| AOP Identifier | AOP Title | AO Classification | OECD Status | Taxonomic applicability | Coverage Score ⓘ The fraction of KEs within the AOP, that are mapped to the chemical-associated toxicological endpoints. | KE Identifier | KE Name |
|---|---|---|---|---|---|---|---|
| AOP:398 | Decreased ALDH1A (RALDH) activity leading to decreased fertility via disrupted meiotic initiation of fetal oogonia | Reproductive system disease | Under Development | Mouse, Rat, Human | 0.17 | KE:1881 | Decreased, all-trans retinoic acid (atRA) concentration |
| AOP:419 | Aryl hydrocarbon receptor activation leading to impaired lung function through P53 toxicity pathway | Respiratory system disease | - | 0.25 | KE:1923 | Altered gene expression, P53 dependent apoptosis pathway | |
| AOP:436 | Inhibition of RALDH2 causes reduced all-trans retinoic acid levels, leading to transposition of the great arteries | Cardiovascular system disease | - | Chicken, Mouse, Vertebrates | 0.2 | KE:1881 | Decreased, all-trans retinoic acid (atRA) concentration |
| AOP:525 | Reduced oligodendrocyte differentiation during neurodevelopment leading to impaired learning and memory | Developmental disorder of mental health | - | 0.08 | KE:2115 | Altered, cholesterol metabolism | |
| AOP:529 | Perfluorooctanesulfonic acid (PFOS) binding to peroxisome proliferator-activated receptors (PPARs) causes dysregulation of lipid metabolism and subsequent liver steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | Vertebrates, Mouse, Rat, Zebrafish | 0.12 | KE:2225 | Disrupted Lipid Storage |
| AOP:550 | Increased LMNA gene mutation leading to heart failure | Cardiovascular system disease | - | Human, Mouse, Rat | 0.2 | KE:2066 | Altered Signaling Pathways |
We have built a comprehensive resource which compiles potential endocrine disrupting chemicals (EDCs) based on the observed adverse effects or endocrine-mediated endpoints in published experiments on humans or rodents to support basic research. We are not responsible for any errors or omissions in the published research articles or supporting literature on potential EDCs compiled in this resource. Users are advised to exercise their own judgement on the weight of evidence for potential EDCs compiled in this resource. Importantly, our sole goal to build this resource on potential EDCs is to enable future basic research towards better understanding of the systems-level perturbations upon chemical exposure rather than influencing regulatory advice on chemical use.