Evidence map›Paper›PMID 22163375›Full record

ArticleToxicological and environmental chemistry2011

The plausibility of a role for mercury in the etiology of autism: a cellular perspective.

Matthew Garrecht, David W Austin

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological and environmental chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
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  6. Article
  7. Article
  8. Associations of Metabolic Genes (International journal of environmental research and public health · 2021
    Article
  9. Correlation between concentrations of four heavy metals in cord blood and childhood blood of Jamaican children.Journal of environmental science and health. Part A, Toxic/hazardous substances & environmental engineering · 2021
    Article
  10. Article
  11. Article
  12. Neurodevelopmental Effects of Mercury.Advances in neurotoxicology · 2018
    Article
  13. A Two-Phase Case-Control Study of Autism Risk Among Children Born From the Late 1990s Through the Early 2000s in the United States.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  14. Chelation for autism spectrum disorder (ASD).The Cochrane database of systematic reviews · 2015
    Article
  15. Interaction betweenResearch in autism spectrum disorders · 2015
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Hair toxic metal concentrations and autism spectrum disorder severity in young children.International journal of environmental research and public health · 2012
    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

2 authors at 1 institution in 1 country.

Matthew GarrechtSwinburne Autism Bio-Research Initiative, Faculty of Life and Social Sciences, Swinburne University of Technology, Hawthorn, Victoria 3122, Australia.
David W Austin
Swinburne University of Technology · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism is defined by a behavioral set of stereotypic and repetitious behavioral patterns in combination with social and communication deficits. There is emerging evidence supporting the hypothesis that autism may result from a combination of genetic susceptibility and exposure to environmental toxins at critical moments in development. Mercury (Hg) is recognized as a ubiquitous environmental neurotoxin and there is mounting evidence linking it to neurodevelopmental disorders, including autism. Of course, the evidence is not derived from experimental trials with humans but rather from methods focusing on biomarkers of Hg damage, measurements of Hg exposure, epidemiological data, and animal studies. For ethical reasons, controlled Hg exposure in humans will never be conducted. Therefore, to properly evaluate the Hg-autism etiological hypothesis, it is essential to first establish the biological plausibility of the hypothesis. This review examines the plausibility of Hg as the primary etiological agent driving the cellular mechanisms by which Hg-induced neurotoxicity may result in the physiological attributes of autism. Key areas of focus include: (1) route and cellular mechanisms of Hg exposure in autism; (2) current research and examples of possible genetic variables that are linked to both Hg sensitivity and autism; (3) the role Hg may play as an environmental toxin fueling the oxidative stress found in autism; (4) role of mitochondrial dysfunction; and (5) possible role of Hg in abnormal neuroexcitory and excitotoxity that may play a role in the immune dysregulation found in autism. Future research directions that would assist in addressing the gaps in our knowledge are proposed.

Identifiers

PMID22163375
PMCPMC3173748
OpenAlexW2003753209

What OpenQuestion holds

Textmetadata
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.