Renal, vascular and cardiac fibrosis in rats exposed to passive smoking and industrial dust fibre amosite

• Published in: Journal of cellular and molecular medicine 2009-11, Vol.13 (11-12), p.4484-4491
• Main Authors: Boor, Peter, Casper, Sandra, Celec, Peter, Hurbánková, Marta, Beňo, Milan, Heidland, August, Amann, Kerstin, Šebeková, Katarína
• Format: Article
• Language: English
• Subjects: Animals; AOPP; Aorta - drug effects; Aorta - pathology; Architecture; Asbestos; Asbestos, Amosite - toxicity; Biomarkers - metabolism; Blood Pressure - drug effects; Blood Vessels - drug effects; Blood Vessels - pathology; Cardiovascular disease; Cardiovascular diseases; Cardiovascular system; Cigarette smoke; Construction; Coronary artery disease; Coronary vessels; Creatinine; Dust; environmental pollutants; Fibrosis; Gene expression; Gene Expression Regulation - drug effects; glomerulosclerosis; Heart; Heart diseases; Humans; Industry; Inflammation - pathology; Inhalation Exposure; Kidney - drug effects; Kidney - metabolism; Kidney - pathology; Kidney - physiopathology; Kidney diseases; Kidney Function Tests; Kidneys; Laboratory animals; Lung cancer; Lung diseases; Macrophages; Male; Monocytes; Morphology; Myocardium - pathology; Oxidation; oxidative stress; Oxidative Stress - drug effects; Passive smoking; Peroxidase; Plasma; Pollutants; Protein structure; Proteins; Pulmonary fibrosis; Rats; Rats, Wistar; Risk factors; RNA, Messenger - genetics; RNA, Messenger - metabolism; Rodents; Smoking; Tobacco smoke; Tobacco Smoke Pollution; Toxicity; Trachea; Tumor necrosis factor-TNF
• ISSN: 1582-1838; 1582-4934
• DOI: 10.1111/j.1582-4934.2008.00518.x

Passive smoking is an independent risk factor for cardiovascular diseases. Industrial fibrous dust, e.g. the asbestos group member, amosite, causes lung cancer and fibrosis. No data are available on renal involvement after inhalational exposure to these environmental pollutants or of their combination, or on cardiovascular and renal toxicity after exposure to amosite. Male Wistar rats were randomized into four groups (n= 6): control and amosite group received initially two intratracheal instillations of saline and amosite solution, respectively. Smoking group was subjected to standardized daily exposure to tobacco smoke for 2 hrs in a concentration resembling human passive smoking. Combined group was exposed to both amosite and cigarette smoke. All rats were killed after 6 months. Rats exposed to either amosite or passive smoking developed significant glomerulosclerosis and tubulointerstitial fibrosis. Combination of both exposures had additive effects. Histomorphological changes preceded the clinical manifestation of kidney damage. In both groups with single exposures, marked perivascular and interstitial cardiac fibrosis was detected. The additive effect in the heart was less pronounced than in the kidney, apparent particularly in changes of vascular structure. Advanced oxidation protein products, the plasma marker of the myeloperoxidase reaction in activated monocytes/macrophages, were increased in all exposed groups, whereas the inflammatory cytokines did not differ between the groups. In rats, passive smoking or amosite instillation leads to renal, vascular and cardiac fibrosis potentially mediated via increased myeloperoxidase reaction. Combination of both pollutants shows additive effects. Our data should be confirmed in subjects exposed to these environmental pollutants, in particular if combined.