可吸入细颗粒物 (PM) 会引发气道炎症反应，并激活单核细胞、组织稳态介质和促肿瘤炎症。我们评估了人类单核细胞和单核细胞衍生的巨噬细胞对标准化空气污染物（炭黑、城市灰尘和纳米颗粒炭黑）的体外反应，重点关注它们的促炎和 DNA 损伤特性。除了诱导氧化应激、部分 DNA 损伤和抑制吞噬作用外，PM（100 μg/mL/24 小时）对细胞没有显着毒性。 TNFα仅略有增加。 PM 纳米粒子增加表达并激活 DNA 损伤相关的组蛋白 H2A.X 以及促炎 NF-κB。我们已经证明，城市灰尘通过 H2A.X 的选择性翻译后磷酸化刺激 DNA 损伤/修复途径，而纳米颗粒炭黑通过激活 NF-κB 增加炎症。此外，在预先暴露于城市灰尘或纳米颗粒炭黑的巨噬细胞中，对脂多糖的炎症反应明显更强。我们的数据表明，空气中的纳米颗粒会诱导培养的单核细胞亚群中 PM 特异性的表观遗传改变，这可以使用二元荧光散点图进行量化。这些变化与炎症信号传导相协调，并凸显了促进肿瘤的炎症的重要分子和细胞特异性表观遗传机制。

Fine inhalable particulate matter (PM) triggers an inflammatory response in the airways and activates mononuclear cells, mediators of tissue homeostasis, and tumour-promoting inflammation. We have assessed ex vivo responses of human monocytes and monocyte-derived macrophages to standardised air pollutants: carbon black, urban dust, and nanoparticulate carbon black, focusing on their pro-inflammatory and DNA-damaging properties. None of the PM (100 μg/mL/24 h) was significantly toxic to the cells, aside from inducing oxidative stress, fractional DNA damage, and inhibiting phagocytosis. TNFα was only slightly increased. PM nanoparticles increase the expression and activate DNA-damage-related histone H2A.X as well as pro-inflammatory NF-κB. We have shown that the urban dust stimulates the pathway of DNA damage/repair via the selective post-translational phosphorylation of H2A.X while nanoparticulate carbon black increases inflammation via activation of NF-κB. Moreover, the inflammatory response to lipopolysaccharide was significantly stronger in macrophages pre-exposed to urban dust or nanoparticulate carbon black. Our data show that airborne nanoparticles induce PM-specific, epigenetic alterations in the subsets of cultured mononuclear cells, which may be quantified using binary fluorescence scatterplots. Such changes intercede with inflammatory signalling and highlight important molecular and cell-specific epigenetic mechanisms of tumour-promoting inflammation.