|
|
||||||||
From the Departments of Nutrition (E.L.T., E.J.O., A.A.), Epidemiology (M.G.W., A.A.), and Environmental Health (M.G.W.), Harvard School of Public Health; Channing Laboratory (A.A.), Department of Medicine, Brigham and Womens Hospital, and Harvard Medical School; and Department of Neurology (M.A.S.), Massachusetts General Hospital, Boston, MA; Epidemiology Branch (H.C.), National Institute of Environmental Health Sciences, Research Triangle Park, NC; and Epidemiology and Surveillance Research Department (M.L.M., E.E.C., M.J.T.), American Cancer Society, Atlanta, GA.
Address correspondence and reprint requests to Mr. Evan L. Thacker, 655 Huntington Ave., Bldg. 2, Boston, MA 02115; e-mail: ethacker{at}post.harvard.edu.
Objective: To characterize further the relationship between smoking history and Parkinson disease (PD) risk by considering temporal and qualitative features of smoking exposure, including duration, average intensity, and recentness, as well as the relative importance of smoking during different periods of life.
Methods: We prospectively assessed incident PD from 1992 to 2001 among 79,977 women and 63,348 men participating in the Cancer Prevention Study II Nutrition Cohort, according to their cigarette smoking status and lifetime smoking histories.
Results: During follow-up, 413 participants had definite or probable PD confirmed by their treating neurologists or medical record review. Compared with never smokers, former smokers had a relative risk (RR) of 0.78 (95% CI 0.64 to 0.95) and current smokers had an RR of 0.27 (95% CI 0.13 to 0.56). On average, participants with more years smoked, more cigarettes per day, older age at quitting smoking, and fewer years since quitting smoking had lower PD risk. The relative risks and trends did not vary significantly by sex. The cumulative incidence of PD was lowest among participants who quit smoking at later ages. A 30% to 60% decreased risk of PD was apparent for smoking as early as 15 to 24 years before symptom onset, but not for smoking 25 or more years before onset.
Conclusions: The lower risk of Parkinson disease among current and former smokers varied with smoking duration, intensity, and recentness. The dependence of this association on the timing of smoking during life is consistent with a biologic effect.
Supported by a grant to Dr. Ascherio from the National Institute of Neurologic Disorders and Stroke (NS048517) and in part by the Intramural Research Program of the NIH, the National Institute of Environmental Health Sciences.
Disclosure: The authors report no conflicts of interest.
Received July 28, 2006. Accepted in final form November 8, 2006.
This article has been cited by other articles:
![]() |
C. Xiao, R. Nashmi, S. McKinney, H. Cai, J. M. McIntosh, and H. A. Lester Chronic Nicotine Selectively Enhances {alpha}4{beta}2* Nicotinic Acetylcholine Receptors in the Nigrostriatal Dopamine Pathway J. Neurosci., October 7, 2009; 29(40): 12428 - 12439. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. J. O'Reilly, H. Chen, H. Gardener, X. Gao, M. A. Schwarzschild, and A. Ascherio Smoking and Parkinson's Disease: Using Parental Smoking as a Proxy to Explore Causality Am. J. Epidemiol., March 15, 2009; 169(6): 678 - 682. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |