Mitochondrial oxidative DNA damage and exposure to particulate air pollution in mother-newborn pairs
Open accessAbstract
BACKGROUND: Studies emphasize the importance of particulate matter (PM) in the formation of reactive oxygen species and inflammation. We hypothesized that PM exposure during different time windows in pregnancy influences mitochondrial 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, which is an established biomarker for oxidative stress, in both maternal and foetal blood. METHODS: We investigated maternal (n = 224) and cord blood (n = 293) from mother-newborn pairs that were enrolled in the ENVIRONAGE birth cohort. We determined mitochondrial 8-OHdG by quantitative polymerase chain reaction (qPCR). Multivariable regression models were used to assess the association between mitochondrial 8-OHdG with PM10 and PM2.5 exposure over various time windows during pregnancy. RESULTS: In multivariable analysis, PM10 exposure during the entire pregnancy was positively associated with levels of mitochondrial 8-OHdG in maternal blood. For an IQR increment in PM10 exposure an increase of 18.3 % (95 % confidence interval (CI): 5.6 to 33.4 %, p = 0.004) in 8-OHdG was observed. PM10 exposure during the last trimester of pregnancy was positively associated with levels of 8-OHdG (28.1, 95 % CI: 8.6 to 51.2 %, p = 0.004, for an IQR increment in PM10). In a similar way, PM2.5 exposure was significantly associated with an increase of mitochondrial 8-OHdG levels in maternal blood during the entire pregnancy (13.9, 95 % CI: 0.4 to 29.4 %, p = 0.04 for an IQR increment in PM2.5 exposure) and third trimester of pregnancy (28.1, 95 % CI: 3.6 to 58.4 %, p = 0.02 for an IQR increment in PM2.5 exposure). In umbilical cord blood, 8-OHdG levels were significantly associated with PM10 exposure during first and second trimester of pregnancy with respectively an increase of 23.0 % (95 % CI: 5.9 to 42.8 %, p = 0.007) and 16.6 % (95 % CI: 1.8 to 33.5 %, p = 0.03) for an IQR increment in PM10 exposure. CONCLUSIONS: We found PM-associated increased mitochondrial oxidative DNA damage during pregnancy in both mothers and their newborns. Accordingly, our study showed that particulate air pollution exposure in early life plays a role in increasing systemic oxidative stress, at the level of the mitochondria, both in mother and foetus.
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PM2.5 exposure during pregnancy was positively associated with markers of mitochondrial DNA damage in maternal blood.
“Grevendonk et al. [161] demonstrated PM2.5 exposure during pregnancy was positively associated with markers of mitochondrial DNA damage in maternal blood.”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [161]
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Result
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“Animal models showed that PM 2.5 (PM with diameter of 2.5 µ m or smaller) can cross the placenta and circulate in fetal blood, inducing oxidative stress and inflammatory responses in the growing fetus, thereby affecting fetal development [43,104,127–129].”
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Effects of maternal exposure to ambient air pollution on newborn telomere length
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Mitochondrial Function in Allergic Disease
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“[18] Exposure to ambient pollution in pregnancy can enhance systemic oxidative stress[19] and impact endocrine and immune system disruption[20] which in turn has implications for neuropsychological functioning in women during the perinatal period.”
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BackgroundCellular mechanisms linking to outdoor and indoor air pollution damage during pregnancy
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“(92) 293 mother-newborn pairs mixture PM2.”
BackgroundThe Impact of Oxidative Stress of Environmental Origin on the Onset of Placental Diseases
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Maternal Particulate Matter Exposure Impairs Lung Health and Is Associated with Mitochondrial Damage
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Neurodevelopmental toxicity induced by airborne particulate matter
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“5 and PM10 during gestation has been shown to induce mitochondrial oxidative stress in human maternal blood and fetal umbilical cord blood when sampled at delivery (Grevendonk et al., 2016).”
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Prenatal Exposure to Ambient Air Pollution and Epigenetic Aging at Birth in Newborns
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“Epidemiological and clinical studies have linked prenatal air pollution exposure to epigenetic alterations, inflammation, and oxidative stress (Janssen et al., 2013; Breton et al., 2016; Grevendonk et al., 2016; Saenen et al., 2016; Gruzieva et al., 2017; Breton et al., 2019).”
BackgroundPremature births in Spain: Measuring the impact of air pollution using time series analyses
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“One likely pathway manifested through inflammatory stress and endothelial function is the cardiovascular mechanisms (Brunst et al. 2018; Grevendonk et al. 2016; Rosa et al. 2017b; Kannan et al. 2006).”
BackgroundEffects of PM2.5 exposure during gestation on maternal gut microbiota and pregnancy outcomes.
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Long-term impact of ambient air pollution on preterm birth in Xuzhou, China: a time series study
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“…stress, inflammation, leading to DNA damage and accumulation in fetal tissues, and changes in the viscosity of the blood and the release of proinflammatory cytokines, including IL-6, IL-8, IL-10, and TNF-α (Clemente et al. 2016; Grevendonk et al. 2016; Peters et al. 1997; Sun et al. 2015).”
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“Air pollution exposure can lead to increased oxidative stress and mtDNA damage (Grevendonk et al., 2016), with several lines of research suggesting that this damage is linked to age-related endothelial and vascular dysfunction (Mikhed et al., 2015; Forstermann, 2008).”
