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Title: | Prenatal particulate air pollution exposure and cord blood homocysteine in newborns: Results from the ENVIRONAGE birth cohort | Authors: | HOGERVORST, Janneke MADHLOUM, Narjes SAENEN, Nelly JANSSEN, Bram PENDERS, Joris Vanpoucke, Charlotte De Vivo, Immaculata VRIJENS, Karen NAWROT, Tim |
Issue Date: | 2019 | Publisher: | ACADEMIC PRESS INC ELSEVIER SCIENCE | Source: | ENVIRONMENTAL RESEARCH, 168, p. 507-513 | Abstract: | Introduction Particulate air pollution is probably causally related to increased risk of cardiovascular disease. Plasma homocysteine is an established cardiovascular disease risk factor. Recent studies show that exposure to particulate air pollution is associated with plasma homocysteine levels in adults but no studies on the association between prenatal air pollution and neonatal homocysteine levels exist. Methods: In 609 newborns of the ENVIRONAGE (ENVIRonmental influence ON early AGEing) birth cohort, we investigated the association between prenatal particulate matter exposure with a diameter <= 2.5 mu m (PM2.5) and cord plasma homocysteine levels, and in a subset (n = 490) we studied the interaction with 11 single nucleotide polymorphism (SNPs) in oxidative stress-related genes (CAT, COMT, GSTP1, SOD2, NQO1 and HFE), through multiple linear regression. PM2.5 levels were obtained using a high resolution spatial temporal interpolation method. Homocysteine levels were measured by the homocysteine enzymatic assay on a Roche/Hitachi cobas c system. SNPs were assessed on the Biotrove OpenArray SNP genotyping platform. Results: In multivariable-adjusted models, cord plasma homocysteine levels were 8.1% higher (95% CI: 1.9 to 14.3%; p = 0.01) for each 5 mu g/m(3) increment in average PM2.5 exposure during the entire pregnancy. With regard to pregnancy trimesters, there was only an association in the 2nd trimester: 3.6% (95% CI: 0.9% to 6.4%; p = 0.01). The positive association between PM2.5 in and homocysteine was (borderline) statistically significantly modified by genetic variants in MnSOD (p interaction = 0.02), GSTP1 (p interaction = 0.07) and the sum score of the 3 studied SNPs in the CAT gene (p interaction = 0.09), suggesting oxidative stress as an underlying mechanism of action. Conclusions: Exposure to particulate air pollution in utero is associated with higher cord blood homocysteine levels, possibly through generating oxidative stress. Increased air pollution -induced homocysteine levels in early life might predispose for cardiovascular and other diseases later in life. | Notes: | [Hogeryorst, Janneke G. F.; Madhloum, Narjes; Saenen, Nelly D.; Janssen, Bram G.; Vrijens, Karen; Nawrot, Tim S.] Hasselt Univ, Ctr Environm Sci, Hasselt, Belgium. [Penders, Joris] Hasselt Univ, Biomed Res Inst, Hasselt, Belgium. [Penders, Joris] East Limburg Hosp, Lab Clin Biol, Genk, Belgium. [Vanpoucke, Charlotte] Belgian Interreg Environm Agcy, Brussels, Belgium. [De Vivo, Immaculata] Brigham & Womens Hosp, Dept Med, Charming Div Network Med, 75 Francis St, Boston, MA 02115 USA. [De Vivo, Immaculata] Harvard Med Sch, Boston, MA USA. [De Vivo, Immaculata] Harvard Sch Publ Hlth, Program Genet Epidemiol & Stat Genet, Boston, MA USA. [Nawrot, Tim S.] Leuven Univ, Dept Publ Hlth & Primary Care, Leuven, Belgium. | Keywords: | PM2.5; homocysteine; in utero; oxidative stress-related SNPs; birth cohort;PM2.5; homocysteine; in utero; oxidative stress-related SNPs; birth cohort | Document URI: | http://hdl.handle.net/1942/29570 | ISSN: | 0013-9351 | e-ISSN: | 1096-0953 | DOI: | 10.1016/j.envres.2018.08.032 | ISI #: | 000452938700054 | Rights: | 2018 Elsevier Inc. All rights reserved. | Category: | A1 | Type: | Journal Contribution | Validations: | ecoom 2020 |
Appears in Collections: | Research publications |
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