Early-life exposure to persistent organic pollutants, gut microbiota diversity and metabolites, and respiratory health in Norwegian children

Abstract

Background: Evidence suggests that early-life exposure to certain environmental chemicals increases the risk of allergic diseases, while gut microbiota diversity and microbiota-derived short-chain fatty acid (SCFA) metabolites may be protective. Objectives: We assessed associations between persistent organic pollutants (POPs), microbial markers, and subsequent risk of asthma and lower respiratory tract infection (LRTI). Methods: We studied a Norwegian birth cohort (HUMIS). Twenty-six POPs [polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs), perfluoroalkyl substances (PFASs), and organochlorine pesticides (OCPs)] were quantified in maternal breastmilk (n=993). Shannon diversity and SCFAs were assessed at multiple time points before 2 years of age in a subset of children. We evaluated registry-based diagnosis of asthma when children were a median age of 10 years, along with maternal-reported asthma and LRTI by 2 years of age. Results: ∑14PCBs was associated with decreased odds and ∑4OCPs with increased odds of asthma; associations between β-HCH (OR=2.99 per 2-SD increase; 95% CI: 1.66, 5.43) and PCB-138 (OR=0.43; 95% CI: 0.20, 0.91) and asthma by age 10 years were most robust. PBDEs and PFASs were not consistently associated with asthma and no POPs were associated with LRTI. There were both inverse and positive associations between diversity and respiratory outcomes, and generally imprecise associations for SCFAs. There was limited evidence that POP exposures perturbed diversity or production of SCFAs, except for an association between ∑14PCBs and reduced diversity at 2 years, and there was no clear evidence of mediation effects. Conclusions: This study provides support for associations between some POPs and risk of childhood asthma, and indications of a potential independent role of gut microbiota.

Competing Interest Statement

The authors have declared no competing interest.

Funding Statement

This research was supported in part by the Research Council of Norway (NevroNor grant agreement number 226402) and by the European Commission's Seventh Framework Program (DENAMIC grant agreement number FP7-ENV-2011-282957).

Author Declarations

I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained.

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The details of the IRB/oversight body that provided approval or exemption for the research described are given below:

The Regional Committees for Medical and Health Research Ethics in Norway and the Norwegian Data Inspectorate gave ethical approval for this work.

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Data Availability

Data cannot be made publicly available as the dataset contains sensitive and identifying information. The data may be made available upon request.

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