In This Article:
Although Parkinson’s disease (PD) poses a serious risk to the quality of life and well-being of those suffering from it, the neurodegenerative illness remains relatively poorly understood. Current medical orthodoxy considers the onset of PD to be the product of interacting genetic and environmental factors. In a recent study of this dynamic in JAMA Network Open, Dayoon Kwon and colleagues consider the interplay of traffic-related air pollution, known genetic predispositions to PD, and the disease’s incidence among two large cohorts in the US and Denmark. Their analysis suggests that air pollution exposure, while showing a more modest positive correlation with new PD diagnoses than genetic risk, does increase the odds of its onset. GlobalData epidemiologists forecast that the diagnosed prevalent cases of PD in the US will increase from nearly 1,031,000 to over 1,238,000 between 2025 and 2033. Research such as that of Kwon and colleagues into PD’s complex aetiology and risk factors may allow for a reduction in the disease’s burden or improvement in its clinical management from a more nuanced understanding of its onset and early detection.
Kwon and colleagues conducted a combined case-control study and meta-analysis of two cohorts of adults with a mean age of 65 based in central California and Denmark. The US study consisted of 634 cases and 733 controls in a two-phase study between 2000 and 2017. In Denmark, 966 cases and 1,045 controls were selected from national hospital records between 1996 and 2009 for retroactive analysis. To measure exposure to traffic-related air pollution, the authors leveraged government pollution monitoring and meteorological data, with a focus on carbon monoxide levels in the event of data gaps. Genetic risk was identified in patients based on commercially available genotyping kits of participants, with 90 genetic loci identified as high risk for the development of PD. In the US, analysis of the above factors in case and control populations showed that individuals with select genetic loci and those exposed to traffic-related air pollution were 1.69 times and 1.10 times, respectively, more likely to develop PD than those without genetic or environmental exposure. Moreover, as seen in Figure 1 (below), those with high genetic risk and air pollution exposure were more than three times as likely to have PD. These results underscore the complex interplay of biological and environmental factors that contribute to PD diagnoses.
The work of Kwon and colleagues brings attention to the risk factors for PD, inviting further inquiry into the role of environmental stressors in its onset. Their findings are particularly resonant for individuals with genetic predispositions to PD, given the notable increase in risk for its development when such participants were exposed to traffic-related air pollution. Provided that a larger body of work is generated and demonstrates stronger correlations between air pollution and PD, it could provide a further rationale for policymakers to more strictly manage air pollution, which has already been associated with myriad negative health endpoints. Furthermore, these findings could be factored into the clinical prediction and management of PD by allowing physicians to identify another risk factor to guide early assessments of individuals with other risk factors living in high-risk areas.