Neurology 1999;52:115
© 1999 American Academy of Neurology
Articles
Smoking and Parkinson’s disease
A dose–response relationship
Jay M. Gorell, MD,
Benjamin A. Rybicki, PhD,
Christine Cole Johnson, PhD and
Edward L. Peterson, PhD
From the Departments of Neurology (Dr. Gorell) and Biostatistics and Research Epidemiology (Drs. Rybicki, Johnson, and Peterson), Henry Ford Health System; and the National Institute of Environmental Health Sciences Center in Molecular and Cellular Toxicology with Human Applications (Drs. Gorell, Rybicki, and Johnson), Wayne State University, Detroit, MI.
Address correspondence and reprint requests to Dr. Jay M. Gorell, Department of Neurology, Henry Ford Hospital and Health Sciences Center, 2799 W. Grand Boulevard, Detroit, MI 48202.
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 case-control study of men and women  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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