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Environ Sci Pollut Res Int. 2019 Jan;26(2):1370-1378. doi: 10.1007/s11356-018-3659-6. Epub 2018 Nov 13.

No evidence of the role of early chemical exposure in the development of β-cell autoimmunity.

Author information

1
Scientific Laboratory, Clinicum, University of Helsinki, Haartmaninkatu 8, 00290, Helsinki, Finland. harri.salo@helsinki.fi.
2
Department of Health Security, National Institute for Health and Welfare (THL), Kuopio, Finland.
3
Scientific Laboratory, Clinicum, University of Helsinki, Haartmaninkatu 8, 00290, Helsinki, Finland.
4
Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
5
Research Programs Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland.
6
Immunogenetics Laboratory, University of Turku, Turku, Finland.
7
Department of Clinical Microbiology, University of Eastern Finland, Kuopio, Finland.
8
Department of Health, National Institute for Health and Welfare, Helsinki, Finland.
9
School of Health Sciences, University of Tampere, Tampere, Finland.
10
Science Centre, Pirkanmaa Hospital District and Center for Child Health Research, Tampere University and University Hospital, Tampere, Finland.
11
Department of Pediatrics, University of Tartu and Tartu University Hospital, Tartu, Estonia.
12
Folkhälsan Research Center, Helsinki, Finland.
13
Tampere Centre for Child Health Research, Tampere University Hospital, Tampere, Finland.

Abstract

Exposure to environmental chemicals can modulate the developing immune system, but its role in the pathogenesis of type 1 diabetes is largely unexplored. Our objective was to study the levels of circulating concentrations of environmental pollutants during the first years of life and their associations with the later risk of diabetes-predictive autoantibodies. From two birth-cohort studies including newborn infants with HLA-conferred susceptibility to type 1 diabetes (FINDIA and DIABIMMUNE), we identified case children with at least one biochemical diabetes-associated autoantibody (n = 30-40) and from one to four autoantibody-negative controls per each case child matched for age, gender, diabetes-related HLA-risk, delivery hospital, and, in FINDIA, also dietary intervention group. Plasma levels of 13 persistent organic pollutants and 14 per- and polyfluorinated substances were analyzed in cord blood and plasma samples taken at the age of 12 and 48 months. Both breastfeeding and the geographical living environment showed association with circulating concentrations of some of the chemicals. Breastfeeding-adjusted conditional logistic regression model showed association between decreased plasma HBC concentration at 12-month-old children and the appearance of diabetes-associated autoantibodies (HR, 0.989; 95% Cl, 0.978-1.000; P = 0.048). No association was found between the plasma chemical levels and the development of clinical type 1 diabetes. Our results do not support the view that exposure to the studied environmental chemicals during fetal life or early childhood is a significant risk factor for later development of β-cell autoimmunity and type 1 diabetes.

KEYWORDS:

Breastfeeding; Chemical exposure; Human; Type 1 diabetes; β-cell autoimmunity

PMID:
30426368
DOI:
10.1007/s11356-018-3659-6

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