ArticleEnvironmental health perspectives2016
Prenatal Ambient Air Pollution, Placental Mitochondrial DNA Content, and Birth Weight in the INMA (Spain) and ENVIRONAGE (Belgium) Birth Cohorts.
Article in Environmental health perspectives, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 3 of them syntheses that pooled it.
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Who cites it
70 citing papers in PubMed, 3 syntheses or guidelines pooled it, 140 citations in OpenAlex.
- Association between atmospheric particulate matter pollution during pregnancy and premature birth in China: a meta-analysis.Frontiers in public health · 2025Pooled it
- Prenatal air pollution exposure in relation to the telomere-mitochondrial axis of aging at birth: A systematic review.Environmental research · 2024Pooled it
- Adverse Birth Outcomes Related to NOInternational journal of environmental research and public health · 2020Pooled it
- Prenatal Household Air Pollution Alters Cord Blood Mononuclear Cell Mitochondrial DNA Copy Number: Sex-Specific Associations.International journal of environmental research and public health · 2018Trial
- Air pollution and adverse birth outcomes: a narrative review of epidemiological and mechanistic findings.Journal of environmental health science & engineering · 2026Review
- Traffic-Related Air Pollution and Birth Weight: The Roles of Noise, Placental Function, Green Space, Physical Activity, and Socioeconomic Status (FRONTIER).Research report (Health Effects Institute) · 2026Article
- An exploratory analysis of miRNAs measured in placental tissue and their associations with prenatal exposure to household air pollution.Environmental epigenetics · 2026Article
- FIGO committee opinion: Environmental drivers of gynecologic and reproductive health.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2025Article
- FIGO committee opinion: Environmental drivers of obstetric health and early childhood development.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2025Article
- Air pollution exposure during pregnancy and low birth weight and macrosomia: the role of gestational diabetes mellitus.Reproductive health · 2025Article
- Ambient Air Pollution and Congenital Heart Disease: Updated Evidence and Future Challenges.Antioxidants (Basel, Switzerland) · 2025Review
- Association of fetal growth trajectory with mitochondrial DNA copy number in the cord blood of newborns: evidence from a birth cohort.Frontiers in pediatrics · 2025Article
- Interpregnancy interval, air pollution, and the risk of low birth weight: a retrospective study in China.BMC public health · 2024Article
- Newborn glomerular function and gestational particulate air pollution.EBioMedicine · 2024Article
- Prenatal PMToxics · 2024Review
- Exosome-encapsulated lncRNA HOTAIRM1 contributes to PMScience China. Life sciences · 2024Article
- Ambient air pollution and adverse birth outcomes: A review of underlying mechanisms.BJOG : an international journal of obstetrics and gynaecology · 2024Review
- Prenatal exposure to air pollution and BWGA Z-score: Modifying effects of placenta leukocyte telomere length and infant sex.Environmental research · 2024Article
- Umbilical cord blood thyroid hormones are inversely related to telomere length and mitochondrial DNA copy number.Scientific reports · 2024Article
- Maternal mitochondrial DNA copy number and methylation as possible predictors of pregnancy outcomes in a Michigan pregnancy cohort.Environmental epigenetics · 2024Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors at 13 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMitochondria are sensitive to environmental toxicants due to their lack of repair capacity. Changes in mitochondrial DNA (mtDNA) content may represent a biologically relevant intermediate outcome in mechanisms linking air pollution and fetal growth restriction.
objectiveWe investigated whether placental mtDNA content is a possible mediator of the association between prenatal nitrogen dioxide (NO2) exposure and birth weight.
methodsWe used data from two independent European cohorts: INMA (n = 376; Spain) and ENVIRONAGE (n = 550; Belgium). Relative placental mtDNA content was determined as the ratio of two mitochondrial genes (MT-ND1 and MTF3212/R3319) to two control genes (RPLP0 and ACTB). Effect estimates for individual cohorts and the pooled data set were calculated using multiple linear regression and mixed models. We also performed a mediation analysis.
resultsPooled estimates indicated that a 10-μg/m3 increment in average NO2 exposure during pregnancy was associated with a 4.9% decrease in placental mtDNA content (95% CI: -9.3, -0.3%) and a 48-g decrease (95% CI: -87, -9 g) in birth weight. However, the association with birth weight was significant for INMA (-66 g; 95% CI: -111, -23 g) but not for ENVIRONAGE (-20 g; 95% CI: -101, 62 g). Placental mtDNA content was associated with significantly higher mean birth weight (pooled analysis, interquartile range increase: 140 g; 95% CI: 43, 237 g). Mediation analysis estimates, which were derived for the INMA cohort only, suggested that 10% (95% CI: 6.6, 13.0 g) of the association between prenatal NO2 and birth weight was mediated by changes in placental mtDNA content.
conclusionOur results suggest that mtDNA content can be one of the potential mediators of the association between prenatal air pollution exposure and birth weight. CITATION: Clemente DB, Casas M, Vilahur N, Begiristain H, Bustamante M, Carsin AE, Fernández MF, Fierens F, Gyselaers W, Iñiguez C, Janssen BG, Lefebvre W, Llop S, Olea N, Pedersen M, Pieters N, Santa Marina L, Souto A, Tardón A, Vanpoucke C, Vrijheid M, Sunyer J, Nawrot TS. 2016. Prenatal ambient air pollution, placental mitochondrial DNA content, and birth weight in the INMA (Spain) and ENVIRONAGE (Belgium) birth cohorts. Environ Health Perspect 124:659-665; http://dx.doi.org/10.1289/ehp.1408981.
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