ReviewNeurotoxicology2025
Cumulative risk assessment as the pathway to public health protection for behavioral neurotoxicity.
Review in Neurotoxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- From toxicogenomics to predictive toxicology and exposomics: defining the next decade of gene-environment research.Frontiers in genetics · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The formulation of adverse outcome pathways (AOPs) based on high-throughput in vitro new approach methods linking biochemical/mechanistic data with an apical endpoint considered an adverse outcome (AO), is increasingly proposed to accelerate the process of risk assessment for environmental chemical exposures. While a laudable goal, this approach ignores the extensive evidence demonstrating context-dependence of neurotoxicological consequences, including behavioral toxicity of chemical exposures. Such contextual modifiers can include environmental conditions (poverty, psychosocial stress, behavioral experience/history), physiological conditions (sex, period of exposure, nutritional status, brain region, exposure parameters), and genetic background. Context dependence represents a serious omission for AOP formulation because an environmental context can alter a chemical's molecular targets, or potentially enhance toxicity through interactions with other contextual conditions, thus leading to potential underestimation of neurological risks due to such exposures. The integrative physiological basis of AOs requires cumulative risk assessments that model environmental contexts across scales of biology, i.e., integration and testing in whole-animal models. AOPs contribute to the derivation of cumulative risk considerations regarding factors to incorporate into cumulative risk assessments by defining risk factors with shared biological targets. Epidemiological and animal model studies can provide information to prioritize interactive effects of greatest magnitude. Additionally, a focus on how a single risk factor in different physiological contexts may attribute risk across multiple neurologic conditions, rather than to a single unique condition, would provide broader public health protection. Realistic acknowledgement of context-dependence is requisite to understanding both the etiological basis of neurological diseases and disorders and to human health protection.
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What OpenQuestion holds
Registered trials
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.