title: 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).
abstract: 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.affiliation: Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. rwood@jhmi.edu
authors.forename: Robert A
authors.initials: RA
authors.lastname: Wood
authors.forename: Gordon R
authors.initials: GR
authors.lastname: Bloomberg
authors.forename: Meyer
authors.initials: M
authors.lastname: Kattan
authors.forename: Kathleen
authors.initials: K
authors.lastname: Conroy
authors.forename: Megan T
authors.initials: MT
authors.lastname: Sandel
authors.forename: Amy
authors.initials: A
authors.lastname: Dresen
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Gergen
authors.forename: Diane R
authors.initials: DR
authors.lastname: Gold
authors.forename: John C
authors.initials: JC
authors.lastname: Schwarz
authors.forename: Cynthia M
authors.initials: CM
authors.lastname: Visness
authors.forename: James E
authors.initials: JE
authors.lastname: Gern
mesh_terms: D000393:Air Pollutants / Q000009:adverse effects*; D000485:Allergens / Q000276:immunology; D000818:Animals; D015142:Baltimore / Q000453:epidemiology; D001900:Boston / Q000453:epidemiology; D015331:Cohort Studies; D016207:Cytokines / Q000276:immunology*; D004485:Eczema / Q000453:epidemiology / Q000209:etiology / Q000276:immunology; D004781:Environmental Exposure / Q000009:adverse effects*; D005260:Female; D005312:Fetal Blood / Q000276:immunology*; D006801:Humans; D006967:Hypersensitivity / Q000453:epidemiology* / Q000209:etiology / Q000276:immunology; D007223:Infant; D008297:Male; D009518:New York / Q000453:epidemiology; D012135:Respiratory Sounds / Q000209:etiology* / Q000276:immunology; D014504:Urban Health
chemical_list: D000393:Air Pollutants; D000485:Allergens; D016207:Cytokines