Nowadays, a large amount and variety of plastic is being produced and consumed by human beings on an enormous scale. Microplastics and nanoplastics (MNPLs) have become ubiquitous since they can be found in many ecosystem components. Plastic particles can be found in soil, water, and air. The routes of human exposure are numerous, mainly involving ingestion and inhalation. Once ingested, these particles interact with the gastrointestinal tract and digestive fluids. They can adsorb substances such as additives, heavy metals, proteins, or even microorganisms on their surface, which can cause toxicity. During inhalation, they can be inhaled according to their respective sizes. Studies have reported that exposure to MNPLs can cause damage to the respiratory tract, creating problems such as bronchitis, asthma, fibrosis, and pneumothorax. The reports of boards and committees indicate that there is little data published and available on the toxicity of MNPLs as well as the exposure levels in humans. Despite the well-established concept of MNPLs, their characteristics, and presence in the environment, little is known about their real effects on human health and the environment.

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 in ammatory disease with autoimmune nature, characterized by the production of autoantibodies that affects several organs, including the heart. Caused by several factors, air pollution, may appear as one of the most important points on the onset and development of SLE. This study aims to investigate whether exposure to air pollution promotes increased in ammation and cardiac remodeling in animals predisposed to SLE. Female mice of NZBWF1, were used in an environmental particle concentrator. Aspects related to cardiac remodeling, in ammation and apoptosis in myocardium were analyzed. Body weight gain, cardiac trophism by heart/body weight ratio, relative area of cardiomyocytes and brotic area of cardiac tissue were evaluated during exposure period. Animals exposed to PM2.5 showed increased area of cardiomyocytes, and area of brosis, in addition, we observed an increase of IL-1 and C3 in cardiac tissue, demonstrating increased in ammation. We suggest that air pollution is capable of promoting cardiac remodeling and increased in ammation in animals predisposed to SLE.

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 with autoimmune nature, characterized by the production of autoantibodies that affects several organs, including the heart. Caused by several factors, air pollution, may appear as one of the most important points on the onset and development of SLE. This study aims to investigate whether exposure to air pollution promotes increased inflammation and cardiac remodeling in animals predisposed to SLE. Female mice of NZBWF1, were used in an environmental particle concentrator. Aspects related to cardiac remodeling, inflammation and apoptosis in myocardium were analyzed. Body weight gain, cardiac trophism by heart/body weight ratio, relative area of cardiomyocytes and fibrotic area of cardiac tissue were evaluated during exposure period. Animals exposed to PM2.5 showed increased area of cardiomyocytes, and area of fibrosis, in addition, we observed an increase of IL-1 and C3 in cardiac tissue, demonstrating increased inflammation. We suggest that air pollution is capable of promoting cardiac remodeling and increased inflammation in animals predisposed to SLE.

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 with autoimmune nature, characterized by the production of autoantibodies that affects several organs, including the heart. Caused by several factors, air pollution, may appear as one of the most important points on the onset and development of SLE. This study aims to investigate whether exposure to air pollution promotes increased inflammation and cardiac remodeling in animals predisposed to SLE. Female mice of NZBWF1, were used in an environmental particle concentrator. Aspects related to cardiac remodeling, inflammation and apoptosis in myocardium were analyzed. Body weight gain, cardiac trophism by heart/body weight ratio, relative area of cardiomyocytes and fibrotic area of cardiac tissue were evaluated during exposure period. Animals exposed to PM2.5 showed increased area of cardiomyocytes, and area of fibrosis, in addition, we observed an increase of IL-1 and C3 in cardiac tissue, demonstrating increased inflammation. We suggest that air pollution is capable of promoting cardiac remodeling and increased inflammation in animals predisposed to SLE.

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