Nicotine was named after J. Nicot (1530-1600), a French ambassador in Lisbon who was sending tobacco leaves to France, thus making tobacco smoking popular. According to the most recent epidemiological data, nicotine causes a greater number of addiction-related deaths than cocaine, heroin and alcohol combined (1-3). Its toxicity also significantly affects the organ of sight (2, 3).

As an irritant, the tobacco smoke can cause conjunctival irritation and symptoms of the dry eye syndrome. This disease occurs frequently in industrialised countries. In the USA there are approximately 59 million patients suffering from this disease, and the number has doubled in the last 10 years (4). Demographic data show that approx. 25-40% of employees are exposed to tobacco smoke at work, due to both active and second-hand smoking and 25% of them exhibit symptoms of the dry eye syndrome. Grus et al. conducted research into the chemical composition of tear film in smokers. In comparison to a control group of non-smokers, a significant increase of lower molecular weight protein content in tears was observed, as well as an overexpression of area of 25-40 kDa molecular weight in electrophoresis. According to the authors, these changes are a result of the toxic effect of tobacco smoke which causes oxidative damage to proteins and might potentially increase the concentration of smaller protein fragments present in the tear film. Smoking can also damage or change the blood flow in this area causing transudation of protein molecules. Moreover, there are indicators of damage caused through free radicals in these patients (4).

In histopathological studies, Satici et al. showed a metaplasia of conjunctival epithelium and its keratinization in persons exposed to tobacco smoke. According to the authors, these changes are caused by a change in the stability of tear film in smokers resulting from lipid layer deficiency, which may additionally intensify lacrimation and cause irritation to eye surface tissues. A decrease of lysozyme content in tears caused by its local binding by toxins present in tobacco smoke has also been described (5). Because smoking intensifies the symptoms of dry eye syndrome it can also cause contact lens intolerance (2, 3). Smoking can be also a risk factor for spinocellular carcinoma of the conjunctiva (6).

Smoking is also risk factor for lens opacification. In Reykjavik Eye Study, the influence of different risk factors for lens opacification in Reykjavik inhabitants was assessed. It was demonstrated that apart from ageing, smoking was the most important variable risk factor for opacifications of this type (not demonstrated in cortico-nuclear opacifications) (2, 3, 7).

Smoking is an acknowledged risk factor for the development of many systemic vessels diseases. Nicotine influences the increase of catecholamines level in blood, which manifests as tachycardia and arterial blood pressure increase. Tobacco smoke contains 2-6% of carbon monoxide among other components. Smoking leads to increased level of carboxyhemoglobin, up to 5-15% (0.5% in non-smokers). This increases the accessibility of oxyhaemoglobin, changes its dissociation curve and decreases the oxygen supply to tissues as a result. Oxygen deficit, through regulatory mechanisms, causes dilation of vessels and increase of blood flow velocity. The changes described also apply to eyeball and retrobulbar vessels. Kaiser et al. described that the increase of the blood flow velocity mostly concerns ophthalmic artery, middle artery, central retinal vein and lateral short posterior ciliary artery in comparison to the non-smoking group. The author also observed a lowered diastolic and systolic blood pressure as well as tachycardia in smokers (2, 3, 8).