摘要
To explore the association of Parkinson抯 disease (PD) with cigarette smoking. Methods One hundred of fourteen PD patients were compared with 205 control subjects who were matched by gender, race and residency. A previously validated questionnaire including smoking, alcohol/tea consumption as well as some other environmental exposure data was administered. Results With never-smokers as the reference category, we observed reduced risk for PD among ever smokers (OR=0.49, 95% CI: 0.30 to 0.79) current smokers (OR=0.44, 95% CI: 0.23 to 0.86) and ex-smokers (OR=0.54, 95% CI: 0.30 to 0.96). When ever smokers were stratified by years of smoking, there was an inverse correlation between those whose smoking history was longer than 20 years (OR=0.40 95% CI: 0.21 to 0.81) and an even mild protective correlation between those who smoked less than 20 years (OR=0.57, 95% CI: 0.33 to 0.99). Those who had quitted smoking for more than 20 years were less likely to have the disease than never smokers, and those who had quitted for less than 20 years were least likely to have PD, while those who were current smokers were still least likely to have the disease. We found significant inverse gradient with pack-day smoking (trend P<0.05), and the inverse correlation between cigarette smoking and PD was not confounded by alcohol/tea consumption and other confounding bias. Conclusions The inverse correlation between Parkinson抯 disease risk and smoking as well as the trend of gradient dose response is again observed in our study. More future researches are needed to confirm these correlations and to explore further biochemical evidence.
To explore the association of Parkinson抯 disease (PD) with cigarette smoking. Methods One hundred of fourteen PD patients were compared with 205 control subjects who were matched by gender, race and residency. A previously validated questionnaire including smoking, alcohol/tea consumption as well as some other environmental exposure data was administered. Results With never-smokers as the reference category, we observed reduced risk for PD among ever smokers (OR=0.49, 95% CI: 0.30 to 0.79) current smokers (OR=0.44, 95% CI: 0.23 to 0.86) and ex-smokers (OR=0.54, 95% CI: 0.30 to 0.96). When ever smokers were stratified by years of smoking, there was an inverse correlation between those whose smoking history was longer than 20 years (OR=0.40 95% CI: 0.21 to 0.81) and an even mild protective correlation between those who smoked less than 20 years (OR=0.57, 95% CI: 0.33 to 0.99). Those who had quitted smoking for more than 20 years were less likely to have the disease than never smokers, and those who had quitted for less than 20 years were least likely to have PD, while those who were current smokers were still least likely to have the disease. We found significant inverse gradient with pack-day smoking (trend P<0.05), and the inverse correlation between cigarette smoking and PD was not confounded by alcohol/tea consumption and other confounding bias. Conclusions The inverse correlation between Parkinson抯 disease risk and smoking as well as the trend of gradient dose response is again observed in our study. More future researches are needed to confirm these correlations and to explore further biochemical evidence.
