Greater Smoking Intensity May Accelerate Retinal Nerve Thinning in Glaucoma

Patients with primary open-angle glaucoma (POAG) experience faster rates of circumpapillary retinal nerve fiber layer (cpRNFL) thinning based on their intensity of tobacco smoking, according to findings published in the British Journal of Ophthalmology. The study shows that the structural change these patients experience can occur more rapidly based on their smoking pack-year index.

Data for this analysis were sourced from the University of California San Diego Diagnostic Innovations in Glaucoma Study and African Descent and Glaucoma Evaluation Study. Researchers looked at 466 eyes of 314 patients with POAG) semiannually using spectral domain optical coherence tomography (SD-OCT). Longitudinal changes to the cpRNFL were evaluated on the basis of ethnicity and pack-years of cigarettes smoked at baseline.

The participants were aged mean 67.0 (95% CI, 65.8-68.2) years, 51.3% were women, 50.6% were of European descent, 41.7% were of African descent, 37.6% reported ever smoking, smoking intensity was 16.5 (95% CI, 13.3-19.8) pack-years, and cpRNFL thickness was 72.9 (95% CI, 71.4-74.5) μm.

Stratified by ethnicity, individuals with African descent were younger and fewer drank alcohol. This participants group also had higher body mass indexes (BMI), more hypertension and diabetes, shorter axial lengths, thinner central corneal thicknesses, thicker cpRNFLs, and higher intraocular pressure (all P ≤.038) compared with individuals with European descent. Stratified by smoking status, the groups had similar demographic and ophthalmologic features, except that more men were smokers (P =.027).

During a mean follow-up of 6.6 years, the slope of cpRNFL change was -0.62 μm/year overall, -0.67 μm/year among those with African descent, -0.64 μm/year among nonsmokers, -0.59 μm/year among those with European descent, and -0.59 μm/year among smokers.

The change in cpRNFL associated with central corneal thickness per 100 μm thinner (coefficient, -0.15 μm/year; P =.030), smoking intensity per 10 pack-year increase (coefficient, -0.06 μm/year; P =.012), mean intraocular pressure per 1 mm Hg increase (coefficient, -0.03 μm/year; P =.002), axial length per 1 mm increase (coefficient, 0.05 μm/year; P =.041), and hypertension (coefficient, 0.13 μm/year; P =.041) in the univariate model.

In the multivariate model that accounted for smoking history, change in cpRNFL associated with African ancestry (coefficient, -0.27 μm/year; P =.012), smoking intensity (coefficient, -0.06 μm/year; P =.031), and baseline 24-2 visual field mean deviation per 1 dB worse (coefficient, 0.02 μm/year; P =.047). In the model that accounted for smoking intensity, more rapid cpRNFL thinning was associated with African ancestry (coefficient, -0.27 μm/year; P =.017).

Risk for moderate to fast RNFL thinning associated with smoking intensity per 10 pack-years (odds ratio [OR], 1.28; P =.006).

“Higher intensity of smoking was significantly associated with faster rates of RNFL thinning over time, supporting that evaluation of smoking intensity might add information to the assessment of risk of glaucoma progression,” the researchers report.

Patients with African descent “experience earlier onset and increased severity of POAG compared with those of [European descent] and are on average 3 times more likely to develop POAG,” the study authors explain, adding that patients with African descent have disproportionately higher rates of tobacco-related disease and death.

The major limitation of this study was that many patients were early in their POAG disease. These findings may not be generalizable for moderate to severe glaucoma.

Disclosure: Multiple authors declared affiliations with industry. Please refer to the original article for a full list of disclosures.