RESUMO
Ambient particles may undergo modifications to their chemical composition as a consequence of climatic variability. The determination of whether these changes modify the toxicity of the particles is important for the understanding of the health effects associated with particle exposure. The objectives were to determine whether low levels of particles promote cardiopulmonary effects, and to assess if the observed alterations are influenced by season. Mice were exposed to 200 µg/m(3) concentrated ambient particles (CAPs) and filtered air (FA) in cold/dry and warm/humid periods. Lung hyperresponsiveness, heart rate, heart rate variability, and blood pressure were evaluated 30 min after each exposure. After 24 h, blood and tissue samples were collected. During both periods (warm/humid and cold/dry), CAPs induced alterations in red blood cells and lung inflammation. During the cold/dry period, CAPs reduced the mean corpuscular volume levels and increased erythrocytes, hemoglobin, mean corpuscular hemoglobin concentration, and red cell distribution width coefficient variation levels compared with the FA group. Similarly, CAPs during the warm/humid period decreased mean corpuscular volume levels and increased erythrocytes, hemoglobin, hematocrit, and red cell distribution width coefficient variation levels compared with the FA group. CAPs during the cold/dry period increased the influx of neutrophils in the alveolar parenchyma. Short-term exposure to low concentrations of CAPs elicited modest but significant pulmonary inflammation and, to a lesser extent, changes in blood parameters. In addition, our data support the concept that changes in climate conditions slightly modify particle toxicity because equivalent doses of CAPs in the cold/dry period produced a more exacerbated response.
Assuntos
Poluentes Atmosféricos/efeitos adversos , Hemodinâmica , Exposição por Inalação/efeitos adversos , Material Particulado/efeitos adversos , Mecânica Respiratória , Estações do Ano , Poluentes Atmosféricos/sangue , Animais , Brasil , Pulmão/patologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Material Particulado/sangue , Hidrocarbonetos Policíclicos Aromáticos/efeitos adversos , Hidrocarbonetos Policíclicos Aromáticos/análise , Hidrocarbonetos Policíclicos Aromáticos/sangueRESUMO
Introdução: Em ambientes urbanos, a exaustão dos carros a diesel é uma importante fonte de partículas e gases que afetam diretamente a saúde das pessoas. Como a adição do biodiesel ao diesel é recente, torna-se necessário avaliar o perfil toxicológico dessas emissões e os possíveis efeitos adversos a saúde. Além do mais, a concentração dos poluentes atmosféricos e sua composição físico-química sofrem influências diretas das condições meteorológicas. Esse estudo tem como foco avaliar o perfil toxicológico dos poluentes primários (emitidos diretamente da fonte) e secundários (gerados a partir das condições atmosféricas) por meio de dois estudos. Objetivos: (Estudo I) Avaliar a exposição aguda da exaustão do diesel e biodiesel no perfil inflamatório pulmonar e sistêmico; (Estudo II) Avaliar se a exposição aguda a baixos níveis de partículas ambientais concentradas (PACs) promovem efeitos cardiopulmonares e sistêmicos; e se a magnitude dessas alterações observadas é influenciada pelos períodos (frio/seco e quente/úmido). Métodos: (Estudo I) Camundongos Balb/C foram expostos ao ar filtrado (AF) e a duas concentrações de MP2,5 (600 e 1200 ?g/m3) tanto da exaustão do combustível diesel (D) quanto do biodiesel (BD). As emissões dos poluentes (MP2,5, NO e NO2), temperatura e umidade foram monitorados em tempo real. Os registros da variabilidade da frequência cardíaca (VFC), frequência cardíaca (FC) e da pressão arterial (PA) foram obtidas 30 minutos após a exposição. Após 24 horas os animais foram eutanasiados e foram coletados o lavado broncoalveolar (LBA), o pulmão, o sangue e a medula óssea para avaliar a inflamação pulmonar e sistêmica. A expressão das citocinas (ET-Ar, ET-Br, INOs, ISO, VCAM, IL-8) foram analisadas nos vasos peribronquiolares e no epitélio brônquico. (Estudo II) Camundongos Balb/C foram expostos ao ar filtrado e as PACs na concentração de 200 ?g/m3 geradas no período frio/seco e quente/úmido. A hiperresponsividade pulmonar, VFC, FC, PA foram...
