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Inhibitory effects of four carbamate insecticides on acetylcholinesterase of male and female Carassius auratus in vitro.

The inhibitory effects of four carbamate insecticides, methomyl, thiodicarb, carbofuran and carbosulfan, on acetylcholinesterase of male and female Carassius auratus were investigated in the laboratory. Kinetic constants, biomolecular rate constant (k(i)), carbamylation rate constant (k2) and decarbamylation rate constant (k3) were determined in vitro. The ratios of bimolecular rate constant (female/male) for AChE reacting with methomyl, thiodicarb, carbofuran and carbosulfan were 1.03, 2.44, 1.03 and 1.106, respectively. The k(i) of AChE for thiodicarb was significantly higher in female fish than in male fish (P<0.05). The ratios of carbamylation rate constant (female/male) for methomyl, thiodicarb, carbofuran and carbosulfan were 1.18, 4.29, 3.53, and 2.07, respectively. The k2 values of AChE for the above four carbamates were significantly higher in females than in males. The ratios of the decarbamylation rate constant (female/male) for methomyl, thiodicarb, carbofuran and carbosulfan were 1.02, 1.39, 1.06, and 1.98, respectively. Only for carbosulfan, the decarbamylation rate of AChE was significantly higher in the female than in the male, indicating that AChE of females inhibited by carbosulfan recovered more quickly than that of males. The above results suggest that the female in the sensitivity of AChE to carbamates was different from the male fish.

Acetylcholinesterase↗

Patterns of insecticide resistance in onion thrips (Thysanoptera: Thripidae) in onion fields in New York.

To develop an insecticide resistance management program for onion thrips, Thrips tabaci Lindeman (Thysanoptera: Thripidae), on onions (Allium spp.), we surveyed populations in commercial onion fields in New York and evaluated their susceptibility to the two most widely used classes of insecticides plus two new insecticides during 2003-2005. All insecticide evaluations were conducted using the Thrips Insecticide Bioassay System (TIBS). As in our surveys conducted during 2002-2003, there were large temporal and spatial variations in susceptibility to the pyrethroid lambda-cyhalothrin (Warrior) across onion-growing regions in 2003. New data indicate that the field rate of methomyl (Lannate LV) still provides control but that the genes for resistance to methomyl are present in some populations. Tests with the two new insecticides, acetamiprid (Assail 70 WP) and spinosad (SpinTor 2CS), indicated they provided > 85% mortality at the field rate. To determine the spatial variation in insecticide susceptibility within a region, a series of systematic assays were conducted with lambda-cyhalothrin and methomyl. In 2004 and 2005, our data indicated that the within-region spatial variation in susceptibility to lambda-cyhalothrin was not large at the field rate or for the 100 ppm rate of methomyl. In 2005, a year in which T. tabaci densities in most fields were much higher than in 2004, growers were unable to control T. tabaci in particular fields and attributed this lack of control to resistance. Yet, we found similar levels of high susceptibility in all fields when using TIBS. This finding suggests that resistance had not developed and that variation in control may have been due to other factors, such as localized higher populations, poor spray coverage, too much time between spray applications, or different onion varieties.

Animals↗

Fungal toxins bind to the URF13 protein in maize mitochondria and Escherichia coli.

Expression of the maize mitochondrial T-urf13 gene results in a sensitivity to a family of fungal pathotoxins and to methomyl, a structurally unrelated systemic insecticide. Similar effects of pathotoxins and methomyl are observed when T-urf13 is cloned and expressed in Escherichia coli. An interaction between these compounds and the membrane-bound URF13 protein permeabilizes the inner mitochondrial and bacterial plasma membranes. To understand the toxin-URF13 effects, we have investigated whether toxin specifically binds to the URF13 protein. Our studies indicate that toxin binds to the URF13 protein in maize mitochondria and in E. coli expressing URF13. Binding analysis in E. coli reveals cooperative toxin binding. A low level of specific toxin binding is also demonstrated in cms-T and cms-T-restored mitochondria; however, binding does not appear to be cooperative in maize mitochondria. Competition and displacement studies in E. coli demonstrate that toxin binding is reversible and that the toxins and methomyl compete for the same, or for overlapping, binding sites. Two toxin-insensitive URF13 mutants display a diminished capability to bind toxin in E. coli, which identifies residues of URF13 important in toxin binding. A third toxin-insensitive URF13 mutant shows considerable toxin binding in E. coli, demonstrating that toxin binding can occur without causing membrane permeabilization. Our results indicate that toxin-mediated membrane permeabilization only occurs when toxin or methomyl is bound to URF13.

