Biomedical subjects
T Frischer
Publications and source records attributed to T Frischer.
Effects of ambient ozone on lung function in children over a two-summer period.
There is a general consensus that short term exposure to ozone (O3) causes a decrease in lung function parameters such as forced vital capacity (FVC) and forced expiratory volume in one second (FEV1). The objective of this study was to assess the reproducibility of lung function decrements after ambient O3 exposure over a two-summer period. The authors studied 797 children with a mean age of 8.2 yrs (95% confidence interval: 6.9-9.5) from the second and third grades of ten elementary schools in Austria and southwestern Germany. At the outset the various study locations were stratified into three groups with low (L), medium (M) and high (H) O3 exposure (range of mean O3 concentration in the locations April-October 1994: 24-30 (L); 33-38 (M); 44-52 (H) parts per billion (ppb)). Four lung function tests were performed on each child between March 1994 and November 1995. The increases in FVC and FEV1 recorded from one test period to the next were expressed as mL x day(-1). A significantly lower FVC and FEV1 increase was observed in children exposed to high ambient O3 concentration during the summer season. (FVC in summer 1994: 0.83 (L); 0.56 (M); 0.55 (H) mL x day(-1); p=0.004; and summer 1995: 0.80 (L); 0.63 (M); 0.56 (H) mL x day(-1); p=0.011; FEV1 in summer 1994: 0.48 (L); 0.34 (M); 0.18 (H) mL x day(-1); p=0.004 and summer 1995: 0.68 (L); 0.45 (M); 0.41 (H) mL x day(-1), p=0.006). There was no significant difference in FVC or FEV1 increase between the groups during the winter period. Adjusting for sex, age, height and passive smoke exposure, linear regression revealed a statistically significant negative association of average ambient O3 concentration with the FVC and FEV1 increase in both summers. During the winter period no association of O3 with FVC or FEV1 was observed. In conclusion, in two consecutive summer periods the authors found reproducible lung function decrements in children exposed to high levels of ambient ozone. Reoccurrence of ozone associated lung function deficits might increase the likelihood of persisting effects on the childrens' airways.
[Consensus guidelines for drug therapy of bronchial asthma in children and adolescents. Austrian Society of Pediatrics and Adolescent Medicine and Austrian Society for Lung Diseases and Tuberculosis].
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Major basic protein, but not eosinophil cationic protein or eosinophil protein X, is related to atopy in cystic fibrosis.
Increased eosinophil granule proteins have been described in serum and sputum samples of patients with cystic fibrosis (CF). It has been assumed that eosinophil degranulation is enhanced in atopic subjects - as in asthmatics. Since in CF no differences in eosinophil cationic protein (ECP), eosinophil protein X (EPX), and eosinophil peroxidase between atopic and nonatopic subjects have been detected, we investigated whether major basic protein (MBP) is increased in serum and sputum samples derived from atopic (n = 14) compared with nonatopic CF subjects (n = 26). In CF patients, high mean serum (sputum) levels of ECP 29.7 microg/l (2.7 mg/l), EPX 53.7 microg/l (7.9 mg/l), and MBP 984.6 microg/l but low sputum MBP levels (57.4 microg/l) were measured. In addition, in serum and in sputum samples, a significant correlation between MBP and ECP (P<0.03 and P<0.0001, respectively) or EPX (P<0.05 and P<0.0004, respectively) was detected. By subdivision of the patients into allergic and nonallergic subjects, significant differences were found for serum MBP values only(mean 1382.2 microg/l vs. 770.5 microg/l; P<0.0001), but not for ECP or EPX serum levels or for eosinophil proteins in sputum. Although no differences between atopic and nonatopic CF patients in ECP and EPX were found, serum MBP levels were higher in patients sensitized to inhalant allergens than in nonsensitized subjects. These results indicate differential release of eosinophil granule proteins in peripheral blood from eosinophils, and they also indicate that MBP in serum likely is to be a better discriminator of atopy in CF.
Upper airway inflammation in children exposed to ambient ozone and potential signs of adaptation.
