Plasma concentrations of lipophilic persistent organic pollutants and glucose homeostasis in youth populations.
Flame retardants
Obesogens
Organochlorines
Pesticides
Polybrominated compounds
Type II diabetes
Journal
Environmental research
ISSN: 1096-0953
Titre abrégé: Environ Res
Pays: Netherlands
ID NLM: 0147621
Informations de publication
Date de publication:
09 2022
09 2022
Historique:
received:
29
11
2021
revised:
15
03
2022
accepted:
09
04
2022
pubmed:
22
4
2022
medline:
22
6
2022
entrez:
21
4
2022
Statut:
ppublish
Résumé
Exposure to lipophilic persistent organic pollutants (POPs) is ubiquitous. POPs are metabolic disrupting chemicals and are potentially diabetogenic. Using a multi-cohort study including overweight adolescents from the Study of Latino Adolescents at Risk (SOLAR, N = 301, 2001-2012) and young adults from the Southern California Children's Health Study (CHS, N = 135, 2014-2018), we examined associations of POPs and risk factors for type 2 diabetes. SOLAR participants underwent annual visits for a median of 2.2 years and CHS participants performed a single visit, during which a 2-h oral glucose tolerance test was performed. Linear mixed models were used to examine associations between plasma concentrations of POPs [4,4'-dichlorodiphenyldichloroethylene (4,4'-DDE), hexachlorobenzene (HCB), PCBs-153, 138, 118, 180 and PBDEs-154, 153, 100, 85, 47] and changes in glucose homeostasis across age and pubertal stage. In SOLAR, exposure to HCB, PCB-118, and PBDE-153 was associated with dysregulated glucose metabolism. For example, each two-fold increase in HCB was associated with approximately 2 mg/dL higher glucose concentrations at 30 min (p = 0.001), 45 min (p = 0.0006), and 60 min (p = 0.03) post glucose challenge. Compared to individuals with low levels of PCB-118, individuals with high levels exhibited a 4.7 mg/dL (p = 0.02) higher glucose concentration at 15 min and a 3.6 mg/dL (p = 0.01) higher glucose concentration at 30 min. The effects observed with exposure to organochlorine compounds were independent of pubertal stages. PBDE-153 was associated with the development of dysregulated glucose metabolism beginning in late puberty. At Tanner stage 4, exposure to PBDE-153 was associated with a 12.7 mg/dL higher 60-min glucose concentration (p = 0.009) and a 16.1 mg*dl Our results suggest that childhood exposure to lipophilic POPs is associated with dysregulated glucose metabolism.
Sections du résumé
BACKGROUND
Exposure to lipophilic persistent organic pollutants (POPs) is ubiquitous. POPs are metabolic disrupting chemicals and are potentially diabetogenic.
METHODS
Using a multi-cohort study including overweight adolescents from the Study of Latino Adolescents at Risk (SOLAR, N = 301, 2001-2012) and young adults from the Southern California Children's Health Study (CHS, N = 135, 2014-2018), we examined associations of POPs and risk factors for type 2 diabetes. SOLAR participants underwent annual visits for a median of 2.2 years and CHS participants performed a single visit, during which a 2-h oral glucose tolerance test was performed. Linear mixed models were used to examine associations between plasma concentrations of POPs [4,4'-dichlorodiphenyldichloroethylene (4,4'-DDE), hexachlorobenzene (HCB), PCBs-153, 138, 118, 180 and PBDEs-154, 153, 100, 85, 47] and changes in glucose homeostasis across age and pubertal stage.
RESULTS
In SOLAR, exposure to HCB, PCB-118, and PBDE-153 was associated with dysregulated glucose metabolism. For example, each two-fold increase in HCB was associated with approximately 2 mg/dL higher glucose concentrations at 30 min (p = 0.001), 45 min (p = 0.0006), and 60 min (p = 0.03) post glucose challenge. Compared to individuals with low levels of PCB-118, individuals with high levels exhibited a 4.7 mg/dL (p = 0.02) higher glucose concentration at 15 min and a 3.6 mg/dL (p = 0.01) higher glucose concentration at 30 min. The effects observed with exposure to organochlorine compounds were independent of pubertal stages. PBDE-153 was associated with the development of dysregulated glucose metabolism beginning in late puberty. At Tanner stage 4, exposure to PBDE-153 was associated with a 12.7 mg/dL higher 60-min glucose concentration (p = 0.009) and a 16.1 mg*dl
CONCLUSION
Our results suggest that childhood exposure to lipophilic POPs is associated with dysregulated glucose metabolism.
Identifiants
pubmed: 35447156
pii: S0013-9351(22)00623-5
doi: 10.1016/j.envres.2022.113296
pmc: PMC9831292
mid: NIHMS1854160
pii:
doi:
Substances chimiques
Environmental Pollutants
0
Hydrocarbons, Chlorinated
0
Dichlorodiphenyl Dichloroethylene
4M7FS82U08
Hexachlorobenzene
4Z87H0LKUY
Polychlorinated Biphenyls
DFC2HB4I0K
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
113296Subventions
Organisme : NIEHS NIH HHS
ID : U2C ES030163
Pays : United States
Organisme : NIEHS NIH HHS
ID : R21 ES029681
Pays : United States
Organisme : NIEHS NIH HHS
ID : P01 ES022845
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES030691
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK059211
Pays : United States
Organisme : NIEHS NIH HHS
ID : R21 ES028903
Pays : United States
Organisme : NIEHS NIH HHS
ID : R21 ES029328
Pays : United States
Organisme : NIEHS NIH HHS
ID : R00 ES027870
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES030364
Pays : United States
Organisme : NIEHS NIH HHS
ID : T32 ES013678
Pays : United States
Organisme : NIEHS NIH HHS
ID : P30 ES019776
Pays : United States
Organisme : NIEHS NIH HHS
ID : R24 ES029490
Pays : United States
Organisme : NIEHS NIH HHS
ID : K12 ES033594
Pays : United States
Organisme : NIEHS NIH HHS
ID : R21 ES031824
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES029944
Pays : United States
Organisme : NIEHS NIH HHS
ID : P30 ES007048
Pays : United States
Organisme : NIEHS NIH HHS
ID : P30 ES023515
Pays : United States
Organisme : NIEHS NIH HHS
ID : R01 ES032189
Pays : United States
Informations de copyright
Copyright © 2022 Elsevier Inc. All rights reserved.
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