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© Borgis - Postępy Nauk Medycznych 12/2013, s. 865-867
*Ewa Czaplicka1, Iwona Grabska-Liberek2, Iwona Rospond1, Jarosław Kocięcki1
Narażenie na dym tytoniowy i jego wpływ na narząd wzroku
Environmental exposure to tobacco smoke and condition of organ of vision
1Department and Clinic of Ophthalmology, Poznań University of Medical Sciences
Head of Department and Clinic: Jarosław Kocięcki, MD, PhD
2Clinic of Ophthalmology, Medical Center of Postgraduate Education, Warszawa
Head of Clinic: Iwona Grabska-Liberek, MD, PhD, assoc. prof.
Streszczenie
Dostępne dane epidemiologiczne sugerują, że nikotyna jest odpowiedzialna za wyższy odsetek zejść śmiertelnych związanych z jej zażywaniem niż kokaina, nikotyna i alkohol łącznie.
Palenie czynne i bierne wywołuje istotny wpływ na struktury gałki ocznej , upośledza fizjologiczne procesy i stymuluje powstanie procesów patologicznych , które są odpowiedzialne za powstawanie chorób oczu. Badania przeprowadzone w obrębie nauk podstawowych umożliwiają głębsze zrozumienie mechanizmów wpływu nikotyny na narząd wzroku oraz ich związek z rozwojem i progresją schorzeń okulistycznych.
Autorzy omawiają toksyczny wpływ nikotyny na szereg struktur narządu wzroku i funkcję widzenia. Wyjaśniają rolę palenia i uzależnienia od nikotyny w patogenezie wielu chorób oczu.
Summary
According to the most recent epidemiological data, nicotine causes a greater number of addiction-related deaths than cocaine, heroin and alcohol combined. Its toxicity also significantly affects the organ of sight.
Smoking exerts a severe influence on all structures of the eyeball, impairing physiological processes as well as stimulating pathological processes which result in eye diseases. Studies conducted within fundamental science allow for a deeper understanding of the mechanisms of nicotine influence on the organ of sight and its connection to the development and progression of ophthalmic diseases.
The authors comment the toxic effect of nicotine on several anatomical structures of the eye and the visual function and discuss the role of smoking and nicotine abuse in the pathogenesis of several ocular diseases.
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).
Smoking also causes changes in microcirculation. Steigerwalt et al. in turn describeda 36% decrease in blood flow velocity in contraction and 52% in decontraction in ophthalmic artery, central retinal artery and posterior ciliary artery. According to the authors, this happens because of a contraction of minute vessels of the retinal and optic disc through sympathetic system excitation. This is why smoking may intensify the course of numerous ophthalmic diseases related to blood flow disorders e.g. diabetes, central retinal vein thrombosis, ischemic optic neuropathy and giant cell arteritis (Horton’s disease) (2, 3, 9).
Apart from cardiovascular factors including arterial hypertension, smoking is an important risk factor for retinal vein thromboses. The most recent studies show that smoking plays an important role in the etiology of thromboses taking place in arteriovenous crossings – in a prospective analysis of 874 eyes such thromboses were the most frequently observed type (2, 3, 10).

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Piśmiennictwo
1. Philips M: Smoke gets in your eyes... and in your breath! Wien Klin Wochenschr 2004; 116(1-2): 1-2.
2. Czaplicka EC, Rospond I: Nikotyna a narząd wzroku. [W:] Florek E, Piekoszewski W (red.): Tytoń a zdrowie. Choroby odtytoniowe. Akademia Medyczna, Poznań 2003: 156-159.
3. Czaplicka EL, Rospond-Kubiak I: Wpływ palenia tytoniu na narząd wzroku. Prz Okulist 2006; 3(3): 3-4.
4. Grus FH, Sabuncuo P, Agustin A et al.: Effect of smoking on tear proteins. Graefe’s Arch Clin Exp Ophthalmol 2002; 240: 889-892.
5. Satici A, Bitiren M, Ozardali I et al.: The effects of chronic smoking on the ocular surface and tear characteristics: a clinical, histological and biochemical study. Acta Ophthalmol Scand 2003; 81: 583-597.
6. Robinson JW, Brownstein S, Jordan DR et al.: Conjunctival mucoepidermoid carcinoma in a patient with ocular cicatricial pemphigoid and a review of the literature. Surv Ophthalmol 2006 Sep-Oct; 51(5): 513-519.
7. Arnarsson A, Jonasson F, Sasaki H et al.: Reykjavik Eye Study Group. Risk factors for nuclear lens opacification: the Reykjavik Eye Study. Dev Ophthalmol 2002; 35: 12-20.
8. Kaiser HJ, Schoetzau A, Flammer J: Blood flow velocity on the extraocular vessels in chronic smokers. Br J Ophthalmol 1997; 81: 133-135.
9. Steigerwalt RD, Laurora G, Incandela L et al.: Ocular and orbital blood flow in cigarette smokers. Retina 2000; 20: 394-397.
10. Beaumont PE, Kang HK: Clinical characteristics of retinal venous occlusions occurring at different sites. Br J Ophthalmol 2002; 86: 572-580.
11. Beratis NG, Varvarigou A, Katsibris J et al.: Vascular retinal abnormalities in neonates of mothers who smoked during pregnancy. J Paediatr 2000; 136: 760-766.
12. Everekliogliu C, Özkiriş A, Alaşehirli B et al.: Effect of gestational nicotine treatment on newborn rat retina: a histopatological and morphometric analysis. Ophthal Physiol Opt 2003; 23: 527-533.
13. Leeuwen van R, Klaver CC, Vingerling JR et al.: Epidemiology of age related maculopathy: a review. Eur J Epidemiol 2003; 18: 845-854.
14. Handelman GJ: The evolving Role of Carotenoids in Human Biochemistry. Nutrition 2001; 17: 818-822.
15. Klein R, Knudtson MD, Cruickshanks KJ, Klein BEK: Further observations on the relationship of smoking to the long-term incidence and progression of age-related macular degeneration. The Beaver Dam Eye Study. Arch Ophthalmol 2008; 126(1): 115-121.
16. Lee AJ, Rochtchina E, Wang JJ et al.: Does smoking affect intraocular pressure? Finding from the Blue Mountains Eye Study. J Glaucoma 2003; 12: 209-212.
17. Kang JH, Pasquale LR, Rosner BA et al.: Prospective Study of Cigarette Smoking and the Risk of Primary Open-angle Glaucoma. Arch Ophthalmol 2003; 121: 1762-1768.
18. Pereira CB, Strupp M, Eggert T et al.: Nicotine-induced nystagmus: Three-dimensional analysis and dependence on head position. Neurology 2000; 55: 1563-1565.
19. Schotthoefer EO, Wallace DK: Strabismus associated with thyroid eye disease. Curr Opin Ophthalmol 2007; 18(5): 361-365.
20. Kański JJ: Okulistyka Kliniczna. Wydawnictwo Urban & Partner, Wrocław 1997: 464-465.
otrzymano: 2013-09-22
zaakceptowano do druku: 2013-11-04

Adres do korespondencji:
*Ewa Czaplicka
Department of Ophthalmology
Autonomous Public Teaching Hospital no. 2
Poznan University of Medical Sciences
ul. Długa 1/2, 68-848 Poznań
tel. +48 618-549-284, fax: +48 618-549-084
e-mail: dreczaplicka@gmail.com

Postępy Nauk Medycznych 12/2013
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