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Are noise and air pollution related to the incidence of dementia? A cohort study in London, England
  1. Iain M Carey1,
  2. H Ross Anderson1,2,
  3. Richard W Atkinson1,
  4. Sean D Beevers2,
  5. Derek G Cook1,
  6. David P Strachan1,
  7. David Dajnak2,
  8. John Gulliver3,
  9. Frank J Kelly2,4
  1. 1 Population Health Research Institute, St George’s, University of London, London, UK
  2. 2 MRC-PHE Centre for Environment and Health, King’s College London, London, UK
  3. 3 UK Small Area Health Statistics Unit, MRC-PHE Centre for Environment and Health, Imperial College, London, UK
  4. 4 NIHR HealthProtection Research Unit in Health Impact of Environmental Hazards, King’s College London, London, UK
  1. Correspondence to Dr Iain M Carey; sgjd450{at}


Objective To investigate whether the incidence of dementia is related to residential levels of air and noise pollution in London.

Design Retrospective cohort study using primary care data.

Setting 75 Greater London practices.

Participants 130 978 adults aged 50–79 years registered with their general practices on 1 January 2005, with no recorded history of dementia or care home residence.

Primary and secondary outcome measures A first recorded diagnosis of dementia and, where specified, subgroups of Alzheimer’s disease and vascular dementia during 2005–2013. The average annual concentrations during 2004 of nitrogen dioxide (NO2), particulate matter with a median aerodynamic diameter ≤2.5 µm (PM2.5) and ozone (O3) were estimated at 20×20 m resolution from dispersion models. Traffic intensity, distance from major road and night-time noise levels (Lnight) were estimated at the postcode level. All exposure measures were linked anonymously to clinical data via residential postcode. HRs from Cox models were adjusted for age, sex, ethnicity, smoking and body mass index, with further adjustments explored for area deprivation and comorbidity.

Results 2181 subjects (1.7%) received an incident diagnosis of dementia (39% mentioning Alzheimer’s disease, 29% vascular dementia). There was a positive exposure response relationship between dementia and all measures of air pollution except O3, which was not readily explained by further adjustment. Adults living in areas with the highest fifth of NO2 concentration (>41.5 µg/m3) versus the lowest fifth (<31.9 µg/m3) were at a higher risk of dementia (HR=1.40, 95% CI 1.12 to 1.74). Increases in dementia risk were also observed with PM2.5, PM2.5 specifically from primary traffic sources only and Lnight, but only NO2 and PM2.5 remained statistically significant in multipollutant models. Associations were more consistent for Alzheimer’s disease than vascular dementia.

Conclusions We have found evidence of a positive association between residential levels of air pollution across London and being diagnosed with dementia, which is unexplained by known confounding factors.

  • air pollution
  • dementia
  • noise
  • primary care
  • alzheimer’s disease

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  • Contributors HRA, RWA, JG, SDB and FJK contributed to the wider study conception and design. HRA, SDB, JG, DD and FJK contributed to exposure assessment. IMC, RWA and DGC acquired linked health data. IMC conceived the specific study design, conducted the data analyses and drafted the initial report. HRA, RWA, DGC and DPS all contributed to the data analysis plan. All authors contributed to interpreting the analyses and to critically revising the article, and approved the final draft. IMC is the guarantor of the work.

  • Funding This work was supported by the UK Natural Environment Research Council, Medical Research Council, Economic and Social Research Council, Department for Environment, Food and Rural Affairs, and Department of Health (NE/I007806/1; NE/I008039/1; NE/I00789X/1) through the Environmental Exposure & Health Initiative . The research was also part funded by the National Institute for Health Research Health Protection Research Unit (NIHR HPRU) in Health Impact of Environmental Hazards at King’s College London in partnership with Public Health England (PHE) and Imperial College London. The views expressed in this paper are those of the authors and not do not reflect the official policy or position of any of the following: the NHS, the NIHR, the Department of Health, Public Health England or the Medicines and Healthcare Products Regulatory Agency (MHRA). Clinical Practice Research Datalink is owned by the Secretary of State of the UK Department of Health and operates within the MHRA. Clinical Practice Research Datalink has received funding from the MHRA, Wellcome Trust, Medical Research Council, NIHR Health Technology Assessment Programme, Innovative Medicines Initiative, UK Department of Health, Technology Strategy Board, Seventh Framework Programme EU, various universities, contract research organisations, and pharmaceutical companies.

  • Competing interests None declared.

  • Patient consent Not required.

  • Ethics approval This study (protocol number 12_026AR) was approved by the Independent Scientific Advisory Committee evaluation of joint protocols of research involving CPRD data in September 2017.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement Due to data restrictions, we are unable to share any aspect of the data.