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Toxicity of pyrethroids

Insecticides are acutely toxic to a wide spectrum of insects while being relatively safe for mammals and harmless to plants.

Hijacking the motor system

Pyrethroids, like many successful insecticides, target the nervous system of insects to incapacitate them, rendering them unable to feed and reproduce, in effect culling the population which would otherwise be feeding on nearby crops. Pyrethroids are not directly cytotoxic, instead they act very selectively to produce a few symptoms, the most devastating of which affect motor activity in the nervous system.

Pyrethroids act to increase the excitability of neuronal tissue outside of the functional range, causing erratic movement and thereby rendering creatures immobile. They act on the membrane ion channels that tightly control ionic gradients between cells and the extracellular matrix. By disrupting ion homeostasis the foundation of neuronal signaling is disturbed, compromising the whole system.

Acute pyrethroid poisoning with near lethal doses produces characteristic symptoms. Type I pyrethroids cause fine muscular tremor, while Type II are more complex including choreoathetosis (writhing, shaking) and salivation. These symptoms underlie assessment of toxicity in vivo and are of diagnostic value is cases of suspected pyrethroid over-exposure.

Species-specific resistance

The doses required to prevent insects feeding are quite small, compared with those that will begin to affect mammals. A number of factors contribute to mammal's resistance to pyrethroid toxicity Firstly mammals metabolise the pyrethroids more efficiently using the cytochrome oxidase family of enzymes, rendering the toxins inactive. Secondly the neuronal ion channels affected by pyrethroids are slightly different in mammals, due to alternate protein sequences and making them less sensitive to pyrethroids' effects. Thirdly the potency of pyrethroids is inversely correlated with temperature - mammals generally have higher body temperatures and so require even higher doses compared with heterothermic insects.

Poisoning types and treatments

Type II pyrethroids are responsible for a greater number of poisonings, due to their higher potency, longer persistence of effects, and perhaps their larger scale of use (buckets rather than spray cans). When poisoning does occur, there are some available treatments, although these are extreme and must be applied rapidly to be effective. Once pyrethroid poisoning is identified as the origin of symptoms, the patient should administered paralysing doses of pentobarbitone and put on an iron-lung ventilator [Ray & Forshaw, 2000]. In this condition the hyperexcitability-syndrome is diminished, and the patient is kept alive until the body is able to detoxify itself.

Effects of exposure

Skin contact with pyrethroids is by far the most common form of exposure, but ingestion is usually necessary to cause poisoning. Pyrethroids are readily absorbed into the lipids of the skin causing odd sensations - paresthesia. This is caused purely by localised excitation of small afferent nerve fibres, and isn't accompanied by tissue inflammation. Paresthesia is characterized by numbness, itching, burning, or tingling of the skin following dermal exposure to a pyrethroids. Paresthesia correlates poorly with signs of systemic intoxication, meaning it is relatively harmless [Soderlund et al, 2002].

Symptoms of acute poisoning

Assessing pyrethroid intoxication is largely done by subjective observation and scoring of symptoms. While qualitative symptoms have defined underlying mechanisms, identifying them in vivo can be tricky; massive doses are often required to precipitate the characteristic symptoms, which must then be interpreted by an experienced observer. Therefore there is limited hope in achieving accurate assessment by using subjective behavioural criteria. This is why paradigms such as paired-pulse inhibition are essential in achieving accurate, mechanistic diagnosis of the level of poisoning.

Chronic exposure and poisoning

While acute toxicity is dominated by hyperexcitability of the nervous system, there are some other effects of relevance caused by cumulative doses over longer time scales [Ray & Fry, 2006]. Direct neuronal death has been seen with daily exposure to permethrin, a Type I pyrethroid, in rats. This effect is only seen during transdermal exposure, and not dietary intake, even at larger doses, which has left some researchers skeptical.

Chronic exposure can also lead to enzyme induction, particularly the cytochrome oxidase type enzymes. Some metabolites of pyrethroids are themselves toxic, which has raised questions about how acute toxicity may differ in individuals who are chronically exposed to small, enzyme inducing quantities.

Developmental toxicity is also apparent: neo-natal rat pups are many times more sensitive to pyrethroids than adults. This is thought to be due to an undeveloped ability to detoxify through metabolism, and an unformed blood brain barrier.


  • Pyrethroids aren't directly poisonous, but disrupt central nervous function such that the organism is compromised.
  • Mammals are less sensitive than insects, due to better metabolism, higher body temperature and different ion channel structures.
  • Two types of poisoning syndromes can be classified, corresponding to different, but overlapping, groups of pyrethroids
  • Assessing the degree of poisoning is done by a visual, subjective rating by someone familiar with the symptoms.
  • Paresthesia is the most common symptom, but is unrelated to life-threatening systemic poisoning.
  • The best therapy is probably pentobarbitone, which acts to quell central hyperexcitability (make sure patient is mechanically respirated!).

References in this page

[Ray & Forshaw, 2000], [Soderlund et al, 2002], [Ray & Fry, 2006]

On to the next section - Cellular mechanisms



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