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. Lung histophatological analysis supported the rise in the number of inflammatory cells in the bronchoalveolar lavage from PM-exposed animals. Also, both PM caused recruitment of inflammatory cells in the liver and heart parenchyma and IL-6 and transaminases augmentation in serum. We have shown that despite morphochemical differences, both urban air PM altered the lung and extrapulmonary organs. Therefore, exposure to urban air PM may distress body metabolism which, in turn could lead to the development and progression of multifactorial diseases.

Oxidative stress response to air particle pollution in a rat nutritional growth retardation model.

Air pollution consisting of gases and particulate matter-(PM) represents a health problem in cities worldwide. However, air pollution does not impact equally all individuals, as children appear to be more vulnerable subpopulations. Air pollution and malnutrition are two distinct factors that have been associated with oxidative damage. Therefore, the interaction between environmental exposure and nutritional status in populations at risk needs to be explored. The aim of this study was to examine oxidative metabolism in lung, heart and liver in malnourished young rats exposed to residual oil fly ash (ROFA). A Nutritional Growth Retardation (NGR) model was developed in weanling male rats placed on a 20% restricted balanced diet for 4 weeks. Then, NGR and control rats were intranasally instilled with either ROFA (1mg/kg BW) or phosphate buffered saline (PBS). Twenty-four hr post-exposure lung, heart and liver were excised, and serum collected. ROFA induced lung and liver inflammation in control and NGR animals as evidenced by lung polymorphonuclear neutrophil (PMN) recruitment and alveolar space reduction accompanied by liver lymphocyte and binucleated hepatocyte level increase. In lung and liver, antioxidant defense mechanisms reduced lipoperoxidation. In contrast, only in NGR animals did ROFA exposure alter heart oxidative metabolism leading to lipid peroxidation. Although histological and biochemical tissue alterations were detected, no marked changes in serum liver and heart systemic biomarkers were observed. In conclusion, NGR animals responded differently to PM exposure than controls suggesting that nutritional status plays a key role in responsiveness to ambient air contaminants.

Acute exposure to Buenos Aires air particles (UAP-BA) induces local and systemic inflammatory response in middle-aged mice: A time course study.

Exposure to air particulate matter (PM) is associated with increased cardiovascular morbimortality. However, PM doesn't affect equally to all people, being the old cohort the most susceptible and studied. We hypothesized that another specific life phase, the middle-aged subpopulation, may be negatively affected. Therefore, the aim of this study was to analyze in vivo the acute biological impact of two environmental particles, Urban Air Particles from Buenos Aires and Residual Oil Fly Ash, on the cardiorespiratory system of middle-aged mice, evaluating oxidative metabolism and inflammation. Both PM provoked a local and systemic inflammatory response, leading to a reduced alveolar area in the lung, an epicard inflammation in the heart, an increment of IL-6, and a reduction on PON 1 activity in serum of middle-aged animals. The positive correlation of local parameters with systemic markers of oxidative stress and inflammation could be responsible for associations of cardiovascular morbimortality in this subpopulation.

Bioaccessible heavy metals-sediment particles from Reconquista River induce lung inflammation in mice.

The Reconquista River (RR), one of the most polluted watercourses in Argentina, receives effluent discharges from heavily industrialized and highly populated settlements. During winter and summer, the floodplain remains dry, producing the oxidation of sulfide and organic matter present in the sediment, making heavy metals more bioaccessible. Dispersion of this sediment occurs, and thus harmful effects on the pulmonary health of residents and workers inhabiting the RR bank may take place. The authors characterized the sediment particles of the RR (RR-PM) morphologically by scanning electron microscopy and its elemental composition by energy dispersive X-ray spectroscopy (EDX) and Community Bureau of Reference (BCR) sequential extraction. Furthermore, the authors evaluated its biological impact on the respiratory system of BALB/c mice, generating four groups: control healthy, sensibilized with ovalbumin, exposed to particles, and sensibilized and exposed to particles. Sediment particles of the Reconquista River contained fine particulate matter, with a high concentration of bioaccessible Cu and Zn. The authors found that animal exposure to RR-PM caused polymorphonuclear cell lung infiltration, augmentation of O2(-), increase of proinflammatory cytokines (tumor necrosis factor alpha [TNFα], interleukin-6 [IL-6]) and apoptosis. This adverse response was more dramatic in the sensibilized and exposed to particles group. Even more, they proved the bioaccessible fraction present in the RR-PM to be responsible for these harmful effects. The authors conclude that RR-PM produces an adverse biological impact on the airways of healthy animals, which is largely aggravated in previously sensibilized animals.

Simvastatin pretreatment prevents ambient particle-induced lung injury in mice.

Air particulate pollution negatively affects the health of the population exposed, being the lung the main target organ. Simvastatin (SV) is widely used for the prevention and risk reduction of coronary disease. Its pleiotropic effects may provide benefit for lung diseases. Here, we investigated the preventive effect of simvastatin pretreatment on acute intranasal exposure to ROFA (Residual Oil Fly Ash), and UAP (Urban Air Particle from Buenos Aires). Male BALB/c mice were randomized in two groups to receive either saline (control, C) solution or SV (1 mg/kg bw /day; ip) for 14 days. After SV treatment, ROFA or UAP (1 mg/kg bw) or saline were intranasally delivered for 24 hours generating 4 subgroups for the ROFA experiment (C, SV, ROFA and SV+ROFA) and 3 subgroups for the UAP experiment (C, SV, UAP and SV+UAP). Biomarkers of lung injury were examined in BAL cells evaluating total cell number (TCN), cell differential (CD) and superoxide anion generation (O2-), in lung homogenates assessing superoxide dismutase activity (SOD) and tumor necrosis factor α (TNFα); and in blood samples determining interleukin 6 (IL-6) production. ROFA and UAP produced an acute pulmonary injury, characterized by an increase in BAL, TCN and neutrophilic inflammatory influx, a rise in O2- generation, and production of the proinflammatory TNFα cytokine. SV pretreatment had no significant effect per se on any of these biomarkers but prevented the pulmonary cytotoxicity and inflammation induced by ROFA and UAP. Our results encourage further studies to determine the preventive effects on lung injury induced by air pollutants.