Ultrastructural nasal pathology in children chronically and sequentially exposed to air pollutants

Ultrastructural nasal pathology in children chronically and sequentially exposed to air pollutants
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DOI:
10.1165/ajrcmb.24.2.4157
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发表时间:
2001-02-01
影响因子:
6.4
通讯作者:
Carson, JL
Carson, JL
中科院分区:
医学1区
文献类型:
--
作者:
Calderón-Garcidueñas, L;Valencia-Salazar, G;Carson, JL

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墨西哥城西南部 (SWMMC) 的儿童反复暴露于复杂的空气污染物混合物中,包括臭氧、颗粒物和醛类。从这些儿童身上采集的鼻活检显示出广泛的组织病理学改变:纤毛细胞和杯状细胞群的显着变化、基底细胞增生、鳞状上皮化生和轻​​度不典型增生。我们研究了从 SWMMC 长大的 4 至 15 岁临床健康儿童获得的 15 例鼻活检样本的超微结构特征。研究结果与 11 名在韦拉克鲁斯长大、接触低污染物水平的儿童的鼻活检进行了比较。鼻活检的超薄切片显示对照儿童的粘液纤毛上皮不明显,而 SWMMC 儿童的上皮由不同数量的基底细胞、纤毛细胞、杯状细胞和鳞状化生细胞以及中间细胞组成。新生纤毛细胞(通过迁移运动体的存在证明)很常见,纤毛异常也很常见,包括中央微管缺失、多余的中央和外周小管、睫状微管不连续性和复合纤毛。紧邻纤毛的中央微管方向改变表明与这些异常纤毛相关的运动障碍。上皮细胞之间有明显的漏出液,表明上皮连接完整性存在潜在缺陷。颗粒物存在于上皮细胞的异溶酶体中,并且也沉积在细胞间隙中。鼻上皮的严重结构改变以及显着的获得性纤毛缺陷可能是慢性气道损伤的结果,其中臭氧、颗粒物和醛被认为起着至关重要的作用。 SWMMC 儿童的鼻上皮从根本上来说是紊乱的,其粘液纤毛防御机制不再完整。受损的鼻上皮保护下呼吸道的能力较差,并且可能使远端腺泡气道更容易受到活性气体的影响。粘膜纤毛清除功能受损可能会增加沉积的诱变颗粒物与上皮表面之间的接触时间,从而增加鼻癌发生的风险。长期接触空气污染物会影响整个呼吸道;鼻上皮是监测有毒或致癌物质暴露的可及且有价值的哨兵。
Southwest Metropolitan Mexico City (SWMMC) children are repeatedly exposed to a complex mixture of air pollutants, including ozone, particulate matter, and aldehydes. Nasal biopsies taken from these children exhibit a wide range of histopathologic alterations: marked changes in ciliated and goblet cell populations, basal cell hyperplasia, squamous metaplasia, and mild dysplasias. We studied the ultrastructural features of 15 nasal biopsies obtained from clinically healthy children 4 to 15 yr of age, growing up in SWMMC. The results were compared with nasal biopsies from 11 children growing up in Veracruz and exposed to low pollutant levels. Ultrathin sections of nasal biopsies revealed an unremarkable mucociliary epithelium in control children, whereas SWMMC children showed an epithelium comprised of variable numbers of basal, ciliated, goblet, and squamous metaplastic as well as intermediate cells. Nascent ciliated cells, as evidenced by the presence of migratory kinetosomes, were common, as were ciliary abnormalities, including absent central microtubules, supernumerary central and peripheral tubules, ciliary microtubular discontinuities, and compound cilia. Dyskinesia associated with these abnormal cilia was suggested by the altered orientation of the central microtubules in closely adjacent cilia. A transudate was evident between epithelial cells, suggesting potential deficiencies in epithelial junction integrity. Particulate matter was present in heterolysosomal bodies in epithelial cells and it was also deposited in intercellular spaces. The severe structural alteration of the nasal epithelium together with the prominent acquired ciliary defects are likely the result of chronic airway injury in which ozone, particulate matter, and aldehydes are thought to play a crucial role. The nasal epithelium in SWMMC children is fundamentally disordered, and their mucociliary defense mechanisms are no longer intact. A compromised nasal epithelium has less ability to protect the lower respiratory tract and may potentially leave the distal acinar airways more vulnerable to reactive gases. Impairment of mucociliary clearance has the potential to increase the contact time between deposited mutagenic particulate matter and the epithelial surface, thus increasing the risk for nasal carcinogenesis. Chronic exposures to air pollutants affect the whole respiratory tract; the nasal epithelium is an accessible and valuable sentinel to monitor exposures to toxic or carcinogenic substances.