Pyrethroids Case Study

PYRETHROID TOXICITY: case study on self poisoning

SUBBURAJ M2, HIMMATH K G1 , SOOPY K1, PRADEEP KUMAR K M1,*
1Department of Medicine, Medical College, Calicut, Kerala, India
2Department of Health & Family welfare, Analytic Laboratory, Calicut, Kerala, India
*corresponding author: [e-mail]

ABSTRACT

Pyrethroids and its derivatives are the most widely used insecticides. It is an important insecticide against mosquitoes and other disease-carrying vectors. They are often used in indoor sprays, pet shampoos and aerosol to kill flying and jumping insects. Pyrethroids are highly lipophilic, have a short life in the environment so it’s not biomagnify like other chemical classes. So the use has increased substantially throughout

They are used widely in and around households, including on pets, in mosquito control, and in agriculture. The use of pyrethrins and pyrethroids has increased during the past decade with the declining use of organophosphate pesticides, which are more acutely toxic to birds and mammals than the pyrethroids. This change to less acutely toxic pesticides, while generally beneficial, has introduced certain new issues. For example, residential uses of pyrethrins and pyrethroids may result in urban runoff, potentially exposing aquatic life to harmful levels in water and sediment. They are neurotoxins that attack the nervous systems of all insects. Generally Pyrethroids are popular for insecticide because exoskeletons of insects are sufficiently porous to pyrethroids. They are axonic poisons and cause paralysis of an organism by keeping the sodium channels open in the neuronal membranes. The sodium channel is a membrane protein with a hydrophilic interior. This interior is a tiny hole which is shaped precisely to strip away the partially charged water molecules from a sodium ion and create a favorable way for sodium ions to pass through the membrane, enter the axon, and propagate an action potential. When the toxin keeps the channels in their open state, the nerves cannot de-excite, so the

Piperonyl butoxide prevents the insect's enzymes from metabolizing the pyrethroid, which would diminish its lethality. Synthetic pyrethroid compounds vary in their toxicity as do the natural pyrethrins. Inhaling high levels of pyrethrum may bring about asthmatic breathing, sneezing, nasal stuffiness, headache, nausea, incoordination, tremors, convulsions, facial flushing and swelling, and burning and itching sensations2. The most severe poisonings have been reported in infants, who are not able to efficiently break down pyrethrum. The lowest lethal oral dose of pyrethrum is 750 mg/kg for children and 1,000 mg/kg for adults2. Oral LD50 values of pyrethrins in rats range from 200 mg/kg to greater than 2,600 mg/kg3. Some of this variability is due to the variety of constituents in the formulation. Mice have a pyrethrum oral LD50 of 370 mg/kg2. Animals exposed to toxic amounts may experience tongue and lip numbness, nausea, and diarrhea. Symptoms may also include incoordination, tremors, convulsions, paralysis, respiratory failure, and death. Pyrethroids can cause two quite different responses at near lethal doses in rats; aggressive sparring and a sensitivity to external stimuli progressing to tremors is the one response and pawing and burrowing behavior, and salivation leading to chronic seizures is the other. Human response to these two different types of