Binding, Competitive↗

Evaluation of selective toxicity of five pesticides against Plutella xylostella (Lep: Plutellidae) and their side-effects against Cotesia plutellae (Hym: Braconidae) and Oomyzus sokolowskii (Hym: Eulophidae).

The toxicities of five pesticides commonly used in vegetable fields to the larvae of the diamondback moth, Plutella xylostella (L) and its two major parasitoids, Cotesia plutellae (Kurdjumov) and Oomyzus sokolowskii (Kurdjumov), were evaluated in the laboratory using several bioassays. When tested at the rates recommended for field application by the manufacturer, fipronil, avermectin and chlorfluazuron produced over 95% mortality on third-instar larvae of P xylostella, but fenvalerate and methomyl did not produce any substantial mortality to such larvae, and over 70% of P xylostella larvae could still pupate normally after feeding on cabbage leaf treated with the two pesticides. In a residual contact assay with adult parasitoids, fipronil and methomyl caused over 93% mortality within 24 h; fenvalerate killed approximately 55% of the adults within 24 h; avermectin and chlorfluazuron showed differential toxicity to the two parasitoids. Avermectin was extremely harmful to O sokolowskii but slightly toxic to C plutellae, while chlorfluazuron was more toxic to C plutellae than to O sokolowskii. In the residue assay with cocoons of C plutellae and pupae of O sokolowskii developed within P xylostella pupae, treatments with pesticides did not reduce adult emergence. However, the mortality of C plutellae adults emerged from the fipronil-treated cocoons increased greatly within 24 h post-emergence; adults from the fenvalerate-treated cocoons parasitized less host larvae. Treatments with fenvalerate and methomyl significantly increased the mortality of O sokolowskii adults within 24 h post-emergence. Recommendations of choosing pesticides for the control of P xylostella are given.

Animals↗

Serum esterase inhibition in birds: a nondestructive biomarker to assess organophosphorus and carbamate contamination.

With the aim of proposing a nondestructive biomarker for monitoring the toxicological risk to birds of exposure to the organophosphorus insecticide azamethiphos and the carbamate insecticide methomyl, laboratory studies were performed on serum "B" esterases in Japanese quail (Coturnix coturnix japonica). The birds received two single dose treatments of each compound (azamethiphos and methomyl), i.e., 50 mg/kg and 250 mg/kg respectively. In the first treatment, serum butyrylcholinesterase (BChE) and carboxylesterase (CbE) were drastically inhibited in the azamethiphos-treated group, 24 h after the dose. No inhibition was detected for BChE and CbE activities in the methomyl-treated group, 24 h after the dose. In the second treatment, the birds died or were sacrificed 3 h after the dose. Serum BChE and brain acetylcholinesterase (AChE) were strongly inhibited after treatment with both insecticides. Serum CbE, hepatic microsomal CbE and 7-ethoxyresorufin dealkylation activities were also inhibited. A statistically significant correlation between serum BChE and brain AChE was found at lethal and sublethal doses of these xenobiotics. The experimental results indicate that the nondestructive biomarker BChE can give an early qualitative and semi-quantitative warning of the toxic effects of organophosphate and carbamate insecticides in birds.

Animals↗

Insecticide-insensitive acetylcholinesterase from a laboratory selected and a field strain of housefly (Musca domestica) (L.).

1. Acetylcholinesterase from the heads of a strain of houseflies selected for resistance to the carbamate insecticide methomyl, and from a methomyl-resistant field strain was found to be less sensitive to inhibition by methomyl than that from a susceptible strain. 2. The enzyme from resistant insects was also more tolerant to malaoxon, dichlorvos and bomyl but not to azamethiphos. 3. The decrease in sensitivity to inhibition appeared to be due to an increase in affinity for substrate.

Acetylcholinesterase↗

Acute poisoning with carbamate pesticides: the Cretan experience.

In Crete, in southern Greece, a number of fatal carbamate poisonings were investigated over a period of 2 years, from 1991 to 1993. Five cases are reported, involving the fatal ingestion of methomyl (Lannate), a cholinesterase-inhibiting carbamate insecticide. Analysis of samples of blood plasma and serum showed more than 90% inhibition of cholinesterase. The blood methomyl concentrations had a mean value of 26.7 mg/l, and a range of 5.6-57.0 mg/l. These values are much higher than those previously reporter in similar cases (0.57-1.4 mg/l). Methomyl concentrations in organs and tissues were found to be significantly lower than those in blood and vitreous humour.

