Eugenol attenuates pulmonary damage induced by diesel exhaust particles

Zin WA, Silva AG, Magalhaes CB, Carvalho GM, Riva DR, Lima CC, Leal-Cardoso JH, Takiya CM, Valen a SS, Saldiva PH, Faffe DS. Eugenol attenuates pulmonary damage induced by diesel exhaust particles. J Appl Physiol 112: 911-917, 2012. First published December 22, 2011; doi: 10.1152/japplphysiol.00764.2011.-Environmentally relevant doses of inhaled diesel particles elicit pulmonary inflammation and impair lung mechanics. Eugenol, a methoxyphenol component of clove oil, presents in vitro and in vivo anti-inflammatory and antioxidant properties. Our aim was to examine a possible protective role of eugenol against lung injuries induced by diesel particles. Male BALB/c mice were divided into four groups. Mice received saline (10 mu l in; CTRL group) or 15 mu g of diesel particles DEP (15 mu g in; DIE and DEUG groups). After 1 h, mice received saline (10 mu l; CTRL and DIE groups) or eugenol (164 mg/kg; EUG and DEUG group) by gavage. Twenty-four hours after gavage, pulmonary resistive (Delta P1), viscoelastic (Delta P2) and total (Delta Ptot) pressures, static elastance (Est), and viscoelastic component of elastance (Delta E) were measured. We also determined the fraction areas of normal and collapsed alveoli, amounts of polymorpho- (PMN) and mononuclear cells in lung parenchyma, apoptosis, and oxidative stress. Est, Delta P2, Delta Ptot, and Delta E were significantly higher in the DIE than in the other groups. DIE also showed significantly more PMN, airspace collapse, and apoptosis than the other groups. However, no beneficial effect on lipid peroxidation was observed in DEUG group. In conclusion, eugenol avoided changes in lung mechanics, pulmonary inflammation, and alveolar collapse elicited by diesel particles. It attenuated the activation signal of caspase-3 by DEP, but apoptosis evaluated by TUNEL was avoided. Finally, it could not avoid oxidative stress as indicated by malondialdehyde.

Anti-inflammatory Effects of Aerobic Exercise in Mice Exposed to Air Pollution

VIEIRA, R. D. P., A. C. TOLEDO, L. B. SILVA, F. M. ALMEIDA, N. R. DAMACENO-RODRIGUES, E. G. CALDINI, A. B. G. SANTOS, D. H. RIVERO, D. C. HIZUME, F. D. T. Q. S. LOPES, C. R. OLIVO, H. C. CASTRO-FARIA-NETO, M. A. MARTINS, P. H. N. SALDIVA, and M. DOLHNIKOFF. Anti-inflammatory Effects of Aerobic Exercise in Mice Exposed to Air Pollution. Med. Sci. Sports Exerc., Vol. 44, No. 7, pp. 1227-1234, 2012. Purpose: Exposure to diesel exhaust particles (DEP) results in lung inflammation. Regular aerobic exercise improves the inflammatory status in different pulmonary diseases. However, the effects of long-term aerobic exercise on the pulmonary response to DEP have not been investigated. The present study evaluated the effect of aerobic conditioning on the pulmonary inflammatory and oxidative responses of mice exposed to DEP. Methods: BALB/c mice were subjected to aerobic exercise five times per week for 5 wk, concomitantly with exposure to DEP (3 mg.mL (1); 10 mu L per mouse). The levels of exhaled nitric oxide, reactive oxygen species, cellularity, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) were analyzed in bronchoalveolar lavage fluid, and the density of neutrophils and the volume proportion of collagen fibers were measured in the lung parenchyma. The cellular density of leukocytes expressing IL-1 beta, keratinocyte chemoattractant (KC), and TNF-alpha in lung parenchyma was evaluated with immunohistochemistry. The levels of IL-1 beta, KC, and TNF-alpha were also evaluated in the serum. Results: Aerobic exercise inhibited the DEP-induced increase in the levels of reactive oxygen species (P < 0.05); exhaled nitric oxide (P < 0.01); total (P < 0.01) and differential cells (P < 0.01); IL-6 and TNF-alpha levels in bronchoalveolar lavage fluid (P < 0.05); the level of neutrophils (P < 0.001); collagen density in the lung parenchyma (P < 0.05); the levels of IL-6, KC, and TNF-alpha in plasma (P < 0.05); and the expression of IL-1 beta, KC, and TNF-alpha by leukocytes in the lung parenchyma (P < 0.01). Conclusions: 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.