In order to investigate nasal inflammation and subsequent adaptation after ambient ozone exposure, nasal lavage (NL) fluid was collected from 170 schoolchildren on 11 occasions (time points) between March and October. Eosinophil cationic protein (ECP), albumin and leukocytes were quantified as markers of nasal inflammation. The highest half-hour outdoor O3 concentration for each individual on the day prior to the NL was used as a measure of exposure (O3indiv). To avoid confounding with exposure to common environmental allergens, the study population was restricted to children without sensitization to inhalant allergens. In the initial period of increased O3 levels in May (time point 4), with a median O3indiv of 135 microg x m(-3) (5th-95th percentile 100-184 microg x m(-3)), the highest medians of all 11 leukocyte and ECP measurements were observed. The highest O3indiv were observed in June at time point 7 (O3indiv 173 microg x m(-3), 5th-95th percentile 120-203 microg x m(-3)). Cross-sectional analysis of all 11 time points revealed no significant association of O3indiv on the one hand and ECP, albumin and leukocyte levels on the other. A multivariable model estimated using generalized estimating equations showed a statistically significant association of O3indiv and leukocytes and ECP as the dependent variable, when time points 1-4 were analysed (p<0.05). In the same model, this association diminished continuously when time points 5-11 were added stepwise, in spite of high O3 exposure. Not even a tendency towards an O3 effect could be recognized when time points 1-8 were considered. The results indicate: 1) acute inflammation of the nasal mucosa after the first increase in ambient ozone levels, with 2) a significant dose-dependent increase in leukocyte and eosinophil cationic protein levels, and 3) possible adaptation of the nasal mucosa in spite of constant high levels of ozone exposure in children during the summer season.
Comparison between serial skin-prick tests and specific serum immunoglobulin E to mite allergens.
Sensitization to dust mite allergens can be determined by means of a skin-prick test (SPT) or by measurement of specific IgE antibodies in serum (sIgE). In our study, concordance of the results of both methods was analyzed on the basis of reproducible SPT results. Three consecutive SPTs were performed on 138 school children (age 6-8 years) at one-year intervals. SIgE was determined at the end of a two-year observation period. Seven common inhalant allergens (Dpt, Df, birch pollens, hazel pollens, grass pollens and cat and dog dander) were analyzed. The majority of subjects with positive SPT reactions to the respective allergen also showed sIgE (Dpt: 82/86; Df: 53/53; cat dander: 31/32; dog dander: 6/9; birch pollens: 29/31; hazel pollens: 22/22; grass pollens: 37/37). A significant correlation between the SPT [weal diameter (P1) or allergen/ histamine ratio (P2)] and sIgE was found for Dpt (P1 = 0.004/ P2 = 0.016), birch pollens (P1 = 0.002/P2 = 0.0001) and grass pollens (P1 = 0.0005/P2 = 0.0001). There was also a significant correlation between sIgE to Dpt and to either Der p 1 (p = 0.0001) or Der p 2 (p = 0.0001), as well as between sIgE of both major allergens (p = 0.0001). In the analysis of co-sensitization of Dpt and Df, most subjects sensitized to Dpt were also sensitized to Df (57/91). Children with sIgE to Dpt (n = 87) usually showed sIgE to Df(n = 83). In this study, SPT and sIgE results are concordant and appear equivalent when using reproducible SPTs. Therefore, in the case of a positive Dpt result, additional testing for sensitization to Df can be regarded as redundant when Dpt and Df are the major contributors to the allergen content of house dust.
Assessment of eosinophil granule proteins in various body fluids: is there a relation to clinical variables in childhood asthma?
