Air pollution exposure is associated with an increased risk of developing Parkinson disease (PD) and dyskinesia, according to study results published in JAMA Network Open.
Researchers conducted a population-based case-control study to examine whether air pollution in the form of particulate matter with a diameter of 2.5 μm or less (PM2.5) and nitrogen dioxide (NO2) is related to the risk for and clinical characteristics of PD. The researchers sourced data from Rochester Epidemiology Project and patients with PD in Minnesota between 1991 and 2015 were identified for study inclusion. Control patients were matched 20:1 with patients with PD. Based on their most prominent feature on examination, patients with PD were divided into 2 subgroups (akinetic rigid and tremor-predominant PD subtypes).
The primary outcome was incident PD risk. Secondary outcomes included all-cause mortality following PD symptom onset, presence of tumor-predominant vs akinetic rigid PD, and development of dyskinesia. Logistic regression and Cox proportional hazards regression models were used in statistical analyses.
A total of 346 incident cases of PD (median age, 72; men, 62.4%; White, 95.4%; non-Hispanic/Latino, 98.0%) were identified for study inclusion and matched with 4183 control patients (median age, 72; men, 61.2%; White, 86.5%; non-Hispanic/Latino, 88.9%).
A positive association was found between PM2.5 and PD risk. Compared with the lowest quintile of PM2.5 exposure, the increased risk of developing PD associated with PM2.5 exposure was 4% in the second quintile (odds ratio [OR], 1.04; 95% CI, 1.02-1.06) and 14% in the top quintile (OR, 1.14; 95% CI, 1.11-1.18).
Similarly, a positive relationship was found between NO2 and PD risk; however, this was only observed in the top 2 quintiles of NO2 exposure. Compared with the lowest quintile of NO2 exposure, the odds of PD were increased by 5% in the fourth quintile (OR, 1.05; 95% CI, 1.01-1.10) and 13% in the top quintile (OR, 1.13; 95% CI, 1.07-1.19).
Increased PM2.5 exposure was associated with a 36% increased risk for akinetic rigid presentation (OR per 1-μg/m3 increase, 1.36; 95% CI, 1.02-1.80; P =.03).
A total of 259 (74.9%) patients with PD were deceased at the time of data abstraction (median time from PD symptom onset to death, 9.0 years). No significant association was observed between level of PM2.5 exposure and mortality risk (hazard ratio [HR] per 1-μg/m3 increase, 0.93; 95% CI, 0.82-1.05; P =.23).
Dyskinesia developed in 54 (15.6%) patients with PD (median time from PD symptom onset to dyskinesia, 5.6 years). Each 1-μg/m3 increase in PM2.5 exposure was linked to a 42% greater risk for dyskinesia (HR, 1.42; 95% CI, 1.17-1.73; P <.001).
Study limitations include the dataset’s limited geographic extent and potential exposure misclassification errors.
“These findings suggest that a reduction in PM2.5 may help reduce the risk of PD and affect the clinical profile of PD and disease complications (modifying the PD phenotype and the risk of dyskinesia in patients with PD),” the study authors concluded.
Disclosure: One study author declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.