Evidence map›Paper›PMID 26792633›Full record

ArticleEnvironmental health : a global access science source2016

Mitochondrial oxidative DNA damage and exposure to particulate air pollution in mother-newborn pairs.

Lotte Grevendonk, Bram G Janssen, Charlotte Vanpoucke, Wouter Lefebvre, Mirjam Hoxha, Valentina Bollati, Tim S Nawrot

Abstract read
In one paragraph

Article in Environmental health : a global access science source, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  15. Ambient air pollution and adverse birth outcomes: A review of underlying mechanisms.BJOG : an international journal of obstetrics and gynaecology · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Lotte GrevendonkEPIGET-Epidemiology, Epigenetics and Toxicology Lab-Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy. lotte.grevendonk@unimi.it.
Bram G JanssenCentre for Environmental Sciences, Hasselt University, Hasselt, Belgium. bram.janssen@uhasselt.be.
Charlotte VanpouckeBelgian Interregional Environment Agency, Brussels, Belgium. vanpoucke@irceline.be.
Wouter LefebvreFlemish Institute for Technological Research (VITO), Mol, Belgium. wouter.lefebvre@vito.be.
Mirjam HoxhaEPIGET-Epidemiology, Epigenetics and Toxicology Lab-Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy. mirjam.hoxha@unimi.it.
Valentina BollatiEPIGET-Epidemiology, Epigenetics and Toxicology Lab-Department of Clinical Sciences and Community Health, Università degli Studi di Milano, Milan, Italy. valentina.bollati@unimi.it.
Tim S NawrotCentre for Environmental Sciences, Hasselt University, Hasselt, Belgium. tim.nawrot@uhasselt.be.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundStudies 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.

methodsWe 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.

resultsIn 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.

conclusionsWe 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.

Indexed as

AdultAir PollutantsCohort StudiesDNA, MitochondrialEnvironmental ExposureFemaleFetal BloodHumansInfant, NewbornMaternal ExposureParticulate MatterPlacentaPregnancyYoung AdultAir PollutantsDNA, MitochondrialParticulate Matter

Identifiers

PMID26792633
PMCPMC4719654

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.