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Beate Ritz, MD, PhD; Alberto Ascherio, MD, DrPH; Harvey Checkoway, PhD; Karen S. Marder, MD, MPH; Lorene M. Nelson, PhD; Walter A. Rocca, MD, MPH; G. Webster Ross, MD; Daniel Strickland, PhD; Stephen K. Van Den Eeden, PhD; Jay Gorell, MD

Arch Neurol. 2007;64(7):990-997.

Context  Epidemiologic studies have reported that cigarette smoking is inversely associated with Parkinson disease (PD). However, questions remain regarding the effect of age at smoking onset, time since quitting, and race/ethnicity that have not been addressed due to sample size constraints. This comprehensive assessment of the apparent reduced risk of PD associated with smoking may provide important leads for treatment and prevention.

Objective  To determine whether race/ethnicity, sex, education, age at diagnosis, and type of tobacco modify the observed effects of smoking on PD.

Design, Setting, and Participants  We conducted the first ever pooled analysis of PD combining individual-level data from 8 US case-control and 3 cohort studies (Nurses' Health Study, Health Professionals Follow-Up Study, and Honolulu-Asia Aging Study) conducted between 1960 and 2004. Case-control studies provided data for 2328 PD cases and 4113 controls matched by age, sex, and ethnicity; cohort studies contributed 488 cases and 4880 controls selected from age- and sex-matched risk sets.

Main Outcome Measure  Incident PD.

Results  We confirmed inverse associations between PD and smoking and found these to be generally stronger in current compared with former smokers; the associations were stronger in cohort than in case-control studies. We observed inverse trends with pack-years smoked at every age at onset except the very elderly (>75 years of age), and the reduction of risk lessened with years since quitting smoking. The risk reductions we observed for white and Asian patients were not seen in Hispanic and African American patients. We also found an inverse association both for smoking cigars and/or pipes and for chewing tobacco in male subjects.

Conclusions  Our data support a dose-dependent reduction of PD risk associated with cigarette smoking and potentially with other types of tobacco use. Importantly, effects seemed not to be influenced by sex or education. Differences observed by race and age at diagnosis warrant further study.

Author Affiliations: Department of Epidemiology and Environmental Health Sciences, University of California, Los Angeles, School of Public Health, Los Angeles (Dr Ritz); Department of Neurology, University of California, Los Angeles, School of Medicine, Los Angeles (Dr Ritz); Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, Massachusetts (Dr Ascherio); Department of Environmental and Occupational Health Sciences, University of Washington, Seattle (Dr Checkoway); Gertrude H. Sergievsky Center, Taub Institute, and Departments of Neurology and Psychiatry, Columbia University College of Physicians and Surgeons, New York, New York (Dr Marder); Division of Epidemiology, Department of Health Research and Policy, Stanford University School of Medicine, Palo Alto, California (Dr Nelson); Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic College of Medicine, Rochester, Minnesota (Dr Rocca); Veterans Affairs Pacific Islands Health Care System, Pacific Health Research Institute, Honolulu, Hawaii (Dr Ross); Research and Evaluation, Kaiser Permanente, Southern California, Pasadena (Dr Strickland); Division of Research, Kaiser Permanente, Oakland, California (Dr Van Den Eeden); and Department of Neurology, Henry Ford Hospital, Detroit, Michigan (Dr Gorell).
Deceased.

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