Abstract

Aim. To evaluate the acute effects of cigarette smoking on photopic and mesopic pupil sizes and wavefront aberrations. Methods. Cigarette smoker volunteers were recruited in the study. Photopic and mesopic pupil sizes and total ocular aberrations were measured before smoking and immediately after smoking. All volunteers were asked to smoke a single cigarette containing 1.0 mg nicotine. Pupil sizes and total ocular aberrations were assessed by optical path difference scanning system (OPD-Scan II ARK-10000, NIDEK). Only the right eyes were considered for statistical analysis. The changes of pupil size and total ocular aberrations after smoking were tested for significance by Wilcoxon signed ranks test. Results. Mean photopic pupil size decreased from 3.52 ± 0.73 mm to 3.29 ± 0.58 mm (P = 0.001) after smoking. Mean mesopic pupil size was also decreased from 6.42 ± 0.75 mm to 6.14 ± 0.75 mm after smoking (P = 0.001). There was a decrease in all the measured components of aberrations (total wavefront aberration, higher-order aberration, total coma, total trefoil, total tetrafoil, total spherical aberration and total higher-order aberration) after smoking; however the differences were insignificant for all (P > 0.05). Conclusion. Our results indicate that pupil constricts after smoking. On the other hand, smoking does not alter ocular aberrations.

Highlights

  • Nicotine is the primary active pharmacological agent in tobacco products, accounting for only acute pharmacological effects of smoking [1]

  • OPD-Scan II ARK-10000 is a refractive power analyzer, wavefront analyzer, corneal topographer, keratometer, autorefractor, and pupillometer all in one unit [13]. In this Journal of Ophthalmology study we aimed to examine the acute effects of cigarette smoking on photopic pupil size, mesopic pupil size, and wavefront aberrations of the eye in a group of young male smokers using OPD-Scan system

  • Mean mesopic pupil size decreased from 6.42 ± 0.75 mm to 6.14 ± 0.75 mm after smoking (P = 0.001)

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Summary

Introduction

Nicotine is the primary active pharmacological agent in tobacco products, accounting for only acute pharmacological effects of smoking [1]. The other compounds of tobacco are responsible for the adverse long-term cardiovascular, pulmonary, and carcinogenic effects. Autonomic nervous system is composed of sympathetic and parasympathetic nervous systems. Sympathetic nervous system has adrenergic receptors at preganglionic and postganglionic terminals. Parasympathetic nervous system has cholinergic nicotinic receptors at somatic motor and preganglionic terminals and cholinergic muscarinic receptors at postganglionic terminals. It is known that iris receives dual innervation from both the sympathetic and the parasympathetic nervous systems, the sphincter iris muscle and the dilatator iris muscle being under the control of sympathetic and parasympathetic nerves, respectively [6, 7]

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