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<p>The synergistic impact of coexisting environmental stressors—air pollution, traffic noise, and diminished green space—on cardiovascular disease (CVD) pathogenesis remains poorly quantified. In the UK Biobank, we developed a composite environmental exposure score by hierarchizing and summing the levels of the abovementioned three exposures. The associations of exposure score with incident risks of hypertension, type 2 diabetes (T2D), and CVD were assessed, and the interaction between exposure score and polygenetic risk score (PRS) was estimated. Per unit elevation of the exposure score was linked to 6% (hazard ratio [HR]: 1.06; 95% confidence interval [CI]: 1.05, 1.07), 8% (1.08; 1.07, 1.09), and 4% (1.04; 1.03, 1.06) increments in incident risks of hypertension, T2D, and CVD, respectively. Gene-environmental interaction was discovered between exposure score and PRS, accounting for 3%, 14%, and 6% of the incident risks of hypertension, T2D, and CVD, respectively. Multistate models suggested that exposure score was significantly associated with the transmission from health to hypertension (HR: 1.10; 95% CI: 1.08, 1.12), T2D (1.12; 1.07, 1.18), and CVD (1.08; 1.04, 1.12) and from hypertension to CVD (1.03; 1.001, 1.06). Hypertension significantly mediated the CVD progression driven by exposure score. These findings suggest that integrated urban planning strategies, which simultaneously mitigate air pollution and traffic noise while enhancing green space, are crucial for preventing hypertension and interrupting its progression to CVD, especially in individuals with high genetic susceptibility.</p>

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Air pollution, road traffic noise, residential green space and hypertension, type 2 diabetes, and cardiovascular disease trajectories

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月3日

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  • Wei Liu,
  • Jiahao Song,
  • Wendi Shi,
  • Shuhui Wan,
  • Da Shi,
  • Xuefeng Lai,
  • Hao Wang,
  • Zhiying Huo,
  • Le Hong,
  • Qing Liu,
  • Shuting Cao,
  • Bin Wang

摘要

The synergistic impact of coexisting environmental stressors—air pollution, traffic noise, and diminished green space—on cardiovascular disease (CVD) pathogenesis remains poorly quantified. In the UK Biobank, we developed a composite environmental exposure score by hierarchizing and summing the levels of the abovementioned three exposures. The associations of exposure score with incident risks of hypertension, type 2 diabetes (T2D), and CVD were assessed, and the interaction between exposure score and polygenetic risk score (PRS) was estimated. Per unit elevation of the exposure score was linked to 6% (hazard ratio [HR]: 1.06; 95% confidence interval [CI]: 1.05, 1.07), 8% (1.08; 1.07, 1.09), and 4% (1.04; 1.03, 1.06) increments in incident risks of hypertension, T2D, and CVD, respectively. Gene-environmental interaction was discovered between exposure score and PRS, accounting for 3%, 14%, and 6% of the incident risks of hypertension, T2D, and CVD, respectively. Multistate models suggested that exposure score was significantly associated with the transmission from health to hypertension (HR: 1.10; 95% CI: 1.08, 1.12), T2D (1.12; 1.07, 1.18), and CVD (1.08; 1.04, 1.12) and from hypertension to CVD (1.03; 1.001, 1.06). Hypertension significantly mediated the CVD progression driven by exposure score. These findings suggest that integrated urban planning strategies, which simultaneously mitigate air pollution and traffic noise while enhancing green space, are crucial for preventing hypertension and interrupting its progression to CVD, especially in individuals with high genetic susceptibility.