The DOI matches its Crossref record; 39 of the 43 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Toxic potential of materials at the nanolevel
Nel, A., Xia, T., Mädler, L., & Li, N. (2006) · Science · doi:10.1126/science.1114397 · Cited by 9,324 · cited 1×
“risk factor for the induction of inflammatory and oxidative stress responses [1–4], especially during the pregnancy period when increased levels of oxidative stress can be expected [5].”
BackgroundHellemans, J., Mortier, G., De Paepe, A., Speleman, F., & Vandesompele, J. (2007) · Genome Biology · doi:10.1186/gb-2007-8-2-r19 · Cited by 4,023 · cited 2×
“qBase software (Biogazelle, Zwijnaarde, BE) was used to normalize data and correct for run-to-run differences [22].”
MethodYakes, F. M., & Van Houten, B. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.2.514 · Cited by 1,854 · cited 1×
“be more extensive and persistent compared to nuclear DNA damage [30].”
Background8-Hydroxyguanine, an abundant form of oxidative DNA damage, causes G-T and A-C substitutions.
Cheng, K. C., Cahill, D. S., Kasai, H., Nishimura, S., & Loeb, L. A. (1992) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)48474-8 · Cited by 1,844 · cited 1×
“the most common one [7].”
Li, N., Xia, T., & Nel, A. E. (2008) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2008.01.028 · Cited by 949
Human mitochondrial DNA: roles of inherited and somatic mutations
Schon, E. A., DiMauro, S., & Hirano, M. (2012) · Nature Reviews Genetics · doi:10.1038/nrg3275 · Cited by 757 · cited 1×
“Besides metabolic disorders, the stochastic accumulation of mtDNA mutations encompasses the pathophysiological basis of disease processes including aging, neurodegenerative diseases, and cancer [38].”
BackgroundChuang, K.-J., Chan, C.-C., Su, T.-C., Lee, C.-T., & Tang, C.-S. (2007) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.200611-1627oc · Cited by 685 · cited 1×
“Consistent with our results, most of these studies observed a positive association between nuclear 8-OHdG levels in urine and PM exposure [14–16, 23–25] or tobacco smoke exposure [16, 26–29].”
ResultMitochondrial DNA Genetics and the Heteroplasmy Conundrum in Evolution and DiseasePreprint
Dc, W., & Chalkia, D. (2013) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a021220 · Cited by 680 · cited 1×
“If accumulation of 8-OHdG and somatic mtDNA mutations exceed a critical threshold, they can cause a biochemical defect in the mitochondrial respiratory chain and could result in a progressive decline of mitochondrial function [10, 34, 36].”
BackgroundLoft, S., Vistisen, K., Ewertz, M., Tjønneland, A., Overvad, K., & Poulsen, H. E. (1992) · Carcinogenesis · doi:10.1093/carcin/13.12.2241 · Cited by 643
Universal heteroplasmy of human mitochondrial DNA
Payne, B. A. I., Wilson, I., Yu‐Wai‐Man, P., Coxhead, J., Deehan, D. J., Horváth, R., Taylor, R. W., Samuels, D. C., Santibanez‐Koref, M., & Chinnery, P. F. (2012) · Human Molecular Genetics · doi:10.1093/hmg/dds435 · Cited by 396 · cited 2×
“Moreover, the mtDNA repair mechanisms work less efficiently resulting in a 5 to 15 times higher mutation rate compared with nDNA [6, 9].”
Background
Research works printed but not linked: 2
- de Souza-Pinto NC, Eide L, Hogue BA, Thybo T, Stevnsner T, Seeberg E, et al. Repair of 8-oxodeoxyguanosine lesions in mitochondrial dna depends on the oxoguanine dna glycosylase (OGG1) gene and 8-oxoguanine accumulates in the mitochondrial dna of OGG1-defective mice. Cancer Res. 2001;61(14):5378–81.
- Sorensen M, Autrup H, Hertel O, Wallin H, Knudsen LE, Loft S. Personal exposure to PM2.5 and biomarkers of DNA damage. Cancer Epidemiol Biomarkers Prev. 2003;12(3):191–6.
Cited by
Sorted by citations
Items 101–120 of 120
Gehring, U., & Gascón, M. (2022) · Environmental Health Perspectives · doi:10.1289/ehp11224 · Cited by 4
Framing Fetal and Early Life Exposome Within Epidemiology
Laine, J. E., & Robinson, O. (2018) · Springer eBooks · doi:10.1007/978-3-319-89321-1_4 · Cited by 6
Chen, B., Chen, S., Duan, L., Zhang, M., Liu, X., & Duan, Y. (2022) · BMC Pediatrics · doi:10.1186/s12887-022-03328-9 · Cited by 2
“PM10 is known as a kind of inhalable particle with aerodynamic diameter of 10 microns or less, and it can enter the human respiratory tract, inducing systematic inflammation [23] and oxidative damage to both mother and fetus[24].”
