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SUNY Upstate researchers offer new evidence into what killed 12,000 people during the Great London Smog of 1952
Examining samples of lung tissues from victims of the Great London Smog of 1952, researchers at SUNY Upstate Medical University and the Royal Hospital of London have identified for the first time the fine particulates that may have played a role in the disaster that killed 12,000 people.
While these lung tissues were known to contain large aggregates of soot, researchers examining these lung slices for the first time using electron microscopes and X-ray microanalysis found embedded in the tissue more than a dozen substances, including manganese, lead, carbon, zinc and tin. The study, which was funded by the American Lung Association, is published in the July issue of Environmental Health Perspectives.
“Our findings indicate the victims were exposed to very fine carbonaceous particles from high temperature emissions and substantial quantities of fine metal particles that can have a toxic effect in the lung,” said Andrew Hunt, Ph.D., a research associate professor at SUNY Upstate at the time of the study.
Study co-author Jerrold Abraham, Ph.D., professor of pathology at SUNY Upstate, said the technology used by researchers enabled them to make definitive identifications of the metallic elements in the lung samples. “In addition to manganese, lead, carbon, zinc and tin, we also found elements of lead, aluminum, copper, titanium, antimony and cadmium,” he said. “These are all the metals that we see in today’s aerosol samples of particulate matter from combustion sources.”
During five days in December 1952, a slow-moving high pressure system stalled over London, trapping smoky coal and diesel emissions, as well as emissions from domestic fires and industrial plants. As the polluted air lingered, Londoners began to get sick and those with already compromised health died from the deadly smog mixture. During the crisis, the daily mortality rate rose from a norm of less than 250 people per day to more than 900 people per day. The incident spurred Great Britain to enact strict clean air laws.
Abraham and Hunt teamed up with researchers at the Royal London Hospital, where preserved autopsy tissue samples of persons known to have died from the smog exposure were stored. The samples, according to Abraham, provide the best evidence of the toxic nature of the London air a half century ago. “It appears that no ambient aerosol samples collected during the Great London Smog of 1952 exist today for analysis,” he said. “By examining these lung tissues we can better understand the composition of the particulate matter in the London smog case and look at its possible connection with the increased mortality rates.”
In addition to identifying the metals present in the lung tissues, researchers were also able to analyze the retention of particulate matter in large and small airways and air spaces of the lung. “What we found were ultrafine particles, less than a tenth of a micron in diameter, still present in the mucus in the small airways compartment of the lung, which represents the particles inhaled most recently before death,” Abraham said. “We found fewer of certain particulates in other, more long-term storage, lung compartments, which indicate that these particles were likely trapped in the mucus and then dissolved or eaten by macrophages.”
Abraham and Hunt hope their study of the Great London Fog of 1952 can further analysis into the mechanism by which fine particulates, especially those uncovered in the research, can kill.
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