Adult↗

N,N'-dicyclohexylcarbodiimide cross-linking suggests a central core of helices II in oligomers of URF13, the pore-forming T-toxin receptor of cms-T maize mitochondria.

URF13 is a mitochondrially encoded, integral membrane protein found only in maize carrying the cms-T cytoplasm. URF13 is associated with cytoplasmic male sterility, Texas type, and causes susceptibility to the fungal pathogens Bipolaris maydis race T and Phyllosticta maydis. URF13 is predicted to contain three transmembrane alpha-helices and is a receptor for the pathotoxins (T-toxins) produced by B. maydis race T and P. maydis. Binding of T-toxin to URF13 leads to membrane permeability. Cross-linking of URF13 oligomers with N,N'-dicyclohexylcarbodiimide (DCCD) protects Escherichia coli cells expressing URF13 and cms-T mitochondria from the permeability caused by T-toxin or methomyl. Using mutated forms of URF13 expressed in E. coli cells, we determined the molecular mechanism of DCCD protection. We separately changed Lys-37 in helix II to isoleucine (K37I-URF13) and Lys-32 in the helix I/helix II loop region to alanine (K32A-URF13). DCCD treatment of K37I-URF13-expressing cells did not protect the cells from permeability caused by T-toxin or methomyl. DCCD cross-linking was greatly reduced in K37I-URF13 and in D39V-URF13-expressing cells, but it was unaffected in K32A-URF13-expressing cells. Binding of methomyl or T-toxin decreases DCCD cross-linking of URF13 oligomers expressed in either E. coli or cms-T mitochondria. We conclude that Asp-39 in helix II is cross-linked by DCCD to Lys-37 in helix II of an adjacent URF13 molecule and that this cross-linking protects against toxin-mediated permeabilization. Our results also indicate that helices II form a central core in URF13 oligomers.

Amino Acid Sequence↗

A 13-kilodalton maize mitochondrial protein in E. coli confers sensitivity to Bipolaris maydis toxin.

The Texas male-sterile cytoplasm (cms-T) of maize carries the cytoplasmically inherited trait of male sterility. Mitochondria isolated from cms-T maize are specifically sensitive to a toxin (BmT-toxin) produced by the fungal pathogen Bipolaris maydis, race T, and the carbamate insecticide methomyl. A mitochondrial gene unique to cms-T maize, which produces a 13-kilodalton polypeptide associated with cytoplasmic male sterility, was expressed in Escherichia coli. After addition of BmT-toxin or methomyl, inhibition of whole cell respiration and swelling of spheroplasts were observed in Escherichia coli cultures producing the novel mitochondrial protein; these effects are similar to those observed with isolated cms-T mitochondria. The amino-terminal region of the 13-kilodalton polypeptide appears to be essential for proper interaction with the BmT-toxin and methomyl. These results implicate the 13-kilodalton polypeptide in conferring toxin sensitivity to mitochondria of cms-T maize.

Bacterial Proteins↗

Assessment of insecticide resistance after the outbreak of diamondback moth (Lepidoptera: Plutellidae) in California in 1997.

During an outbreak of the diamondback moth, Plutella xylostella (L.), in California in 1997, nine populations were collected from the major broccoli areas throughout the state. Populations were assayed for their susceptibility to currently used materials (Bacillus thuringiensis subsp. kurstaki, permethrin, and methomyl) and to newer materials that had not yet been commercially used in California (spinosad, emamectin benzoate, and chlorfenapyr). For the currently used insecticides, elevated levels of resistance were seen only with permethrin and seven of the nine populations had tolerance ratios (TR) of > 100. With the newer chemistries, TR values were all < 15. To compare potential cross-tolerance, TR values of the currently used insecticides were compared with TR values of the newer insecticides. There were significant relationships found between: methomyl and emamectin benzoate, methomyl and spinosad, and permethrin and spinosad. Further biochemical studies are needed to confirm the actual mechanisms that lead to these relationships and field tests are needed to determine what impact, if any, such TR levels would have on control in the field. These data indicate that resistance to at least one of the commonly used insecticides (permethrin) may have played a role in the outbreak during 1997. However, other factors may have been at least equally important. The winter of 1996-1997 was warmer than normal, and during the period from February through August of 1997 the amount of rainfall was < 50% of normal. Hot and dry conditions are known to be conducive to outbreaks of P. xylostella. These data add to an overall knowledge about the geographic variation of resistance in P. xylostella populations within the United States. They also serve as a baseline for monitoring changes in susceptibility to these newer insecticides and can also help explain the occurrence of outbreaks caused by factors other than insecticide resistance.