BackgroundEpigenetic Epidemiology for Cancer Risk
Barrow, T. M. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-809552-2.00008-5 · Cited by 2
Hahad, O., Kuntić, M., Al-Kindi, S. G., Lelieveld, J., Cheng, Y., Schmitt, V. H., Hobohm, L. H., Keller, K., Kerahrodi, J. G., Faridi, S., et al. (2026) · Journal of Environmental Health Science and Engineering · doi:10.1007/s40201-026-00990-4 · Cited by 2
“A significant source and target of oxidative stress is air pollution-induced mitochondrial damage and dysfunction, which has been observed in human studies [61 –64 ].”
InfluentialParikh, G., Chhapia, P., Maity, P., & Patel, B. M. (2026) · Methods · doi:10.1016/j.ymeth.2026.05.002 · Cited by 1
Peuters, C., Birulés, J., Galmés, T., Basagaña, X., Domínguez, A., Foraster, M., Gómez-Herrera, L., Gómez‐Roig, M. D., Llurba, E., Rivas, I., et al. (2025) · Environmental Pollution · doi:10.1016/j.envpol.2025.127496 · Cited by 1
Yu, Z., Wang, C., Lv, Y., Chang, M., Wang, H., Du, Y., Li, X., Jin, J., & Guan, S. (2025) · Toxics · doi:10.3390/toxics13110983 · Cited by 1
Rasking, L., Vanbrabant, K., Vangeneugden, M., Pee, T. V., Cassee, F., Bové, H., Vusser, K. D., Plusquin, M., & Nawrot, T. (2025) · Journal of Hazardous Materials Advances · doi:10.1016/j.hazadv.2025.100790 · Cited by 1
Self-citationMorris, R. H., Chabrier, G., Counsell, S. J., McGonnell, I. M., & Thornton, C. (2022) · Developmental Neuroscience · doi:10.1159/000524829 · Cited by 3
Rodulfo-Cárdenas, R., Biosca-Brull, J., Barberà-Parada, S., Gabaldón-Díaz, R., Ruiz-Sobremazas, D., Blanco, J., Cabré, M., Domingo, J. L., López-Granero, C., Sánchez-Santed, F., et al. (2026) · Neurotoxicology · doi:10.1016/j.neuro.2026.103580
Breathing in harm: current insights into the effects of air pollution on cardiorespiratory health
Michou, V., Tsamos, D., Itziou, A., & Tsanaktsidis, C. (2026) · Medical Gas Research · doi:10.4103/mgr.medgasres-d-25-00201
Shajravi, A., Chamani, A., Sobhanardakani, S., & Zamanpour, Z. (2026) · International Journal of Environmental Health Research · doi:10.1080/09603123.2026.2701102
Ilia, E., Papoutsis, D., Michou, V., & Itziou, A. (2026) · Current Issues in Molecular Biology · doi:10.3390/cimb48060575
“Our findings align with previous research that supports the impact of air pollution on systemic oxidative stress in pregnant women [30].”
Chen, J., Wang, Y., Zhu, J., Fang, J., Li, P., Guo, L., & Wu, S. (2026) · Journal of Hazardous Materials · doi:10.1016/j.jhazmat.2026.142402
Cho, S., Oh, J., Kim, E., Kim, H., 조은혜, Kim, J., Ha, E., & Kim, Y. (2026) · Environmental Research · doi:10.1016/j.envres.2026.124720
Li, X., Zhu, X., Chen, D., Zhao, Y., Deng, X., Zhan, Y., Guo, B., Xu, T., & Wang, X. (2025) · Atmospheric Environment · doi:10.1016/j.atmosenv.2025.121511
Yang, S., Zhang, G., Hong, X., Li, T., Liu, Y., Hong, H., Liu, L., Wang, H., Wu, S.-P., Wang, Y., et al. (2025) · Reproductive Toxicology · doi:10.1016/j.reprotox.2025.108906
Huang, S., Chen, Y., Huang, Y., Li, J., Liu, S., Chen, Z., Jiang, C., Li, L., & Zhou, C. (2020) · doi:10.21203/rs.3.rs-31608/v1
“Recent studies have suggested that prenatal PM10 exposure during the last trimester of pregnancy may cause mitochondrial dysfunction and shorten the lengths of telomeres in the cells of newborns [33, 34, 35].”
BackgroundAir Pollution and Cigarettes Cloud Development
Finch, C. E. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-813102-2.00004-2
Metadata
- 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 ›
Are you an author, or do you see a problem with this page? Request a review
