Document Detail


Relationships among environmental exposures, cord blood cytokine responses, allergy, and wheeze at 1 year of age in an inner-city birth cohort (Urban Environment and Childhood Asthma study).
MedLine Citation:
PMID:  21333343     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: The Urban Environment and Childhood Asthma study was established to investigate the immunologic and environmental causes of asthma in inner-city children.
OBJECTIVE: We sought to evaluate potential atopic outcomes in the first 12 months and their relationships to environmental exposures and immune development.
METHODS: A birth cohort of 560 children with at least 1 parent with allergy or asthma was established in Baltimore, Boston, New York, and St Louis. Wheezing is assessed every 3 months, allergen-specific IgE yearly, and mononuclear cell cytokine responses at birth and yearly; environmental assessments include dust allergen and endotoxin, maternal stress, and indoor nicotine and nitrogen dioxide levels.
RESULTS: Key outcomes in the first year include wheeze in 49%, 2 or more episodes of wheeze in 23%, eczema in 30%, and detectable IgE to milk, egg, and/or peanut in 32% and to cockroach in 4%. Household dust revealed levels of greater than 2 μg/g to cockroach in 40%, mite in 19%, cat in 25%, and mouse in 29%, and 66% of homes housed at least 1 smoker. Positive associations were detected between multiple wheeze and cotinine levels, maternal stress, and maternal depression, whereas cytokine responses to a variety of innate, adaptive, and mitogenic stimuli were inversely related to eczema.
CONCLUSIONS: This high-risk cohort of inner-city infants is exhibiting high rates of wheeze, eczema, and allergic sensitization. Low cytokine responses at birth might be a risk factor for eczema, whereas a variety of adverse environmental exposures contribute to the risk of wheezing in infancy. These findings provide evidence of specificity in the interactions between immune development, environmental exposures, and the development of early features that might predict future asthma.
Authors:
Robert A Wood; Gordon R Bloomberg; Meyer Kattan; Kathleen Conroy; Megan T Sandel; Amy Dresen; Peter J Gergen; Diane R Gold; John C Schwarz; Cynthia M Visness; James E Gern
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-02-18
Journal Detail:
Title:  The Journal of allergy and clinical immunology     Volume:  127     ISSN:  1097-6825     ISO Abbreviation:  J. Allergy Clin. Immunol.     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-04-04     Completed Date:  2011-05-31     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  1275002     Medline TA:  J Allergy Clin Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  913-9.e1-6     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2011 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
Affiliation:
Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. rwood@jhmi.edu
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MeSH Terms
Descriptor/Qualifier:
Air Pollutants / adverse effects*
Allergens / immunology
Animals
Baltimore / epidemiology
Boston / epidemiology
Cohort Studies
Cytokines / immunology*
Eczema / epidemiology,  etiology,  immunology
Environmental Exposure / adverse effects*
Female
Fetal Blood / immunology*
Humans
Hypersensitivity / epidemiology*,  etiology,  immunology
Infant
Male
New York / epidemiology
Respiratory Sounds / etiology*,  immunology
Urban Health
Grant Support
ID/Acronym/Agency:
1UL1RR024156/RR/NCRR NIH HHS; 1UL1RR025771/RR/NCRR NIH HHS; 5UL1RR024992-02/RR/NCRR NIH HHS; HHSN272200900052C/AI/NIAID NIH HHS; M01RR00071/RR/NCRR NIH HHS; M01RR00533/RR/NCRR NIH HHS; N01-AI-25482/AI/NIAID NIH HHS; N01-AI-25496/AI/NIAID NIH HHS; P30 ES000002/ES/NIEHS NIH HHS; RR00052/RR/NCRR NIH HHS; UL1 RR024992/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Air Pollutants; 0/Allergens; 0/Cytokines
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