Prenatal exposure to environmental contaminants and cord serum metabolite profiles in future immune-mediated diseases Show others and affiliations
2024 (English) In: Journal of Exposure Science and Environmental Epidemiology, ISSN 1559-0631, E-ISSN 1559-064X, Vol. 34, no 4, p. 647-658Article in journal (Refereed) Published
Abstract [en]
BACKGROUND: Prenatal exposure to environmental contaminants is a significant health concern because it has the potential to interfere with host metabolism, leading to adverse health effects in early childhood and later in life. Growing evidence suggests that genetic and environmental factors, as well as their interactions, play a significant role in the development of autoimmune diseases.
OBJECTIVE: In this study, we hypothesized that prenatal exposure to environmental contaminants impacts cord serum metabolome and contributes to the development of autoimmune diseases.
METHODS: We selected cord serum samples from All Babies in Southeast Sweden (ABIS) general population cohort, from infants who later developed one or more autoimmune-mediated and inflammatory diseases: celiac disease (CD), Crohn's disease (IBD), hypothyroidism (HT), juvenile idiopathic arthritis (JIA), and type 1 diabetes (T1D) (all cases, N = 62), along with matched controls (N = 268). Using integrated exposomics and metabolomics mass spectrometry (MS) based platforms, we determined the levels of environmental contaminants and metabolites.
RESULTS: Differences in exposure levels were found between the controls and those who later developed various diseases. High contaminant exposure levels were associated with changes in metabolome, including amino acids and free fatty acids. Specifically, we identified marked associations between metabolite profiles and exposure levels of deoxynivalenol (DON), bisphenol S (BPS), and specific per- and polyfluorinated substances (PFAS).
IMPACT STATEMENT: Abnormal metabolism is a common feature preceding several autoimmune and inflammatory diseases. However, few studies compared common and specific metabolic patterns preceding these diseases. Here we hypothesized that exposure to environmental contaminants impacts cord serum metabolome, which may contribute to the development of autoimmune diseases. We found differences in exposure levels between the controls and those who later developed various diseases, and importantly, on the metabolic changes associated with the exposures. High contaminant exposure levels were associated with specific changes in metabolome. Our study suggests that prenatal exposure to specific environmental contaminants alters the cord serum metabolomes, which, in turn, might increase the risk of various immune-mediated diseases.
Place, publisher, year, edition, pages Nature Publishing Group, 2024. Vol. 34, no 4, p. 647-658
Keywords [en]
Autoimmune disease, environmental contaminants, exposome, lipidomics, metabolomics, type 1 diabetes
National Category
Occupational Health and Environmental Health
Identifiers URN: urn:nbn:se:oru:diva-113407 DOI: 10.1038/s41370-024-00680-z ISI: 001208827800002 PubMedID: 38678133 Scopus ID: 2-s2.0-85191718574 OAI: oai:DiVA.org:oru-113407 DiVA, id: diva2:1854857
Funder Swedish Research Council, 2020-03674; K2005-72 × -11242-11A; K2008-69 × -20826-01-4; K2008-69 × -20826-01-4 Swedish Research Council Formas, 2019-00869 EU, Horizon Europe, 101094099 Swedish Child Diabetes Foundation Forte, Swedish Research Council for Health, Working Life and Welfare, FAS2004-1775; FAS2004–1775 Medical Research Council of Southeast Sweden (FORSS) Region Östergötland Örebro University
Note This work was supported by the Swedish Research Council [grant number 2020-03674; to TH], Formas [grant number 2019-00869; to TH], and by the “Inflammation in human early life: targeting impacts on life-course health” (INITIALISE) consortium funded by the Horizon Europe Program of the European Union under Grant Agreement 101094099 (to T.H., E.W.T., M.O., and J.L.). The ABIS cohort study (JL) was supported by Barndiabetesfonden (Swedish Child Diabetes Foundation), the Swedish Council for Working Life and Social Research [grant numbers FAS2004-1775 and FAS2004–1775], Swedish Research Council [Grant/Award Numbers: K2005-72 × -11242-11A and K2008-69 × -20826-01-4, K2008-69 × -20826-01-4], Östgöta Brandstodsbolag, Medical Research Council of Southeast Sweden (FORSS), JDRF Wallenberg Foundation [Grant/Award Number: K 98-99D-12813-01A], Joanna Cocozza Foundation and ALF-and LfoU grants from Region Östergötland and Linköping University, Sweden. Open access funding provided by Örebro University.
2024-04-292024-04-292024-09-02 Bibliographically approved