Particulate matter (PM) pollution adversely affects the airways, with asthmatic subjects thought to be especially sensitive. The authors hypothesised that exposure to diesel exhaust (DE), a major source of PM, would induce airway neutrophilia in healthy subjects, and that either these responses would be exaggerated in subjects with mild allergic asthma, or DE would exacerbate pre-existent allergic airways.Healthy and mild asthmatic subjects were exposed for 2 h to ambient levels of DE (particles with a 50% cut-off aerodynamic diameter of 10 mm (PM10) 108 mg?m -3 ) and lung function and airway inflammation were assessed.Both groups showed an increase in airway resistance of similar magnitude after DE exposure. Healthy subjects developed airway inflammation 6 h after DE exposure, with airways neutrophilia and lymphocytosis together with an increase in interleukin-8 (IL-8) protein in lavage fluid, increased IL-8 messenger ribonucleic acid expression in the bronchial mucosa and upregulation of the endothelial adhesion molecules. In asthmatic subjects, DE exposure did not induce a neutrophilic response or exacerbate their preexisting eosinophilic airway inflammation. Epithelial staining for the cytokine IL-10 was increased after DE in the asthmatic group.Differential effects on the airways of healthy subjects and asthmatics of particles with a 50% cut-off aerodynamic diameter of 10 mm at concentrations below current World Health Organisation air quality standards have been observed in this study. Further work is required to elucidate the significance of these differential responses. Numerous epidemiological studies have demonstrated clear associations between increased ambient particulate matter (PM) concentrations and indices of pulmonary and cardiac morbidity and mortality within the general population [1]. These adverse effects appear to be magnified in populations with pre-existing respiratory disease, such as asthma [2]. During PM pollution episodes, asthmatic subjects demonstrate increased respiratory symptoms, bronchoconstriction, medication use, bronchial hyperreactivity and emergency care visits [2,3]. The mechanism underlying this difference remains unclear.Exposure to particles with a 50% cut-off aerodynamic diameter of 10 mm (PM10) at concentrations above the USA National Air Quality Standards of 150 mg?m -3 (24 h average) occurs frequently in many cities throughout the world, due to a combination of vehicle traffic and industrial processes. The transport sector, especially diesel-powered vehicles, is a major source of urban PM pollution. Diesel exhaust (DE) is a complex mixture containing carbonaceous particles, oxides of nitrogen, carbon monoxide, aldehydes and other volatile organic carbon species. In addition, DE particles may act as vectors for the delivery to the lung of toxic materials, including heavy metal ions, hydrocarbons and allergens [4,5].The authors have previously shown airway inflammatory responses in healthy volunteers exposed to DE at a PM10 concentration of 300 mg?m -3 [6,7]...

The AEC systems available in modern CT scanners can contribute to a significant reduction in radiation exposure to the patient and the image noise becomes more uniform within any given scan.

The six evaluated IR algorithms all improve the image quality in brain CT but show different strengths and weaknesses.

Nitrogen dioxide (NO2) is a common indoor and outdoor air pollutant that may induce deterioration of respiratory health. In this study the effects of repeated daily exposure to NO2 on airway antioxidant status, inflammatory cell and mediator responses, and lung function were examined. Healthy nonsmoking subjects were exposed under controlled conditions to air (once) and to 2 ppm of NO2 for 4 h on four consecutive days. Lung function measurements were made before and immediately after the end of each exposure. Bronchoscopy with endobronchial biopsies, bronchial wash (BW), and bronchoalveolar lavage (BAL) was carried out 1.5 h after the air exposure and after the last exposure to NO2. Repeated NO2 exposure resulted in a decrease in neutrophil numbers in the bronchial epithelium. The BW revealed a twofold increase in content of neutrophils (p < 0.05) and a 1.5-fold increase in myeloperoxidase (MPO) (p < 0.01) indicative of both migration and activation of neutrophils in the airways. After the fourth NO2 exposure, antioxidant status of the airway fluid was unchanged. Significant decrements in FEV1 and FVC were found after the first exposure to NO2, but these attenuated with repeated exposures. Together, these data indicate that four sequential exposures to NO2 result in a persistent neutrophilic inflammation in the airways, whereas changes in pulmonary function and airway antioxidants are resolved. We conclude that NO2 is a proinflammatory air pollutant under conditions of repeated exposure.