Nasal epithelium as a sentinel for airborne environmental pollution
Nasal epithelium as a sentinel for airborne environmental pollution
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DOI：
10.1093/toxsci/46.2.352
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发表时间：
1998-12-01
影响因子：
3.8
通讯作者：
Morgan, KT
中科院分区：
文献类型：
--
作者：
Calderón-Garcidueñas, L;Rodríguez-Alcaraz, A;Morgan, KT
城市大气中存在各种各样的化学品、颗粒物质和气态空气污染物，可能对人类构成重大健康风险。鼻道是呼吸道与环境接触的第一个部位，通过调节吸入的空气对下呼吸道提供重要的保护。这项活动，包括清除某些污染物，将鼻子置于包括癌症在内的病理变化的风险之中，墨西哥城的居民暴露在复杂的空气污染物混合物中。基于预测的鼻腔空气如何特征，我们选择了4个鼻腔活检地点，对来自低污染城镇（n = 12）和墨西哥西南部大都市常住居民（n = 54）的成年男性志愿者进行研究。临床资料强调鼻症状和组织病理学改变，包括基底细胞和杯状细胞增生、鳞状化生、上皮异常增生和新生血管。免疫组织化学染色评估p53蛋白的积累。对照组没有呼吸道症状，活检结果也不显著。墨西哥城居民抱怨鼻出血、鼻漏、鼻结痂、干燥和鼻塞。活检显示纤毛斑片状缩短，纤毛脱落区，基底细胞增生，鳞状化生。发育不良病变主要位于下鼻甲后部的中央区鳞状上皮和鳞状化生上皮，并表现为p53核积聚。5年或更长时间每日户外暴露时间达10小时以上的个体患发育不良的几率最高。鼻出血患者更容易出现发育不良和新生血管。本研究结果表明：(a)墨西哥城居民的鼻损可能是许多潜在有毒和/或致癌污染物的结果，包括臭氧、醛类物质、颗粒物和未测量的污染物；(b)鼻粘膜纤毛防御机制的改变以及反应性和/或水溶性物质和颗粒的影响可能在鼻病理中起主要作用；(c)在长期暴露于空气污染物的情况下，在发育不良的鼻病变中p53蛋白的积累提高了p53突变已经存在的可能性，并为鳞状细胞提供了克隆扩增的选择优势；(d)鼻腔为检测有毒空气污染物提供了宝贵的前哨组织。(C) 1998毒理学学会。
A wide range of chemicals, particulate matter, and gaseous air pollutants are present in urban atmospheres and may pose a significant health risk for human populations. Nasal passages are the first site of contact of the respiratory tract with the environment and offer significant protection to the lower respiratory tract by conditioning the inspired air. This activity, which includes removal of certain pollutants, places the nose at risk of pathological changes, including cancer, Mexico City residents are exposed to a complex mixture of air pollutants. Based on predicted nasal air how characteristics, four nasal biopsy sites were selected for study in adult male volunteers from a control low polluted town (n = 12) and southwest metropolitan Mexico City permanent residents (n = 54). Clinical data with emphasis on nasal symptoms and histopathological changes including basal and goblet cell hyperplasia, squamous metaplasia, epithelial dysplasia, and neovascularization were evaluated. Immunohistochemical staining was used to assess accumulation of p53 protein. Control individuals had no respiratory symptoms and their biopsies were unremarkable. Mexico City residents complained of epistaxis, rhinorrea, nasal crusting, dryness, and nasal obstruction. Their biopsies showed patchy shortening of cilia, deciliated areas, basal cell hyperplasia, and squamous metaplasia. Dysplastic lesions were predominantly located on antral squamous epithelium and in squamous metaplastic epithelium of the posterior inferior turbinates and they exhibited p53 nuclear accumulation. Individuals with > 10 h of daily outdoor exposure for 5 years or more had the highest rate of dysplasia. Subjects with epistaxis were more likely to have dysplasias and neovascularization. Results of this study suggest: (a) Nasal lesions in Mexico City residents are likely the result of many potentially toxic and/or carcinogenic pollutants, including ozone, aldehydes, particulate matter, and unmeasured pollutants; (b) the alteration of the nasal mucociliary defense mechanisms and the effects of reactive and/or water-soluble materials and particulates could be playing a major role in the nasal pathology; (c) the accumulation of p53 protein in dysplastic nasal lesions in the context of prolonged exposure to air pollutants raises the possibility that p53 mutations are already present and are providing the squamous cells with a selective advantage for clonal expansion; and (d) the nasal passages provide a valuable sentinel tissue for the detection of toxic air pollutants. (C) 1998 Society of Toxicology.