Heavy on the metals: parsing the particulate content of the London Smog.

Half a century after the 1952 London Smog debacle, in which an estimated 12,000 people were killed in the months following a particularly intense early December bout of air pollution, a team of English and U.S. researchers has sliced through samples of old evidence to unveil a few hints about which fine particulates may have played a role in the disaster [EHP 111:1209-1214]. Although the final evidence is scant, it may help today's researchers discover the exact mechanism by which fine particulates, found to be harmful in more than 100 studies, actually damage and kill.

The team from the Royal London Hospital and the State University of New York Upstate Medical University in Syracuse knew that the thick London Smog likely contained a variety of fine particulates from coal, diesel, and other sources. They also knew from a preliminary review that autopsy diagnoses of chronic obstructive pulmonary disease (COPD) following the London Smog episode were about double the rates in the winters before and after. Given these clues, they decided to investigate the presence of particulates in archived autopsy tissues for the period of December 1952 through March 1953.

The team began by picking only those people who had a COPD diagnosis at the time of death, and winnowed that group further by selecting only people generally considered more vulnerable to pollutants--those older than 45 or younger than 1. From these, they selected those subjects for whom pulmonary tissue had been preserved in blocks that could be sliced and analyzed. The tissue had to be from one of four pulmonary compartments so the team could gauge how long the particulates may have been in the body. Their premise was that the most recently inhaled particulates--those taken in within a few hours before death--would have lodged in the airway (bronchiole) compartment, whereas particles inhaled earlier would reside progressively deeper, in the airspace (alveolar) macrophages, interstitial macrophages, or lymph nodes.

The researchers ended up with tissue samples from 18 people who died at the time of or shortly after the London Smog. Examination of samples from 2 infants did not yield readily quantifiable amounts of particulate matter. But the tiny, embedded evidence in 16 adult tissue samples included more than a dozen substances, including carbon, lead, tin, zinc, manganese, antimony, and silicon.

However, the team found ultrafine and fine particulates in the airways of only 2 adult subjects. This paucity can be attributed in part to chance, says primary author Andrew Hunt, because the tissue available was limited and was not necessarily representative of each compartment. The same may hold true for the airspace macrophages, assumed to illustrate the next-most-recent exposures, for which 5 subjects yielded particulates. The deeper interstitial macrophages were more productive, yielding particulates in 15 subjects, while the lymph nodes yielded particulates in only 2 subjects.

Within the context of the limitations noted, the team concludes that the range of carbonaceous, heavy metal, and other fine particulates they found provides fodder for future investigations, even though the particulate sources of today may differ in quantity and content. Perhaps most intriguing is the finding that, in the 2 cases where fine particulates were found in the airway compartment--marking them as components breathed by the individuals shortly before death--the same substances (including lead and a zinc-tin mixture) were rarely found in other compartments. The researchers believe this is most likely explained by the solubility of these metals--that they can dissolve into the body as the particles they are attached to pass through the airway compartment. If soluble components of particulate matter affect physiologic processes, they write, it may be a factor in particulate matter-mediated mortality and morbidity.