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The effects of hourly differences in air pollution on the risk of myocardial infarction: case crossover analysis of the MINAP database

BMJ 2011; 343 doi: (Published 20 September 2011) Cite this as: BMJ 2011;343:d5531
  1. Krishnan Bhaskaran, lecturer in statistical epidemiology,
  2. Shakoor Hajat, senior lecturer in epidemiology and medical statistics,
  3. Ben Armstrong, professor of epidemiological statistics,
  4. Andy Haines, professor of public health and primary care,
  5. Emily Herrett, research degree student,
  6. Paul Wilkinson, reader in environmental epidemiology,
  7. Liam Smeeth, professor of clinical epidemiology
  1. 1London School of Hygiene and Tropical Medicine, London, UK
  1. Correspondence to: K Bhaskaran, Department of Non-communicable Diseases Epidemiology, London School of Hygiene and Tropical Medicine, London WC1E 7HT krishnan.bhaskaran{at}
  • Accepted 4 August 2011


Objectives To investigate associations between air pollution levels and myocardial infarction (MI) on short timescales, with data at an hourly temporal resolution.

Design Time stratified case crossover study linking clinical data from the Myocardial Ischaemia National Audit Project (MINAP) with PM10, ozone, CO, NO2, and SO2 data from the UK National Air Quality Archive. Pollution effects were investigated with delays (lags) of 1–6, 7–12, 13–18, 19–24, and 25–72 hours in both single and multi-pollutant models, adjusted for ambient temperature, relative humidity, circulating levels of influenza and respiratory syncytial virus, day of week, holidays, and residual seasonality within calendar month strata.

Setting Population based study in 15 conurbations in England and Wales.

Subjects 79 288 diagnoses of myocardial infarction recorded over the period 2003–6.

Main outcome measures Excess risk of myocardial infarction per 10 µg/m3 increase in pollutant level.

Results In single pollutant models, PM10 and NO2 levels were associated with a very short term increase in risk of myocardial infarction 1–6 hours later (excess risks 1.2% (95% confidence interval 0.3 to 2.1) and 1.1% (0.3 to 1.8) respectively per 10 μg/m3 increase); the effects persisted in multi-pollutant models, though with only weak evidence of an independent PM10 effect (P=0.05). The immediate risk increases were followed by reductions in risk at longer lags: we found no evidence of any net excess risk associated with the five pollutants studied over a 72 hour period after exposure.

Conclusions Higher levels of PM10 and NO2, which are typically markers of traffic related pollution, seem to be associated with transiently increased risk of myocardial infarction 1–6 hours after exposure, but later reductions in risk suggest that air pollution may be associated with bringing events forward in time (“short-term displacement”) rather than increasing overall risk. The well established effect of air pollution on cardiorespiratory mortality may not be mediated through increasing the acute risk of myocardial infarction, but through another mechanism.


  • Contributors: KB, SH, BA, AH, PW, and LS were involved in the design of the study. KB and EH prepared and cleaned the data. KB did the statistical analysis and wrote the first draft. SH, BA AH, EH, PW, and LS contributed to further drafts. KB and LS are the guarantors for the study; KB had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

  • Funding: This work was supported by the British Heart Foundation (grant number FS/04/045) and the Garfield Weston Foundation. LS is supported by a Wellcome Trust Senior Research Fellowship in Clinical Science (grant number 082178). SH is funded by a Wellcome Trust Research Career Development Fellowship (grant number 076583/Z/05/Z). The funding bodies had no role in the design or conduct of this study or in the preparation, review, approval, or decision to submit the manuscript. All authors carried out this research independently of the funding bodies.

  • Competing interests: All authors have completed the unified competing interest form at (available on request from the corresponding author) and declare: KB, EH, and LS had support for the submitted work from the British Heart Foundation, the Garfield Weston Trust, and the Wellcome Trust respectively; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; no other relationships or activities that could appear to have influenced the submitted work

  • Ethical approval: The study was approved by the London School of Hygiene and Tropical Medicine Ethics Committee (application number 5218).

  • Data sharing: No additional data available.

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