Our data provide anatomical and functional support to the concept that chronic exposure to urban PM affects lung growth.

Analysis of fuel emissions is crucial for understanding the pathogenesis of mortality because of air pollution. The objective of this study is to assess cardiovascular and inflammatory toxicity of diesel and biodiesel particles. Mice were exposed to fuels for 1 h. Heart rate (HR), heart rate variability, and blood pressure were obtained before exposure, as well as 30 and 60 min after exposure. After 24 h, bronchoalveolar lavage, blood, and bone marrow were collected to evaluate inflammation. B100 decreased the following emission parameters: mass, black carbon, metals, CO, polycyclic aromatic hydrocarbons, and volatile organic compounds compared with B50 and diesel; root mean square of successive differences in the heart beat interval increased with diesel (p < 0.05) compared with control; low frequency increased with diesel (p < 0.01) and B100 (p < 0.05) compared with control; HR increased with B100 (p < 0.05) compared with control; mean corpuscular volume increased with B100 compared with diesel (p < 0.01), B50, and control (p < 0.001); mean corpuscular hemoglobin concentration decreased with B100 compared with B50 (p < 0.001) and control (p < 0.05); leucocytes increased with B50 compared with diesel (p < 0.05); platelets increased with B100 compared with diesel and control (p < 0.05); reticulocytes increased with B50 compared with diesel, control (p < 0.01), and B100 (p < 0.05); metamyelocytes increased with B50 and B100 compared with diesel (p < 0.05); neutrophils increased with diesel and B50 compared with control (p < 0.05); and macrophages increased with diesel (p < 0.01), B50, and B100 (p < 0.05) compared with control. Biodiesel was more toxic than diesel because it promoted cardiovascular alterations as well as pulmonary and systemic inflammation.

We conclude that long-term aerobic exercise presents protective effects in a mouse model of DEP-induced lung inflammation. Our results indicate a need for human studies that evaluate the pulmonary responses to aerobic exercise chronically performed in polluted areas.

Beers are a source of dietary flavonoids; however, there exist differences in composition, alcohol concentration, and beneficial activities. To characterize these differences, three kinds of lager beer of habitual consumption in Spain, dark, blond, and alcohol-free, were assayed for total phenolic content, antioxidant activity, superoxide and hydroxyl radical scavenging activities, and in vitro inhibitory effect on DNA oxidative damage. Furthermore, their melanoidin content and correlation with antioxidant activity were evaluated. Dark beer contained the highest total phenolic (489 +/- 52 mg/L) and melanoidin (1.49 +/- 0.02 g/L) contents with a 2-fold difference observed when compared to the alcohol-free beer. For the three kinds of beer, the antioxidant activity measured as N,N-dimethyl-p-phenylenediamine dihydrochloride concentration was strongly correlated with the total polyphenol content (R(2) = 0.91102, p < 0.005) and with the melanoidin content (R(2) = 0.7999, p < 0.05). The results support a positive effect of beers on the protection of DNA oxidative damage, by decreasing the deoxyribose degradation, DNA scission (measured by electrophoresis), and inhibition of 8-hydroxydeoxyguanosine (8-OH-dG) formation. Furthermore, a correlation between the total melanoidin content (R(2) = 0.7309, p < 0.01) and inhibition of 8-OH-dG was observed.

The mechanisms involved in the association between air pollution and increased cardiovascular morbidity are not fully understood. The objective of this study was to test the hypothesis that fine particulate matter (PM(2.5)) induces systemic inflammation and vasoconstriction of small arteries in the lung and heart of rats. Thirty-eight healthy Wistar rats were anesthetized, intubated, and submitted to the instillation of 1 ml of distilled water diluted in the following solution: blank filter, 100 microg and 500 microg of PM(2.5). PM(2.5) was collected in glass fiber filters with a high-volume sampler. The animals were sacrificed 24 h after instillation when blood, heart, and lung samples were collected for morphological and wet-to-dry weight ratio analysis. PM(2.5) consisted of the following elements: sulphur, arsenic, bromine, chlorine, cobalt, iron, lanthanum, manganese, antimony, scandium, and thorium. Total reticulocytes significantly increased at both PM(2.5) doses (p < 0.05) while hematocrit levels increased in the 500 microg group (p < 0.05). Quantification of segmented neutrophils and fibrinogen levels showed a significant decrease, while lymphocytes counting increased with 100 microg of PM(2.5) (p < 0.05). A significant dose-dependent decrease of intra-acinar pulmonary arteriole lumen/wall ratio (L/W) was observed in PM groups (p < 0.001). Peribronchiolar arterioles L/W showed a significant decrease in the 500 microg group (p < 0.001). A significant increase in heart wet-to-dry weight ratio was observed in the 500 microg group (p < 0.001). In conclusion, fine environment particles in the city of São Paulo promote pulmonary and cardiac histological alterations. Pulmonary vasculature was markedly affected by particle instillation, resulting in significant vasoconstriction in healthy rats.