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Background Outdoor and indoor air pollutants are suspected to induce harmful effects on respiratory health, raising the question of their involvement in allergic asthma and rhinitis. Objective The potential effect of short-term personal exposure to particulate matter with a diameter of less than 2.5 μm (PM2.5) on nasal inflammation was examined in children living in the Paris area. Methods Forty-one children with allergic asthma and 44 healthy children participated in this study. They were monitored during 48 hours for their personal exposure to PM2.5. At the end of the measurement period, children underwent one nasal lavage. Nasal lavage fluid was investigated for cellular (neutrophils and eosinophils) and soluble (albumin, urea, elastase, α1-antitrypsin, IL-6, and IL-8) mediators. Results Pollutant concentrations did not differ between the 2 groups. In asthmatic subjects, but not in healthy children, personal PM2.5 levels were correlated to nasal percentage of eosinophils and to albumin, urea, and α1-antitrypsin concentrations after adjustment for confounders (age, sex, house dust mites, pollens, cat, environmental tobacco smoke through urinary cotinine, barometric pressure, and respiratory infection). Conclusion The association observed with the percentage of eosinophils supports recent speculations on fine particle involvement in allergic phenotype overexpression. Clinical implications This study highlights the link between personal fine particle exposures and nasal inflammation in asthmatic allergic children living in urban areas. Because the view of united airways is still not completely understood, the question of pulmonary inflammation in such a situation deserves further investigation.

We measured personal exposure to nitrogen dioxide (NO(2)), nitrogen monoxide (NO), and ozone (O(3)), using personal passive samplers during three 4-day periods, in a panel study of asthmatics continuing the normal activities of everyday life. Fifty-five adults, mean age 42 years, 53% men, and 39 children, mean age 11 years, 67% boys, wore two Ogawa passive samplers simultaneously: one for O(3), the other for NO(2) and NO. Mean outdoor pollution was measured at a regional monitoring network. Personal exposure levels were scattered; they were (on average) higher than stationary-site levels for NO and lower for NO(2) and O(3). In adults, 41% of the variance of personal exposure to NO(2) was explained by mean stationary-site measurement levels (P0.0001). Twenty-one percent additional variance was explained by living near a main road, not having an extractor fan over the cooker, older age, and male sex. NO and O(3) personal exposures correlated poorly with stationary-site measurements. In panel studies of the health effects of air pollution, personal exposure to NO(2) and NO can be measured satisfactorily by passive samplers: such measurements are necessary for NO but not for NO(2). For O(3), accurate personal exposure measurement remains a challenge and further technical development is required.

Proteinase 3 (PR3), a serine proteinase which can degrade lung tissue, is present in the cystic fibrosis (CF) sputum. In the present study, PR3 protein and mRNA expression was determined in circulating neutrophils and monocytes. CF neutrophils contained similar PR3 concentrations as healthy controls and poorly expressed PR3 mRNA. In contrast, CF monocytes showed significantly higher PR3 concentrations than controls, together with an upregulation of PR3 mRNA expression especially during pulmonary exacerbation. Interestingly, antibiotic treatment fully abrogated PR3 mRNA expression and decreased PR3 protein in monocytes. Our findings highlight a potential role of monocyte-derived PR3 in CF-associated airway inflammation.

Persistent asthma in adults starts often early in childhood and is associated with alterations in respiratory function that occur early in life.The aim of this study was to evaluate the importance of innate and environmental factors associated with occurrence of asthma during childhood in a population of recurrent wheezing infants followed prospectively.A cohort of infants less than 30 months old with recurrent wheezing was established in order to assess severity of respiratory symptoms and to look for the presence of atopy and environmental risk factors. At the age of 6 years, they were reevaluated with respect to remission or persistence of wheezing over the previous 12-month period.Data were available for 219 subjects aged 15 +/- 5 months. In 27% of the infants with recurrent wheeze, wheezing persisted until the age of 6 years. In multivariate analysis, stepwise logit analysis showed that the risk factors for persistent wheezing are eosinophiliaor=470/mm(3), allergenic sensitization, and a father with asthma. Environmental factors present during the first year of life that protect from persistence of wheezing are ( 1 ) breastfeeding for longer than 3 months, ( 2 ) pets at home, and ( 3 )or=3 siblings. The detection rate for persistent wheezing in this model is 72%. The persistence score showed good specificity 91% but low sensitivity 35%.This study confirms the role of atopic host factors on wheezing persistence during childhood and detected protective environmental factors.

To evaluate the relationship between clinical parameters and differential cell counts, bronchoalveolar lavage was performed in 79 asthmatic infants and children with unusual asthma. Multivariate analysis showed significant associations between (1) allergic asthma and the presence of alveolar eosinophils and (2) persistent and longer asthma and an increased number of alveolar neutrophils. Our results provide the first evidence that in asthmatic infants and children eosinophilic inflammation is related to allergic sensitization.

Right pneumonectomy can lead to severe respiratory impairment due to stenosis of the left main bronchus. This syndrome is usually treated by inserting a fixed-volume prosthesis but, in children, expandable prostheses have the advantage of being adaptable to growth and permit progressive recentering of the mediastinum. We report 3 such cases, with the results of pulmonary function tests. The patients were aged 11, 17, and 22 years at the time of implantation and had undergone pneumonectomy during childhood for either bronchiectasis or complete pulmonary sequestration. All 3 patients are doing well, with a follow-up of 1 to 3 1 2 years. Pulmonary function tests have shown a substantial improvement in the obstructive syndrome in 2 patients whereas, in the third patient, in whom the contralateral lung was not perfectly healthy, the functional improvement was only moderate.

