title: Prenatal and early postnatal environments are significant predictors of total immunoglobulin E concentration in Filipino adolescents.
abstract: BACKGROUND
  Recent evidence suggests that atopic disease may in part be mediated by fetal growth, as well as exposure to infectious disease early in life. Few studies have been able to evaluate these associations simultaneously, or to investigate prospectively the long-term effects of early environments while adequately controlling for potentially confounding variables.
  
  
  OBJECTIVE
  To examine how prenatal growth and infectious disease in infancy are related to total IgE production in adolescence.
  
  
  METHODS
  Ninety-nine adolescents (aged 14-15 years) were selected from a larger cohort study according to the following criteria: full-term birth, currently healthy, and small-for-gestational age (N=53) or appropriate-for-gestational age (N=46). Plasma total IgE was measured with ELISA, and analysed in relation to anthropometric, nutritional, and environmental quality data collected prospectively beginning in the third trimester prior to birth.
  
  
  RESULTS
  Each episode of infectious morbidity recorded at bimonthly intervals in the first 6 months of life was associated with a 0.12 log IU/mL reduction in total IgE in adolescence (P=0.004). Prenatal undernutrition was associated with increased adolescent IgE, but only under conditions of an unsanitary household environment (P=0.002). Each additional kilogram gained per month in the first 6 months of life was associated with an increase in adolescent IgE of 0.74 log IU/mL (P=0.03). Each quartile increase in weekly household income at the time of blood sampling was associated with a 0.10 log IU/mL reduction in total IgE (P=0.02).
  
  
  CONCLUSIONS
  Infectious disease in infancy, as well as interactions between prenatal and postnatal environments, appear to have long-term effects on adolescent total IgE production. Future research should investigate the mechanisms behind these effects, and their implications for symptoms of atopic disease.
authors.affiliation: Laboratory for Human Biology Research, Department of Anthropology, Northwestern University, Evanston, IL 60208-1310, USA. t-mcdade@northwestern.edu
authors.forename: T W
authors.initials: TW
authors.lastname: McDade
authors.forename: C W
authors.initials: CW
authors.lastname: Kuzawa
authors.forename: L S
authors.initials: LS
authors.lastname: Adair
authors.forename: M A
authors.initials: MA
authors.lastname: Beck
mesh_terms: D000293:Adolescent; D001942:Breast Feeding; D003141:Communicable Diseases / Q000276:immunology*; D003967:Diarrhea / Q000453:epidemiology / Q000276:immunology; D005314:Embryonic and Fetal Development; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D005260:Female; D005317:Fetal Growth Retardation / Q000276:immunology*; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood*; D015994:Incidence; D007227:Infant Nutritional Physiological Phenomena; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011446:Prospective Studies; D012141:Respiratory Tract Infections / Q000453:epidemiology / Q000276:immunology; D012923:Social Class
chemical_list: D007073:Immunoglobulin E