AHA Scientific Sessions 2026 Abstract · Nov 2, 2026
Transportation Noise Exposure Associates with Cardiovascular Events and Risk Factors Independently of Sleep
By Nguyen J, Saeed F, Bellinge JW et al.
Background: Elevated transportation noise exposure is independently linked to increased risk of major adverse cardiovascular events (MACE) and development of cardiovascular disease risk factors (CVDRFs). One mechanism by which noise exposure is hypothesized to impact cardiovascular (CV) health is through its impact on sleep; yet recent studies suggest that noise exposure associates with adverse cardiovascular effects independently of sleep. We evaluated whether the relationship between noise exposure and risk of developing MACE and/or incident CVDRFs differed between those with normal vs abnormal sleep. Methods: We studied participants from the Mass General Brigham Biobank (2010-2020). Presence and timing of MACE, sleep disorders, CVDRFs (i.e., diabetes mellitus, hypertension, and hyperlipidemia), and key confounders were assessed from medical records, optional lifestyle surveys, and US government data. Annual 24-hour average transportation noise exposure was estimated using a US Department of Transportation tool. Elevated noise exposure was assessed at thresholds of >50 and >45 dBA based on the relationship of these thresholds with CVD. Abnormal sleep was defined as a diagnosis of a sleep disorder (i.e., sleep apnea, insomnia, parasomnia, hypersomnia, narcolepsy, or cataplexy) at any time or sleeping <7 or >9 hours per night. Patients who developed MACE prior to study start were excluded. Results: Among 108,051 individuals (median age 57; 57.6% female), 34.7% had abnormal sleep, 33.0% had noise exposure >50 dBA, and 54.5% had noise exposure >45 dBA. Noise exposure >50 dBA associated with incident MACE in those with normal sleep (odds ratio (OR) [95% confidence interval (CI)]: 1.083 [1.027, 1.142], p = 0.003), abnormal sleep (1.102 [1.040, 1.167], p < 0.001), and all participants (1.091 [1.049, 1.135], p < 0.001) in models adjusted for age, sex, and abnormal sleep. This relationship largely persisted with further adjustment for baseline CVDRFs, socioenvironmental variables, and psychiatric disorders (Table 1A) and using a noise threshold of >45 dBA (Table 1B). Noise exposure >50 dBA also associated with the number of incident CVDRFs (HTN, HLD, DM) developed prior to MACE in those with normal sleep (standardized β [95% CI]: 0.028 [0.014, 0.043], p < 0.001), abnormal sleep (0.035 [0.013, 0.058], p = 0.002), and all participants (0.031 [0.018, 0.043], p < 0.001) in models adjusted for age, sex, abnormal sleep, and baseline CVDRFs. These relationships largely persisted with further adjustment for socioenvironmental, psychiatric, and lifestyle factors (Table 2A), and when using a noise threshold of >45 dBA (Table 2B). Conclusions: The relationships between noise exposure and heightened risk of MACE and incident CVDRFs are similar among individuals with and without unhealthy sleep, suggesting that healthy sleep is not protective against the adverse CV impact of noise exposure.