Pyrethrum is an exogenous solid with the formula C22H28O5 and an average molecular weight of 372.46 g/mol. Pyrethrum belongs to the fatty acid esters, a subclass of fatty acyls within the organic compounds. It is utilized as a phytogenic insecticide.
The compound interacts with 18 recorded protein targets, including the nuclear receptor subfamily 1 group I member 2 (NR1I2), calcium-activated potassium channel subunit alpha-1 (KCNMA1), and sodium channel protein type 1 subunit alpha (SCN1A), sodium channel protein type 2 subunit alpha (SCN2A), sodium channel protein type 10 subunit alpha (SCN10A), and sodium channel protein type 11 subunit alpha (SCN11A). As an axonic poison, this pyrethroid prolongs the open phase of sodium channel gates during nerve cell excitation, blocking the closing of the gates and prolonging the return of the membrane potential to its resting state. This action leads to nervous system hyperactivity, which can result in death and/or paralysis. Type I Pyrethroid esters that lack alpha-cyano substituents affect sodium channels in nerve membranes. Additionally, the compound inhibits Ca2+ and Mg2+ ATPase and Na+/K+ ATPase, which are essential for transporting calcium across membranes. This inhibition results in the accumulation of intracellular free calcium ions, promoting the release of neurotransmitters from storage vesicles, the depolarization of adjacent neurons, and the propagation of stimuli throughout the central nervous system.
belongs to the class of organic compounds known as pyrethrins. These are pyrethroids with a structure based on a skeleton that is characterized by the presence of a chrysanthemic acid esterified with a cyclopentenone derivative.
Both type I and type II pyrethroids exert their effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. They appear to bind to the membrane lipid phase in the immediate vicinity of the sodium channel, thus modifying the channel kinetics. This blocks the closing of the sodium gates in the nerves, and thus prolongs the return of the membrane potential to its resting state. The repetitive (sensory, motor) neuronal discharge and a prolonged negative after potential produce effects quite similar to those produced by DDT, leading to hyperactivity of the nervous system which can result in paralysis and/or death. Other mechanisms of action of pyrethroids include antagonism of gamma-aminobutyric acid (GABA)-mediated inhibition, modulation of nicotinic cholinergic transmission, enhancement of noradrenaline release, and actions on calcium ions. They also inhibit calcium channels and Ca2+, Mg2+-ATPase. (4, 5, 2)
Metabolism
Following ingestion, pyrethriods are hydrolysed by various digestive enzymes in the gastro-intestinal tract. However, a small portion of the insecticidally active compounds or its derivatives are absorbed, as shown by their toxicity and their effect on the liver. Pyrethriods may also be absorbed following inhalation or dermal contact. They are rapidly distributed to most tissues, particularly to those with a high lipid content, and are concentrated in central and peripheral nervous tissues. Pyrethriods or their metabolites are not known to be stored in the body or to be excreted in the milk, but no study of the matter has employed modern methods. The major metabolic pathways for pyrethriods are hydrolysis of the central ester bond, oxidative attacks at several sites, and conjugation reactions, to produce a complex array of primary and secondary water-soluble metabolites that undergo urinary excretion. Metabolism is believed to involve nonspecific microsomal carboxyesterases and microsomal mixed function oxidases, which are located in nearly all tissue types, with particularly high activities in the liver. Metabolites are excreted in the urine and faeces. (2, 3)
Pyrethroid effects typically include rapid onset of aggressive behavior and increased sensitivity to external stimuli, followed by fine tremor, prostration with coarse whole body tremor, elevated body temperature, coma, and death. Paresthesia, severe corneal damage, hypotension and tachycardia, associated with anaphylaxis, can also occur following pyrethriod poisoning. (2)
Symptoms
Spilling on the head, face and eyes can result in pain, lacrimation, photophobia, congestion, and edema of the conjunctiva and eyelids. Ingestion causes epigastric pain, nausea, vomiting, headache, dizziness, anorexia, fatigue, tightness in chest, blurred vision, paresthesia, palpitations, coarse muscular fasciculations, and disturbances of conciousness. In severe poisonings, convulsive attacks with opisthotonos and loss of conciousness have occurred. (4)
Treatment
Following oral exposure, the treatment is symptomatic and supportive and includes monitoring for the development of hypersensitivity reactions with respiratory distress. Provide adequate airway management when needed. Gastric decontamination is usually not required unless the pyrethrin product is combined with a hydrocarbon. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist, the patient should be seen in a health care facility. If the contamination occurs through dermal exposure, remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. Vitamin E topical application is highly effective in relieving parenthesis. (6)
