymph node) approach, we differentiated exposures contemporary with death from those of earlier origin. Electron microscopic analyses revealed the dominance of retained soot and a surfeit of other particle types. A variety of metal-bearing particle types were found in all compartments, but Pb, Zn, and SnZn types appeared the least biopersistent. The results support the acute toxicologic importance of ultrafine carbonaceous and metal PM.

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