Incidence of pulmonary carcinogenic changes after one hundred weeks of solitary α-quartz exposure in albino Wistar rats (in vivo study)

Abstract

Introduction: Quartz is one of the most well-known compounds in earth crust which could be inhaled causing silicosis which is an occupational lung disease marked by pulmonary inflammation and scarring mainly in the upper lobes of the lungs. Many researchers linked between chronic repetitive quartz exposure and pulmonary histopathological changes in the form of hyperplasia and neoplastic lesions, but in our present study we aim to examine the carcinogenic effect of single exposure of quartz in two years period. Material and Methods: 80 Albino Wistar rats were divided into four groups. Q-60 and Q-100 groups received single dose of quartz (5 mg) by intratracheal injection and sacrificed after 60 and 100 weeks of exposure respectively. S-60 and S-100 groups received intratracheal 0.2 ml saline injection and sacrificed after 60 and 100 weeks of exposure respectively. Lungs were collected for histopathological and immunohistochemical studies. Results: Lung tissue of Q60 and Q100 showed inflammatory cells infiltrations, pulmonary edema and pulmonary fibrosis. Pulmonary edema and fibrosis are significantly apparent in Q60 than in Q 100. Q60 and S60 groups showed inflammatory cells infiltration but neither hyperplastic nor neoplastic changes were detected. Q100 and S100 groups showed inflammatory cells infiltration together with hyperplastic changes, adenoma, adenocarcinoma and papillomatous formation. Q100 group showed higher incidence of adenoma and adenocarcinoma if compared to S100, inflammatory cells infiltration was positively correlated with formation of hyperplastic and neoplastic changes. Examination of anti Napsin A and anti-CD-86 stained sections showed negative reaction in S60 and S100 groups while reaction in Q60 and Q100 groups was significantly strong positive. Conclusion:Our study revealed that quartz can be detected in lung tissue after two years of this solitary exposure inducing hyperplastic and precancerous lesions which could be reflected on quartz workers health.

Comparing α-Quartz-Induced Cytotoxicity and Interleukin-8 Release in Pulmonary Mono- and Co-Cultures Exposed under Submerged and Air-Liquid Interface Conditions

“…Inflammation and cell injury appear to be early markers for the onset of various lung pathologies, especially silicosis [ 5 , 6 ]. The release of cytokines and chemokines, the infiltration of inflammatory cells, and the development of fibrotic changes as the driving force of pulmonary disease upon quartz exposure in vivo have been covered extensively in the literature [ 7 , 8 , 9 , 10 ]. Similar conclusions were drawn from several in vitro investigations assessing cytotoxicity, DNA damage, and inflammation in macrophages [ 11 , 12 , 13 , 14 ], epithelial cells [ 15 , 16 , 17 ], and pulmonary fibroblasts [ 18 , 19 ].…”