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Short-term associations between outdoor air pollution and mortality in London 1992-4.
  1. S A Bremner,
  2. H R Anderson,
  3. R W Atkinson,
  4. A J McMichael,
  5. D P Strachan,
  6. J M Bland,
  7. J S Bower
  1. Department of Public Health Sciences, St George's Hospital Medical School, London, UK.


    OBJECTIVES: A previous study of the short term effects of air pollution in London from April 1987 to March 1992 found associations between all cause mortality and black smoke and ozone, but no clear evidence of specificity for cardiorespiratory deaths. London data from 1992 to 1994 were analysed to examine the consistency of results over time and to include particles with a mean aerodynamic diameter of 10 microns (PM10) and carbon monoxide. METHODS: Poisson regression was used of daily mortality counts grouped by age and diagnosis, adjusting for trend, seasonality, calendar effects, deaths from influenza, meteorology, and serial correlation. The pollutants examined were particles (PM10 and black smoke), nitrogen dioxide, ozone, sulphur dioxide, and carbon monoxide with single and cumulative lags up to 3 days. RESULTS: No significant associations were found between any pollutant and all cause mortality, but, with the exception of ozone, all estimates were positive. Each pollutant apart from ozone was significantly associated with respiratory mortality; PM10 showed the largest effect (4% increase in deaths of all ages for a 10th-90th percentile increment). The pollutants significantly associated with cardiovascular deaths were nitrogen dioxide, ozone, and black smoke but there was no evidence of an association with PM10. In two pollutant models of respiratory deaths, the effect of black smoke, which in London indicates fine particles of diesel origin, was independent of that of PM10, but not vice versa. CONCLUSION: These results from a new data set confirm a previous report that there are associations between various air pollutants and daily mortality in London. This new study found greater specificity for associations with respiratory and cardiovascular deaths, and this increases the plausibility of a causal explanation. However, the effects of ozone found in the earlier study were not replicated. The fraction of PM10 which comprises black smoke accounted for much of the effect of PM10.

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