BACKGROUND: The eosinophil plays a central role in the inflammatory process in bronchial asthma. Recent studies have indicated that the assessment of eosinophil-derived proteins in various body fluids could be used for monitoring disease activity of childhood asthma. Till now, no study exists which compared the levels of eosinophil-derived proteins in various body fluids such as serum, nasal lavage fluid (NALF) and urine. OBJECTIVE: To investigate whether eosinophil granule proteins in different compartments were correlated and whether there is a relationship between disease activity, pulmonary function and bronchial hyperreactivity. METHODS: Twenty-eight children with atopic bronchial asthma were recruited. Serum, NALF and urine samples were obtained and assessed for eosinophil cationic protein (ECP) and eosinophil protein X (EPX). The levels of eosinophil proteins were analysed for a relationship with lung function variables, bronchial hyperreactivity and disease activity. Eleven healthy control subjects were used as controls. RESULTS: Median ECP and EPX concentrations in serum (31.4 and 74.8 microg/L vs 15.8 and 24.3 microg/L, respectively), NALF (9.9 and 44. 9 microg/L vs 0 and 2.5 microg/L, respectively) and urine (49.4 vs 16.5 microg/mmol creatinine) were significantly raised in children with bronchial asthma compared with healthy control subjects. In addition, ECP and EPX levels in serum and urine samples were significantly higher in symptomatic patients compared with asymptomatic subjects with asthma. Although no relationship between eosinophil-derived proteins in serum, NALF or urine and the level of nonspecific bronchial hyperreactivity could be detected, the concentrations of EPX in serum and urine were correlated with variables of pulmonary function. CONCLUSION: Our findings demonstrate increased eosinophil activity in serum, NALF and urine derived from children with bronchial asthma. Due to the relationship between levels of eosinophil proteins in serum/urine samples and lung function, as well as significant concentration differences between symptomatic and asymptomatic asthmatic children, the assessment of eosinophil proteins in serum or urine samples appear to be more appropriate in monitoring disease activity than measurement of ECP or EPX in NALF. Thus, the determination of serum ECP/EPX or urinary EPX may be preferentially used in monitoring eosinophilic inflammation in childhood asthma.
Lack of relationship between eosinophil cationic protein and eosinophil protein X in nasal lavage and urine and the severity of childhood asthma in a 6-month follow-up study.
BACKGROUND: Recent studies suggest that eosinophil cationic protein (ECP) and eosinophil protein X (EPX) may be valuable markers of airway inflammation in various body fluids of asthmatic children. Most of these studies have relied on a single measure of inflammatory markers. OBJECTIVE: We measured ECP and EPX in nasal lavage fluids (NALF) and urine samples in children with asthma over a 6-month period to study the relationship between inflammatory markers and clinical severity. METHODS: Fourteen children with mild persisting asthma (mean age 11.7 years, SD 2.2) were recruited. All patients were on therapy including inhaled steroids. For a 6-month period asthma severity was monitored by at least monthly physical examination and pulmonary function tests. Daily morning and evening PEF, asthma symptoms and medication were recorded in diaries for the whole study period. Telephone interviews were performed between visits and additional visits were done in case of an increase in asthmatic symptoms or drop of PEF values under 80% of best value. An exacerbation was defined by a fall of FEV1 > 10% and an increase in asthma symptoms and additional need of beta2-agonist. NALF and urine samples were obtained at each visit and analysed for ECP (NALF only) and EPX. RESULTS: Mean observation time was 186.4 days (SD 19.8). Thirteen patients completed the study. During the study period 11 exacerbations were observed in six patients. No significant associations between PEF, PEF variability (amplitude % of mean), daily symptoms, additional beta2-agonist, FEV1 and MEF50 and nasal ECP, nasal EPX and urinary EPX were found. However, at exacerbations an average increase of nasal ECP (9.3 vs 50.3 microg/L) and EPX (nasal EPX 36.4 vs 141.7 microg/L, urinary EPX 46.4 vs 74.1 microg/mmol creatinine) was observed. CONCLUSION: Serial measurements of ECP and EPX in NALF and urine samples do not provide additional information for the practical management in monitoring childhood asthma.
Lung function growth and ambient ozone: a three-year population study in school children.
