Background/Aims To investigate the relationship between smoking and smoking intensity, and the rate of retinal nerve fibre layer (RNFL) thinning in patients with primary open angle glaucoma (POAG).
Methods In this longitudinal study, patients with POAG who had at least 3 years of follow-up with a minimum of 5 visits of optical coherence tomography (OCT) were enrolled. The smoking intensity was calculated as the pack-year at the baseline OCT. Univariable and multivariable linear mixed models were used to determine the effect of each parameter on the rates of RNFL thinning over time. Non-linear least-squares estimation with piecewise regression model was used to investigate the cut-off point for the relationship between circumpapillary RNFL thinning and smoking intensity.
Results A total of 466 eyes of 314 patients were included over the mean (95% CI) follow-up of 6.6 (6.4 to 6.7) years. Of the 314 patients, 121 (39%) had reported any history of smoking. Greater smoking intensity was associated with faster RNFL thinning (−0.06 (95% CI −0.11 to 0.00) µm/year per 10 pack-year higher; p=0.031) after adjusted for confounding factors. RNFL thinning became significantly faster when smoking intensity was >8 pack-year.
Conclusions Smoking intensity is associated with faster rates of RNFL thinning. Evaluation of smoking intensity might add information to the assessment of risk of glaucoma progression. Future studies are required to explore if withdrawing smoking as a modifiable risk factor can decrease progression in patients with glaucoma.
Data availability statement
Data are available on reasonable request. The datasets generated and/or analysed during the current study are available from the corresponding author on reasonable request.
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Contributors Involved in design and conduct of study: TN, RW and SM; data collection: TN and SM; analysis or interpretation of data: TN, RW and SM; writing: TN, GM, RW and SM; critical revision of the manuscript: all authors; approval of the manuscript: all authors; Guarantor of work: SM.
Funding National Institutes of Health/National Eye Institute Grants R01EY029058, R01EY011008, R01EY034148, U10EY14267, R01EY026574, R01EY019869, R01EY027510, R01EY028284, P30EY022589, and 5K12EY024225; Tobacco Related Disease Research Programme Grant T31IP1511; Core Grant P30EY022589, an unrestricted grant from Research to Prevent Blindness (New York, New York); EyeSight Foundation of Alabama and participant retention incentive grants in the form of glaucoma medication at no cost from Novartis/Alcon Laboratories, Allergan, Akorn and Pfizer.
Competing interests RW: financial support—National Eye Institute. Research instruments: Carl Zeiss Meditec, Centervue, Heidelberg Engineering, Konan, Optovue, Consultant—Aerie Pharmaceuticals, Allergan, Eyenovia, Nicox, Novartis; JML: research support—Carl Zeiss Meditec, Heidelberg Engineering, National Eye Institute, Optovue; Consultant—Alcon, Allergan, Carl Zeiss Meditec, Heidelberg Engineering; CAG: financial support—EyeSight Foundation of Alabama; National Eye Institute; Research to Prevent Blindness; MAF: financial support—EyeSight Foundation of Alabama; National Eye Institute; Research to Prevent Blindness; LMZ: research support—Carl Zeiss Meditec, Heidelberg Engineering, National Eye Institute, Topcon, Optovue.
Provenance and peer review Not commissioned; externally peer reviewed.
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