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tooluniverse-toxicology

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Drug and chemical toxicity assessment via adverse outcome pathways (AOPs), real-world FAERS adverse event signals, FDA labels, toxicogenomic associations, and EPA CompTox quantitative hazard/high-throughput bioactivity data. Triangulates molecular initiating event to cellular outcome to organ-level toxicity to clinical adverse event. Use for hepatotoxicity/cardiotoxicity/nephrotoxicity prediction and toxicology reports.

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# Toxicology Assessment via Adverse Outcome Pathways & Signal Detection

Systematic toxicology analysis that links molecular initiating events (MIEs) through adverse outcome
pathways (AOPs) to apical adverse outcomes, then triangulates with real-world FAERS signals, FDA
label data, and toxicogenomic associations.

## Domain Reasoning

Toxicity has many mechanisms, and the first interpretive question is temporal: is this acute toxicity (immediate effect from a high dose) or chronic toxicity (cumulative damage from long-term low-dose exposure)? Acute and chronic toxicity operate through different mechanisms — acute hepatotoxicity may reflect direct mitochondrial damage, while chronic hepatotoxicity may involve fibrosis from repeated low-level inflammation. They also have different regulatory frameworks: acute toxicity is captured by LD50 and emergency protocols, while chronic toxicity requires long-term carcinogenicity and repeat-dose studies.

## LOOK UP DON'T GUESS

- Adverse outcome pathways for a chemical: query `AOPWiki_list_aops` and `AOPWiki_get_aop`; do not describe mechanisms from memory.
- FAERS adverse event signals: retrieve from `FAERS_count_reactions_by_drug_event` and `FAERS_calculate_disproportionality`; never estimate PRR values.
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