Long-Term Road Traffic Noise Exposure and Its Association with Parkinson Disease Risk: Insights from a Danish Nationwide Cohort Study

Highlight

• Long-term residential exposure to road traffic noise is associated with a modest but statistically significant increase in Parkinson disease (PD) risk.
• Having a quiet side of the residence (a noise difference of ≥10 dB between the most and least exposed facades) mitigates the risk associated with traffic noise.
• The association remains robust after adjusting for air pollution, green space, sociodemographic factors, smoking, and physical activity.
• Findings suggest noise pollution as a novel environmental risk factor for PD, emphasizing the importance of urban noise mitigation strategies.

Study Background

Parkinson disease is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms, significantly impacting quality of life among older adults. While aging and genetic predisposition are established risk factors, environmental exposures are increasingly recognized contributors to PD pathogenesis. Among various urban environmental stressors, road traffic noise has been proposed to impact neurological health through mechanisms involving stress response, sleep disturbance, and possibly neuroinflammation. Despite hypothesized associations, epidemiological evidence linking long-term noise exposure to PD risk has been limited and inconsistent, necessitating comprehensive prospective studies.

Study Design

This investigation was a Danish nationwide prospective cohort study examining the association between residential road traffic noise exposure and the incidence of Parkinson disease. The study leveraged the complete residential address history of Danish residents aged 40 years and older from 1990 onward, enabling calculation of 10-year time-weighted average exposure to road traffic noise (expressed as LDEN) at both the most and least exposed facades of each residence. Incident PD cases were identified through the National Patient Register between 2000 and 2017. Cox proportional hazards models were used to estimate hazard ratios (HRs) adjusting for a comprehensive panel of individual-level and area-level sociodemographic factors, air pollution indicators (fine particulate matter ≤2.5 µm [PM2.5] and ultrafine particles), and access to green space. Sensitivity analyses adjusted for smoking and physical activity in a subset of participants to address potential residual confounding.

Key Findings

Among 3,103,577 participants (mean age 50.9 years, 51.2% female), 20,587 incident PD cases occurred during follow-up. The study found a statistically significant association between road traffic noise at the most exposed facade (LDEN-Max) and increased PD risk, with a hazard ratio (HR) of 1.03 (95% CI, 1.00–1.05) per interquartile range (11.5 dB) increment. Adjusting for the noise difference between the facades (Δnoise), an indicator of having a quiet side of the residence, strengthened this association (HR 1.06; 95% CI, 1.02–1.09), indicating that noise exposure is a nuanced exposure metric.

Importantly, having a quiet facade defined as a noise difference of 10 dB or more was associated with a decreased risk of PD across various levels of high LDEN-Max exposure (>50 dB), suggesting a protective effect of reduced noise exposure within the same dwelling. Noise exposure at the least exposed facade also showed a similar association, with an HR of 1.04 (95% CI, 1.02–1.07) per interquartile increment of 8.9 dB.

These associations were consistent across subgroups defined by sex, education, income, cohabitation status, and population density. Additional adjustment for lifestyle factors such as smoking and physical activity did not materially alter the findings, supporting the robustness of the observed associations.

Expert Commentary

This study offers compelling evidence supporting road traffic noise as an environmental risk factor for Parkinson disease. The large sample size, nationwide scope, and comprehensive exposure assessment enhance the internal validity and generalizability within similar urban settings. Mechanistically, chronic noise exposure may induce neurodegenerative pathways via stress-mediated neuroinflammation, oxidative stress, or sleep disruption – all proposed contributors to PD pathogenesis.

Notably, the study highlights the value of considering the heterogeneous noise exposure within residences, underscoring that a “quiet side” may mitigate adverse health effects through improved sleep and reduced stress. These findings align with emerging public health policies advocating for urban planning strategies that preserve quiet residential spaces to promote neurological as well as cardiovascular health.

Study limitations include potential exposure misclassification inherent in modeled noise data, residual confounding due to unmeasured factors, and generalizability limited to populations with similar urban infrastructure and healthcare systems. Further research integrating biological markers of exposure and mechanistic studies would strengthen causal inference.

Conclusion

This Danish nationwide cohort study demonstrates that long-term exposure to residential road traffic noise is associated with a modestly increased risk of Parkinson disease. The presence of a quieter side of the residence attenuates this risk, illuminating the importance of nuanced exposure assessment. These findings introduce noise as a novel environmental risk factor for PD and have significant implications for public health and urban policy, advocating for noise mitigation interventions and architectural design strategies that foster quieter living environments. Continued research is warranted to explore underlying biological mechanisms and to inform targeted preventive measures.

Funding and Clinical Trials

The study was supported by Danish national research institutions and did not involve interventional clinical trial registration.

References

1. Sørensen M, Poulsen AH, Raaschou-Nielsen O, et al. Road Traffic Noise, Noise Difference Between Residential Facades, and Risk of Parkinson Disease. JAMA Neurol. 2026; Published July 20, 2026. doi:10.1001/jamaneurol.2026.42475104
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