C. Gartner
Boston Children's Hospital
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Featured researches published by C. Gartner.
European Respiratory Journal | 2002
F. Horak; Michael Studnicka; C. Gartner; John D. Spengler; E. Tauber; Radvan Urbanek; A. Veiter; Thomas Frischer
The effects of particulate matter <10 µm in diameter (PM10) and other air pollutants on lung function were assessed in 975 schoolchildren, from eight communities in Lower Austria between 1994–1997. In each community, air pollution data were collected. Spirometry was performed twice a year. PM10 concentration (mean concentration between two subsequent lung-function measures in spring and autumn (summer interval) or between autumn and spring (winter interval)) showed a mean value of 17.36 µg·m−3 in the summer interval and 21.03 µg·m−3 in the winter interval. A slower increase in the forced expiratory volume in one second (FEV1) and midexpiratory flow between 25 and 75% of the forced vital capacity (MEF25–75) with age in children exposed to higher summer PM10 was observed in the 3-yr study period. After adjusting for potential confounders (sex, atopy, passive smoking, initial height, height difference, site, initial lung function) an increase of summer PM10 by 10 µg·m−3 was associated with a decrease in FEV1 growth of 84 mL·yr−1 and 329 mL·s−1·yr−1 for MEF25–75. Nitrogen dioxide and ozone also showed a negative effect on lung-function growth, confirming previous work. The authors concluded that long-term exposure to particulate matter <10 µm in diameter had a significant negative effect on lung-function proxy for the development of large (forced expiratory volume in one second) and small (midexpiratory flow between 25 and 75% of the forced vital capacity) airways, respectively, with strong evidence for a further effect of ozone and nitrogen dioxide on the development of forced vital capacity and forced expiratory volume in one second.
Pediatric Allergy and Immunology | 2002
G. Halmerbauer; C. Gartner; M. Schierl; Hassan Arshad; Tara Dean; D. Y. Koller; Wilfried Karmaus; Joachim Kuehr; J. Forster; Radvan Urbanek; Thomas Frischer
Several studies have demonstrated that early intervention may modulate the natural course of atopic disease. Our objective was to prevent sensitization to house‐dust mite and food allergens, as well as the development of atopic symptoms during infancy, by the combination of an educational package and the use of mite allergen‐impermeable mattress encasings. A multicentre European, population‐based, randomized, controlled study of children at increased atopic risk [Study on the Prevention of Allergy in Children in Europe (SPACE)] was performed in five countries (Austria, Germany, Greece, the UK, and Lithuania), and included three cohorts – schoolchildren, toddlers, and newborns. We report on the newborn cohort. A total of 696 newborns were included from Austria, the UK, and Germany. Inclusion criteria were: a positive history of parental allergy; and a positive skin‐prick test or specific immunoglobulin E (IgE) (IgE ≥ 1.43 kU/L) against at least one out of a panel of common aeroallergens in one or both parents. At 1 year of age, the overall sensitization rate against the tested allergens [dust‐mite allergens: Dermatophagoides pteronyssinus and Dermatophagoides farinae (Der p and Der f)] and food allergens (egg, milk) in the prophylactic group was 6.21% vs. 10.67% in the control group. The prevalence of sensitization against Der p was 1.86% in the prophylactic group vs. 5% in the control group. In conclusion, we were able to demonstrate, in a group of newborns at risk for atopic diseases, that the sensitization rate to a panel of aero‐ and food allergens could be effectively decreased through the use of impermeable mattress encasings and the implementation of easy‐to‐perform preventive measures.
Clinical & Experimental Allergy | 2002
F. Horak; M. Studnicka; C. Gartner; A. Veiter; E. Tauber; Radvan Urbanek; Thomas Frischer
Background There is growing evidence that the development of allergic sensitization can be influenced by environmental co‐factors. Studies showed that growing up on a farm can protect children against allergic sensitization. However, little is known whether this ‘farming effect’ can only be observed in early lifetime or whether it also plays a role in later childhood.
Clinical & Experimental Allergy | 2001
Thomas Frischer; M. Studnicka; G. Halmerbauer; F. Horak; C. Gartner; E. Tauber; D. Y. Koller
Background Eosinophil activation is characteristic for allergic airways disease. However, eosinophilic airways inflammation has also been observed subsequent to ambient ozone exposure.