Animals↗

Carbamate and organophosphate resistance in cotton pests in India, 1995 to 1999.

Monitoring for organophosphate and carbamate resistance was carried out on five major insect pests of cotton collected from 22 cotton-growing districts across India. Resistance was monitored in Helicoverpa armigera (Hübner) and Pectinophora gossypiella (Saunders) for the period 1995-1999 and for Spodoptera litura (Fabricius), Earias vittella (Fabricius) and Bemisia tabaci (Gennadius) in a survey conducted during the 1997-98 cropping season. Of the 53 field strains of H. armigera, only four were found to exhibit resistance to quinalphos, the highest 15-fold, whereas all 16 field strains tested were found to be resistant to monocrotophos. Similarly, out of 40 field strains tested, only eight were found to express appreciable resistance to methomyl. Resistance in P. gossypiella to quinalphos was high in the majority of the strains tested. Of the seven strains of E. vittella tested, two strains from northern India exhibited > 70-fold resistance to monocrotophos. Of the 11 S. litura strains tested, only four were found to exhibit resistance factors of 10 to 30-fold to quinalphos and monocrotophos. All of the B. tabaci field strains exhibited resistance to methomyl and monocrotophos and susceptibility to triazophos. Practical implications for pest control resulting from the observed patterns of cross-resistance between quinalphos, monocrotophos and methomyl are discussed.

Animals↗

[Assessment on acute toxicity of combined pesticides].

The acute oral toxicity (LD50) of two pesticides combined from 3 categories of insecticides, i.e. organophosphates(OPs), pyrethroids and carbamates, was evaluated by Harris method on equal toxicity doses. The OPs compounds studied included: methylparathion, omethoate, methamidophos, phoxim, dichlorvos, profenofos, isocarbophos and malathion; the pyrethroids: alpha-cypermethrin, deltamethrin, fenvalerate and fenpropathrin; the carbamates: methomyl, isoprocarb and metolcarb. The mixtures of two OPs on the combination of dichlorvos plus omethoate and methamidophos plus profenofos showed additive effects, but methylparathion plus phoxim showed antagonistic effect. Most of the combination of OPs with pyrethroids showed synergistic effects, such as the mixtures of phoxim plus deltamethrin, phoxim plus alpha-cypermethrin, methlyparathion plus alpha-cypermethrin and ioscoarbphos plus fenpropthrin, with the exception of two mixtures showed additive effects: phoxim plus fenvalerate resulting in 1.5 times higher toxicity than expected, while dichlorvos plus deltamethrin resulting in less toxicity than expected. The effects of the mixtures of OPs and carbamates: phoxim plus methomyl and methamidophos plus metolcarb, were all additive, but the mixtures of he methylparathion plus methomyl showed antagonistic effect and malathion plus isoprocarb were synergistic. The biochemical mechanisms of changed toxicity of pesticides mixtures were discussed based on their toxicokinetics and toxicodynamics. It was concluded that the combined effects of insecticide mixtures were additive for OPs plus OPs or plus carbamates in most cased, but synergistic for OPs plus pyrethroids.

Animals↗

Carbamate poisoning and oxime treatment in children: a clinical and laboratory study.

