Exposure to urban PM1 in rats: development of bronchial inflammation and airway hyperresponsiveness.

BACKGROUND: Several epidemiological and laboratory studies have evidenced the fact that atmospheric particulate matter (PM) increases the risk of respiratory morbidity. It is well known that the smallest fraction of PM (PM1 - particulate matter having a diameter below 1 µm) penetrates the deepest into the airways. The ratio of the different size fractions in PM is highly variable, but in industrial areas PM1 can be significant. Despite these facts, the health effects of PM1 have been poorly investigated and air quality standards are based on PM10 and PM2.5 (PM having diameters below 10 µm and 2.5 µm, respectively) concentrations. Therefore, this study aimed at determining whether exposure to ambient PM1 at a near alert threshold level for PM10 has respiratory consequences in rats. METHODS: Rats were either exposed for 6 weeks to 100 µg/m(3) (alert threshold level for PM10 in Hungary) urban submicron aerosol, or were kept in room air. End-expiratory lung volume, airway resistance (Raw) and respiratory tissue mechanics were measured. Respiratory mechanics were measured under baseline conditions and following intravenous methacholine challenges to characterize the development of airway hyperresponsiveness (AH). Bronchoalveolar lavage fluid (BALF) was analyzed and lung histology was performed. RESULTS: No significant differences were detected in lung volume and mechanical parameters at baseline. However, the exposed rats exhibited significantly greater MCh-induced responses in Raw, demonstrating the progression of AH. The associated bronchial inflammation was evidenced by the accumulation of inflammatory cells in BALF and by lung histology. CONCLUSIONS: Our findings suggest that exposure to concentrated ambient PM1 (mass concentration at the threshold level for PM10) leads to the development of mild respiratory symptoms in healthy adult rats, which may suggest a need for the reconsideration of threshold limits for airborne PM1.

Respiratory consequences of red sludge dust inhalation in rats.

The environmental disaster following flooding by red sludge in the Ajka region in Hungary poses a serious public health threat with particular concern regarding the potentially adverse respiratory effects of the inhalation of red sludge dust (RSD). The respiratory consequences of the inhalation of RSD obtained from field samples were investigated in rats. Rats were either exposed to RSD at a high concentration (2 weeks, 8h/day), or kept in room air. After the exposures, the airway resistance (R(aw)) and the respiratory tissues mechanics were measured under baseline condition, and following methacholine (MCh) challenges with the aim of establishing airway hyper-responsiveness (AH). Histopathology was performed to assess lung morphologic alterations. The physical properties and the chemical composition of the RSD were also characterized. The size distribution, chemical composition and topology of the RSD particles applied in our experiments were similar to those observed at the site of the disaster. The inhalation of RSD did not alter the basal respiratory mechanics, whereas it led to greater MCh-induced responses in R(aw), demonstrating the progression of mild AH. Histopathological investigations revealed fine, granular particles in the alveolar macrophages, as evidence that RSD had reached the lower respiratory tract and induced mild inflammation around the alveoli and the pulmonary vasculature. The mild respiratory symptoms that developed following short-term exposure of healthy individuals to high concentrations of airborne RSD do not appear to pose a greater respiratory hazard than the inhalation of urban dust at a comparable concentration.