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Editorial: The impact of exposure to environmental chemicals, pharmaceuticals and particles via human breast milk: a focus on health effects and underlying mechanisms
No full textThe author(s) declare that financial support was received for the research and/or publication of this article. Charlotte Cosemans was financially supported by the Research Foundation Flanders (FWO; 1249025N)
The role of the exposome on molecular biomarkers: focus on mitochondria and telomeres in different stages of life
No full textThe exposome refers to the totality of life-course environmental exposures from
conception onwards and evolves throughout the lifetime of an individual. It offers
an opportunity to better understand the impact of the environment on human
health in different stages of life, ultimately leading to better prevention strategies.
It has already been known that environmental exposures, such as air pollution,
have detrimental effects on molecular biomarkers, like mitochondria and
telomeres. However, the role of mitochondria and telomeres in the exposome is
still underexplored. In this dissertation, we aim to tackle some of these knowledge
gaps between different domains of the exposome and mitochondria and telomeres
in newborns, childhood, adolescence, and adulthood.
In the first section, we investigate the influence of lifestyle exposure on
mitochondria. One example of a lifestyle exposure is the diet. In Chapter 1, we
aim to investigate the link between breastfeeding during infancy and blood
mitochondrial DNA content in adolescents.
The second section focuses on the influence of physical & chemical exposures
on both mitochondria and telomeres. In Chapter 2, we aim to investigate the
impact of prenatal air pollution exposure on a specific mitochondrial variant
(ND4L10550A>G) in newborns by studying cord blood. Furthermore, the link of this
variant with childhood overweight is examined. Since prenatal air pollution might
also influence other mitochondrial mutations, the link between prenatal air
pollution and mitochondrial heteroplasmy in cord blood is investigated in Chapter
3. Lastly, in Chapter 4, we study another type of physical & chemical exposure,
namely the herbicide glyphosate. In this chapter, we aim to investigate the
association between both glyphosate and its degradation metabolite
aminomethylphosphonic acid (AMPA) on mitochondria, as well as on telomeres in
peripheral blood of adults.
The key findings of this dissertation are concisely summarized in Table 1. In
summary, we found several environmental exposures to be linked with
mitochondria and telomeres. Breastfeeding during infancy and prenatal air
pollution were both associated with mitochondrial biology. When focusing on telomeres, we found an association between AMPA exposure and longer leukocyte
telomere length.
Based on the findings of this thesis, we formulate advice for policy and our society:
i) keep promoting breastfeeding as the optimal nutrition for developing infants;
ii) reduce ambient air pollution concentrations for example to levels of the new
WHO guidelines; and iii) consider and further investigate the possible carcinogenic
mechanism as demonstrated by longer leukocyte telomere length associated with
AMPA exposure, for extending the permission of glyphosate use from December
2022 onwards.Het exposoom verwijst naar het geheel van milieublootstellingen gedurende de
levensloop, startend vanaf de conceptie, en evolueert gedurende het leven van
een individu. Het biedt de mogelijkheid om de impact van de omgeving op de
menselijke gezondheid in verschillende levensfasen beter te begrijpen, wat
uiteindelijk leidt tot betere preventiestrategieën. Het is al bekend dat
milieublootstellingen, zoals luchtvervuiling, schadelijke effecten hebben op
moleculaire biomarkers, zoals mitochondriën en telomeren. De rol van
mitochondriën en telomeren in het exposoom is echter nog steeds onvoldoende
onderzocht. In dit proefschrift willen we een aantal van deze kenniskloven
aanpakken tussen de verschillende domeinen van het exposoom en mitochondriën
en telomeren bij pasgeborenen, de kindertijd, de adolescentie en de
volwassenheid.
In het eerste deel onderzoeken we de invloed van de levensstijl op
mitochondriën. Eén van de factoren van de levensstijl is voeding. In Hoofdstuk
1 willen we het verband onderzoeken tussen borstvoeding tijdens de kindertijd en
mitochondriaal DNA-inhoud in bloed bij adolescenten.
Het tweede deel richt zich op de invloed van fysische en chemische
blootstellingen op zowel mitochondriën als telomeren. In Hoofdstuk 2 willen we
de impact onderzoeken van prenatale blootstelling aan luchtverontreiniging op
een specifieke mitochondriale variant (ND4L10550A>G) in pasgeborenen door het
bestuderen van navelstrengbloed. Verder wordt het verband van deze variant met
overgewicht bij kinderen onderzocht. Aangezien prenatale luchtverontreiniging
ook andere mitochondriale mutaties kan beïnvloeden, wordt het verband tussen
prenatale luchtverontreiniging en mitochondriale heteroplasmie in
navelstrengbloed onderzocht in Hoofdstuk 3. Ten slotte bestuderen we in
Hoofdstuk 4 een ander type fysieke en chemische blootstelling, namelijk het
herbicide glyfosaat. In dit hoofdstuk willen we de associatie onderzoeken tussen
zowel glyfosaat als zijn afbraakmetaboliet aminomethylfosfonzuur (AMPA) op
zowel mitochondriën als telomeren in bloed van volwassenen.
De belangrijkste bevindingen van dit proefschrift zijn beknopt samengevat in
Tabel 1. We toonden aan dat verschillende blootstellingen geassocieerd waren met mitochondriën. Borstvoeding tijdens de kindertijd en prenatale luchtvervuiling
waren beide geassocieerd met mitochondriale biologie. Als we kijken naar
telomeren, vonden we een verband tussen AMPA-blootstelling en een langere
telomeerlengte.
