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Purpose of Review <p>Ambient air pollution drives cardiovascular disease (CVD), yet single-pollutant models overlook how risk emerges within broader environmental and structural contexts. This review applies the Public Health Exposome (PHE) framework, which integrates natural, built, social, and policy environments, to show how multilevel systems shape CVD vulnerability.</p> Recent Findings <p>Extreme heat, humidity, and climate variability modify pollutant toxicity, while structural inequities, discriminatory policies, and inadequate planning intensify exposures in marginalized communities. Cumulative psychosocial stress further amplifies inflammatory responses, activating the endo-exposome. Multi-omics studies reveal that pollution alters epigenomic, transcriptomic, and metabolomic pathways linked to inflammation, oxidative stress, and endothelial dysfunction. Emerging tools like machine learning, high-resolution exposure modeling, graph-based analytics, and wearable sensing, enable integration of environmental data and support systems-level approaches.</p> Summary <p>The PHE framework illustrates how layered environmental and structural stressors accumulate to elevate CVD risk. Reducing this burden requires coupling PHE science with equitable public policy.</p>

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Air Pollution Within the Public Health Exposome Framework: Impacts on Cardiovascular Health

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月27日

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  • Lucia D. Juarez,
  • Andrzej Kulczycki,
  • Gabriela R. Oates,
  • Kai Zhang,
  • Gokhan M. Mutlu,
  • Sairam Parthasarathy

摘要

Purpose of Review

Ambient air pollution drives cardiovascular disease (CVD), yet single-pollutant models overlook how risk emerges within broader environmental and structural contexts. This review applies the Public Health Exposome (PHE) framework, which integrates natural, built, social, and policy environments, to show how multilevel systems shape CVD vulnerability.

Recent Findings

Extreme heat, humidity, and climate variability modify pollutant toxicity, while structural inequities, discriminatory policies, and inadequate planning intensify exposures in marginalized communities. Cumulative psychosocial stress further amplifies inflammatory responses, activating the endo-exposome. Multi-omics studies reveal that pollution alters epigenomic, transcriptomic, and metabolomic pathways linked to inflammation, oxidative stress, and endothelial dysfunction. Emerging tools like machine learning, high-resolution exposure modeling, graph-based analytics, and wearable sensing, enable integration of environmental data and support systems-level approaches.

Summary

The PHE framework illustrates how layered environmental and structural stressors accumulate to elevate CVD risk. Reducing this burden requires coupling PHE science with equitable public policy.