Long-term air pollution mixture exposure accelerates hypertension onset: modification by neighborhood social vulnerability

Background Hypertension (HTN) is the leading modifiable risk factor for cardiovascular disease globally. Although air pollution is an established cardiovascular risk factor, prior studies have largely examined single pollutants or short-term exposures, overlooking the cumulative effects of real-world pollutant mixtures. Whether long-term mixture exposure accelerates HTN onset, particularly among socially vulnerable populations exposed to compounded environmental and psychosocial stressors, remains unclear. Purpose We examined the association between long-term air pollution mixture exposure and incident HTN, assessed its impact on age at onset, and tested whether this association is modified by neighborhood social vulnerability. Methods We performed a longitudinal cohort study of adults in the Mass General Brigham Biobank (2010–2020) free of HTN at baseline. Incident HTN was identified using validated natural language processing (PPV >95%). Ten-year moving average exposures to PM₂.₅, PM₁₀, NO₂, and SO₂ were estimated at the sub-neighborhood level using geocoded residential addresses. An air pollution mixture (APM) score was derived via principal component analysis to reflect a cumulative multi-pollutant burden. Neighborhood social vulnerability was quantified using the CDC Social Vulnerability Index (SVI; quartiles). Multivariable Cox and linear regression models adjusted for demographic, socioeconomic, lifestyle, and clinical covariates were applied. Nonlinearity was assessed using restricted cubic splines (RCS), and effect modification by SVI was tested. Results Among 36,145 participants (median [IQR] age 49 [33–61] years; 41% male; 14% non-White), 19,091 (52.8%) developed HTN over 10 years of follow-up. In fully adjusted models, higher APM exposure (per 1-IQR increase) was associated with a 6% higher risk of HTN (HR 1.06, 95% CI 1.04–1.09; p<0.001). The association was stronger among individuals residing in highly vulnerable neighborhoods (SVI-Q4: HR 1.15 vs. Q1: HR 1.02; p-interaction=0.06; Fig. 1). Higher APM exposure was also associated with earlier HTN onset by approximately 2.5 years (β −2.46 years, 95% CI −2.80 to −2.13; p<0.001), with a greater effect among those in SVI-Q4 compared with Q1 (−3.49 vs. −2.25 years; p-interaction<0.001; Fig. 1). RCS analyses demonstrated a linear dose–response relationship (p-nonlinearity>0.05; Fig. 2). Similar associations, to varying degrees, were observed for individual pollutants. Conclusion Long-term exposure to air pollution mixtures accelerates hypertension onset, particularly among socially vulnerable populations, underscoring the intersection of environmental and social inequities in driving early cardiometabolic disease. Targeting cumulative environmental burden may represent a scalable strategy for reducing premature hypertension and cardiovascular disparities.