The environment and childhood asthma (ECA) study in Oslo: ECA-1 and ECA-2.
An observed increase in asthma admissions in Oslo during the 1980s prompted a prospective birth cohort study to ask the following question: was air pollution (outdoor and indoor) (in a broad sense) associated with asthma development in young children? During 12 months from 1 January 1992, 3,754 children (birth weight > or = 2,000 g) in Oslo were enrolled at birth into the Environment and Childhood Asthma (ECA) study and followed to 2 years of age (ECA-part I). Cord blood, a detailed questionnaire (family and pregnancy history of disease, environmental exposures, socio-economic status) completed by the mother and lung function measurements (n = 803) were collated at birth. Detailed questionnaires completed every 6 months for 2 years included the child's disease history, feeding habits and environmental exposures. A nested case-control study comprised 306 children with confirmed minimum two episodes of bronchial obstruction (rBO) and 306 controls (without lower respiratory tract disease) with clinical investigations (including tidal breathing lung function, beta-2 responsiveness and allergy assessment) and environmental exposure assessments (indoor and outdoor). Home dampness and low ventilation, as well as maternal smoking in pregnancy, but not outdoor air pollution increased the risk of rBO. Lung function at birth was decreased among newborns whose mother smoked during pregnancy. To understand better the early risk factors for asthma and allergy development, a follow-up study started (in 2001; ECA-part II) of all cases and controls, and those with lung function measured at birth (total 1,230 invited) (9-10 years of age). This involved clinical investigation, allergy assessments, lung function, airway hyper responsiveness measures, exhaled nitric oxide and immunological as well as allergen exposure investigations.
Lødrup Carlsen
Karin C
KC
Department of Paediatrics, Division of Woman and Child Health, Ullevål, University Hospital, Oslo, Norway. karinloedrup.carlsen@ulleval.no
D000280:Administration, Inhalation; D000420:Albuterol / Q000008:administration & dosage; D001249:Asthma / Q000097:blood / Q000453:epidemiology / Q000209:etiology*; D015415:Biomarkers / Q000097:blood; D001798:Blood Proteins / Q000032:analysis; D001993:Bronchodilator Agents / Q000008:administration & dosage; D016022:Case-Control Studies; D015331:Cohort Studies; D004781:Environmental Exposure / Q000009:adverse effects*; D047091:Eosinophil Granule Proteins; D005500:Follow-Up Studies; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D007229:Infant Welfare; D007231:Infant, Newborn; D009664:Norway; D009195:Peroxidase / Q000097:blood; D011446:Prospective Studies; D012129:Respiratory Function Tests; D012260:Ribonucleases; D013990:Tidal Volume / Q000187:drug effects / Q000502:physiology
D015415:Biomarkers; D001798:Blood Proteins; D001993:Bronchodilator Agents; D047091:Eosinophil Granule Proteins; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D007073:Immunoglobulin E; D009195:Peroxidase; D012260:Ribonucleases; D000420:Albuterol