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By the administration of radioactively labelled compounds, the metabolic products of pyrethrin I, pyrethrin II, and allethrin in the rat have been identified. This paper describes the structures of the metabolites.
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Pyrethrins are widely used insecticides in both agriculture and households. In many commercial formulations piperonyl butoxide (PBO) is used with pyrethrins. PBO is a well-known synergist of pyrethrins, used to intensify their effects. One of the cellular targets of pyrethrins is the sodium channel in the membrane. In the present study, the activity of the membrane-bound integral protein ATPase was studied as a biomarker for the membrane effects of pyrethrin and PBO. Cerebral synaptosomes of rat brain were used in the study. The isolation of synaptosomes was performed with the Percoll gradient method. Both total ATPase and Mg2+ activated ATPase were studied by determining inorganic phosphate. Exposure to 0.1-1000 microM of pyrethrin and to 0.4-4000 microM of PBO decreased ATPase activity dose-dependently. The most efficient mixture was the one consisting of one part of pyrethrin and four parts of PBO. The activity of total ATPase decreased 15% in concentrations of 0.1-10 microM pyrethrin, and a 50% decrease was found at 100 microM pyrethrin. The mixture of pyrethrin and PBO caused a 15-60% decrease in the total ATPase activity at 0.1-10 microM pyrethrin and 0.4-40 microM PBO. A 85% decrease was found after exposure to the mixture of 100 microM pyrethrin and 400 microM PBO. PBO alone had no effect at 0.4-40 microM concentrations, but a marked effect was seen at over 40 microM concentrations. The results indicate that PBO is an effective synergist of pyrethrin and that it is very toxic in high concentrations. The results also confirm that neuronal sodium homeostasis is one target of the neurotoxic effect of pyrethroid compounds.
Prolonged treatment with high doses of Pyrethrins results in thyroid gland tumors in the rat. To elucidate the mode of action for tumor formation, the effect of Pyrethrins on rat thyroid gland, thyroid hormone levels and hepatic thyroxine UDPglucuronosyltransferase activity was investigated. Male Sprague-Dawley CD rats were fed diets containing 0 (control) and 8000 ppm Pyrethrins and female rats diets containing 0, 100, 3000 and 8000 ppm Pyrethrins for periods of 7, 14 and 42 days and for 42 days followed by 42 days of reversal. As a positive control, rats were also fed diets containing 1200-1558 ppm sodium Phenobarbital (NaPB) for 7 and 14 days. The treatment of male rats with 8000 ppm Pyrethrins, female rats with 3000 and 8000 ppm Pyrethrins and both sexes with NaPB resulted in increased thyroid gland weights, which were associated with follicular cell hypertrophy. Thyroid follicular cell replicative DNA synthesis was increased by treatment with Pyrethrins and NaPB for 7 and/or 14 days. Treatment with Pyrethrins and NaPB increased hepatic microsomal thyroxine UDPglucuronosyltransferase activity and serum thyroid stimulating hormone levels (TSH), but reduced serum levels of either thyroxine (T4) and/or triiodothyronine (T3). The effects of Pyrethrins in female rats were dose-dependent, with 100 ppm being a no-effect level, and on cessation of treatment were essentially reversible in both sexes. The concordance between the effects of Pyrethrins and NaPB suggests that the mode of action for Pyrethrins-induced rat thyroid gland tumors is similar to that of some other non-genotoxic inducers of hepatic xenobiotic metabolism.
High doses of Pyrethrins produce liver tumors in female rats. To elucidate the mode of action for tumor formation, the hepatic effects of Pyrethrins have been investigated. Male Sprague-Dawley CD rats were fed diets containing 0 (control) and 8000 ppm Pyrethrins and female rats' diets containing 0, 100, 3000 and 8000 ppm Pyrethrins for periods of 7, 14 and 42 days and 42 days followed by 42 days of reversal. As a positive control, rats were also fed diets containing 1200-1558 ppm sodium Phenobarbital (NaPB) for 7 and 14 days. The treatment of male rats with 8000 ppm Pyrethrins, female rats with 3000 and 8000 ppm Pyrethrins and both sexes with NaPB resulted in increased liver weights, which were associated with hepatocyte hypertrophy. Hepatocyte replicative DNA synthesis was also increased by treatment with Pyrethrins and NaPB. The treatment of male and female rats with Pyrethrins and NaPB produced significant increases in hepatic microsomal cytochrome P450 (CYP) content and a marked induction of CYP2B-dependent 7-pentoxyresorufin O-depentylase and testosterone 16beta-hydroxylase activities. Significant increases were also observed in CYP3A-dependent testosterone 6beta-hydroxylase activity. The hepatic effects of Pyrethrins were dose-dependent in female rats with 100 ppm being a no effect level and on cessation of treatment were reversible in both sexes. This study demonstrates that Pyrethrins are mitogenic CYP2B form inducers in rat liver. The mode of action for Pyrethrins-induced rat liver tumor formation appears to be similar to that of NaPB and some other non-genotoxic CYP2B inducers of hepatic xenobiotic metabolism.
