Aim To examine the associations of air pollution with both self-reported age-related macular degeneration (AMD), and in vivo measures of retinal sublayer thicknesses.
Methods We included 115 954 UK Biobank participants aged 40–69 years old in this cross-sectional study. Ambient air pollution measures included particulate matter, nitrogen dioxide (NO2) and nitrogen oxides (NOx). Participants with self-reported ocular conditions, high refractive error (< −6 or > +6 diopters) and poor spectral-domain optical coherence tomography (SD-OCT) image were excluded. Self-reported AMD was used to identify overt disease. SD-OCT imaging derived photoreceptor sublayer thickness and retinal pigment epithelium (RPE) layer thickness were used as structural biomarkers of AMD for 52 602 participants. We examined the associations of ambient air pollution with self-reported AMD and both photoreceptor sublayers and RPE layer thicknesses.
Results After adjusting for covariates, people who were exposed to higher fine ambient particulate matter with an aerodynamic diameter <2.5 µm (PM2.5, per IQR increase) had higher odds of self-reported AMD (OR=1.08, p=0.036), thinner photoreceptor synaptic region (β=−0.16 µm, p=2.0 × 10−5), thicker photoreceptor inner segment layer (β=0.04 µm, p=0.001) and thinner RPE (β=−0.13 µm, p=0.002). Higher levels of PM2.5 absorbance and NO2 were associated with thicker photoreceptor inner and outer segment layers, and a thinner RPE layer. Higher levels of PM10 (PM with an aerodynamic diameter <10 µm) was associated with thicker photoreceptor outer segment and thinner RPE, while higher exposure to NOx was associated with thinner photoreceptor synaptic region.
Conclusion Greater exposure to PM2.5 was associated with self-reported AMD, while PM2.5, PM2.5 absorbance, PM10, NO2 and NOx were all associated with differences in retinal layer thickness.
- public health
Data availability statement
Researchers wishing to access UK Biobank data can register and apply at https://www.ukbiobank.ac.uk/.
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PJF and PJP are joint senior authors.
Contributors SYLC 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. PJF and PJP led conception and design of the study. SYLC, PJF and PJP contributed to the data analyses, data interpretation and wrote the draft of the manuscript. All authors reviewed the results, read and critically revised the manuscript. All authors approved the final manuscript. The corresponding author attests that all listed authors meet authorship criteria and that no others meeting the criteria have been omitted.
Funding The UK Biobank Eye and Vision Consortium is supported by grants from Moorfields Eye Charity, The NIHR Biomedical Research Centre at Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, the Alcon Research Institute and the International Glaucoma Association (UK). SYLC, PTK, PJF and PJP received salary support from the NIHR BRC at Moorfields Eye Hospital. PTK is supported in part by the Helen Hamlyn Trust. PJF received support from the Richard Desmond Charitable Trust, via Fight for Sight, London. APK is supported by a Moorfields Eye Charity Career Development Fellowship. This research used data from the UK Biobank Resource, under data access request number 2112.
Competing interests CR reports employment by Topcon Healthcare Solutions, Inc, outside the submitted work. PJF reports personal fees from Allergan, Carl Zeiss, Google/DeepMind and Santen, a grant from Alcon, outside the submitted work. PJP reports grants from Topcon Inc, outside the submitted work.
Patient and public involvement statement Not commissioned; externally peer reviewed.
Provenance and peer review Not commissioned; externally peer reviewed.
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