The impacts of acute arsenic exposure (i.e. vomiting, diarrhea, and renal failure) are distinct from those brought about by sustained, low level exposure from environmental sources or drinking of contaminated well water. Chronic arsenic exposure is a risk factor for the development of pulmonary diseases, including lung cancer. How arsenic exposure leads to pulmonary disease is not fully understood. Both acute versus chronic arsenic exposure increase EGFR expression, but do so via distinct molecular mechanisms. BEAS-2B cells were exposed to either acute sodium arsenite (5 μM for 24 h) or chronic sodium arsenite (100 nM for 24 weeks). Cells treated with acute arsenic exhibited a decrease in viability, changes in morphology, and increased mRNA level of BTC. In contrast, during 24 weeks of arsenic exposure, the cells had increased EGFR expression and activity, and increased mRNA and protein levels of TGFα. Further, chronic arsenic treatment caused an increase in cell migration in the absence of exogenous ligand. Elevated TGFα and EGFR expression are features of many non-small cell lung cancers. We propose that lung epithelial cells chronically exposed to low level arsenic increases EGFR signaling via TGFα production to enhance ligand-independent cell migration.

急性砷暴露（即呕吐、腹泻和肾功能衰竭）的影响不同于持续、低水平暴露于环境来源或饮用受污染的井水所带来的影响。慢性砷暴露是肺部疾病发展的危险因素，包括肺癌。砷暴露如何导致肺部疾病尚不完全清楚。急性和慢性砷暴露都会增加 EGFR 的表达，但这是通过不同的分子机制实现的。BEAS-2B 细胞暴露于急性亚砷酸钠（5 μM，持续 24 小时）或慢性亚砷酸钠（100 nM，持续 24 周）。用急性砷处理的细胞表现出活力降低、形态变化和 BTC mRNA 水平增加。相比之下，在 24 周的砷暴露期间，这些细胞的 EGFR 表达和活性增加，TGFα 的 mRNA 和蛋白质水平增加。此外，在没有外源配体的情况下，慢性砷处理会导致细胞迁移增加。升高的 TGFα 和 EGFR 表达是许多非小细胞肺癌的特征。我们建议长期暴露于低水平砷的肺上皮细胞通过 TGFα 产生增加 EGFR 信号传导，以增强不依赖配体的细胞迁移。