Rajesh Kumar1, Ryan P Ferrie2, Lauren C Balmert2, Matthew Kienzl2, Sheryl L Rifas-Shiman3, Diane R Gold4, Joanne E Sordillo3, Ken Kleinman5, Carlos A Camargo6, Augusto A Litonjua7, Emily Oken3, Joan M Cook-Mills8. 1. Lurie Children's Hospital, Chicago, Ill; Northwestern University, Chicago, Ill. 2. Northwestern University, Chicago, Ill. 3. Division of Chronic Disease Research across the Lifecourse, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, Mass. 4. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, Mass; Channing Division of Network Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, Mass. 5. Department of Biostatistics and Epidemiology, University of Massachusetts, Amherst, Mass. 6. Channing Division of Network Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, Mass; Department of Emergency Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Mass. 7. Division of Pediatric Pulmonary Medicine, University of Rochester Medical Center, Rochester, NY. 8. Herman B. Wells Center for Pediatric Research, Departments of Pediatrics and Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Ind. Electronic address: joancook@iu.edu.
Abstract
BACKGROUND: Tocopherol isoforms may regulate child lung growth and spirometric measures. OBJECTIVE: Our aim was to determine the extent to which plasma α-tocopherol (α-T) or γ-tocopherol (γ-T) isoform levels in early childhood or in utero are associated with childhood lung function. METHODS: We included 622 participants in the Project Viva cohort who had lung function at a mid-childhood visit (age 6-10 years). Maternal and child tocopherol isoform levels were measured by HPLC at the second trimester and 3 years of age, respectively. Multivariable linear regression models (adjusted for mid-childhood body mass index z scores, maternal education, smoking in pregnancy, and prenatal particulate matter with diameter of <2.5 micrometers (PM2.5) particulate exposure) stratified by tertiles of child γ-T level were used to assess the association of α-T levels with FEV1 and forced vital capacity (FVC) percent predicted. Similarly, models stratified by child α-T tertile evaluated associations of γ-T levels with lung function. We performed similar analyses with maternal second trimester tocopherol isoform levels. RESULTS: The median maternal second trimester α-T level was 63 μM (interquartile range = 47-82). The median early-childhood level was 25 μM (interquartile range = 20-33 μM). In the lowest tertile of early-childhood γ-T, children with a higher α-T level (per 10 μM) had a higher mid-childhood FEV1 percent predicted (β = 3.09; 95% CI = 0.58-5.59 and a higher FVC percent predicted (β = 2.77; 95% CI = 0.47-5.06). This protective association of α-T was lost at higher γ-T levels. We did not see any consistent associations of second trimester levels of either α-T or γ-T with mid-childhood FEV1 or FVC. CONCLUSION: When γ-T levels were in the lowest tertile, a higher early-childhood α-T level was associated with better lung function at mid-childhood. Second trimester maternal plasma α-T concentration was 3-fold higher than in the adult nonpregnant female population.
BACKGROUND: Tocopherol isoforms may regulate child lung growth and spirometric measures. OBJECTIVE: Our aim was to determine the extent to which plasma α-tocopherol (α-T) or γ-tocopherol (γ-T) isoform levels in early childhood or in utero are associated with childhood lung function. METHODS: We included 622 participants in the Project Viva cohort who had lung function at a mid-childhood visit (age 6-10 years). Maternal and child tocopherol isoform levels were measured by HPLC at the second trimester and 3 years of age, respectively. Multivariable linear regression models (adjusted for mid-childhood body mass index z scores, maternal education, smoking in pregnancy, and prenatal particulate matter with diameter of <2.5 micrometers (PM2.5) particulate exposure) stratified by tertiles of child γ-T level were used to assess the association of α-T levels with FEV1 and forced vital capacity (FVC) percent predicted. Similarly, models stratified by child α-T tertile evaluated associations of γ-T levels with lung function. We performed similar analyses with maternal second trimester tocopherol isoform levels. RESULTS: The median maternal second trimester α-T level was 63 μM (interquartile range = 47-82). The median early-childhood level was 25 μM (interquartile range = 20-33 μM). In the lowest tertile of early-childhood γ-T, children with a higher α-T level (per 10 μM) had a higher mid-childhood FEV1 percent predicted (β = 3.09; 95% CI = 0.58-5.59 and a higher FVC percent predicted (β = 2.77; 95% CI = 0.47-5.06). This protective association of α-T was lost at higher γ-T levels. We did not see any consistent associations of second trimester levels of either α-T or γ-T with mid-childhood FEV1 or FVC. CONCLUSION: When γ-T levels were in the lowest tertile, a higher early-childhood α-T level was associated with better lung function at mid-childhood. Second trimester maternal plasma α-T concentration was 3-fold higher than in the adult nonpregnant female population.
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