Risk assessment of PM2.5 to child residents in Brazilian Amazon region with biofuel production

Background: Exposure to fine fractions of particulate matter (PM2.5) is associated with increased hospital admissions and mortality for respiratory and cardiovascular disease in children and the elderly. This study aims to estimate the toxicological risk of PM2.5 from biomass burning in children and adolescents between the age of 6 and 14 in Tangara da Serra, a municipality of Subequatorial Brazilian Amazon. Methods: Risk assessment methodology was applied to estimate the risk quotient in two scenarios of exposure according to local seasonality. The potential dose of PM2.5 was estimated using the Monte Carlo simulation, stratifying the population by age, gender, asthma and Body Mass Index (BMI). Results: Male asthmatic children under the age of 8 at normal body rate had the highest risk quotient among the subgroups. The general potential average dose of PM2.5 was 1.95 mu g/kg.day (95% CI: 1.62 - 2.27) during the dry scenario and 0.32 mu g/kg. day (95% CI: 0.29 - 0.34) in the rainy scenario. During the dry season, children and adolescents showed a toxicological risk to PM2.5 of 2.07 mu g/kg. day (95% CI: 1.85 - 2.30). Conclusions: Children and adolescents living in the Subequatorial Brazilian Amazon region were exposed to high levels of PM2.5 resulting in toxicological risk for this multi-pollutant. The toxicological risk quotients of children in this region were comparable or higher to children living in metropolitan regions with PM2.5 air pollution above the recommended limits to human health.

Endothelial dysfunction in the pulmonary artery induced by concentrated fine particulate matter exposure is associated with local but not systemic inflammation

Clinical evidence has identified the pulmonary circulation as an important target of air pollution. It was previously demonstrated that in vitro exposure to fine particulate matter (aerodynamic diameter <= 2.5 mu m, PM2.5) induces endothelial dysfunction in isolated pulmonary arteries. We aimed to investigate the effects of in vivo exposure to urban concentrated PM2.5 on rat pulmonary artery reactivity and the mechanisms involved. For this, adult Wistar rats were exposed to 2 weeks of concentrated Sao Paulo city air PM2.5 at an accumulated daily dose of approximately 600 mu g/m(3). Pulmonary arteries isolated from PM2.5-exposed animals exhibited impaired endothelium-dependent relaxation to acetylcholine without significant changes in nitric oxide donor response compared to control rats. PM2.5 caused vascular oxidative stress and enhanced protein expression of Cu/Zn- and Mn-superoxide dismutase in the pulmonary artery. Protein expression of endothelial nitric oxide synthase (eNOS) was reduced, while tumor necrosis factor (TNF)-alpha was enhanced by PM2.5 inhalation in pulmonary artery. There was a significant positive correlation between eNOS expression and maximal relaxation response (E-max) to acetylcholine. A negative correlation was found between vascular TNF-alpha expression and E-max to acetylcholine. Plasma cytokine levels, blood cells count and coagulation parameters were similar between control and PM2.5-exposed rats. The present findings showed that in vivo daily exposure to concentrated urban PM2.5 could decrease endothelium-dependent relaxation and eNOS expression on pulmonary arteries associated with local high TNF-alpha level but not systemic pro-inflammatory factors. Taken together, the present results elucidate the mechanisms underlying the trigger of cardiopulmonary diseases induced by urban ambient levels of PM2.5. (C) 2012 Elsevier Ireland Ltd. All rights reserved.

Relações entre experiências anômalas tipicamente contemporâneas, transtornos mentais e experiências espirituais

Background: The anomalous experiences are often an explanatory challenge for psychiatry and psychology about how and why they occur, in addition to signaling gaps in knowledge about human psychological functioning, as hallucinations in non-clinical populations. Objective: It aims to investigate possible psychopathological dimensions of Brazilian samples of persons who claim distinctively contemporary anomalous experiences. Methods: It was used the Mini International Neuropsychiatric Interview, detailed version (MINI PLUS) and the nine diagnostic criteria for the distinction between spiritual experiences and mental disorders with religious content developed by Menezes Junior and Moreira-Almeida. Results: There was evidence that the experiences are typically healthy, although there are indicators of pre-morbid characteristics in the childhood and adolescence of the protagonists of the more complex experiments. There is profitable intersections with healthy squizotype profile, which is still poorly understood. Discussion: The absence of formal mental disorders does not exhaust the possible relations between contemporary anomalous experiences and the mental health field, but reveals complexities that characterize the everyday culture. Martins LB, Zangari W / Rev Psiq Clin. 2012; 39(6): 198-202

An overview of biodiesel soil pollution: Data based on cytotoxicity and genotoxicity assessments

Biodiesel production has received considerable attention in the recent past as a nonpolluting fuel. However, this assertion has been based on its biodegradability and reduction in exhaust emissions. Assessments of water and soil biodiesel pollution are still limited. Spill simulation with biodiesel and their diesel blends in soils were carried out, aiming at analyzing their cytotoxic and genotoxic potentials. While the cytotoxicity observed may be related to diesel contaminants, the genotoxic and mutagenic effects can be ascribed to biodiesel pollutants. Thus, taking into account that our data stressed harmful effects on organisms exposed to biodiesel-polluted soils, the designation of this biofuel as an environmental-friendly fuel should be carefully reviewed to assure environmental quality. (C) 2011 Elsevier B.V. All rights reserved.