OBJECTIVE: (1) Retrospective evaluation of the clinical course of carbamate poisoning and the effect of oxime therapy in children. (2) In vitro study of the effect of oximes on the reactivation of carbamylated cholinesterase. DESIGN: (1) Clinical survey: The records of 26 children intoxicated with carbamates were examined retrospectively. The poisoning agents in all cases were positively identified as methomyl or aldicarb by gas chromatography-mass spectrometry. (2) Laboratory study: The direct effect of obidoxime and of pralidoxime on acetylcholinesterase activity in vitro was investigated in normal human packed red blood cells pretreated with an organophosphate (paraoxon) or a carbamate (aldicarb or methomyl). CLINICAL SETTING: Pediatric intensive care unit of a teaching hospital. PATIENTS: Twenty-six infants and young children (aged 1 to 8 years) admitted to the pediatric intensive care unit with severe carbamate intoxication. INTERVENTIONS: All cases had been treated with repeated doses of atropine sulfate (0.05 mg/kg) administered every 5 to 10 minutes until muscarinic symptoms disappeared. Obidoxime chloride (Toxogonin, 6 mg/kg) was administered on admission, and again after 4 to 5 hours. RESULTS: Predominant symptoms were related to central nervous system and nicotinic effects. All the patients showed marked improvement within several hours and recovered completely within 24 hours. None of the children deteriorated and none showed exacerbation of cholinergic symptoms after obidoxime treatment. In vitro, oximes reactivated acetylcholinesterase inhibited with paraoxon, whereas no significant effect of oximes on carbamylated enzyme activity was observed. CONCLUSIONS: Based on the recovery of all cases, as compared with other reports of carbamate poisoning treated with atropine alone, it is concluded that, in the case of aldicarb or methomyl poisoning, oxime therapy apparently does not contribute to the recovery of poisoned patients. In cases of poisoning by an unknown pesticide or of mixed poisoning, oxime therapy can prove beneficial because no negative effects of the therapy can be discerned.

Aldicarb↗

Cross-linking of the cms-T maize mitochondrial pore-forming protein URF13 by N,N'-dicyclohexylcarbodiimide and its effect on URF13 sensitivity to fungal toxins.

URF13 is a membrane protein unique to mitochondria from maize having the Texas male-sterile cytoplasm (cms-T), which is capable of permeabilizing biological membranes in the presence of a family of pathotoxins (T-toxins) produced by certain fungi or the insecticide methomyl. The carboxylate-specific reagent dicyclohexylcarbodiimide has been shown previously to protect URF13-containing membranes against the permeabilizing effects of added T-toxin or methomyl. Dicyclohexylcarbodiimide was found to covalently cross-link URF13 into higher order oligomers, including dimers, trimers, and tetramers, in isolated cms-T mitochondria and Escherichia coli cells expressing URF13. In intact E. coli cells and isolated spheroplasts, the observed protection against the effects of methomyl was not associated with the appearance of dimers but was correlated with the appearance of cross-linked trimers and tetramers. Following treatment of E. coli cells expressing URF13 with dicyclohexylcarbodiimide, the specific binding of tritiated T-toxin was reduced by 50% and all binding cooperativity was lost. A similar decrease in the level of T-toxin binding and loss of binding cooperativity were observed with site-directed, T-toxin-insensitive URF13 mutants at aspartate 39, the residue known to undergo reaction with dicyclohexylcarbodiimide. When coupled with a postulated three membrane-spanning helical model of URF13, these results provide initial insights into the intermolecular interactions involved in URF13 oligomer formation.

Aspartic Acid↗

The status and development of insecticide resistance in Danish populations of the housefly Musca domestica L.

Samples of housefly (Musca domestica) field populations were collected from Danish livestock farms in 1997. The tolerance of the first-generation offspring was determined for a number of insecticides. Dose-response values were obtained by topical application for the pyrethroids bioresmethrin and pyrethrum, both synergised with piperonyl butoxide, and the organophosphate dimethoate. The organophosphates azamethiphos and propetamphos and the carbamate methomyl were tested in discriminating dose feeding bioassays. Resistance was low to moderate in most of the populations for most of the compounds tested, but this study also revealed the existence of high resistance to pyrethroid, organophosphate and carbamate insecticides in some populations. The resistance factors at LD50 for bioresmethrin/piperonyl butoxide ranged between 2 and 98, and for pyrethrum/piperonyl butoxide between 2 and 29. Our results indicate that pyrethroid resistance in Denmark is increasing, since four of the 21 farms showed more than 100-fold resistance at LD95, a level of resistance only observed once before. Resistance factors at LD50 for dimethoate ranged from 9 to 100, and showed two distinct trends: populations with either decreasing or increasing resistance. Resistance to azamethiphos was found to be widespread and high. Although two strains with high methomyl and propetamphos resistance were observed, methomyl and propetamphos resistance is moderate and appears not to be increasing.

Animals↗

URF13, a ligand-gated, pore-forming receptor for T-toxin in the inner membrane of cms-T mitochondria.

