Inhalation exposures to polycyclic aromatic hydrocarbons (PAHs) have been associated with various adverse health effects, including chronic lung diseases and cancer. Using human bronchial epithelial cell line HBE1, we investigated the effects of structurally different PAHs on tissue homeostatic processes, namely gap junctional intercellular communication (GJIC) and MAPKs activity. Rapid (<1 h) and sustained (up to 24 h) inhibition of GJIC was induced by low/middle molecular weight (MW) PAHs, particularly by those with a bay- or bay-like region (1- and 9-methylanthracene, fluoranthene), but also by fluorene and pyrene. In contrast, linear low MW (anthracene, 2-methylanthracene) or higher MW (chrysene) PAHs did not affect GJIC. Fluoranthene, 1- and 9-methylanthracene induced strong and sustained activation of MAPK ERK1/2, whereas MAPK p38 was activated rather nonspecifically by all tested PAHs. Low/middle MW PAHs can disrupt tissue homeostasis in human airway epithelium via structure-dependent nongenotoxic mechanisms, which can contribute to their human health hazards.

吸入暴露于多环芳烃 (PAH) 与各种不良健康影响有关，包括慢性肺病和癌症。使用人支气管上皮细胞系 HBE1，我们研究了结构不同的 PAHs 对组织稳态过程的影响，即间隙连接细胞间通讯 (GJIC) 和 MAPKs 活性。GJIC 的快速（<1 小时）和持续（长达 24 小时）抑制是由低/中分子量 (MW) PAH 诱导的，特别是那些具有海湾或海湾样区域（1-和 9-甲基蒽，荧蒽），但也由芴和芘。相比之下，线性低分子量（蒽、2-甲基蒽）或更高分子量（屈）的多环芳烃不影响 GJIC。荧蒽、1- 和 9-甲基蒽诱导 MAPK ERK1/2 的强烈和持续激活，而 MAPK p38 被所有测试的多环芳烃非特异性激活。低/中 MW 多环芳烃可以通过结构依赖的非基因毒性机制破坏人类气道上皮的组织稳态，这可能会危害人类健康。