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“Several studies have linked in-utero PM exposure to mitochondrial oxidative dysfunction (Grevendonk et al. 2016; Brunst et al. 2018; Cosemans et al. 2022).”
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“As previously shown, exposure to ambient PM during pregnancy has been found to be associated with increased levels of mitochondrial 8-hydroxy 2-deoxyguanine, which is considered to be a marker of oxidative DNA damage (Grevendonk et al., 2016) which was found to be correlated with loss of mtDNA (Qian and Van Houten, 20…”
BackgroundCentral metabolism of functionally heterogeneous mesenchymal stromal cells
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Does PM1 exposure during pregnancy impact the gut microbiota of mothers and neonates?
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“PM10 exposure is also associated with systemic inflammation [24]: inhalation of particles”
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Ambient Air Pollution and Congenital Heart Disease: Updated Evidence and Future Challenges
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“…vulnerability to environmental toxins, and it has been suggested that PM 2.5 exposure during the first trimester promotes mitochondrial DNA damage at the placenta, leading to oxidative stress, and interfering with the barrier function of this structure (Grevendonk et al., 2016; Tapia et al., 2020).”
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“5 and psychosocial stress during pregnancy are associated with oxidative stress.(10,11,27) Oxidative stress may influence AD pathogenesis.”
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“Upon inhalation, these DEP cause oxidative stress with accompanying in fl ammatory processes and DNA damage (Grevendonk et al., 2016; Ito et al., 2000; Ma and Ma, 2002; Shukla et al., 2000; Zhao et al., 2009).”
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Detection of Mitochondrial Toxicity of Environmental Pollutants UsingCaenorhabditis elegans
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Self-citationPrenatal Exposure to Fine Particulate Matter Components and Autism Risk in Childhood
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The telomere-mitochondrial axis of aging in newborns
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“The characteristic indexes were selected and detected from the aspects of oxidative stress, the level of inflammatory factors, and the intercellular communication between gap junctions (Bekki et al., 2016; Grevendonk et al., 2016).”
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“…via the olfactory nerve, where they instigate immune dysfunction via glial cells of the central nervous system, leading to oxidative DNA damage (Grevendonk et al., 2016), lipid peroxidation (Ambroz et al., 2016; Bernardi et al., 2021), and pathological white matter changes (Allen et al., 2017;…”
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“Exposure to ambient AP during pregnancy may further increase systemic oxidative stress [12, 13] and disrupt immune and endocrine system [14], which may have implications for women ’ s perinatal neuropsychological functioning [15].”
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“Air pollutants can inflict a range of cellular injuries by inducing the endoplasmic reticulum (ER) stress, promoting the accumulation of misfolded proteins [45] and causing DNA damage that can initiate repair mechanisms, enforce cell cycle arrest, or trigger apoptosis [46, 47].”
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“12 13–15 Air pollution particles can pass placenta and translocate directly toward fetus, 16,17 which induces inflammation, 18,19 oxidative/nitrosative stress, 13,14 and epigenetic alterations.”
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Effect Of Atmospheric Particulate Matter On The Functional State Of Mitochondria
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“This phenomenon can be observed in cells exposed to pollutants or in people living in a highly polluted environment [42-44].”
Background
- Authors
- Grevendonk, L., Janssen, B. G., Vanpoucke, C., Lefebvre, W., Hoxha, M., Bollati, V., & Nawrot, T. S.
- Affiliations
- University of Milan (IT)
- Hasselt University (BE)
- Flemish Institute for Technological Research (BE)
- Corresponding author
- Nawrot, Tim S.
- Venue
- Environmental Health
- Published
- 2016-01-20
- Volume
- 15
- Issue
- 1
- Pages
- 10-10
- ISSN
- 1476-069X (ISSN-L)
- PMC
- PMC4719654
- OpenAlex
- W2286090902
- Cited by
- 145
- References
- 43
- Citations by year
- 2026: 6 · 2025: 17 · 2024: 13 · 2023: 16 · 2022: 16 · 2021: 28 · 2020: 8 · 2019: 13 · 2018: 12 · 2017: 12 · 2016: 4
- FWCI
- 8.59
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Environmental Health (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Lirias (KU Leuven) (submittedVersion, cc-by)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- Document Server@UHasselt (UHasselt) (submittedVersion, cc-by)
- Funders
- EU Programme “Ideas” (ERC-2011-StG 282413)
- EU Program “Ideas” (ERC-2012-StG 310898)
- Flemish Scientific Fund (FWO) (N1516112/G.0.873.11.N.10)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Health, Environment, Cognitive Aging
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Indoor Air Quality and Microbial Exposure
- Keywords
- particulate matter, PM10, PM2.5, prenatal air pollution exposure, 8-hydroxy-2'-deoxyguanosine, oxidative stress, maternal blood, umbilical cord blood, pregnancy trimesters, ENVIRONAGE birth cohort, prenatal exposure, birth cohort studies, biomarkers of exposure, inflammation, reactive oxygen species
- MeSH terms
- Adult, Air Pollutants, DNA, Mitochondrial, Environmental Exposure, Female, Fetal Blood, Humans, Infant, Newborn, Placenta, Pregnancy, Cohort Studies, Maternal Exposure, Particulate Matter, Young Adult
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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