Evidence map›Paper›PMID 35902457›Full record

ReviewCurrent environmental health reports2022

Environmental Chemical Exposures and Mitochondrial Dysfunction: a Review of Recent Literature.

Aalekhya Reddam, Sarah McLarnan, Allison Kupsco

Open access · hybridAbstract readReview
In one paragraph

Review in Current environmental health reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
11.2field-weighted citation impact, top 1% 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

75 citing papers in PubMed, 141 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Cellular responses of human Muller glia exposed to test dust pollution.Environmental pollution (Barking, Essex : 1987) · 2026
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

15 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Aalekhya ReddamDepartment of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722 W 168th St, New York, NY, 10032, USA.
Sarah McLarnanDepartment of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722 W 168th St, New York, NY, 10032, USA.
Allison KupscoDepartment of Environmental Health Sciences, Mailman School of Public Health, Columbia University, 722 W 168th St, New York, NY, 10032, USA. ak4181@cumc.columbia.edu.ORCID 0000-0001-8760-2730
Columbia University · US

Funding

Prenatal Exposures to Flame-Retardants: Mitochondrial Signatures and Childhood ObesityR00ES030749 · NIEHS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI KUPSCO, ALLISON · 2021 to 2023
$639k
NIEHS NIH HHS R00 ES030749
6 · The paper itself

Abstract

purpose of reviewMitochondria play various roles that are important for cell function and survival; therefore, significant mitochondrial dysfunction may have chronic consequences that extend beyond the cell. Mitochondria are already susceptible to damage, which may be exacerbated by environmental exposures. Therefore, the aim of this review is to summarize the recent literature (2012-2022) looking at the effects of six ubiquitous classes of compounds on mitochondrial dysfunction in human populations. RECENT

findingsThe literature suggests that there are a number of biomarkers that are commonly used to identify mitochondrial dysfunction, each with certain advantages and limitations. Classes of environmental toxicants such as polycyclic aromatic hydrocarbons, air pollutants, heavy metals, endocrine-disrupting compounds, pesticides, and nanomaterials can damage the mitochondria in varied ways, with changes in mtDNA copy number and measures of oxidative damage the most commonly measured in human populations. Other significant biomarkers include changes in mitochondrial membrane potential, calcium levels, and ATP levels. This review identifies the biomarkers that are commonly used to characterize mitochondrial dysfunction but suggests that emerging mitochondrial biomarkers, such as cell-free mitochondria and blood cardiolipin levels, may provide greater insight into the impacts of exposures on mitochondrial function. This review identifies that the mtDNA copy number and measures of oxidative damage are commonly used to characterize mitochondrial dysfunction, but suggests using novel approaches in addition to well-characterized ones to create standardized protocols. We identified a dearth of studies on mitochondrial dysfunction in human populations exposed to metals, endocrine-disrupting chemicals, pesticides, and nanoparticles as a gap in knowledge that needs attention.

Indexed as

Environmental ExposureHumansMitochondriaEnvironmental chemicalsHeteroplasmyMitochondrial dysfunctionmtDNAOxidative stress

Identifiers

PMID35902457
PMCPMC9729331
OpenAlexW4288441895

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.