Pilot exposure to pyrethrin was monitored after 2 aerial applications of a ultra-low-volume (ULV) pyrethrin insecticide for the control of adult mosquitoes. Pyrethrin exposure was estimated by measuring the excretion in urine of a common metabolite, trans-chrysanthemumdicarboxylic acid, of the natural pyrethrin mixture. Pyrethrin exposure estimated by total daily urine volume was well correlated (R2 = 0.8) with exposure estimated by the creatinine-adjusted volume of combined workday urine voids, indicating that a postapplication spot urine sample would be sufficient to measure pyrethrin exposure. Pilot exposure to pyrethrin was very low after both insecticide applications. The highest exposure was found on day 1, with a dose of 2.05 microg pyrethrin equivalents/day or a dosage of 0.03 microg pyrethrin equivalents/kg/day. These exposure rates represent approximately 1/2,800,000th of the low observed adverse effect level and 1/1,000th of the acceptable daily intake for pyrethrin. The aerial application of ULV pyrethrin insecticide for the control of adult mosquitoes does not result in undue exposure to a pilot who is trained and certified to conduct such control operations.
Prolonged storage of harvested Tasmanian pyrethrum crop from Tanacetum cinerariaefolium has resulted in substantial losses of the pyrethrin esters due to the environmental conditions in the storage shed. The generation of heat, the presence of moisture and oxygen, and the microbial activity were identified as possible causes. A pyrethrum crop sample was divided up and stored in different conditions relating to these variables, and the pyrethrins content was monitored over time using a standard method. Temperature was determined to be a critical factor in the rate of the degradation of the natural pyrethrins. Moisture, oxygen, and microbial activity unexpectedly did not play a major role in the degradation. An initial rapid loss of the natural pyrethrins was observed before the pyrethrins content stabilized at a loss of around 65%. This suggests that the plant structure may provide chemical or physical protection to the pyrethrins. In all cases, the majority of the loss was attributed to the pyrethrin I and pyrethrin II esters.
Pyrethrins, natural extracts of Chrysanthemum cinerariaefolium and Chrysanthemum cocineum flowers, and pyrethroids, synthetic analogues and derivatives of pyrethrins, are powerful insecticides. They are widely used in households and insect control in pets or livestock, in textiles such as carpets, wallpapers, furniture and clothes, as well as in agriculture, forestry and public health services. This article brings a list of pyrethrin and pyrethroid insecticides registered for use in plant protection in Croatia. Pyrethrins and pyrethroids can enter the organism by ingestion (accidental or suicidal ingestion or in food), by inhalation and/or by skin contact. Although these pesticides pose a relatively low risk to mammals due to rapid metabolism with no significant accumulation, they can induce adverse health effects, more often in acute poisoning, but also due to chronic exposure. The primary target of pyrethrin and pyrethroid toxicity is the nervous system, since they act directly on the sodium channels of nerve cell axons, leading to hyperexcitation. Another important toxicological mechanism is allergenicity, which is more pronounced with pyrethrins than with synthetic pyrethroids. Because there is no antidote for pyrethrin and pyrethroid poisoning, treatment is symptomatic and supportive. The article discusses the measures for poisoning prevention and alleviation of exposure to pyrethrins and pyrethroids in occupational settings and in general population.
Field control failures with pirimiphos-methyl against the rice moth, Corcyra cephalonica (Stainton), in Weslaco, Texas, USA, led us to investigate the susceptibility of this particular strain to pirimiphos-methyl, spinosad, pyrethrins synergized with piperonyl butoxide, and pirimiphos-methyl combined with synergized pyrethrins. In laboratory bioassays, 50 eggs of C cephalonica were exposed to untreated and insecticide-treated corn and sunflower seeds to determine larval survival after 21 days, egg-to-adult emergence after 49 days, and larval damage to seeds at both exposure periods. Pirimiphos-methyl at both 4 and 8 mg kg(-1) did not prevent larval survival or egg-to-adult emergence of C cephalonica on either corn or sunflower seeds, and seed damage was evident at both rates. The C cephalonica strain was highly susceptible to spinosad at 0.5 and 1 mg kg(-1). At both spinosad rates, reduction in larval survival, egg-to-adult emergence, and seed damage relative to the control treatment was > or = 93% on both corn and sunflower seeds. Pirimiphos-methyl and spinosad were generally more effective against C cephalonica on corn than sunflower seeds. The C cephalonica strain was completely controlled on corn treated with 1.5 mg kg(-1) of pyrethrins synergized with 15 mg kg(-1) of piperonyl butoxide. Many larvae survived and became adults on corn treated with synergized pyrethrins at < or = 0.75 mg kg(-1). Corn treated with pirimiphos-methyl at 4, 6 or 8 mg kg(-1) in combination with 0.38 to 1.5 mg kg(-1) of synergized pyrethrins reduced larval survival by > or = 95%, egg-to-adult emergence by > or = 97%, and seed damage by > or = 94%. Our results suggest that the C cephalonica strain can be controlled on corn by combining pirimiphos-methyl with synergized pyrethrins or with synergized pyrethrins at the labeled rate. Although spinosad is not currently labeled for use on stored corn and sunflower seeds, it appears to be effective against C cephalonica on both commodities at very low rates.