Nitrous oxide emissions from gasohol, ethanol and CNG light duty vehicles

A sample of 21 light duty vehicles powered by Otto cycle engines were tested on a chassis dynamometer to measure the exhaust emissions of nitrous oxide (N2O). The tests were performed at the Vehicle Emission Laboratory of CETESB (Environmental Company of the State of Sao Paulo) using the US-FTP-75 (Federal Test Procedure) driving cycle. The sample tested included passenger cars running on three types of fuels used in Brazil: gasohol, ethanol and CNG. The measurement of N2O was made using two methods: Non Dispersive InfraRed (NDIR) analyzer and Fourier Transform InfraRed spectroscopy (FTIR). Measurements of regulated pollutants were also made in order to establish correlations between N2O and NOx. The average N2O emission factors obtained by the NDIR method was 78 +/- 41 mg.km(-1) for vehicles running with gasohol, 73 +/- 45 mg.km(-1) for ethanol vehicles and 171 +/- 69 mg.km(-1) for CNG vehicles. Seventeen results using the FTIR method were also obtained. For gasohol vehicles the results showed a good agreement between the two methods, with an average emission factor of 68 +/- 41 mg.km(-1). The FTIR measurement results of N2O for ethanol and CNG vehicles were much lower than those obtained by the NDIR method. The emission factors were 17 +/- 10 mg.km(-1) and 33 +/- 17 mg.km(-1), respectively, possibly because of the interference of water vapor (present at a higher concentration in the exhaust gases of these vehicles) on measurements by the NDIR method.

Influence of urban activities on polycyclic aromatic hydrocarbons in precipitation: Distribution, sources and depositional flux in a developing metropolis, Fortaleza, Brazil

We measured polycyclic aromatic hydrocarbons (PAHs) in bulk precipitation in the Fortaleza metropolitan area, Ceara, Brazil, for the first time. Because little information is available concerning PAHs in tropical climatic regions, we assessed their spatial distribution and possible sources and the influence of urban activities on the depositional fluxes of PAHs in bulk precipitation. The concentrations of individual and total PAHs (Sigma(PAHs)) in bulk precipitation ranged from undetectable to 133.9 ng.L-1 and from 202.6 to 674.8 ng.L-1, respectively. The plume of highest concentrations was most intense in a zone with heavy automobile traffic and favorable topography for the concentration of emitted pollutants. The depositional fluxes of PAHs in bulk precipitation calculated in this study (undetectable to 0.87 mu g.m(-2).month(-1)) are 4 to 27 times smaller than those reported from tourist sites and industrial and urban areas in the Northern Hemisphere. Diagnostic ratio analyses of PAH samples showed that the major source of emissions is gasoline exhaust, with a small percentage originating from diesel fuel. Contributions from coal and wood combustion were also found. Major economic activities appear to contribute to pollutant emissions. (C) 2011 Elsevier B.V. All rights reserved.

HEPATOTOXICITY ASSESSMENT OF THE AZO DYES DISPERSE ORANGE 1 (DO1), DISPERSE RED 1 (DR1,) AND DISPERSE RED 13 (DR13) IN HEPG2 CELLS

During the dyeing process in baths approximately 10 to 15% of the dyes used are lost and reach industrial effluents, thus polluting the environment. Studies showed that some classes of dyes, mainly azo dyes and their by-products, exert adverse effects on humans and local biota, since the wastewater treatment systems and water treatment plants were found to be ineffective in removing the color and reducing toxicity of some dyes. In the present study, the toxicity of the azo dyes disperse orange 1 (DO1), disperse red 1 (DR1), and disperse red 13 (DR13) was evaluated in HepG2 cells grown in monolayers or in three dimensional (3D) culture. Hepatotoxicity of the dyes was measured using 3-(4,5-dimethylthiazol-2yl)2,5-diphenyltetrazolium (MTT) and cell counting kit 8 (CCK-8) assays after 24, 48, and 72 h of incubation of cells with 3 different concentrations of the azo dyes. The dye DO1 only reduced the mitochondrial activity in HepG2 cells grown in a monolayer after 72 h incubation, while the dye DR1 showed this deleterious effect in both monolayer and 3D culture. In contrast, dye DR13 decreased the mitochondrial activity after 24, 48, and 72 h of exposure in both monolayer and 3D culture. With respect to dehydrogenase activity, only the dye DR13 diminished the activity of this enzyme after 72 h of exposure in both monolayer and 3D culture. Our results clearly demonstrated that exposure to the studied dyes induced cytotoxicity in HepG2 cells.