We followed a cohort of 1,150 children for 3 yr to investigate long-term effects of ambient ozone. Nine study sites were selected on the basis of air-quality data to represent a broad range of ozone exposure. In 1994, 1995, and 1996 lung function was recorded biannually, always before and after summertime. The effect of ozone was analyzed with regression analyses and study-site, a child's sex, atopy, passive smoking, baseline lung function, and increase in height were considered as confounding variables. A negative effect of summertime ozone on the pre- to post-summer-time change in FEV(1) (ml/d) was present in 1994 (beta = -0.019 ml/d/ppb; p < 0.01) and in 1995 (beta = -0.017 ml/d/ ppb; p < 0.05), but not in 1996 (beta = 0. 004 ml/d/ppb; p = 0.6); corresponding estimates for FVC were in 1994: beta = -0.022 ml/d/ppb, p < 0.005; 1995: beta = -0.018 ml/d/ppb, p < 0.05; and 1996: beta = 0.006 ml/d/ppb, p = 0.46. When all three study years were considered simultaneously, i.e., the changes in lung function between each of two subsequent surveys being the dependent variable, summertime ozone was associated with a lesser increase in FEV(1) (beta = -0.029 ml/d/ppb; p < 0.001), FVC (beta = -0.018 ml/d/ppb; p < 0.001), and MEF(50) (beta = -0.076 ml/s/d; p = 0.001). No consistent associations were observed for lung function and NO(2), SO(2) and PM(10). Long-term ambient ozone exposure might negatively influence lung function growth.
Necrotizing sarcoid granulomatosis in a 14-yr-old female.
A case of a 14-yr-old female with necrotizing sarcoid granulomatosis (NSG) is presented. She was referred because of chest pain and malaise, and radiography revealed multiple pulmonary nodules. Her history showed seasonal sensitization to aeroallergens and hay fever. Infectious agents or malignancies did not characterize these nodules. However, she was treated with macrolide antibiotics because of suspected infection with Chlamydia pneumoniae. Open lung biopsy showed histological findings of NSG, with epithelioid granulomatous inflammation, including giant cells, and vasculitis. No further treatment was performed, and symptoms disappeared within a few weeks. The chest radiograph showed gradual improvement. The aetiology of NSG is poorly understood, and is postulated to represent either sarcoidosis or rare forms of pulmonary vasculitis such as Wegener's granulomatosis or the Churg-Strauss syndrome. In the case presented, a coincidence of infection with Chlamydia pneumoniae suggests an involvement of infectious agents in the pattern of formation of immune complexes in the aetiology of NSG.
Cytokine expression in bronchial biopsies of cystic fibrosis patients with and without acute exacerbation.
In patients with cystic fibrosis (CF), the progression of pulmonary disease differs considerably, even in identical cystic fibrosis transmembrane conductance regulator-genotypes which could reflect an additional influence of the host's immune response. This study therefore measured cytokine expression patterns in CF patients with different clinical presentation. Expression of interleukin (IL)-8, interferon gamma (IFN-gamma), IL-4, IL-10, and transforming growth factor (TGF)beta(I) was assessed in bronchial mucosal biopsies of eight CF patients with acute exacerbation (age 6.0-14.2 yrs), eight CF patients with chronic stable disease (age 7.3-17.4 yrs), and in five normal control subjects by semiquantitative and quantitative reverse transcriptase polymerase chain reaction combined with histopathological assessment and immunohistochemical staining. All CF patients expressed IL-8. In acute exacerbation, expression of TGF-beta1 and IFN-gamma was either absent or extremely low. In contrast, all patients with stable disease strongly expressed TGF-beta1. The highest expression of TGF-beta1 and IFN-gamma was found in CF patients with mild disease and a history of infrequent exacerbations. No correlation was found between the expression of IL-4 and IL-10 and patient history. In normal control subjects, only a weak expression of TGF-beta1 was observed. These results show a remarkable correlation between cytokine pattern and the clinical course of cystic fibrosis. High expression of transforming growth factor-beta1 and interferon gamma was associated with mild disease, whereas no or very weak expression of these cytokines was typical for patients with acute disease and frequent exacerbations suggesting a contribution of the immune response to the progression of pulmonary disease in cystic fibrosis.
