Margaret A Adgent1, Tebeb Gebretsadik2, Cordelia R Elaiho3, Ginger L Milne4, Paul Moore5, Terryl J Hartman6, Whitney Cowell7, Cecilia S Alcala7, Nicole Bush8, Robert Davis9, Kaja Z LeWinn10, Frances A Tylavsky11, Rosalind J Wright12, Kecia N Carroll13. 1. Department of Health Policy, Vanderbilt University Medical Center, Nashville, TN, USA. 2. Department of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, USA. 3. Department of Pediatrics, Kravis Children's Hospital, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 4. Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, TN, USA. 5. Division of Allergy, Immunology and Pulmonary Medicine, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN, USA. 6. Department of Epidemiology, Emory University Rollins School of Public Health, Atlanta, GA, USA. 7. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 8. Department of Psychiatry, University of California, San Francisco, San Francisco, CA, USA; Department of Pediatrics, University of California, San Francisco, San Francisco, CA, USA. 9. Center for Biomedical Informatics, University of Tennessee Health Science Center, Memphis, TN, USA. 10. Department of Psychiatry, University of California, San Francisco, San Francisco, CA, USA. 11. Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, TN, USA. 12. Department of Pediatrics, Kravis Children's Hospital, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 13. Department of Pediatrics, Kravis Children's Hospital, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Division of General Pediatrics, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN, USA. Electronic address: kecia.carroll@mssm.edu.
Abstract
BACKGROUND: Childhood wheeze, asthma, and allergic rhinitis are common and likely have prenatal origins. Oxidative stress is associated with respiratory disease, but the association of oxidative stress during the prenatal period with development of respiratory and atopic disease in childhood, particularly beyond the infancy period, is unknown. This study aims to investigate associations between prenatal oxidative stress, measured by maternal urinary F2-isoprostanes, and child respiratory outcomes, including effect modification by maternal race. METHODS: We prospectively studied Black (n = 717) and White (n = 363) mother-child dyads. We measured F2-isoprostanes in 2nd-trimester urine (ng/mg-creatinine). At approximately age 4, we obtained parent report of provider-diagnosed asthma (ever), current wheeze, current asthma (diagnosis, symptoms and/or medication), and current allergic rhinitis (current defined as previous 12 months). We used multivariable logistic regression to estimate adjusted odds ratios (aOR) and 95% confidence intervals (95%CI) per interquartile range (IQR) increase in F2-isoprostane concentration, controlling for confounders. We examined modification by maternal race using interaction terms. RESULTS: The prevalence of provider-diagnosed asthma and current wheeze, asthma and allergic rhinitis was 14%, 19%, 15%, and 24%, respectively. Median (IQR) F2-isoprostane levels were 2.1 (1.6, 2.9) ng/mg-creatinine. Associations between prenatal F2-isoprostanes and provider-diagnosed asthma, current wheeze, and current asthma were modified by maternal race. Results were strongest for current wheeze (aOR [95%CI]: 1.55 [1.16, 2.06] for White; 0.98 [0.78, 1.22] for Black; p-interaction = 0.01). We observed no association between F2-isoprostanes and allergic rhinitis. CONCLUSION: Prenatal urinary F2-isoprostanes may be a marker associated with childhood wheeze/asthma in certain populations. Research is needed to understand underlying mechanisms and racial differences.
BACKGROUND: Childhood wheeze, asthma, and allergic rhinitis are common and likely have prenatal origins. Oxidative stress is associated with respiratory disease, but the association of oxidative stress during the prenatal period with development of respiratory and atopic disease in childhood, particularly beyond the infancy period, is unknown. This study aims to investigate associations between prenatal oxidative stress, measured by maternal urinary F2-isoprostanes, and child respiratory outcomes, including effect modification by maternal race. METHODS: We prospectively studied Black (n = 717) and White (n = 363) mother-child dyads. We measured F2-isoprostanes in 2nd-trimester urine (ng/mg-creatinine). At approximately age 4, we obtained parent report of provider-diagnosed asthma (ever), current wheeze, current asthma (diagnosis, symptoms and/or medication), and current allergic rhinitis (current defined as previous 12 months). We used multivariable logistic regression to estimate adjusted odds ratios (aOR) and 95% confidence intervals (95%CI) per interquartile range (IQR) increase in F2-isoprostane concentration, controlling for confounders. We examined modification by maternal race using interaction terms. RESULTS: The prevalence of provider-diagnosed asthma and current wheeze, asthma and allergic rhinitis was 14%, 19%, 15%, and 24%, respectively. Median (IQR) F2-isoprostane levels were 2.1 (1.6, 2.9) ng/mg-creatinine. Associations between prenatal F2-isoprostanes and provider-diagnosed asthma, current wheeze, and current asthma were modified by maternal race. Results were strongest for current wheeze (aOR [95%CI]: 1.55 [1.16, 2.06] for White; 0.98 [0.78, 1.22] for Black; p-interaction = 0.01). We observed no association between F2-isoprostanes and allergic rhinitis. CONCLUSION: Prenatal urinary F2-isoprostanes may be a marker associated with childhood wheeze/asthma in certain populations. Research is needed to understand underlying mechanisms and racial differences.
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