Evidence map›Paper›PMID 32926486›Full record

ArticleEnvironmental and molecular mutagenesis2020

Genotoxicity as a toxicologically relevant endpoint to inform risk assessment: A case study with ethylene oxide.

Bala Bhaskar Gollapudi, Steave Su, Abby A Li, George E Johnson, Richard Reiss, Richard J Albertini

Open access · bronzeAbstract read
In one paragraph

Article in Environmental and molecular mutagenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Use of updated mortality study of ethylene oxide manufacturing workers to inform cancer risk assessment.Risk analysis : an official publication of the Society for Risk Analysis · 2025
    Article
  5. Review
  6. Benchmark Response (BMR) Values for In Vivo Mutagenicity Endpoints.Environmental and molecular mutagenesis · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
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

6 authors at 3 institutions in 2 countries.

Bala Bhaskar GollapudiExponent, Inc., Center for Health Sciences, Alexandria, Virginia, USA.
Steave SuExponent, Inc., Center for Health Sciences, New York, New York, USA.
Abby A LiExponent, Inc., Center for Health Sciences, Oakland, California, USA.
George E JohnsonSwansea University Medical School, Swansea, Wales, UK.ORCID 0000-0001-5643-9942
Richard ReissExponent, Inc., Center for Health Sciences, Alexandria, Virginia, USA.
Richard J AlbertiniDepartment of Pathology, University of Vermont College of Medicine, Burlington, Vermont, USA.
Exponent (United States) · USSwansea University · GBUniversity of Vermont · US

Funding

American Chemistry CouncilEthylene Oxide Task ForceLyondellBasell
6 · The paper itself

Abstract

The purpose of the present investigation is to analyze the in vivo genotoxicity dose-response data of ethylene oxide (EO) and the applicability of the derived point-of-departure (PoD) values when estimating permitted daily exposure (PDE) values. A total of 40 data sets were identified from the literature, and benchmark dose analyses were conducted using PROAST software to identify a PoD value. Studies employing the inhalation route of exposure and assessing gene or chromosomal mutations and chromosomal damage in various tissues were considered the most relevant for assessing risk from EO, since these effects are likely to contribute to adverse health consequences in exposed individuals. The PoD estimates were screened for precision and the values were divided by data-derived adjustment factors. For gene mutations, the lowest PDE was 285 parts per trillion (ppt) based on the induction of lacI mutations in the testes of mice following 48 weeks of exposure to EO. The corresponding lowest PDE value for chromosomal mutations was 1,175 ppt for heritable translocations in mice following 8.5 weeks of EO exposure. The lowest PDE for chromosomal aberrations was 238 ppt in the mouse peripheral blood lymphocytes following 48 weeks of inhalation exposure. The diverse dose-response data for EO-induced genotoxicity enabled the derivation of PoDs for various endpoints, tissues, and species and identified 238 ppt as the lowest PDE in this retrospective analysis.

Indexed as

AnimalsChromosome AberrationsDose-Response Relationship, DrugEthylene OxideMiceMutagenicity TestsMutagensMutationRatsRisk AssessmentTranslocation, GeneticEthylene OxideMutagensbenchmark dosechromosomal aberrationgenotoxicitymutationpermitted daily exposure

Identifiers

PMID32926486
PMCPMC7756744
OpenAlexW3086677416

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.