Evidence map›Paper›PMID 41012374›Full record

ReviewToxics2025

Toxicology of Airborne Inorganic Arsenic: Oxidative Stress, Molecular Mechanisms, and Organ-Specific Pathologies.

Qingyang Liu

Abstract readReview
In one paragraph

Review in Toxics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Qingyang LiuCollege of Ecology and Environment, Nanjing Forestry University, Nanjing 210037, China.ORCID 0000-0003-3193-5856

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arsenic, a naturally occurring metalloid, poses a significant global public health threat due to widespread environmental contamination. Despite its well-documented carcinogenicity, critical gaps remain in understanding the health impacts of chronic low-level airborne exposure and the multi-modal mechanisms driving inorganic arsenic toxicity. This narrative review synthesizes recent molecular research and population health data to explain how airborne inorganic arsenic causes harm through multiple biological pathways. Key novel insights include (1) a comprehensive analysis of inorganic arsenic-induced oxidative stress and epigenetic dysregulation, revealing transgenerational effects via germline epigenetic markers; (2) a critical evaluation of the linear no-threshold (LNT) model, demonstrating its overestimation of low-dose risks by 2-3× compared to threshold-based evidence; and (3) descriptions of mechanistic links between inorganic arsenic speciation, organ-specific pathologies (e.g., neurodevelopmental impairments, cardiovascular diseases), and pollution mitigation strategies. This study connects molecular mechanisms with public health strategies to improve arsenic risk assessment. It focuses on how inorganic arsenic alters gene regulation (epigenetics) and combines exposure from multiple sources, while also clarifying uncertainties about low-dose effects and refining safety standards.

Indexed as

airborne inorganic arseniccarcinogenrisk assessmenttoxicological mechanisms

Identifiers

PMID41012374
PMCPMC12474278

What Socratic 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 Socratic graph.