Search

Antecedentes La contaminacion atmosferica se asocia a una carga sustancial para la salud humana; sin embargo, los contaminantes de mayor importancia pueden variar segun el lugar. Es necesaria una monitorizacion adecuada para determinar el efecto de dichos contaminantes sobre la salud respiratoria. Objetivos Este estudio se diseno para evaluar el papel de la exposicion en el exterior, en el interior y personal a los contaminantes derivados de la combustion NO2 y O3 sobre la salud respiratoria de los ninos en una zona urbana economicamente poco favorecida de Sao Paulo (Brasil). Metodos Se determinaron de forma continua los niveles de NO2 y O3 en el aire del exterior, el interior, y tambien en la exposicion personal, durante 30 dias con el empleo de aparatos de medicion pasiva. Se evaluo la salud respiratoria con una version en brasileno del cuestionario ISAAC. Resultados Se dispuso de datos completos de 64 ninos de 6 a 10 anos de edad. La morbilidad respiratoria fue alta, con 43 (67,2%) ninos en los que habia habido sibilancias en alguna ocasion, 27 (42,2%) con sibilancias en el mes anterior, 17 (26,6%) con asma en alguna ocasion y 21 (32,8%) con neumonia en alguna ocasion. Las correlaciones entre los niveles de NO2 y O3 determinados en las 3 localizaciones evaluadas fueron bajas. Los niveles de NO2 en el area de interior y la exposicion personal a O3 mostraron una asociacion independiente con el asma (p=0,02 en ambos casos), la neumonia (O3, p=0,02) y la presencia de sibilancias en alguna ocasion (p

INTRODUÇÃO. Estudos epidemiológicos têm demonstrado que a exposição à poluição atmosférica está associada ao aumento de doenças cardiorrespiratórias. Trabalhos experimentais anteriores, utilizaram uretana para induzir a formação de nódulos pulmonares em camundongos e expor estes animais à poluição de \"mundo real\". Ou seja, os animais foram expostos a gases e partículas da mesma forma com que a população está exposta na cidade de São Paulo. Evidenciou-se então, o papel promotor e dose dependente da atmosfera poluída na progressão dos tumores de pulmão. Sabe-se que substâncias carcinogênicas como hidrocarbonetos policíclicos aromáticos (HPA), metais, ácidos graxos e aldeídos, estão presentes na fração particulada respirável da poluição (material particulado fino - MP 2,5), e a exposição prolongada a este último vem sendo considerada um risco para o desenvolvimento do câncer de pulmão. O objetivo deste estudo é verificar se a exposição crônica ao MP2,5 concentrado, a partir do ar ambiente da cidade de São Paulo, tem potencial carcinogênico. MÉTODOS. Foram utilizados 60 camundongos machos suíços (30g); e 60 AJ (20g), com quatro a seis semanas de vida. Os camundongos suíços foram pré-tratados com um carcinógeno completo, o ácido carbâmico (uretana-U), enquanto que os AJ receberam um carcinógeno iniciador 4-(methylnitrosamino)-1-(3-pyridil)-1-butanona (NNK), por serem pré-dispostos ao desenvolvimento de tumores de pulmão. Em seguida todos os animais foram expostos no Concentrador de Partículas Atmosféricas Harvard ao MP 2,5 diariamente, por 2 horas, durante quatro meses. Cada linhagem foi dividida em quatro grupos (n=15 cada): 2 controles com salina e carcinógeno (CsS e CsU ou CajS e CajNNK) e 2 expostos com salina e carcinógeno (EsS e EsU ou EajS e EajNNK). Foi realizada a análise histopatológica dos pulmões, a contagem e classificação das lesões pulmonares encontradas. Foi feito estudo imunoistoquimico para p53 e PCNA. RESULTADOS. Os animais dos grupos expostos, em ambas as linhagens, apresentaram maior número de lesões neoplásicas. As médias de lesões (nódulos e hiperplasia) obtidas foram: CsU: 1,07( DP+ 1,54), CsSl: 0( DP+ 0), EsU: 2,57 ( DP+ 2,77) e EsS: 0,40 ( DP+ 1,12), com p < 0,001; CajNNK: 4,94( DP+ 3,54), CajS: 0,15( DP+ 0,37), EajNNK: 9,14 ( DP+ 7,70) e EajS:0,80 ( DP+ 1,93), com p

Air pollution is associated with a substantial burden on human health; however, the most important pollutants may vary with location. Proper monitoring is necessary to determine the effect of these pollutants on respiratory health.This study was designed to evaluate the role of outdoor, indoor and personal exposure to combustion-related pollutants NO(2) and O(3) on respiratory health of children in a non-affluent urban area of São Paulo, Brazil.Levels of NO(2) and O(3) were continuously measured in outdoor and indoor air, as well as personal exposure, for 30 days using passive measurement monitors. Respiratory health was assessed with a Brazilian version of the ISAAC questionnaire.Complete data were available from 64 children, aged 6-10 years. Respiratory morbidity was high, with 43 (67.2%) reporting having had wheezing at any time, 27 (42.2%) wheezing in the last month, 17 (26.6%) asthma at any time and 21 (32.8%) pneumonia at any time. Correlations between levels of NO(2) and O(3) measured in the three locations evaluated were poor. Levels of NO(2) in indoor air and personal exposure to O(3) were independently associated with asthma (both cases P=.02), pneumonia (O(3), P=.02) and wheezing at any time (both cases P.01). No associations were seen between outdoor NO(2) and O(3) and respiratory health.Exposure to higher levels of NO(2) and O(3) was associated with increased risk for asthma and pneumonia in children. Nonetheless, the place where the pollutants are measured influences the results. The measurements taken in indoor and personal exposure were the most accurate.

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 ≤2.5μm, 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 São Paulo city air PM2.5 at an accumulated daily dose of approximately 600μg/m3. 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)-α was enhanced by PM2.5 inhalation in pulmonary artery. There was a significant positive correlation between eNOS expression and maximal relaxation response (Emax) to acetylcholine. A negative correlation was found between vascular TNF-α expression and Emax 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-α 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.