Prenatal arachidonic acid exposure and selected immune-related variables in childhood.
Arachidonic acid (AA) is considered essential in fetal development and some of its metabolites are thought to be important mediators of the immune responses. Therefore, we studied whether prenatal exposure to AA is associated with some immune-related clinical conditions and plasma markers in childhood. In 280 children aged 7 years, atopy, lung function and plasma inflammation markers were measured and their relationships with early AA exposure were studied by linear and logistic regression analyses. AA exposure was deduced from AA concentrations in plasma phospholipids of the mothers collected at several time points during pregnancy and at delivery, and in umbilical cord plasma and arterial and venous wall phospholipids. In unadjusted regression analyses, significant positive associations were observed between maternal AA concentrations at 16 and 32 weeks of pregnancy (proxies for fetal AA exposure) and peak expiratory flow decline after maximal physical exercise and plasma fibrinogen concentrations of their children, respectively. However, after correction for relevant covariables, only trends remained. A significant negative relationship was observed between AA concentrations in cord plasma (reflecting prenatal AA exposure) and the average daily amplitude of peak expiratory flow at rest, which lost significance after appropriate adjustment. Because of these few, weak and inconsistent relationships, a major impact of early-life exposure to AA on atopy, lung function and selected plasma inflammation markers of children at 7 years of age seems unlikely.
Dirix
Chantal E H
CE
Department of Human Biology, Faculty of Health, Medicine and Life Sciences, Maastricht University, Maastricht, The Netherlands.
Hogervorst
Janneke G F
JG
Rump
Patrick
P
Hendriks
Johannes J E
JJ
Bruins
Maaike
M
Hornstra
Gerard
G
D016718:Arachidonic Acid / Q000097:blood / Q000502:physiology*; D001249:Asthma / Q000175:diagnosis; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D002648:Child; D002657:Child Development / Q000502:physiology*; D005260:Female; D005312:Fetal Blood / Q000737:chemistry; D005340:Fibrinogen / Q000032:analysis; D005500:Follow-Up Studies; D006801:Humans; D006967:Hypersensitivity / Q000175:diagnosis; D007231:Infant, Newborn; D020738:Leptin / Q000097:blood; D016014:Linear Models; D010366:Peak Expiratory Flow Rate; D011247:Pregnancy; D011262:Pregnancy Trimester, Second; D011263:Pregnancy Trimester, Third; D011297:Prenatal Exposure Delayed Effects; D011446:Prospective Studies; D012129:Respiratory Function Tests; D014841:von Willebrand Factor / Q000032:analysis
D015415:Biomarkers; D020738:Leptin; D014841:von Willebrand Factor; D016718:Arachidonic Acid; D005340:Fibrinogen; D002097:C-Reactive Protein