Allergy | 2000
Thomas Frischer; G. Halmerbauer; C. Gartner; R. Rath; E. Tauber; M. Schierl; D. Y. Koller; Radvan Urbanek; J. Forster; J. Kühr
BACKGROUND Eosinophilic airways inflammation forms the pathophysiologic basis for a proportion of children at risk of developing recurrent wheezing. Early preventive measures and/or anti-inflammatory treatment may be guided by the identification of such children. METHODS We studied upper-airways inflammation by nasal lavage in a cohort of 397 infants within the first 4 weeks of life. They participated in an international multicenter study on the prevention of allergy in Europe (SPACE-Biomed II Program). A volume of 2 ml of prewarmed 0.9% saline was instilled into each nasal cavity and immediately re-collected by a suction device. The average recovery was 502 microl (SD: 311 microl). The concentrations of eosinophil cationic protein (ECP) and eosinophil protein X (EPX) were determined by RIA analysis. RESULTS ECP was detectable (>2 microg/l) in 47% of samples (173/365) and EPX (>3 microg/l) in 54.7% (197/360). Children with a doctors diagnosis of a wheezy bronchitis within the first 6 months of life (n = 40) had significantly higher ECP and EPX concentrations in the nasal lavage at 4 weeks of age (median ECP: 14 microg/l; 5-95th percentile: 0-122.4 microg/l) than children without such diagnosis (median ECP: 0 microg/l; 5-95th percentile: 0-86.6 microg/l; P<0.05). Corresponding figures for EPX were 12.14 microg/l (0-148.98 microg/l) vs 7.5 microg/l (0-81.46 microg/l; P<0.05). No associations between nasal ECP/EPX and the development of food allergy or eczema were observed. CONCLUSIONS Increased nasal ECP and EPX in the first 4 weeks of life are associated with wheezing in 6-month-old infants at increased risk of atopic disease. We suggest that this might be related to a general tendency for a Th2 cytokine pattern in these young infants and subsequent trafficking of eosinophils into the nasal mucosa, or it might be a consequence of intrauterine allergen exposure.
Allergy | 2000
E. Tauber; G. Halmerbauer; Thomas Frischer; C. Gartner; F. Horak; A. Veiter; D. Y. Koller; M. Studnicka
Background: In epidemiologic studies, it may be difficult to identify children with bronchial asthma. Since this is the most common chronic respiratory disease in childhood, and its prevalence is still increasing, reliable methods for identification of asthmatic children are required. This study evaluates the use of urinary eosinophil protein X (U‐EPX) in epidemiologic studies in identifying atopic and asthmatic children.
Allergy | 2001
Claudia Wojnarowski; G. Halmerbauer; E. Mayatepek; C. Gartner; Thomas Frischer; J. Forster; Joachim Kuehr
Background: Eosinophilic airways inflammation forms the pathophysiologic basis for a proportion of children at risk of developing recurrent wheezing. Early preventive measures and/or anti‐inflammatory treatment may be guided by the identification of such children. We aimed to study the relationship between respiratory symptoms and indirect markers of airway inflammation.
Allergy | 2000
G. Halmerbauer; C. Gartner; D. Y. Koller; M. Schierl; J. Kühr; J. Forster; Radvan Urbanek; Thomas Frischer
Eosinophil cationic protein (ECP) and eosinophil protein X (EPX) are well established as markers of eosinophil activation. We analyzed ECP and EPX concentrations in nasal lavage fluids (NALF) of 378 neonates during their first 4 weeks of life. Inclusion criteria were a positive history of parental allergy and a positive skin prick test or specific IgE (RAST class ≥2) against at least one out of a panel of common aeroallergens in one or both parents. Twenty‐four infants with no history of parental allergy were used as controls. A volume of 2 ml of 0.9% saline was instilled into each nostril and immediately recovered by a suction device. ECP and EPX were analyzed by radioimmunoassay. In 65 samples of three consecutive lavages, EPX was detected in nine samples (13.8%) in the control group, whereas it was detected in 197/360 samples (54.7%) in the study population. The corresponding figures for ECP were 17/65 (26.2%) in the control group and 173/365 (47.4%) in the study group. Both proteins showed a skewed distribution (median/5–95th percentiles for ECP: 0 µg/l [0–69.4] and EPX: 6.6 µg/l [0–73.2]). The differences between the control group and the study group were statistically significant, regardless of the allergic disease of the parents. In children of allergic parents, activation proteins of the eosinophil granulocyte are released on the nasal mucosal surface in about 50% of the studied population at the age of 4 weeks. This early onset of eosinophil activation in the nasal respiratory epithelium may reflect a genetic predisposition to allergy or early exposure to allergens.
American Journal of Respiratory and Critical Care Medicine | 1999
Thomas Frischer; Michael Studnicka; C. Gartner; E. Tauber; Fritz Horak; Andreas Veiter; John D. Spengler; J. Kühr; Radvan Urbanek
American Journal of Respiratory and Critical Care Medicine | 1997
C Wojnarowski; I Eichler; C. Gartner; M Götz; S Renner; D Y Koller; Thomas Frischer