Scholarlink

<p>Global warming increases water evaporation rates from planetary ecosystems. Here, we show that evaporation rates encountered during human breathing in dehydrating atmospheres promote airway inflammation and potentially exacerbate lung diseases. Continuum mathematical analysis predicts that water evaporation thins airway mucus layers and compresses epithelial cells during tidal breathing. Experiments using human tracheal-bronchial cells confirm that exposure to air with progressive degrees of dryness (relative humidities of 95%, 60%, and 30% at 37 °C) causes the mucus layer to progressively thin (by 5%, 35%, and 58%). Associated compression of epithelial cells elevates secretion of inflammatory cytokines (TNF-α, IL-33, and IL-6). Exposing mice with a muco-inflammatory phenotype to intermittent dry air for&#xa0;14 days results in histopathological changes and alteration of inflammatory infiltrates. Together with climate model simulations, these findings suggest that most of the United States will be at elevated risk of airway inflammation by the latter half of this century.</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

Global warming risks dehydrating and inflaming human airways

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年3月17日

查看全文
  • David A. Edwards,
  • Aurélie Edwards,
  • Dan Li,
  • Linying Wang,
  • Kian Fan Chung,
  • Deen Bhatta,
  • Andreas Bilstein,
  • Justin Hanes,
  • Indika Edirisinghe,
  • Britt Burton Freeman,
  • Mark Gutay,
  • Alessandra Livraghi-Butrico,
  • Brian Button

摘要

Global warming increases water evaporation rates from planetary ecosystems. Here, we show that evaporation rates encountered during human breathing in dehydrating atmospheres promote airway inflammation and potentially exacerbate lung diseases. Continuum mathematical analysis predicts that water evaporation thins airway mucus layers and compresses epithelial cells during tidal breathing. Experiments using human tracheal-bronchial cells confirm that exposure to air with progressive degrees of dryness (relative humidities of 95%, 60%, and 30% at 37 °C) causes the mucus layer to progressively thin (by 5%, 35%, and 58%). Associated compression of epithelial cells elevates secretion of inflammatory cytokines (TNF-α, IL-33, and IL-6). Exposing mice with a muco-inflammatory phenotype to intermittent dry air for 14 days results in histopathological changes and alteration of inflammatory infiltrates. Together with climate model simulations, these findings suggest that most of the United States will be at elevated risk of airway inflammation by the latter half of this century.