Maria José Rosa1, Marcela Tamayo-Ortiz2, Adriana Mercado Garcia3, Nadya Y Rivera Rivera4, Douglas Bush5, Alison G Lee6, Maritsa Solano-González7, Chitra Amarasiriwardena8, Martha Maria Téllez-Rojo9, Robert O Wright10, Rosalind J Wright11. 1. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1057, 10029, New York, NY, USA. Electronic address: maria.rosa@mssm.edu. 2. Occupational Health Research Unit, Mexican Institute of Social Security (IMSS), Av. Cuahtemoc 330, Col. Doctores, 06720, Mexico City, Mexico. Electronic address: marcela.tamayo@imss.gob.mx. 3. Center for Nutrition and Health Research, National Institute of Public Health, Av. Universidad #655 Col, Santa Maria Ahuacatitlan C.P, 62100, Cuernavaca, Morelos, Mexico. Electronic address: adrianam@insp.mx. 4. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1057, 10029, New York, NY, USA. Electronic address: nadya.riverarivera@mssm.edu. 5. Kravis Children's Hospital, Department of Pediatrics, Division of Pediatric Pulmonology, Icahn School of Medicine at Mount Sinai, 1184 Fifth Avenue, 10029, New York, NY, USA. Electronic address: douglas.bush@mssm.edu. 6. Division of Pulmonary, Critical Care and Sleep, Department of Medicine, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, 10029, New York, NY, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1057, New York, NY, 10029, USA. Electronic address: alison.lee@mssm.edu. 7. Center for Nutrition and Health Research, National Institute of Public Health, Av. Universidad #655 Col, Santa Maria Ahuacatitlan C.P, 62100, Cuernavaca, Morelos, Mexico. Electronic address: msolano@insp.mx. 8. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1057, 10029, New York, NY, USA. Electronic address: chitra.amarasiriwardena@mssm.edu. 9. Center for Nutrition and Health Research, National Institute of Public Health, Av. Universidad #655 Col, Santa Maria Ahuacatitlan C.P, 62100, Cuernavaca, Morelos, Mexico. Electronic address: mmtellez@insp.mx. 10. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1057, 10029, New York, NY, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1057, New York, NY, 10029, USA. Electronic address: robert.wright@mssm.edu. 11. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1057, 10029, New York, NY, USA; Division of Pulmonary, Critical Care and Sleep, Department of Medicine, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, 10029, New York, NY, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1057, New York, NY, 10029, USA. Electronic address: rosalind.wright@mssm.edu.
Abstract
INTRODUCTION: Maternal hypothalamic-pituitary-adrenal (HPA) axis disruption in pregnancy may contribute to the programming of childhood respiratory disease and may modify the effect of chemical toxins, like lead (Pb), on lung development. Child sex may further modify these effects. We sought to prospectively examine associations between maternal HPA axis disruption, prenatal Pb and childhood lung function and explore potential effect modification by maternal cortisol and child sex on the association between prenatal Pb and lung function outcomes. MATERIALS AND METHODS: Analyses included 222 mothers and children enrolled in a longitudinal birth cohort study in Mexico City. Maternal diurnal salivary cortisol was assessed in pregnancy; cortisol awakening response (CAR) and diurnal slope were calculated. Blood Pb was measured during the second trimester of pregnancy. Post-bronchodilator lung function was tested at ages 8-11 years. Associations were modeled using generalized linear models with interaction terms, adjusting for covariates. RESULTS: A higher (flatter) diurnal slope was associated with lower FEV1/FVC ratio (β: 0.433, 95%CI [-0.766, -0.101]). We did not find any main effect associations between prenatal Pb and lung function outcomes. We report an interaction between Pb and cortisol in relation to FEV1/FVC and FEF25-75% (pinteraction<0.05 for all). Higher prenatal Pb was associated with reduced FEV1/FVC only in children whose mothers had a high CAR. Higher prenatal Pb was also associated with reduced FEV1/FVC and FEF25-75% in mothers with a flatter diurnal slope. A 3-way interaction between prenatal Pb, CAR and sex on FEV1/FVC, indicated that boys born to women with high CAR and higher prenatal Pb levels had lower FEV1/FVC ratios (pinteraction = 0.067). CONCLUSIONS: Associations between prenatal Pb and childhood lung function were modified by disrupted maternal cortisol in pregnancy and child sex. These findings underscore the need to consider complex interactions to fully elucidate effects of prenatal Pb exposure on childhood lung function.
INTRODUCTION: Maternal hypothalamic-pituitary-adrenal (HPA) axis disruption in pregnancy may contribute to the programming of childhood respiratory disease and may modify the effect of chemical toxins, like lead (Pb), on lung development. Child sex may further modify these effects. We sought to prospectively examine associations between maternal HPA axis disruption, prenatal Pb and childhood lung function and explore potential effect modification by maternal cortisol and child sex on the association between prenatal Pb and lung function outcomes. MATERIALS AND METHODS: Analyses included 222 mothers and children enrolled in a longitudinal birth cohort study in Mexico City. Maternal diurnal salivary cortisol was assessed in pregnancy; cortisol awakening response (CAR) and diurnal slope were calculated. Blood Pb was measured during the second trimester of pregnancy. Post-bronchodilator lung function was tested at ages 8-11 years. Associations were modeled using generalized linear models with interaction terms, adjusting for covariates. RESULTS: A higher (flatter) diurnal slope was associated with lower FEV1/FVC ratio (β: 0.433, 95%CI [-0.766, -0.101]). We did not find any main effect associations between prenatal Pb and lung function outcomes. We report an interaction between Pb and cortisol in relation to FEV1/FVC and FEF25-75% (pinteraction<0.05 for all). Higher prenatal Pb was associated with reduced FEV1/FVC only in children whose mothers had a high CAR. Higher prenatal Pb was also associated with reduced FEV1/FVC and FEF25-75% in mothers with a flatter diurnal slope. A 3-way interaction between prenatal Pb, CAR and sex on FEV1/FVC, indicated that boys born to women with high CAR and higher prenatal Pb levels had lower FEV1/FVC ratios (pinteraction = 0.067). CONCLUSIONS: Associations between prenatal Pb and childhood lung function were modified by disrupted maternal cortisol in pregnancy and child sex. These findings underscore the need to consider complex interactions to fully elucidate effects of prenatal Pb exposure on childhood lung function.
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