Early life exposure to mercury and relationships with telomere length and mitochondrial DNA content in European children
(2024) In Science of the Total Environment 932.- Abstract
Background: Telomere length (TL) and mitochondrial function expressed as mitochondrial DNA copy number (mtDNAcn) are biomarkers of aging and oxidative stress and inflammation, respectively. Methylmercury (MeHg), a common pollutant in fish, induces oxidative stress. We hypothesized that elevated oxidative stress from exposure to MeHg decreases mtDNAcn and shortens TL. Methods: Study participants are 6–11-year-old children from the HELIX multi-center birth cohort study, comprising six European countries. Prenatal and postnatal total mercury (THg) concentrations were measured in blood samples, TL and mtDNAcn were determined in child DNA. Covariates and confounders were obtained by questionnaires. Robust regression models were run,... (More)
Background: Telomere length (TL) and mitochondrial function expressed as mitochondrial DNA copy number (mtDNAcn) are biomarkers of aging and oxidative stress and inflammation, respectively. Methylmercury (MeHg), a common pollutant in fish, induces oxidative stress. We hypothesized that elevated oxidative stress from exposure to MeHg decreases mtDNAcn and shortens TL. Methods: Study participants are 6–11-year-old children from the HELIX multi-center birth cohort study, comprising six European countries. Prenatal and postnatal total mercury (THg) concentrations were measured in blood samples, TL and mtDNAcn were determined in child DNA. Covariates and confounders were obtained by questionnaires. Robust regression models were run, considering sociodemographic and lifestyle covariates, as well as fish consumption. Sex, ethnicity, and fish consumption interaction models were also run. Results: We found longer TL with higher pre- and postnatal THg blood concentrations, even at low-level THg exposure according to the RfD proposed by the US EPA. The prenatal association showed a significant linear relationship with a 3.46 % increase in TL for each unit increased THg. The postnatal association followed an inverted U-shaped marginal non-linear relationship with 1.38 % an increase in TL for each unit increased THg until reaching a cut-point at 0.96 μg/L blood THg, from which TL attrition was observed. Higher pre- and postnatal blood THg concentrations were consistently related to longer TL among cohorts and no modification effect of fish consumption nor children's sex was observed. No association between THg exposure and mtDNAcn was found. Discussion: We found evidence that THg is associated with TL but the associations seem to be time- and concentration-dependent. Further studies are needed to clarify the mechanism behind the telomere changes of THg and related health effects.
(Less)
- author
- organization
- publishing date
- 2024-07-01
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Fish consumption, Mercury, Mitochondrial DNA content, Oxidative stress, Telomere length
- in
- Science of the Total Environment
- volume
- 932
- article number
- 173014
- publisher
- Elsevier
- external identifiers
-
- scopus:85192957158
- pmid:38729362
- ISSN
- 0048-9697
- DOI
- 10.1016/j.scitotenv.2024.173014
- language
- English
- LU publication?
- yes
- id
- 26d9cba1-0224-412e-9be4-eff2259e8ed6
- date added to LUP
- 2024-05-23 15:53:48
- date last changed
- 2024-12-20 15:11:50
@article{26d9cba1-0224-412e-9be4-eff2259e8ed6, abstract = {{<p>Background: Telomere length (TL) and mitochondrial function expressed as mitochondrial DNA copy number (mtDNAcn) are biomarkers of aging and oxidative stress and inflammation, respectively. Methylmercury (MeHg), a common pollutant in fish, induces oxidative stress. We hypothesized that elevated oxidative stress from exposure to MeHg decreases mtDNAcn and shortens TL. Methods: Study participants are 6–11-year-old children from the HELIX multi-center birth cohort study, comprising six European countries. Prenatal and postnatal total mercury (THg) concentrations were measured in blood samples, TL and mtDNAcn were determined in child DNA. Covariates and confounders were obtained by questionnaires. Robust regression models were run, considering sociodemographic and lifestyle covariates, as well as fish consumption. Sex, ethnicity, and fish consumption interaction models were also run. Results: We found longer TL with higher pre- and postnatal THg blood concentrations, even at low-level THg exposure according to the RfD proposed by the US EPA. The prenatal association showed a significant linear relationship with a 3.46 % increase in TL for each unit increased THg. The postnatal association followed an inverted U-shaped marginal non-linear relationship with 1.38 % an increase in TL for each unit increased THg until reaching a cut-point at 0.96 μg/L blood THg, from which TL attrition was observed. Higher pre- and postnatal blood THg concentrations were consistently related to longer TL among cohorts and no modification effect of fish consumption nor children's sex was observed. No association between THg exposure and mtDNAcn was found. Discussion: We found evidence that THg is associated with TL but the associations seem to be time- and concentration-dependent. Further studies are needed to clarify the mechanism behind the telomere changes of THg and related health effects.</p>}}, author = {{Lozano, Manuel and McEachan, Rosemary R.C. and Wright, John and Yang, Tiffany C. and Dow, Courtney and Kadawathagedara, Manik and Lepeule, Johanna and Bustamante, Mariona and Maitre, Lea and Vrijheid, Martine and Brantsæter, Anne Lise and Meltzer, Helle Margrete and Bempi, Vasiliki and Roumeliotaki, Theano and Thomsen, Cathrine and Nawrot, Tim and Broberg, Karin and Llop, Sabrina}}, issn = {{0048-9697}}, keywords = {{Fish consumption; Mercury; Mitochondrial DNA content; Oxidative stress; Telomere length}}, language = {{eng}}, month = {{07}}, publisher = {{Elsevier}}, series = {{Science of the Total Environment}}, title = {{Early life exposure to mercury and relationships with telomere length and mitochondrial DNA content in European children}}, url = {{http://dx.doi.org/10.1016/j.scitotenv.2024.173014}}, doi = {{10.1016/j.scitotenv.2024.173014}}, volume = {{932}}, year = {{2024}}, }