Determinants of reproducibility of lung function tests in children aged 7 to 10 years.
Lung function (LF) tests are part of many investigations in childhood lung disease. However, individual reproducibility of LF will confound between-subject differences. At the same time, increased LF variability has been linked to respiratory disease. In a sample of 598 children, two LF tests, separated by a 5-min interval, were recorded, and reliability (Rel) of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), and maximal expiratory flow at 50% of FVC (MEF50) was determined. Rel was also assessed in children trained and untrained in the performance of LF. To investigate determinants of reproducibility for FEV1, the absolute difference between two repeated tests was calculated. Whenever this difference was > 120 ml, a child was considered to demonstrate excessive variability (poor reproducibility) in FEV1. For volume parameters coefficients of reliability (Crel) were found to be better than for MEF50 (FEV1: 0.96; FVC: 0.94, MEF50: 0.91). In untrained children Crel for FEV1 was only 0.91, but it was increased in subsequent visits (0.98, 0.97, and 0.97 at the second, third, and fourth tests, respectively). Excessive variability in FEV1 was observed in 10% of children and was related to the presence of wheeze [odds ratio (OR) 6.31; 95% confidence interval (CI) 1.78-22.4), shortness of breath (OR 3.14; 95% CI 1.00-9.93), a diagnosis of asthma (OR 6.25; 95% CI 1.76-22.1), and bronchial hyperresponsiveness (OR 4.30; 95% CI 2.07-8.94). We conclude that increased variability of LF is likely to be present in young children not accustomed to the testing procedure and in children with respiratory symptoms. Therefore, before guidelines for LF testing are applied, children should be trained to perform the tests and we should be cautious in the interpretation of test results in children who present with symptoms.
Cord blood mononuclear cells and milk-specific T-cell clones are tools to evaluate the residual immunogenicity of hydrolyzed milk formulas.
BACKGROUND: Hydrolyzed milk formulas (HFs) are given to infants allergic to cow's milk proteins and, for preventive reasons, to atopy-prone newborns for which breast feeding is not feasible. The ultimate properties of HFs are not only a reduced allergenicity but also decreased immunogenic capacity combined with good taste and caloric value. No information is available concerning the capacity of HFs to induce immune responses. OBJECTIVE: We sought to determine the residual immunogenic capacity of partially (pHF) and extensively hydrolyzed milk formula (eHF), and we studied the cellular reactivity of cord blood-derived (n = 71) mononuclear cells induced by 10 different HFs. METHODS: To test the effect of HF on T-helper cells, beta-casein-specific T-cell clones (TCCs, n = 21) from individuals allergic to milk were established, and T-cell proliferation and cytokine profiles (interferon-gamma and IL-4) were determined on stimulation with HF. RESULTS: We found significantly reduced proliferative responses of eHF compared with milk proteins. Whey-based pHF displayed the same proliferative capacity as unmodified milk proteins. As expected, extensively processed whey products displayed lower cellular responses compared with partially hydrolyzed products (pHF whey vs eHF whey, p < 0.0001). No difference in cellular response was found between casein-based pHF and casein-based eHF. Beta-casein-specific TCCs (n = 21) proliferated in response to casein-derived hydrolysates (14% with casein/whey-based pHF, 4% with casein-based pHF, and 0% with casein-based eHF). Whey-based pHF was also found to induce proliferation in beta-casein-specific TCCs, indicating the presence or the generation of peptides displaying cross-reactivity with these whey-derived hydrolysates. TCCs stimulated with whey- or casein-based pHF or eHF produced the same amount of cytokines (IL-4, interferon-gamma) as the same clones stimulated with unmodified products. CONCLUSION: Our data indicate that whey- and casein-derived eHFs display highly reduced immunogenic properties at the T-cell level. In contrast, pHFs display residual immunogenic properties detectable at the T-cell level, reflecting a potential for the induction of pathogenetically important T-cell responses.
Determinants of eosinophil cationic protein in nasal lavages in children.
