Evidence map›Paper›PMID 38565416›Full record

ArticleEnvironmental research2024

Joint effects of prenatal exposure to indoor air pollution and psychosocial factors on early life inflammation.

Grace M Christensen, Michele Marcus, Petrus J W Naudé, Aneesa Vanker, Stephanie M Eick, W Michael Caudle, Susan Malcolm-Smith, Shakira F Suglia, Howard H Chang, Heather J Zar and 2 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Environmental research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
2.5field-weighted citation impact, top 12% of its field
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

1 citing paper in PubMed, 8 citations in OpenAlex.

  1. Review
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

12 authors at 3 institutions in 2 countries.

Grace M ChristensenDepartment of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
Michele MarcusDepartment of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, USA; Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
Petrus J W NaudéDepartment of Psychiatry and Mental Health, University of Cape Town, Cape Town, South Africa; Neuroscience Institute, University of Cape Town, Cape Town, South Africa.
Aneesa VankerDepartment of Paediatrics and Child Health, Red Cross War Memorial Children's Hospital, University of Cape Town, Cape Town, South Africa.
Stephanie M EickDepartment of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, USA; Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
W Michael CaudleGangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
Susan Malcolm-SmithDepartment of Psychiatry and Mental Health, University of Cape Town, Cape Town, South Africa; Neuroscience Institute, University of Cape Town, Cape Town, South Africa.
Shakira F SugliaDepartment of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
Howard H ChangGangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA; Department of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
Heather J ZarDepartment of Paediatrics and Child Health, Red Cross War Memorial Children's Hospital, University of Cape Town, Cape Town, South Africa; South African Medical Research Council (SAMRC) Unit on Risk and Resilience in Mental Disorders, University of Cape Town, Cape Town, South Africa.
Dan J SteinDepartment of Psychiatry and Mental Health, University of Cape Town, Cape Town, South Africa; Neuroscience Institute, University of Cape Town, Cape Town, South Africa; South African Medical Research Council (SAMRC) Unit on Risk and Resilience in Mental Disorders, University of Cape Town, Cape Town, South Africa.
Anke HülsDepartment of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA, USA; Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA. Electronic address: anke.huels@emory.edu.
Emory University · USUniversity of Cape Town · ZASouth African Medical Research Council · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is hypothesized that air pollution and stress impact the central nervous system through neuroinflammatory pathways Despite this, the association between prenatal exposure to indoor air pollution and psychosocial factors on inflammatory markers in infancy has been underexplored in epidemiology studies. This study investigates the individual and joint effects of prenatal exposure to indoor air pollution and psychosocial factors on early life inflammation (interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α)). We analyzed data from the South African Drakenstein Child Health Study (N = 225). Indoor air pollution and psychosocial factor measurements were taken in the 2nd trimester of pregnancy. Circulating inflammatory markers (IL-1β, Il-6, and TNF-α) were measured in serum in the infants at 6 weeks postnatal. Linear regression models were used to investigate associations between individual exposures and inflammatory markers. To investigate joint effects of environmental and psychosocial factors, Self-Organizing Maps (SOM) were used to create exposure profile clusters. These clusters were added to linear regression models to investigate the associations between exposure profiles and inflammatory markers. All models were adjusted for maternal age, maternal HIV status, and ancestry to control for confounding. Most indoor air pollutants were positively associated with inflammatory markers, particularly benzene and TNF-α in single pollutant models. No consistent patterns were found for psychosocial factors in single-exposure linear regression models. In joint effects analyses, the SOM profile with high indoor air pollution, low SES, and high maternal depressive symptoms were associated with higher inflammation. Indoor air pollutants were consistently associated with increased inflammation in both individual and joint effects models, particularly in combination with low SES and maternal depressive symptoms. The trend for individual psychosocial factors was not as clear, with mainly null associations. As we have observed pro- and anti-inflammatory effects, future research should investigate joint effects of these exposures on inflammation and their health effects.

Indexed as

Air Pollution, IndoorInflammationPrenatal Exposure Delayed EffectsAdultBiomarkersFemaleHumansInfantMaleMaternal ExposurePregnancySouth AfricaYoung AdultBiomarkersAir pollutionInflammatory markersNeuroinflammationPsychosocial factors

Identifiers

PMID38565416
PMCPMC11188991
OpenAlexW4393359373

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.