Background: In urban environments, the exhaust of diesel cars is an important source of particles and gases that directly affect people's health. As the addition of biodiesel to diesel is recent, it is necessary to evaluate the toxicological profile of these emissions and the possible adverse health effects. Moreover, the concentration of air pollutants and their physico-chemical composition suffer direct influences of weather conditions. This study aims to evaluate the toxicological profile of primary pollutants (emitted directly from the source) and secondary (generated from the weather conditions) through two studies. Objectives: (Study I) Evaluate the acute exposure of diesel and biodiesel exhaust in pulmonary and systemic inflammatory profile. (Study II) Evaluated whether acute exposure to low levels of concentrated ambient particles (CAPs) promotes cardiopulmonary and systemic effects; and whether the magnitude of these observed changes is influenced by periods (cold/dry and warm/humid). Methods: (Study I) Balb/C mice were exposed for two hours to filtered air (FA) and two doses (600 and 1200 ?g/m3) of both diesel (D) and biodiesel (BD) fuels. The PM2.5, NO, and NO2 concentrations, air temperature and humidity were monitored in real time. HRV (time and frequency domain), HR and BP parameters were collected after 30 minutes of exposure. After 24 hours were available the bronchoalveolar lavage (BALf), lung histology, blood and bone marrow for pulmonar and systemic inflammation analysis. The cytokines expression (ET-Ar, ET-Br, INOs, ISO, VCAM, IL-8) were available on peribronchiolar vessels and bronchial epithelium. (Study II) Balb/C mice were exposed to 200 ?g/m3 to concentrated ambient particles (CAPs) and filtered air (FA) in cold/dry and warm/humid periods. Lung hyper-responsiveness, heart rate, heart rate variability and blood pressure were evaluated 30 minutes after the exposures. After 24 hours, blood and tissue sampling were...
Assuntos
Animais , Camundongos , Poluentes Atmosféricos , Sistema Cardiovascular , Inflamação , Exposição por Inalação , Camundongos , Material Particulado , Emissões de VeículosRESUMO
BACKGROUND: Experimental hemorrhagic shock (HS) is based on controlling bleeding and the treatment of fluid resuscitation to restore tissue oxygenation and perfusion. The HS could promote ischemia/reperfusion injury, which induces a general exacerbation of the inflammatory process, initially compromising the lungs. N-acetylcysteine (NAC), an antioxidant, may attenuate ischemia/reperfusion injury. This study evaluated the effect of NAC in association with fluid resuscitation on pulmonary injury in a controlled HS model in rats. METHODS: Male Wistar rats were submitted to controlled HS (mean arterial pressure of 35 mm Hg for 60 min). Two groups were constituted according to resuscitation solution administered: RLG (Ringer's lactate solution) and RLG+NAC (Ringer's lactate in association with 150 mg/kg NAC. A control group was submitted to catheterization only. After 120 min of resuscitation, bronchoalveolar lavage was performed to assess intra-alveolar cell infiltration and pulmonary tissue was collected for assessment of malondialdehyde, interleukin 6, and interleukin 10 and histopathology. RESULTS: Compared with the RLG group, the RLG+NAC group showed lower bronchoalveolar lavage inflammatory cell numbers, lower interstitial inflammatory infiltration in pulmonary parenchyma, and lower malondialdehyde concentration. However, tissue cytokine (interleukin 6 and interleukin 10) expression levels were similar. CONCLUSION: N-acetylcysteine was associated with fluid resuscitation-attenuated oxidative stress and inflammatory cell infiltration in pulmonary parenchyma. N-acetylcysteine did not modify cytokine expression.