Effect of chronic exposure to fine particulate matter on cardiac tissue of NZBWF1 mice

• Published in: International journal of experimental pathology Vol. 104; no. 4; pp. 177 - 187
• Main Authors: Waked, Dunia, Rodrigues, Ana Clara B., Silva, Thamires Moraes, Yariwake, Victor Yuji, Farhat, Sylvia Costa Lima, Veras, Mariana Matera
• Format: Journal Article
• Language: English
• Published: England Wiley Subscription Services, Inc 01.08.2023; John Wiley and Sons Inc
• Subjects: Air pollution; Animal tissues; Animals; Apoptosis; Autoantibodies; autoimmune disease; Body Weight; Body weight gain; cardiac remodelling; Cardiomyocytes; Cardiovascular diseases; Chronic conditions; Chronic exposure; Epidemiology; Exposure; Female; Fibrosis; Health risks; Heart; Inflammation; Inflammatory diseases; Inhalation; Life expectancy; Life span; Lupus Erythematosus, Systemic - chemically induced; Mice; Myocardium; Original; Particulate emissions; Particulate matter; Particulate Matter - analysis; Particulate Matter - toxicity; Respiration; Systemic lupus erythematosus; Toxicity testing; Ventricular Remodeling; cardiac remodelling; particulate matter; systemic lupus erythematosus; air pollution; cardiovascular diseases; autoimmune disease
• ISSN: 0959-9673; 1365-2613
• DOI: 10.1111/iep.12473

Epidemiological and toxicological studies have shown that inhalation of particulate matter (PM) is associated with development of cardiovascular diseases. Long‐term exposure to PM may increase the risk of cardiovascular events and reduce life expectancy. Systemic lupus erythematosus (SLE) is a chronic inflammatory disease, autoimmune in nature, that is characterized by the production of autoantibodies that affects several organs, including the heart. Air pollution ‐ which can be caused by several different factors ‐ may be one of the most important points both at the onset and the natural history of SLE. Therefore this study aims to investigate whether exposure to air pollution promotes increased inflammation and cardiac remodelling in animals predisposed to SLE. Female NZBWF1 mice were exposed to an environmental particle concentrator. Aspects related to cardiac remodelling, inflammation and apoptosis were analysed in the myocardium. Body weight gain, cardiac trophism by heart/body weight ratio, relative area of cardiomyocytes and the fibrotic area of cardiac tissue were evaluated during the exposure period. Animals exposed to PM2.5 showed increased area of cardiomyocytes, and area of fibrosis; in addition, we observed an increase in IL‐1 and C3 in the cardiac tissue, demonstrating increased inflammation. We suggest that air pollution is capable of promoting cardiac remodelling and increased inflammation in animals predisposed to SLE.