Smoking and Parkinson's disease - A dose-response relationship

被引:180
作者
Gorell, JM
Rybicki, BA
Johnson, CC
Peterson, EL
机构
[1] Henry Ford Hlth Syst, Dept Neurol, Detroit, MI USA
[2] Henry Ford Hlth Syst, Dept Biostat & Res Epidemiol, Detroit, MI USA
[3] Wayne State Univ, Natl Inst Environm Hlth Sci, Ctr Mol & Cellular Toxicol Human Applicat, Detroit, MI USA
关键词
D O I
10.1212/WNL.52.1.115
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objective: To determine whether an inverse dose-response relationship exists between cigarette smoking and PD among ever-smokers and ex-smokers. Methods: Smoking and alcohol consumption were analyzed in 144 PD patients and 464 control subjects, who were frequency matched for sex, race, and age (+/-5 years), in a population-based ease-control study of men and women greater than or equal to 50 years old in the Henry Ford Health System. Results: With never-smokers as the reference category, there was an inverse association between current light smokers (>0 to 30 pack-years) and PD patients (odds ratio [OR], 0.59; 95% CI, 0.23 to 1.53), and a stronger inverse association of PD with current heavy smokers (>30 pack-years; OR, 0.08; 95% CI, 0.01 to 0.62). When former >30-pack-year smokers were stratified by the interval since quitting, there was an inverse association between those who stopped >20 years ago and PD (OR, 0.86; 95% CI, 0.42 to 1.75), and a greater inverse relationship with those who stopped 1 to 20 years ago (OR, 0.37; 95% CI, 0.19 to 0.72). Alcohol consumption had no independent, significant association with PD, but heavy drinking (>10 drink-years) had a greater effect than light-moderate drinking in reducing but not eliminating the inverse association between smoking and PD. Conclusions: The inverse dose-response relationship between PD and smoking and its cessation is unlikely to be due to bias or confounding, as discussed, providing indirect evidence that smoking is biologically protective.
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页码:115 / 119
页数:5
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