Acute exposure to diesel and sewage biodiesel exhaust causes pulmonary and systemic inflammation in mice.

Biodiesel is a renewable energy source that reduces particle emission, but few studies have assessed its effects. To assess the effects of acute inhalation of two doses (600 and 1200 µg/m3) of diesel (DE) and biodiesel (BD) fuels on the inflammatory pulmonary and systemic profile of mice. Animals were exposed for 2 h in an inhalation chamber inside the Container Laboratory for Fuels. Heart rate, heart rate variability (HRV) and blood pressure were determined 30 min after exposure. After 24 h, we analyzed the lung inflammation using bronchoalveolar lavage fluid (BALF); neutrophil and macrophage quantification in the lung parenchyma was performed, and blood and bone marrow biomarkers as well as receptor of endothelin-A (ET-Ar), receptor of endothelin-B (ET-Br), vascular cell adhesion molecule 1 (VCAM-1), inducible nitric oxide synthase (iNOs) and isoprostane (ISO) levels in the pulmonary vessels and bronchial epithelium were evaluated. HRV increased for BD600, D600 and D1200 compared to filtered air (FA). Both fuels (DE and BD) produced alterations in red blood cells independent of the dose. BALF from the BD600 and BD1200 groups showed an increase in neutrophils compared to those of the FA group. Numeric density of the polymorphonuclear and mononuclear cells was elevated with BD600 compared to FA. In the peribronchiolar vessels, there was an increase in ET-Ar and ET-Br expression following BD600 compared to FA; and there was a reduction in the iNOs expression for BD1200 and the VCAM-1 for D1200 compared to FA. In the bronchial epithelium, there was an increase in ETAr at BD600, ET-Br at two doses (600 and 1200 µg/m3) of DE and BD, iNOs at D600 and VCAM-1 at BD1200 and D600; all groups were compared to the FA group. Acute exposure to DE and BD derived from sewage methyl esters triggered pulmonary and cardiovascular inflammatory alterations in mice.

Effects of ambient levels of air pollution generated by traffic on birth and placental weights in mice.

OBJECTIVE: To examine whether there is an association between fetal and/or placental weight and exposure to ambient levels of air pollution in mice. DESIGN: Chronic experiments on mice that were exposed to polluted vs. clean air. SETTING: Environmental exposure to atmospheric pollution. ANIMAL(S): Female Swiss mice (n = 70) were maintained at different stages of gestation in an exposure chamber located at an intersection with heavy traffic in a major city in Brazil. Control mice were maintained in a similar chamber, located adjacent to the exposure chamber but equipped with filters for particles and reactive gases. INTERVENTION(S): Animals were divided into six groups as follows: no exposure, exposure to a polluted chamber throughout gestation, exposure to a polluted chamber during the 1st week of pregnancy, exposure to a polluted chamber during the 2nd and 3rd weeks, exposure to a polluted chamber during the 1st and 2nd week, and exposure to a polluted chamber during the 3rd week. MAIN OUTCOME MEASURE(S): At the end of the gestational period, the determination of fetal and placental weight was performed after cesarean section. RESULT(S): Exposure to air pollution during the 1st week of pregnancy promoted a significant reduction in fetal weight. Mice exposed to polluted air, in any phase of gestation, presented with lower placental weight in comparison to mice maintained in clean chambers. CONCLUSION(S): Exposure to ambient levels of traffic pollution at early phases of gestation is a determinant for decreased final fetal weight. Placental weight is reduced with exposure to air pollution at any phase of gestation.

Increased levels of air pollution and a decrease in the human and mouse male-to-female ratio in São Paulo, Brazil.

A significant negative association (R(2) = 0.7642; P=.013) between particulate matter and secondary sex ratio was found when evaluating people in the city of São Paulo, Brazil. An animal model with male mice raised in nonfiltered open-top chambers showed a significant reduction in the secondary sex ratio (P=.041), suggesting that ambient air pollution may interfere with sex distribution by altering the X:Y sperm proportion in pollution-exposed males.