In order to determine the human in vivo percutaneous absorption of pyrethrin and piperonyl butoxide, a commercial formulation containing either [14C]pyrethrin (3.8 mCi/mmol) or [14C]piperonyl butoxide (3.4 mCi/mmol) was applied to the ventral forearm of six human volunteers. The formulation contained 0.3% pyrethrin and 3.0% piperonyl butoxide. Spreadability studies showed that concentrations of 5.5 micrograms pyrethrin/cm2 and 75.8 micrograms piperonyl butoxide/cm2 (used in this study) would be consistent with levels found in actual use. The forearms were thoroughly cleansed with soap and water 30 min after application (as recommended for actual use). Percutaneous absorption was determined by urinary cumulative excretion following dose application. With a 7-day urinary accumulation, 1.9 +/- 1.2% (SD) of the dose of pyrethrin and 2.1 +/- 0.6% of the dose of piperonyl butoxide applied was absorbed through the forearm skin. 1 hr after application blood samples contained no detectable radioactivity. The percutaneous absorption of pyrethrin and piperonyl butoxide from the scalp was calculated to be 7.5% of the applied dose for pyrethrin and 8.3% for piperonyl butoxide. The calculated half-life of 14C excretion was 50 hr for pyrethrin and 32 hr for piperonyl butoxide. The data should be of relevance to appropriate risk assessment in extrapolating animal data to humans.
The dried flower heads of Tanacetum cinerariifolium Trev. (Family: Compositae) contain insecticidal compounds collectively called "pyrethrins." Pyrethrins are the subject of intense interest for use in crop protection because their toxicological properties permit control of certain insect species at application rates as low as 5-10 g AI acre(-1). Seedlings of sweet pepper, Capsicum annuum L. cv. Bell Boy Hybrid and tomato, Lycopersicon esculentum Mill. cv. Mountain Spring F1 Hybrid were planted and sprayed with a Multi-Purpose Insecticide formulation that contains 0.2% pyrethrins, 1.0% piperonyl butoxide (PBO), 88% diatomaceous earth, and 10.8% inert ingredients. The formulation was sprayed on pepper and tomato foliage when tomato fruits became red ripe and pepper became mature green at the rate of 6 lbs of formulated product per acre (5.4 and 27.2 g AI of pyrethrins and PBO, respectively). Following spraying, pepper and tomato leaves and fruits were collected at different time intervals for residue analysis using a high performance liquid chromatograph (HPLC) equipped with a UV detector. Residues of pyrethrins and PBO were generally higher on the leaves than fruits. Initial deposits (1 h following spraying) of pyrethrins were significantly higher on pepper than tomato fruits. Half-life (T1/2) values on pepper and tomato fruits did not exceed 2 h. Where concern exists over synthetic pesticide residues on treated crops and in the environment, pyrethrins are suitable alternatives that can be used to reduce the risk of exposure to synthetic pesticide residues.
The pyrethrins have a long and fascinating history. They were derived from dried chrysanthemum flower heads that were found to have pesticidal activity centuries ago. They comprise a complex mixture of six main chemicals. Commercial formulations usually contain piperonyl butoxide, which inhibits metabolic degradation of the active ingredients. Pyrethrins are readily absorbed from the gut and respiratory tract but poorly absorbed through skin. The active components are rapidly and extensively metabolised in the liver. Pyrethrins probably act on sodium channels resulting in nervous system overactivity. The possibility that they also induce hypersensitivity, which may be fatal when the respiratory tract is involved, has been debated for many years. A few clinical reports support this suggestion but the limited epidemiological evidence available is against it. The number of reports of toxicity caused by pyrethrins has greatly decreased over recent years. The pyrethrins are generally of low acute toxicity but convulsions may occur if substantial amounts are ingested. Two deaths from acute asthma have been attributed to pyrethrins and clinical reports suggest that they may also cause a variety of forms of dermatitis. Ocular exposure has resulted in corneal erosions. Management of pyrethrin toxicity is supportive and symptomatic.