| 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:321 | Reduced environmental pH leading to thinner shells in Mytilus edulis | Unclassified | - | 0.09 | KE:592 | Reduced, survival | |
| AOP:348 | Inhibition of 11β-Hydroxysteroid Dehydrogenase leading to decreased population trajectory | Unclassified | Under Development | Fish | 0.2 | KE:406 | decreased, Fertility |
| AOP:349 | Inhibition of 11β-hydroxylase leading to decresed population trajectory | Unclassified | Under Development | Fish | 0.12 | KE:406 | decreased, Fertility |
| AOP:465 | Alcohol dehydrogenase leading to reproductive dysfunction | Unclassified | - | 0.12 | KE:748 | Increased, Estrogen receptor (ER) activity |
| 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:7 | Aromatase (Cyp19a1) reduction leading to impaired fertility in adult female | Reproductive system disease; Endocrine system disease; Reproductive system disease | Under Review | Rat, Mouse, Human | 0.2 | KE:406 | decreased, Fertility |
| AOP:18 | PPARα activation in utero leading to impaired fertility in males | Reproductive system disease | Under Review | Human, Rat, Mouse | 0.12 | KE:406 | decreased, Fertility |
| AOP:21 | Aryl hydrocarbon receptor activation leading to early life stage mortality, via increased COX-2 | Unclassified | WPHA/WNT Endorsed | Zebrafish, Medaka, Gallus gallus | 0.2 | KE:947 | Increase, Early Life Stage Mortality |
| AOP:64 | Glucocorticoid Receptor (GR) Mediated Adult Leydig Cell Dysfunction Leading to Decreased Male Fertility | Reproductive system disease | - | Rattus norvegicus | 0.14 | KE:406 | decreased, Fertility |
| AOP:91 | Sodium channel inhibition leading to reduced survival | Unclassified | - | Medaka, Gammarus pulex, Hydra | 0.17 | KE:592 | Reduced, survival |
| AOP:95 | Ether-a-go-go (ERG) voltage-gated potassium channel inhibition leading to reduced survival | Unclassified | - | 0.17 | KE:592 | Reduced, survival | |
| AOP:99 | Histamine (H2) receptor antagonism leading to reduced survival | Unclassified | - | Zebrafish | 0.14 | KE:636 | Decreased, survival |
| AOP:124 | HMG-CoA reductase inhibition leading to decreased fertility | Reproductive system disease | - | Rattus rattus | 0.17 | KE:330 | Decrease, Fertility |
| AOP:150 | Aryl hydrocarbon receptor activation leading to early life stage mortality, via reduced VEGF | Unclassified | WPHA/WNT Endorsed | Chicken, Zebrafish, Mouse, Rattus norvegicus | 0.14 | KE:947 | Increase, Early Life Stage Mortality |
| AOP:242 | Inhibition of lysyl oxidase leading to enhanced chronic fish toxicity | Unclassified | - | Fish | 0.12 | KE:636 | Decreased, survival |
| AOP:323 | PPARalpha Agonism Leading to Decreased Viable Offspring via Decreased 11-Ketotestosterone | Unclassified | - | Teleost fish | 0.17 | KE:2147 | Decreased, Viable Offspring |
| AOP:345 | Androgen receptor (AR) antagonism leading to decreased fertility in females | Endocrine system disease; Reproductive system disease; Reproductive system disease | Under Development | Mammals | 0.17 | KE:406 | decreased, Fertility |
| 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:406 | decreased, Fertility |
| AOP:455 | Aryl hydrocarbon receptor activation leading to early life stage mortality via sox9 repression induced impeded craniofacial development | Musculoskeletal system disease | Under Review | Zebrafish, Mouse, Human, Sebastiscus marmoratus, Salmo salar, Chicken | 0.17 | KE:947 | Increase, Early Life Stage Mortality |
| AOP:456 | Aryl hydrocarbon receptor activation leading to early life stage mortality via sox9 repression induced cardiovascular toxicity | Unclassified | Under Review | Zebrafish, Mouse, Human, Chicken | 0.17 | KE:947 | Increase, Early Life Stage Mortality |
| AOP:492 | Glutathione conjugation leading to reproductive dysfunction via oxidative stress | Reproductive system disease | - | Mammals, Fish | 0.2 | KE:406 | decreased, Fertility |
| AOP:504 | SULT1E1 inhibition leading to uterine adenocarcinoma via increased estrogen availability at target organ level | Unclassified | - | Mammals | 0.33 | KE:1065 | Activation, estrogen receptor alpha |
| AOP:521 | Essential element imbalance leads to reproductive failure via oxidative stress | Unclassified | - | Murinae gen. sp. | 0.14 | KE:2147 | Decreased, Viable Offspring |
| AOP:561 | Aromatase induction leading to estrogen receptor alpha activation via increased estradiol | Unclassified | - | Vertebrates | 0.2 | KE:1065 | Activation, estrogen receptor alpha |
| 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:16 | Acetylcholinesterase inhibition leading to acute mortality | Unclassified | Under Development | 0.14 | KE:12 | Acetylcholinesterase (AchE) Inhibition | |
| AOP:167 | Early-life estrogen receptor activity leading to endometrial carcinoma in the mouse. | Reproductive system disease; Cancer | - | Mouse, Homo sapiens | 0.29 | KE:1065 | Activation, estrogen receptor alpha |
| KE:1064 | prepubertal increase, Estrogen receptor (ER) activity | ||||||
| AOP:281 | Acetylcholinesterase Inhibition Leading to Neurodegeneration | Nervous system disease | - | 0.1 | KE:12 | Acetylcholinesterase (AchE) Inhibition | |
| AOP:312 | Acetylcholinesterase Inhibition leading to Acute Mortality via Impaired Coordination & Movement | Unclassified | - | 0.17 | KE:12 | Acetylcholinesterase (AchE) Inhibition | |
| AOP:314 | Binding to estrogen receptor (ER)-α in immune cells leading to exacerbation of systemic lupus erythematosus (SLE) | Immune system disease; Musculoskeletal system disease | Under Development | Homo sapiens | 0.2 | KE:1710 | Binding to estrogen receptor (ER)-α in immune cells |
| AOP:405 | Organo-Phosphate Chemicals induced inhibition of AChE leading to impaired cognitive function | Cognitive disorder | - | Rattus norvegicus, Mus musculus, Homo sapiens | 0.2 | KE:12 | Acetylcholinesterase (AchE) Inhibition |
| AOP:445 | Estrogen Receptor Alpha Agonism leads to Impaired Reproduction | Reproductive system disease | - | 0.12 | KE:1065 | Activation, estrogen receptor alpha | |
| AOP:450 | Inhibition of AChE and activation of CYP2E1 leading to sensory axonal peripheral neuropathy and mortality | Nervous system disease | - | Rattus norvegicus, Mus musculus, Homo sapiens | 0.14 | KE:12 | Acetylcholinesterase (AchE) Inhibition |
| AOP:503 | Activation of uterine estrogen receptor-alfa leading to endometrial adenocarcinoma, via epigenetic modulation | Reproductive system disease; Cancer | Under Review | Human, Mouse | 0.17 | KE:1065 | Activation, estrogen receptor alpha |
| AOP:559 | Inhibition of acetylcholinesterase (AChE) leading to arrhythmias | Symptom | - | Human and other cells in culture, Rattus norvegicus, Dogs, Sus scrofa, Zebrafish, Insecta sp. BOLD:AAN5199 | 0.2 | KE:12 | Acetylcholinesterase (AchE) Inhibition |
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.