Decreased immune response in undernourished rats after air pollution exposure.

Children are highly vulnerable subpopulation to malnutrition and air pollution. We investigate, in a rat nutritional growth retardation (NGR) model, the impact of Residual Oil Fly Ash (ROFA) on the lung immune response using in vitro and ex vivo methods. In vitro: Alveolar macrophages (AM) were isolated from Control (C) and NGR animals, cultured and treated with ROFA (1-100 µg/ml) for 24 h.

Changes in extrapulmonary organs and serum enzyme biomarkers after chronic exposure to Buenos Aires air pollution.

Urban air pollution is a serious environmental problem in developing countries worldwide, and health is a pressing issue in the megacities in Latin America. Buenos Aires is a megacity with an estimated moderate Air Quality Index ranging from 42 to 74 μg/m. Exposure to Urban Air Particles from Buenos Aires (UAP-BA) induces morphological and physiological respiratory alterations; nevertheless, no studies on extrapulmonary organs have been performed.

Hazardous effects of urban air particulate matter acute exposure on lung and extrapulmonary organs in mice.

Air particulate matter (PM) can lead to extrapulmonary adverse reactions in organs such as liver and heart either by particle translocation from the lung to the systemic circulation or by the release of lung mediators. Young BALB/c mice were intranasal instilled with 1mg/BW of Urban Air Particles from Buenos Aires or Residual Oil Fly Ash. Histopathology, oxidative metabolism and inflammation on lungs and extrapulmonary organs and the systemic response were evaluated.

Direct and Indirect Effect of Air Particles Exposure Induce Nrf2-Dependent Cardiomyocyte Cellular Response In Vitro.

Air particulate matter has been associated with adverse effects in the cardiorespiratory system leading to cytotoxic and pro-inflammatory effects. Particulate matter-associated cardiac effects may be direct or indirect. While direct interactions may occur when inhaled ultrafine particles and/or particle components cross the air-blood barrier reaching the cardiac tissue, indirect interactions may occur as the result of pulmonary inflammation and consequently the release of inflammatory and oxidative mediators into the blood circulation.