Background -Improvement of allergic

This study examined the safety of sputum induction and the relation between sputum cell counts and clinical parameters in adolescents with severe persistent asthma.Within 5 days, induced sputum and reversibility in forced expiratory volume in one second (FEV1), quality of life, provocative concentration causing a 20% fall in FEV1 (PC20) of adenosine monophosphate and histamine, exercise-induced bronchoconstriction, overall asthma severity index, and blood eosinophils were collected in 20 atopic adolescents with moderate-to-severe persistent asthma (12±18 yrs of age, FEV1 65±110% of predicted, on 500±2,000 mg inhaled steroids daily).FEV1 was reversible by 13.32.3% pred. After sputum induction, FEV1 was still increased by 9.02.6% pred as compared to the pre-salbutamol baseline. Sputum contained, median (range): 12.4 (0.4±59.5)% squamous cells, 47.3 (6.8±84.0)% macrophages, 39.0 (4.6±84.8)% neutrophils, 4.8 (1.0±12.4)% lymphocytes, 0.4 (0±10.8)% eosinophils and 3.6 (0±23.4)% bronchial epithelial cells. Sputum eosinophils showed a trend towards a significant association with the overall asthma severity index (r=0.46, p=0.06) and correlated inversely with baseline FEV1 (r=-0.51, p=0.03).In conclusion, sputum can be induced safely in adolescents with moderate-to-severe persistent asthma, if pretreated with b 2 -agonists. Despite relatively low sputum eosinophil counts in these patients on inhaled steroids, the association of eosinophil numbers with baseline forced expiratory volume in one second and asthma severity index favours a role of induced sputum in monitoring adolescents with severe asthma. Eur Respir J 1999; 13: 647±653.

Epidemiological studies have observed statistical associations between short-term exposure to increased ambient particulate air pollution and increased hospital admissions, medication use, pulmonary morbidity, and mortality. To examine the effects of particle air pollution in animals, rats with a preexisting pulmonary inflammation (induced by 1600 microg/m(3) ozone) or hypertension (induced by monocrotaline, MCT) were nose-only exposed to concentrated freshly generated diesel exhaust particles (DEP) mixed with ambient air (CDP). It was hypothesized that a single 6-h exposure to PM exacerbates respiratory inflammatory processes, which affects health parameters in the blood. Histopathology of lung and nose, bronchiolar lavage (BAL), and blood analyses were performed at 1, 2, and 4 days after of the CDP exposure. Morphometry of BrdU-labeled cells in lung and nose was performed at 4 days postexposure. One day after ozone exposure, a mild inflammatory reaction in the centriacinar area was present, consisting of an increase in cellularity of septa and in the number of alveolar macrophages, decreasing in time. Additional CDP exposure did not influence this pattern, except for alveolar macrophages that were loaded with CDP. The only effect seen in the nose after ozone exposure was a slight hypertrophy of the septal mucous cells. Additional exposure to CDP did not change this appearance. MCT-treated rats showed hypertrophy of the media of the pulmonary muscular arteries that was not effected by CDP. BrdU labeling of predominantly Clara cells in the terminal bronchioles was significantly increased after ozone exposure as well as after MCT treatment, whereas this labeling index was markedly enhanced after an additional exposure to CDP. However, no increases in Clara cell protein (CC16) levels were measured of Clara cell protein (CC16) in either BAL or blood. BrdU labeling in the nasal epithelium was not influenced by exposure to ozone or ozone + CDP. CDP exposures did not induce significant toxic effects in the lungs. CDP exposures clearly induced an oxidative stress that was indicated by increasing glutathione levels in BAL with time. In addition, blood fibrinogen levels were enhanced in pulmonary hypertensive rats exposed to CDP. The present study demonstrates that very high CDP concentrations are needed to result in pulmonary changes in animal models with a preexisting pulmonary inflammation or hypertension that continue for days after a single exposure. In addition, CDP has the potential to induce changes in blood. It has not yet been determined how the effects seen with CDP would compare to similar levels of ambient particles.

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