Cigarette Smoking and Parkinson's Disease

Abstract

Scientific Background: Despite intensive research, the aetiology of Parkinson's disease (PO) still remains obscure but most likely it is multifactorial. The majority of the studies concerned with the relation between tobacco consumption and PD have come to the same conclusion that tobacco smoking decreases the risk of PD. This was considered as a protective effect of tobacco for PD, however some authors have pointed out that, the early mortality associated with smoking related diseases like cancer and myocardial infarction might be responsible for the relatively reduced presence of smoker population in PH studies. Objectives: In this respect we compared smoker and non-smoker patients for parameters related to PD and investigated the association between tobacco smoking and PD for the Turkish population. Material and Methods: The study group included 118 patients with PD followed by Ankara University, Department of Neurology, Out-patient Clinic of Movement Disorders. Patients were classified as smokers if they had ever smoked for a period of more than 6 months throughout their lives and the quantity ofsmoking was given as cigarette-year value, which was defined as the number of smoking years multiplied by the number of cigarettes consumed per day. All the patients were then evaluated for age, sex, accommodation (urban, rural), education status (years) and alcohol consumption and PD related parameters such as age of onset (the age when the patient experienced his/her first symptom of PD), duration, severity of the disease evaluated according to the "Unified Parkinson's Disea se Rating Scale (UPDRS)" and the rate of progression that was defined as the final UPDRS score divided by the duration of disease in years. Results: Among 118 patients with PD, 45 (38%) cases were female while 73 (62%) were male. For the total population the mean age, age of onset, durationof the disease, UPDRS and the rate of progression values were found as 62.7 (rang e 39-87 std.dev.±9.4) years, 583 (range 29-81 std.dev.± 10 8) years, 4.5 (range 0.1-24 std.dev.±4.1) years, 35.3 (range 11- 105, stddev.± 14.8) and 19.1 (range 1.5-360 std.dev.±36.5) respectively Forty-two (35.6%) patients were smokers while 76(64.4%) were non-smokers and the mean cigarette-year value was 436 (range 10-1200, std.dev.±358.5). No correlation was identified between the age of onset and sex, accommodation, education level and alcohol consumption. There was a positive correlation between ciga rette -year value and the age of onset (Spearman's rho= 0.4, p=0.02) so that the higher the amount of smoking the la ter the age of initiation for PD. However no difference was present between smokers and non-smokers with regard to the rate of progression and no correlation existed between the rate of progression andthe quantity of smoking (Spearman rho=0 .9). Conclusions: The bene ficial effect of cigarette smoking rela ted to the late development of Pd should not make us overlook the potential hazards of tobacco smoking and related clinical morbidity due to infarction, malignancy, pulmonary and vascular diseases.