Fatty acids from cooking fumes and hypochlorous acid (HOCl) released from indoor cleaning adversely affect respiratory health, but the molecular-level mechanism remains unclear. Here, the effect of cooking oil fumes [palmitic acid (PA), oleic acid (OA), and linoleic acid (LA)] on lung model phospholipid (POPG) hydrochlorination mediated by HOCl at the air–water interface of the hanged droplets was investigated. Interfacial hydrochlorination of POPG was impeded by OA and LA, while that of POPG was facilitated by PA. The effect on POPG hydrochlorination increased with the decrease in oil fume concentration. A potential mechanism with respect to the chain length of these oil fumes, regardless of their saturation, was proposed. PA with a short carbon chain looses the POPG packing and leads to the exposure of the C=C double bonds of POPG, whereas OA and LA with a long carbon chain hinder HOCl from reaching the C=C bonds of POPG. These results for short chain and low concentration dependence suggest that the decay of oil fumes or the conversion of short-chain species by indoor interfacial chemistry might be adverse to lung health. These results provide insights into the relationship between indoor multicomponent pollutants and the respiratory system.

中文翻译：

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室内环境中脂肪酸介导的脂质非均相氢氯化反应

烹饪油烟中的脂肪酸和室内清洁释放的次氯酸 (HOCl) 对呼吸系统健康产生不利影响，但其分子水平机制仍不清楚。此处，烹饪油烟 [棕榈酸 (PA)、油酸 (OA) 和亚油酸 (LA)] 对悬挂液滴的空气-水界面处 HOCl 介导的肺模型磷脂 (POPG) 氢氯化作用的影响为调查了。 OA和LA阻碍POPG的界面氢氯化，而PA则促进POPG的界面氢氯化。随着油烟浓度的降低，对POPG氢氯化的影响增大。提出了与这些油烟的链长有关的潜在机制，无论其饱和度如何。碳链短的PA会松散POPG的堆积，导致POPG的C=C双键暴露，而碳链长的OA和LA会阻碍HOCl到达POPG的C=C键。这些短链和低浓度依赖性的结果表明，油烟的衰变或室内界面化学对短链物质的转化可能对肺部健康不利。这些结果为了解室内多组分污染物与呼吸系统之间的关系提供了见解。