Epidemiologic studies1-3 of the association between cancer and Parkinson disease (PD) have generally found a lower risk of cancer after PD and vice versa. Most studies1-3 have examined primarily white or Western populations. In contrast, Lin et al4 analyzed a Taiwanese population and found elevated risks for total and most cancer sites after PD. They attributed the elevated risks to ethnicity or environmental exposures. In a comment5 on the article by Lin et al,4 we suggested that the authors examine whether medical surveillance contributed to the risks.
In our US study of PD and cancer using data from Surveillance, Epidemiology, and End Results (SEER) and Medicare, we adjusted for a surrogate for surveillance (number of physician visits) and found the odds of cancer in the total population after PD was reduced.6 Notably, however, the reduced odds were similar to those of cancer after automobile crashes, although cancer and automobile crashes are unlikely to be biologically related. We concluded that these associations were consistent with a bias in ascertaining cancer after serious medical conditions rather than an association between PD and cancer. In this study, we undertake a similar analysis in SEER-Medicare restricted to Asian Americans, the population most likely to be ethnically similar to the Taiwanese study population examined by Lin et al.4
Using SEER-Medicare linked data (January 1, 1992, through December 31, 2005) of adults 66 years and older, we conducted a case-control study of 20 627 first primary cancer cases and 5558 controls (selected from a 5% random sample) to assess cancer after PD in Asian Americans. We estimated odds ratios (ORs) from unconditional logistic regression models for PD preceding cancer (0 to <5 years), adjusted for physician visits, sex, age at diagnosis or selection, and selection years, with P values based on 2-sided tests. To explore biases in ascertaining cancer in SEER-Medicare, we examined associations between cancer and automobile crash injuries (International Classification of Diseases, Ninth Revision, code E810-819), which we expected to be null. We also examined risks for individual cancer sites with more than 10 PD events among both cancer cases and controls. The National Institutes of Health Office of Human Subjects Research determined that this study using SEER-Medicare data was exempt from the regulatory requirements for human subject research, including requirements for informed consent and institutional review board approval, under the exemption applicable to deidentified data.
Table 1 gives the demographic and other characteristics of cancer cases and controls. Overall, there was no association between PD and subsequent cancer (OR, 0.95; 95% CI, 0.56-1.59) (Table 2). In addition, there was no association between automobile crashes and subsequent cancer (OR, 1.04; 95% CI, 0.76-1.41).
No association between PD and cancer was seen in men or women (Table 2). The only 2 cancer sites with more than 10 PD events were colon and prostate cancer, which were also unrelated to earlier PD (Table 2).
Both cancer and PD occur primarily at advanced ages and can be debilitating. Consequently, medical surveillance for cancer could be influenced by a prior PD diagnosis, which may bias the observed PD-cancer associations. Moreover, patterns of medical surveillance may differ by health care system (eg, US Medicare and Taiwan National Health Insurance Research Database). It is therefore important that in evaluating PD-cancer associations investigators adjust for medical surveillance and include negative controls.
Although we cannot rule out small risks attributable to sample size, we did not find a positive association between PD and subsequent cancer in Asian Americans in SEER-Medicare data. Although according to SEER-Medicare data Asian Americans are ethnically more diverse than the Taiwanese population, our null findings do not support the hypothesis that ethnicity is a major contributor to the elevated risk in the study by Lin et al.4 The elevated risks observed in the study by Lin et al4 could reflect various factors, including possibly more cancer surveillance after PD.
Corresponding Author: D. Michal Freedman, PhD, MPH, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 9609 Medical Center Dr, 7E538, Rockville, MD 20850 (email@example.com).
Published Online: May 19, 2016. doi:10.1001/jamaoncol.2016.0729.
Author Contributions: Drs Freedman and Pfeiffer had full access to all the data in the study and takes responsibility for the integrity of the data and the integrity of the data analysis.
Study concept and design: Both authors.
Acquisition, analysis, or interpretation of data: Both authors.
Drafting of the manuscript: Both authors.
Critical revision of the manuscript for important intellectual content: Both authors.
Statistical analysis: Pfeiffer.
Conflict of Interest Disclosures: None reported.
Funding/Support: This work was supported by the Intramural Research Program of the National Cancer Institute, National Institutes of Health, and the US Public Health Service.
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