Agriculture Reference
In-Depth Information
Table 5.3
continued
Highly toxic*:
Moderately toxic (continued):
Methamidophos (Monitor)
profenofos (Curacron)
Dicrotophos (Bidrin)
formothion (Anthio)
Monocrotophos (Azodrin)
Pyrazophos (Afugan, Curamil)
Methidathion (Supracide, Ultracide)
naled (Dibrom)
EPN
phenthoate (dimephenthoate, Phenthoate)
Isofenphos (Amaze, Oftanol)
cyanophos (Cyanox)
Endothion, bomyl (Swat)
crufomate (Ruelene)
famphur (Famfos, Bo-Ana, Bash)
merphos (Folex, Easy off-D)
Fenophosphon (trichloronate, Agritox)
pirimiphos-methyl (Actellic)
dialifor (Torak)
iodofenphos (Nuvanol-N)
Cyanofenphos (Surecide)
chlorphoxim (Baythion-C)
Dioxathion (Delnav)
propyl thiopyrophosphate (Aspon)
mipafox (Isopestox, Pestox XV)
bromophos (Nexion)
tetrachlorvinphos (Gardona, Appex, Stirofos)
Moderately toxic*:
temephos (Abate, Abathion)
Bromophos-ethyl (Nexagan),
fenitrothion
(Accothion,
Agrothion,
Su-
mithion)
Leptophos (Phosvel), pyridaphenthion (Ofunack)
Dichlorvos (DDVP, Vapona), acephate (Orthene)
ethoprop (Mocap), malathion (Cythion)
demeton-S-methyl
+
(Duratox, Metasystox (i)), ronnel (fenchlorphos, Korlan)
Triazophos (Hostathion) etrimfos (Ekamet),
Oxydemeton-methyl
+
(Metasystox-R) phoxim (Baythion)
*
Compounds are listed approximately in order of descending toxicity. "Highly toxic" organo-
phosphates have listed oral LD
50
values (rat) less than 50 mg/kg; "moderately toxic" agents
have LD
50
values in excess of 50 mg/kg.
+
These organophosphates are systemic; they are taken up by the plant and translocated into
foliage and sometimes into the fruit.
Toxicology and Mode of Action
Organophosphates poison insects and mammals primarily by phosphoryla-
tion of the acetylcholinesterase enzyme (ACHE) at nerve endings. The en-
zyme is critical to normal control of nerve impulse transmission from nerve
fibers to muscle and gland cells, and also to other nerve cells in autonomic
ganglia and in the brain. Some critical portion of the tissue enzyme mass
must be inactivated by phosphorylation before symptoms and signs of poison-
ing are manifested. At sufficient dosage, loss of enzyme function allows ac-
cumulation of acetylcholine (Ach, the impulse-transmitting substance) at cho-
linergic neuroeffector junctions (muscarinic effects), at skeletal nerve-muscle
junctions and autonomic ganglia (nicotinic effects), and in the brain. At cho-
linergic nerve junctions with smooth muscle and gland cells, high ACh con-
centration causes muscle contraction and secretion, respectively. At skeletal
muscl e junct ions, exces s ACh may be excit atory (may cause muscle twitch-
ing), but may also weaken or paralyze the cell by depolarizing the end-plate.
In the brain, high ACh concentrations cause sensory and behavioral distur-
bances, incoordination and depressed motor function. Depression of res-
piration and pulmonary edema are the usual causes of death from organophos-