BACKGROUND: Nasal lavages are increasingly used to assess airways inflammation in children. However, there are no studies assessing how measurement error as well as biological influences contribute to the concentration of nasal inflammatory parameters in a population based survey. OBJECTIVE: To investigate determinants of concentration of eosinophil cationic protein (ECP) in nasal lavages we studied 147 schoolchildren (mean age 8.1 years, SD 0.6 years) by repeated nasal lavages/year over a 2 year period. METHODS: Standardized questionnaires were completed by the parents each year. A skin-prick test with seven aeroallergens (birch, cat, dog, hazel, weeds, Dermatophagoides pteronyssinus and D. farinae) was performed. One hundred and one children could perform valid lavages at least five times a year. As a measure of reproducibility the intraclass coefficient of reliability was calculated. RESULTS: The intraclass coefficient of reliability was 0.27 over all observations suggesting that about a quarter of total variance is due to between-subject variance. Taking means over each year increased reliability to 0.60. Linear regression analyses with ECP being the dependent variable demonstrated significant higher values for boys (beta=12.26; P < 0.01), children sensitized to seasonal (beta=34.27; P=0.02) but not to perennial allergens (beta=-4.44; P=0.57), and for children with a serous (beta=10.01; P=0.01) or purulent rhinitis (beta=22.45; P < 0.001). CONCLUSION: Assessment of inflammatory mediators in nasal lavages is a useful tool for epidemiological paediatric studies. However, due to the relatively high intraindividual variability of ECP concentrations multiple lavages are necessary to characterize the individual.
Accumulation of atopic disorders within families: a sibling effect only in the offspring of atopic fathers.
BACKGROUND: Several studies have reported an association between a child's risk of atopic disorders and family size. However, the inverse association might not be the same in populations with a different genetic disposition for atopic disorders. OBJECTIVE: This longitudinal study was designed to assess risk factors of atopy. METHODS: Lifetime prevalence of asthma, hay fever and eczema of 1440 families including 3165 offspring was ascertained by means of standardized questionnaires. RESULTS: After possible confounders had been controlled for, an inverse association between atopic disorders and the number of older siblings was found only in the offspring of atopic fathers (trend for older siblings: chi2 = 13.38, degrees of freedom [d.f.] = 1, P= 0.0002; odds ratio 'no older sibling'= 2.87 (95% confidence interval 2.18-3.78); '1 older sibling' = 2.11 [1.52-2.92], '2 older siblings' = 1.29 [0.74-2.23]; '3 or more older siblings' = 0. 15 [0.02-0.981). No such relationship was found for children without a history of paternal atopy (trend for older siblings: chi2 = 1.5 1, d.f. = 1, P = 0.22; odds ratio 'no older sibling' = 1 [reference]; '1 older sibling' =0.82 [0.63-1.06]; '2 older siblings' = 0.97 [0.67-1.40]; '3 or more older siblings' = 0.64 [0.31-1.33]). The trend for older siblings in the case of paternal atopy was significantly different from the trend for older siblings without a history of paternal atopy (chi2 = 8.68, d.f. = 1, P = 0.003). The number of younger siblings was not related to child's risk of atopy (trend for younger siblings: chi2 = 0.001, d.f. = 1, P = 0.97). CONCLUSIONS: Data from this study suggest a protective effect of sibship size only in children with a history of paternal atopy and if older siblings are present. The reason for this combined effect remains unclear. Thus, further investigations are needed to interpret the biological cause of the so called 'sibling effect'.
Cotinine excretion as a predictor of peak flow variability.
