Inhibition, Acetylcholinesterase (AchE) leads to Increased, Respiratory distress/arrest
Upstream eventInhibition, Acetylcholinesterase (AchE)
Increased, Respiratory distress/arrest
Key Event Relationship Overview
AOPs Referencing Relationship
|AOP Name||Directness||Weight of Evidence||Quantitative Understanding|
|Acetylcholinesterase inhibition leading to acute mortality||indirectly leads to||Moderate||Weak|
Life Stage Applicability
How Does This Key Event Relationship Work
- Needs further development.
Weight of Evidence
- Plausible links between acetylcholinesterase inhibition and respiratory distress or failure include:
- Acetylcholine accumulation at neuromuscular junctions associated with the diaphragm, potentially leading to inability to regulate movements of the diaphragm.
- Acetylcholine accumulation in cardiac tissue, leading to reduced heart rate and thus stimulation of respiratory stress in relation to reduced systemic oxygen availability.
- Likely others
Empirical Support for Linkage
Include consideration of temporal concordance here
- A study examining respiratory-cardiovascular responses in rainbow trout found that OPs and carbamates caused an increase in oxygen uptake, heart rate and ventilation volume (McKim et al., 1987b). Authors postulated the causation of these physiological responses was due to inhibition of AChE by the pesticides, although no concurrent measurement of AChE levels was conducted (McKim et al., 1987b).
- Within one hour of exposure of broiler chicks to dichlorvos or diazinon symptoms indicative of cholinergic poisoning were observed including respiratory difficulty (gasping), tremors and convulsions (Al-Zubaidy et al. 2011).
Uncertainties or Inconsistencies
Quantitative Understanding of the Linkage
We are unaware of any correlative relationships of significant predictive value with regard to this KER.