Fenthion toxicity

If poisoning is suspected, one should not wait for symptoms to develop. A physician, the nearest hospital, or the nearest Poison Control Center should be contacted immediately. Signs and symptoms of fenthion toxicity include ... 

Another way for OPPs to transform in mammals is linked to their direct oxidation, accompanying the formation of sulfoxide and sulfone, more toxic products. This takes place particularly when using the insecticide fenthion [21]. The systemic insecticide and acaricide demeton is an interesting case. 

Uses Pure fenthion is a colorless liquid. Technical fenthion is a yellow or brown oily liquid with a weak garlic odor. It is grouped by the USEPA under RUP and requires handling by qualified, certified, and trained workers. Fenthion is used for the control of sucking and biting pests (e.g., fruitflies, stem borers, mosquitoes, cereal bugs). In mosquitoes, it is toxic to both the adult and the immature forms (larvae). The formulations of fenthion include dust, emulsifiable concentrate, granular, liquid concentrate, spray concentrate, ultra-low volume, and wettable powder.28... 

Toxicity Fenthion is moderately toxic to mammals and highly toxic to birds. The acute oral LD50 of fention for rats is 250 mg/kg and the acute dermal LD50 for rats is 700 mg/kg. It is slightly toxic via inhalation for rats, with an acute LC50... 

High doses of OPs cause similar toxic effects independent of the identity of the OPs. However, low-dose effects are not identieal for all OPs (Moser, 1995). For example, a low dose of fenthion decreased motor aetivity in rats by 86% but did not alter the tail-pinch response, whereas a low dose of parathion did not affect motor activity but did decrease the... 

Recent work with models both in vivo and in vitro shows that fenthion also has antiandrogenic activity and can produce oxidative stress. More research is needed to establish whether these mechanisms are responsible for significant toxic effects. 

Chronic toxicity studies on fenthion are available in the rat, dog, and monkey. The dog and monkey studies did not reveal any systemic signs of toxicity due to prolonged exposure to fenthion with the exception of cholinesterase inhibition. In the rat study, however, pathology was noted in the epididymis, the nasolacrimal duct, and in ocular tissue. Fenthion is not considered to be a carcinogen. While one test of carcinogenicity in mice indicated that fenthion may be a carcinogen in male mice, further studies in mice and rats did not support this. 

Developmental toxicity studies in rat and rabbit do not show signs of enhanced sensitivity of the developing fetus to fenthion. Dams exhibited clinical signs and decreased body weights at the same dosages that induced fetal effects. In addition, plasma, erythrocyte, and brain cholinesterase inhibition was seen in dams at doses lower than those causing fetal effects. For this reason, the Food Quality Protection Act safety factor for fenthion was reduced from a default 10x to lx. ... 

Fenthion is very highly toxic to birds. The use of fenthion for control of mosquitos has been implicated in several bird kills, including recent incidents on Marco Island, Florida. The major metabolites, fenthion phenol sulfoxide and fenthion phenol sulfone, have very low toxicity to birds. 

Fenthion is classified as a Toxicity Category II chemical for acute oral, dermal, and inhalation toxicity. It is classified in Toxicity Category III for eye irritation and Category IV for dermal irritation. It is not considered by the US EPA to be a carcinogen, and is therefore classified as a Group E chemical, that is, not likely to be carcinogenic in humans via relevant routes of exposure. 

Table 5.3 Toxicity of Fenitrothion, Parathion, and Fenthion according to G. Schrader (1963)...

Of the other older dialkyl-aryl phosphorothionates, fenthion is still widely used. Fenthion has a better residual efficiency than parathion and methyl parathion and is probably less toxic to fish — 0.01 mg/1 at 24 hours exposure results in 100% mortality in mosquitoes (Aedes aegypti), whereas 1 mg/1 does not kill any guppy (Lebistes reticulatus) during 48 hours exposure. 

The above reactions show how fenthion is successively oxidized to the sulfon of the oxon, which is the most toxic metabolite. 

Fenthion is oxidised in the organism to its more effective sulfoxide derivative (37). Oxidation results in an increase in the insecticidal effect and simultaneously, toxicity to warm-blooded animals also increases by about three fold. Further metabolism leads to the formation of sulfone 38, the toxicity of which to warmblooded animals is similar to that of the sulfoxide, but its insecticidal efficiency is lower. 

OP insecticide-induced intermediate syndrome (IMS) was reported for the first time in human patients in Sri Lanka in 1987 (Senanayake and Karalliede, 1987). Since then, this syndrome has been diagnosed in OP-poisoned patients in South Africa (1989), Turkey (1990), Belgium (1992), the United States (1992), Venezuela (1998), France (2000), and elsewhere. IMS is usually observed in individuals who have ingested a massive dose of an OP insecticide either accidentally or in a suicide attempt. IMS is clearly a separate clinical entity from acute toxicity and delayed neuropathy. A similar syndrome has also been observed in dogs and cats poisoned maliciously or accidentally with massive dosc.s of certain OPs. OPs that are known to cause IMS include bromophos, chlorpyrifos, diazinon, dicrotophos, dimethoatc, fenthion, malathion, merphos, methamidophos, methyl parathion, monocrotophos, omethoate, parathion, phosmet, and trichlorfon. These compounds and IMS are discussed further in Chapter 26. 

Our group compared in Wistar rats the acutely toxic organophosphate (OP) paraoxon with fenthion, one of the agents frequently involved in human IMS. The clinical symptoms, the occurrence of muscle fiber necrosis and histochemical assessment of neuromuscular junction AChE activity in muscle biopsies, biochemical assessment of brain AChE activity, and EMG parameters including repetitive nerve stimulation at various frequencies were studied at various lime points. 

Reactive Oxygen Species (ROS) may serve as common mediators in programmed cell death w apoptosis in response to many toxicants and pathological conditions. Studies have demonstrated that ROS may be involved in the cytotoxicity of widely used OP pesticides, such as chlorpyrifos and fenthion. Highly toxic chlorpyrifos and fenthion are organic triesters of phosphoric acid and phosphorothioic acid and arc also lipophilic (Murphy, 1986). Neuroiransmitter systems play a key role in behavioral function and disturbances. Other OPs, such as phosphamidon, irichlorfon, and dichlor-vos, have also been reported to induce oxidative stress, both... 

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