Environmental tobacco smoke (ETS) is suspected to be an important risk factor for bronchial hyperresponsiveness. In order to test the effect of ETS, we measured expiratory flow rates and urine cotinine excretion (UCE) within a narrow time window in two consecutive years. Maternal smoking habits and medical history were ascertained by standardized questionnaires. The percentage ratio of the amplitude over the mean (AVAM) of the diurnal peak flow rates of children (complete values from at least five consecutive days) was calculated as an indicator of bronchial responsiveness. The association of UCE and log10AVAM was analyzed by multiple linear regression. Complete data were available for a sample of 417 children. The median of UCE in children of parents who smoked (3.2 ng/mg and 2.9 ng/mg creatinine, Surveys 1 and 2, respectively) was higher than the median in children of nonsmoking parents (0 ng/mg in both surveys). With increasing UCE the log10AVAM rose in the first and second surveys, as well as in the longitudinal analysis (p = 0.003). This association, however, showed up only in boys (p = 0.0001) and not in girls (p = 0.31). Our data suggest that there is a need both for further analysis of the gender difference and for more support of strategies against passive smoking as far as children are concerned, since airway hyperresponsiveness is a risk factor for chronic airway impairment.
Longitudinal predictors of airway responsiveness to distilled water: the role of atopy and maternal smoke exposure.
Airway responsiveness is an objectively measurable clinical trait related to the presence of asthma. Although risk factors for this trait have been evaluated cross-sectionally, little is known about its longitudinal predictors. A population cohort of 539 children, aged 8 yrs at the start of follow-up, underwent 3-7 bronchial challenge tests spaced at 3-9 month intervals. Airway responsiveness was assessed by a single-step distilled water challenge. To investigate responsiveness as a continuous trait, the ratio of the postchallenge to prechallenge forced expiratory volume in one second was calculated. A child's repeated ratios were then regressed on the time of follow-up. The resulting child-specific regression coefficient was the outcome variable to assess longitudinal predictors of airway responsiveness (AR). Results were based on 2,267 repeated challenge tests, and indicated an overall decrease in responsiveness. Children with a diagnosis of asthma (mean+/-SD, longitudinal change in AR + yr(-1): -0.060+/-0.149), those with a positive skin-prick test (-0.018+/-0.106) and those with reported exposure to maternal smoking (-0.004+/-0.083) demonstrated increased airway responsiveness over time. All of these changes in airway responsiveness were found to be significant in multiple linear regression analysis (p<0.05). Stratified analysis further indicated that the effect of maternal smoking was observed primarily in nonatopic children and was greatest at an exposure level of > or =10 cigarettes x day(-1). In conclusion, atopy and exposure to maternal smoking can predict longitudinal change in childhood airway responsiveness.
Effects of ambient ozone exposures during the spring and summer of 1994 on pulmonary function of schoolchildren.
To investigate the effect of natural exposure to ambient ozone over time, a follow-up study of school-aged children was performed in two small towns in southwestern Germany (Freudenstadt and Villingen) between March and October of 1994. Ozone half-hour mean concentrations were measured continuously and pulmonary function was tested in each child on four occasions (April, June, August, and September). To obtain an average short-term ozone effect, we first analyzed the data from the four time points separately and then constructed a model that included all information. During the study period the median (5th to 95th percentile) of all half-hour values of the ozone concentration was 101 micrograms/m3 or 50.6 ppb (45-179 micrograms/m3 or 22.5-89.8 ppb) in Freudenstadt and 64 micrograms/m3 or 32.1 ppb (1 to 140 micrograms/m3 or 0.5-70.1 ppb) in Villingen. To assess the effects of an individual ozone exposure we related the highest ozone concentration in the respective 24 hours before lung function testing to the results of the subconcentration in the respective 24 hours before lung function testing to the results of the subsequent pulmonary function tests. In the lung function test following the highest ozone exposure, the results of our cross-sectional linear regression analysis showed a significant negative correlation (P = 0.0181) between ozone exposure and forced vital capacity (FVC). In the longitudinal linear regression model we observed a negative statistical correlation between ozone exposure and lung function for the subpopulation living in the town with the high ozone levels (Freudenstadt). The association was more pronounced in boys than girls. For the children in Freudenstadt the decrement of FVC was -12.31 ml/10 micrograms/m3 ozone and the decrease in the forced expiratory volume in 1 second (FEV1) was -11.29 ml/10 micrograms/m3 ozone.