Cement Dust Inhalation Induces Hepato-Renal Dysfunction Via Tissue Heavy Metal Bioaccumulation, Histopathological and Biochemical Mechanisms

Systemic degradations of various forms have been adduced to cement dust exposure and Inhalation is the most considerable route. We deployed inhalation method to investigate the possible reno-hepatic effect of cement dust exposure. Thirty male Wistar rats weighing between 150 and 180g acquired were acclimatized and randomized into three groups of 10 animals each. Group 1 was the control, group 2: 14-day exposed, and group 3: 28-day exposed. Relative organs weights, heavy metal analysis, hepatic and renal functions tests, fibrotic index, lipid peroxidation (MDA), superoxide dismutase (SOD), catalase (CAT), nitric oxide (NO), sulfhydryl group, histopathology, and histomorphometry were assessed using standard procedures. There was increase in organ weight and significant (p < 0.05) tissue bioaccumulation of heavy metals. There were significant increases in urea, creatinine, hepatic aspartate aminotransferase, Alanine aminotransferase and Alkaline phosphatase values in the exposed groups compared with control. Inhaled cement dust was observed to induce lipid peroxidation and deplete SOD and CAT levels. There was also significant upregulation of renal and hepatic NO in the 14-day (0.38 ± 0.05 nmol/g to 0.55 ± 0.17 nmol/g) and 28-day (0.48 ± 0.11 nmol/g to 0.80 ± 0.04 nmol/g) groups when compared with their respective control groups (0.78 ± 0.01 nmol/g to 1.33 ± 0.17 nmol/g). A significant reduction in renal and hepatic sulfhydryl groups was also observed in the exposed groups when compared with the controls. Histopathology showed an array of alterations ranging from vascular congestion, necrosis to neutrophil infiltration. Cement dust exposure by inhalation induced reno-hepatic functional alteration via increased organ weight, heavy metal bioaccumulation, histopathological, and biochemical mechanisms. Biochemically, cement dust inhalation depleted antioxidant capacity and generated oxidative and nitrosative stress.