URF13 is the product of a mitochondrial-encoded gene (T-urf13) found only in maize plants containing the Texas male-sterile cytoplasm (cms-T), and it is thought to be responsible for both cytoplasmic male sterility and the susceptibility of cms-T maize to the fungal pathogens Bipolaris maydis race T and Phyllosticata maydis. Mitochondria isolated from cms-T maize are uniquely sensitive to pathotoxins (T-toxin) produced by these fungi and to methomyl (a commercial insecticide). URF13 acts as a receptor that specifically binds T-toxin to produce hydrophilic pores in the inner mitochondrial membrane. When expressed in Escherichia coli cells, URF13 also forms hydrophilic pores in the plasma membrane if exposed to T-toxin or methomyl. Topological studies established that URF13 contains three membrane-spanning alpha-helices, two of which are amphipathic and can contribute to pore formation. Chemical cross-linking of URF13 was used to demonstrate the existence of URF13 oligomers in cms-T mitochondria and E. coli cells. The ability of the carboxylate-specific reagent, N,N'-dicyclohexycarbodiimide, to cross-link URF13 was used in conjunction with site-directed mutagenesis to establish that the URF13 tetramer has a central core consisting of a four-alpha-helical bundle which undergoes a conformational change after interaction with T-toxin or methomyl. Overall, the experimental evidence indicates that URF13 functions as a ligand-gated, pore-forming T-toxin receptor in cms-T mitochondria.

Amino Acid Sequence↗

Relationship between toxicity of selected insecticides and expression of stress proteins (HSP, GRP) in cultured human cells: effects of commercial formulations versus pure active molecules.

Three carbamate (formetanate, methomyl, pyrimicarb) and one pyrethroid (bifenthrin) insecticides were investigated both as pure chemicals and as commercial formulations in order to unveil possible toxic effects of additives and solvents present in the commercial formulations and to evaluate the cellular stress response as a defense mechanism. Toxic effects were evaluated on A549 cells, derived from a human lung carcinoma, by measuring (1) threshold concentrations leading to a decrease of the growth rate (LOEC), (2) sublethal concentrations (SC) which arrested growth without killing the cells, and (3) expression levels of several stress proteins, i.e., HSP27, HSP72/73, HSP90, GRP78, and GRP94. As compared to the pure active molecule, LOEC appeared at lower concentrations when using the commercial formulations, i.e., Dicarzol (formetanate), Lannate20 (methomyl) and Talstar or Kiros EV (bifenthrin). Propylene glycol and propylene glycol monomethyl ether, respectively, present in Talstar and kiros, do not account for the high toxicity of these commercial formulations and do not potentiate the toxicity of bifenthrin. Additive but not synergistic adverse effects were observed when cells are exposed to a mixture of 4 different commercial formulations. Our results show that the concentrations of active molecules recommended in flori-cultural general use or for spray preparations are much higher than SC concentrations, as determined on A549 pulmonary cells. GRP78 was up-regulated by all the insecticides, commercial preparations being more efficient to trigger the stress reaction. This suggests that insecticides and additives present in commercial formulations disrupt ER functions. Conversely, HSP72/73 was found to be down-regulated by all the insecticides. This seems to be related with a decrease of protein synthesis in the cytosol, as a result of the ER unfolded protein response. Indeed, tunicamycin, known to inhibit N-linked glycosylation in the ER, was found to induce a similar inverse correlation between GRP78 overexpression and HSP72/73 under-expression. Expression of GRP94 was found to be increased and HSP27 lowered by the highest concentrations of bifenthrin commercial formulations. Methomyl and Lannate20 only induced an under-expression of HSP90.

Cell Line, Tumor↗

N-methyl carbamate pesticide residues in conventional and organic infant foods available on the Canadian retail market, 2001-03.

Seven parent N-methyl carbamate insecticides, in addition to two transformation products of aldicarb (aldicarb sulfoxide and aldicarb sulfone), and a single transformation product of carbofuran (3-hydroxycarbofuran) were measured in infant and junior foods available on the Canadian retail market between 2001 and 2003. Carbaryl and methomyl were the only analytes present at levels above the limits of detection in juice, cereals, fruit, vegetables or meat samples analysed. Carbaryl was the most frequently (7.6%) detected compound and concentrations ranged from 0.6 to 18 ng g-1. Detectable levels of carbaryl were most frequently found in foods prepared with fruit. Methomyl was detected (0.8 ng g-1) in one chicken with broth sample analysed in the present study. In all cases, the concentrations observed were orders of magnitude below the maximum residue limits established for these compounds in the corresponding raw food commodities in Canada (100-10 000 ng g-1). Dietary intakes of carbaryl and methomyl based on the consumption of infant foods tested ranged between 0.2-343 and 0.4-2.0 ng kg-1 body weight day-1, respectively.

Carbamates↗