电子垃圾处理车间中细颗粒物在模拟肺液中的沉积及其细胞毒性研究
- Sedimentation and Cytotoxicity of Fine Particulate Matter in Alveolar Fluid from Electronic Waste Recycling Workshops
- 摘要：电子垃圾是全球增长速度最快的废弃物之一,其回收过程中会释放细颗粒物(PM2.5)。PM2.5经过呼吸作用进入肺部,会在肺泡中沉积,对人体呼吸系统造成健康威胁。基于废家电拆解和破碎两类处理工艺,采用体外模拟实验研究PM2.5在模拟肺液(SLF)中的沉降特征,分析牛血清蛋白和磷脂等肺泡表面活性剂对颗粒物沉降速率的影响。对人肺上皮细胞A549进行PM2.5曝毒,研究拆解和破碎车间PM2.5的细胞毒性。结果表明,在SLF中加入磷脂能够加快PM2.5的沉降,而加入牛血清蛋白会使颗粒物的沉降速度变慢。两个车间颗粒物均显著抑制A549细胞的存活率,并呈剂量-效应关系。PM2.5暴露还会导致乳酸脱氢酶水平上升和细胞凋亡率增加,且这种变化与暴露剂量呈现正相关。PM2.5的全组分溶液对A549细胞存活率的影响均大于可溶性组分溶液的影响。经PM2.5可溶性组分溶液暴露,细胞与PM2.5颗粒接触,A549细胞膜的完整性受到破坏,导致细胞内活性氧含量增多,最终会导致细胞凋亡。本研究结果为电子垃圾回收过程中PM2.5的健康影响效应提供基础数据。
- Abstract：Electronic waste (e-waste) is recognized as the fastest-growing component of the solid waste stream, with its recycling processes generating fine particulate matter (PM2.5). When inhaled, PM2.5 can deeply penetrate the respiratory system, reaching and settling in the alveoli of the lungs, posing significant health risks. This study explored the deposition of PM2.5 in simulated lung fluid using in vitro experiments, specifically examining the roles of bovine serum albumin (BSA) and phospholipid (DPPC) in influencing the deposition rates of PM2.5 collected from the disassembly and crushing processes of e-waste. Human lung epithelial cells (A549) were exposed to PM2.5 to evaluate effects on cell viability and apoptosis. The results revealed that DPPC enhances PM2.5 deposition in simulated lung fluid, whereas BSA tends to inhibit it. Exposure to PM2.5 significantly reduced A549 cell survival in a dose-dependent manner. Additionally, elevated levels of lactate dehydrogenase and increased apoptosis rates were observed, both of which correlated positively with the exposure dose. The impact of the complete PM2.5 component solution on cell viability was more severe than that of its soluble components alone. After exposure to the soluble component solution, A549 cells interacted with PM2.5 particles, resulting in compromised cell membrane integrity, a rise in intracellular reactive oxygen species, and ultimately, cell apoptosis. These findings offer vital insights into the health risks associated with PM2.5 exposure during e-waste recycling.
