Scholarlink

<p>Air pollution represents an evolving environmental crisis with profound systemic, developmental, and molecular effects. Emission majorly from all sources such as industrial emission, vehicular exhaust, biomass fuel use and livestock emission remains as the dominant contributors. This review explores its role as both an epigenetic modifier and a multisystem disruptor that influences disease susceptibility and transgenerational health outcomes. Focusing on fine particulate matter (PM<sub>2.5</sub>), ozone (O<sub>3</sub>), and indoor pollutants, we examine air pollution’s impact on cardiovascular, pulmonary, neurological, metabolic, and reproductive systems. We describe mechanisms involving oxidative stress, neuroinflammation, blood–brain barrier (BBB) disruption, and ferroptosis. At the molecular level, pollution-induced epigenetic modifications such as DNA methylation, histone changes, and altered non-coding RNA expression are implicated in various chronic diseases, including Alzheimer’s disease. We explore biomarkers (e.g., p-tau217, ferroptosis indicators) and therapeutic avenues involving Nrf2, GLP-1R agonists, and glymphatic restoration. Integrating insights from genome-wide association studies (GWAS), we propose a systems biology framework for understanding and mitigating pollution-induced pathophysiology. Strategies combining behavioral change, policy, synthetic biology, and green infrastructure are crucial for planetary and human health resilience.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Air pollution as a multisystem disruptor: pollution impacts in human health and epigenetic framework

  • 期刊论文

  • 发表日期：

    2025年11月19日

查看全文
  • Vidhya Sivaramganesh,
  • Rajalakshmi Subramaniyam

摘要

Air pollution represents an evolving environmental crisis with profound systemic, developmental, and molecular effects. Emission majorly from all sources such as industrial emission, vehicular exhaust, biomass fuel use and livestock emission remains as the dominant contributors. This review explores its role as both an epigenetic modifier and a multisystem disruptor that influences disease susceptibility and transgenerational health outcomes. Focusing on fine particulate matter (PM2.5), ozone (O3), and indoor pollutants, we examine air pollution’s impact on cardiovascular, pulmonary, neurological, metabolic, and reproductive systems. We describe mechanisms involving oxidative stress, neuroinflammation, blood–brain barrier (BBB) disruption, and ferroptosis. At the molecular level, pollution-induced epigenetic modifications such as DNA methylation, histone changes, and altered non-coding RNA expression are implicated in various chronic diseases, including Alzheimer’s disease. We explore biomarkers (e.g., p-tau217, ferroptosis indicators) and therapeutic avenues involving Nrf2, GLP-1R agonists, and glymphatic restoration. Integrating insights from genome-wide association studies (GWAS), we propose a systems biology framework for understanding and mitigating pollution-induced pathophysiology. Strategies combining behavioral change, policy, synthetic biology, and green infrastructure are crucial for planetary and human health resilience.