The clinical course of sarcoidosis in children has not been well defined. Eight children with symptomatic sarcoidosis included in this study underwent pulmonary function tests and bronchoscopy with bronchoalveolar lavage (BAL) before treatment and during steroid therapy. At the start of therapy, functional parameters, mostly dynamic lung compliance and lung transfer factor for CO, were impaired. This was associated with abnormalities of BAL cell populations: increased total cell number with a high proportion of lymphocytes, modifications of lymphocyte subpopulation with an elevated CD4+/CD8+ ratio, and enhanced ability of alveolar macrophages to release hydrogen peroxide. Although respiratory abnormalities seemed to be similar at the initial stage of sarcoidosis in children and adults, the course of the disease appeared to be different. Despite the absence of respiratory symptoms and disappearance of chest radiographic abnormalities on prolonged steroid treatment, we found slow improvement of pulmonary functions associated with persistence of BAL lymphocytosis and elevated CD4+/CD8+ ratios. However, the ability of alveolar macrophages to release hydrogen peroxide was significantly reduced after 6 months of steroid treatment, and it remained identical to the control group. Therefore, the evaluation of disease activity appears to be critical for therapy in pediatrics, and for this purpose studies of alveolar macrophage activation may be of particular interest. Pediatr Pulmonol. 1993; 16:41–47. © 1993 Wiley-Liss, Inc.

Fourteen children aged between 6 months and 7 years (mean age = 3.5 years) were treated by CO2 broncholaser in the ENT Department of Trousseau Hospital. Three groups of diagnostic indication were identified: 1. Granulomas treated after mucosal trauma (tracheotomy, foreign body). 2. Granulomas due to pulmonary and/or lymph node tuberculosis. 3. Adhesions and stenosis secondary to neonatal ventilation. The operative and anesthetic technique is described in detail, together with any possible adverse events. The CO2 broncholaser appears to be a technique of choice in this age group, in which the narrowness of the airways makes any endoscopic procedure difficult. The broncholaser allows the early treatment of obstructive tracheobronchial pathology with its risks of severe ventilatory sequelae.

International audience; The ability of alveolar macrophages (AM) to release O2 metabolites was studied in 8 children with interstitial lung disease (ILD), and in 11 children without lung parenchyma disorder. AM were collected by bronchoalveolar lavage. The experiments were performed on unstimulated AM and on AM stimulated by phorbol myristate acetate (PMA) or zymosan. Our results indicated that, with or without triggering agent, the amount of O2 metabolites release was a linear function pattern with time. The accumulation of superoxide anion (O2-) and hydrogen peroxide (H2O2) into the extracellular medium differed depending on the triggering agent used: with PMA, the amount of O2- released was threefold the amount of H2O2 detected in the medium, whereas with zymosan the O2- accumulation was tenfold higher than the amount of H2O2 measured. In patients with ILD, a significant increase in the amount of H2O2 release was observed for both unstimulated and stimulated AM (p less than 0.001). In this group, the measurement was repeated after a 2-month steroid treatment: prednisone had markedly improved the clinical, radiologic, and functional status of the patients, and this improvement was in good correlation with the decrease of O2 metabolite production. The amount of H2O2 release in each case was within the range of control values. Evaluation of O2 metabolite release by AM could be a useful parameter in the assessment of the activity of ILD.

The ability of alveolar macrophages (AM) to release hydrogen peroxide (H2O2), an indicator of AM function, was studied in five children with the acquired immunodeficiency syndrome (AIDS) related complex and, for comparison, in 11 children without disorders of the lung parenchyma. In the AIDS-related complex group, pulmonary manifestations were mild, and lung involvement was suspected by moderate clinical and/or radiological features. None had a past history of opportunistic infections; neither did any have lymphopenia. Cytologic study of the bronchoalveolar lavage (BAL) fluid revealed increased cellularity with increased percentage of lymphocytes. The study of H2O2 release was performed on unstimulated AM and on AM stimulated by phorbol myristate acetate (PMA). Under both experimental conditions, the amount of H2O2 accumulated in the medium was significantly increased in the group with AIDS-related complex (P less than 0.001). As no enhanced oxidative activity has been reported in AM from patients with full-blown AIDS, an increased ability of AM to release oxygen metabolites from children with AIDS-related complex may reflect an initial and temporary step in the course of the LAV/HTLV-III pulmonary disease. Determining AM activation might be a reliable method of assessing the evolution of lung disorder in AIDS.

International audience; A genome-wide search was conducted in 107 nuclear families with at least two siblings with asthma, as part of the French EGEA study. A two-stage analysis strategy was applied to the 107 families divided into two independent subsets of 46 and 61 families, where all regions detected in the first set of families were tested for replication in the second set. In addition, all regions reported by published genome scans in different populations were examined in the total sample. A total of 254 markers were typed in the first set of families and 70% of them in the second set. Linkage was investigated by model-free methods for asthma and four asthma-related phenotypes: bronchial responsiveness (BR), skin test response, total immunoglobulin E (IgE) levels, and eosinophil count. The two-stage analysis led to the detection of three regions: 11p13 for IgE, 12q24 for eosinophils, and 17q12-21 for asthma and skin tests. Among the regions reported by published genome screens, seven were found in the 107 French EGEA families: three being already detected by the two-stage analysis, 11p13 (p = 0.005), 12q24 (p = 0.0008), and 17q12-21 (p = 0.001), and four additional ones, 1p31 (p = 0.005) for asthma, 11q13 (p = 0.006) for IgE, 13q31 (p = 0.001) for eosinophils, and 19q13 (p = 0.02) for BR.