Op basis van de bevindingen van dit proefschrift formuleren we adviezen voor
beleidsmakers en onze samenleving: i) borstvoeding te blijven promoten als de
optimale voeding voor zuigelingen in ontwikkeling; ii) de concentraties van
luchtverontreiniging in de lucht te verlagen tot bijvoorbeeld het niveau van de
nieuwe WHO-richtlijnen; en iii) het mogelijk kankerverwekkend mechanisme
aangetoond door langere telomeerlengte geassocieerd met AMPA-blootstelling te
overwegen en verder te onderzoeken, alvorens de toestemming voor
glyfosaatgebruik vanaf december 2022 te verlengen
Prenatal particulate matter exposure is linked with neurobehavioral development in early life
No full textExploring mitochondrial heteroplasmy in neonates: implications for growth patterns and overweight in the first years of life
No full textBackground: Mitochondrial heteroplasmy reflects genetic diversity within individuals due to the presence of varying mitochondrial DNA (mtDNA) sequences, possibly affecting mitochondrial function and energy production in cells. Rapid growth during early childhood is a critical development with long-term implications for health and well-being. In this study, we investigated if cord blood mtDNA heteroplasmy is associated with rapid growth at 6 and 12 months and overweight in childhood at 4-6 years.
Methods: This study included 200 mother-child pairs of the ENVIRONAGE birth cohort. Whole mitochondrial genome sequencing was performed to determine mtDNA heteroplasmy levels (in variant allele frequency; VAF) in cord blood. Rapid growth was defined for each child as the difference between WHO-SD scores of predicted weight at either 6 or 12 months and birth weight. Logistic regression models were used to determine the association of mitochondrial heteroplasmy with rapid growth and childhood overweight. Determinants of relevant cord blood mitochondrial heteroplasmies were identified using multiple linear regression models.
Results: One % increase in VAF of cord blood MT-D-Loop16362T > C heteroplasmy was associated with rapid growth at 6 months (OR = 1.03; 95% CI: 1.01-1.05; p = 0.001) and 12 months (OR = 1.02; 95% CI: 1.00-1.03; p = 0.02). Furthermore, this variant was associated with childhood overweight at 4-6 years (OR = 1.01; 95% CI 1.00-1.02; p = 0.05). Additionally, rapid growth at 6 months (OR = 3.00; 95% CI: 1.49-6.14; p = 0.002) and 12 months (OR = 4.05; 95% CI: 2.06-8.49; p C heteroplasmy.
Conclusions: Our findings, based on mitochondrial DNA genotyping, offer insights into the molecular machinery leading to rapid growth in early life, potentially explaining a working mechanism of the development toward childhood overweight.The ENVIRONAGE birth cohort is supported by the Methusalem Fund, the Research
Foundation Flanders (FWO, grant numbers 1516112N, G.0873.11.N.10), and Kom op
Tegen Kanker. CC was financially supported by the Special Research Fund of Hasselt
University (grant number BOF22PD04) and Fund Orcadia (grant number 2022-
E2210890-228297), managed by the King Baudouin Foundation. FWO financially
supported RA (grant number 1296523N) and DSM (grant number 12X9623N). The
authors are extremely grateful to the participating women and neonates, as well as
the staff of the maternity ward, midwives, and the staff of the clinical laboratory of
East-Limburg Hospital in Genk
Prenatal particulate matter exposure is linked with neurobehavioral development in early life
No full textPrenatal particulate matter exposure is linked with neurobehavioral development in early life
No full textPrenatal particulate matter exposure is linked with neurobehavioral development in early life
No full text
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
The association between newborn cord blood steroids and ambient prenatal exposure to air pollution: findings from the ENVIRONAGE birth cohort
No full textAbstract Knowledge of whether prenatal exposure to ambient air pollution disrupts steroidogenesis is currently lacking. We investigated the association between prenatal ambient air pollution and highly accurate measurements of cord blood steroid hormones from the androgenic pathway. This study included 397 newborns born between the years 2010 and 2015 from the ENVIRONAGE cohort in Belgium of whom six cord blood steroid levels were measured: 17α-hydroxypregnenolone, 17α-hydroxyprogesterone, dehydroepiandrosterone, pregnenolone, androstenedione, and testosterone. Maternal ambient exposure to PM2.5 (particles with aerodynamic diameter ≤ 2.5 μm), NO2, and black carbon (BC) were estimated daily during the entire pregnancy using a high-resolution spatiotemporal model. The associations between the cord blood steroids and the air pollutants were tested and estimated by first fitting linear regression models and followed by fitting weekly prenatal exposures to distributed lag models (DLM). These analyses accounted for possible confounders, coexposures, and an interaction effect between sex and the exposure. We examined mixture effects and critical exposure windows of PM2.5, NO2 and BC on cord blood steroids via the Bayesian kernel machine regression distributed lag model (BKMR-DLM). An interquartile range (IQR) increment of 7.96 µg/m3 in PM2.5 exposure during pregnancy trimester 3 was associated with an increase of 23.01% (99% confidence interval: 3.26–46.54%) in cord blood levels of 17α-hydroxypregnenolone, and an IQR increment of 0.58 µg/m³ in BC exposure during trimester 1 was associated with a decrease of 11.00% (99% CI: -19.86 to -0.012%) in cord blood levels of androstenedione. For these two models, the DLM statistics identified sensitive gestational time windows for cord blood steroids and ambient air pollution exposures, in particular for 17α-hydroxypregnenolone and PM2.5 exposure during trimester 3 (weeks 28–36) and for androsterone and BC exposure during early pregnancy (weeks 2–13) as well as during mid-pregnancy (weeks 18–26). We identified interaction effects between pollutants, which has been suggested especially for NO2. Our results suggest that prenatal exposure to ambient air pollutants during pregnancy interferes with steroid levels in cord blood. Further studies should investigate potential early-life action mechanisms and possible later-in-life adverse effects of hormonal disturbances due to air pollution exposure
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