Anindita Dutta1, Katherine Brito1, Galina Khramstova2, Ariel Mueller3, Sireesha Chinthala4, Donee Alexander5, Damilola Adu6, Tope Ibigbami6, John Olamijulo6, Abayomi Odetunde7, Kehinde Adigun8, Liese Pruitt9, Olufunmilayo Olopade1, Oladosu Ojengbede10, Sarosh Rana4, Christopher O Olopade11. 1. Center for Global Health, University of Chicago, 5841 S. Maryland Avenue, Chicago, IL 60637, USA; Center for Clinical Cancer Genetics and Department of Medicine, University of Chicago, IL 60637, USA. 2. Center for Clinical Cancer Genetics and Department of Medicine, University of Chicago, IL 60637, USA. 3. Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. 4. Department of Obstetrics and Gynecology, University of Chicago, Chicago, IL 60637, USA. 5. Center for Global Health, University of Chicago, 5841 S. Maryland Avenue, Chicago, IL 60637, USA. 6. Healthy Life for All Foundation, Ibadan, Nigeria. 7. Institute for Medical Research and Training, University of Ibadan, Ibadan, Nigeria. 8. Department of Family Medicine, University College Hospital, Ibadan, Nigeria. 9. Department of Surgery, University of Utah, Salt Lake City, UT, USA. 10. Department of Obstetrics and Gynecology, University of Ibadan, Ibadan, Nigeria; Centre for Population and Reproductive Health, College of Medicine/University College Hospital, University of Ibadan, Nigeria. 11. Center for Global Health, University of Chicago, 5841 S. Maryland Avenue, Chicago, IL 60637, USA; Center for Clinical Cancer Genetics and Department of Medicine, University of Chicago, IL 60637, USA. Electronic address: solopade@bsd.uchicago.edu.
Abstract
BACKGROUND: Maternal exposure to ambient air pollution affects placental growth markers. OBJECTIVES: Investigate impact of household air pollution (HAP) on placental growth markers. METHODS:Two groups of pregnant women were identified: firewood/kerosene stove-users (A, n=33) andbioethanol stove-users (B, n=44) that participated in a randomized control trial in Ibadan, Nigeria. A third group of non-smoking and presumed liquefied petroleum gas-using Chicago women (C, n=19) were included in this exploratory pilot to assess for possible differences between similar racial groups. Levels of placental growth factor (PlGF) and soluble fms-like tyrosine kinase 1 (sFlt-1) were measured in maternal and cord plasma using ELISA. RESULTS:Maternal and cord blood sFlt-1 and PlGF did not differ significantly between women of groups A and B. Nevertheless, both groups differed significantly from the Chicago group in that group A women had lower maternal sFlt-1 (1372.50 vs. 3194.19) but higher PlGF (1607.87 vs. 442.80), and higher cord blood sFlt-1 (2925.02 vs. 107.53) and PlGF (223.68 vs. 6.92), all p≤0.001. Group B showed similar trends (all p≤0.002). Maternal PlGF levels were positively correlated to minutes of HAP exposure when PM2.5 concentration was above 100μg/m3 in Nigerian women. CONCLUSIONS:Maternal levels of PlGF and cord blood levels of sFlt-1 and PlGF in Nigerian women with varying HAP exposures were significantly higher than Chicago-based women who had no presumed HAP exposure. It suggests that in-utero exposure to HAP influenced levels of angiogenic factors involved in normal placentation and growth and could represent compensation for pollutants exposure to preserve fetal viability.
RCT Entities:
BACKGROUND: Maternal exposure to ambient air pollution affects placental growth markers. OBJECTIVES: Investigate impact of household air pollution (HAP) on placental growth markers. METHODS: Two groups of pregnant women were identified: firewood/kerosene stove-users (A, n=33) and bioethanol stove-users (B, n=44) that participated in a randomized control trial in Ibadan, Nigeria. A third group of non-smoking and presumed liquefied petroleum gas-using Chicago women (C, n=19) were included in this exploratory pilot to assess for possible differences between similar racial groups. Levels of placental growth factor (PlGF) and soluble fms-like tyrosine kinase 1 (sFlt-1) were measured in maternal and cord plasma using ELISA. RESULTS: Maternal and cord blood sFlt-1 and PlGF did not differ significantly between women of groups A and B. Nevertheless, both groups differed significantly from the Chicago group in that group A women had lower maternal sFlt-1 (1372.50 vs. 3194.19) but higher PlGF (1607.87 vs. 442.80), and higher cord blood sFlt-1 (2925.02 vs. 107.53) and PlGF (223.68 vs. 6.92), all p≤0.001. Group B showed similar trends (all p≤0.002). Maternal PlGF levels were positively correlated to minutes of HAP exposure when PM2.5 concentration was above 100μg/m3 in Nigerian women. CONCLUSIONS: Maternal levels of PlGF and cord blood levels of sFlt-1 and PlGF in Nigerian women with varying HAP exposures were significantly higher than Chicago-based women who had no presumed HAP exposure. It suggests that in-utero exposure to HAP influenced levels of angiogenic factors involved in normal placentation and growth and could represent compensation for pollutants exposure to preserve fetal viability.
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