Implication in the control of malaria vectors with insecticides in tropical countries of South-East Asia region. Part II--Consequences of insecticide use.
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This study was undertaken to investigate the possibility that mechanisms other than cholinesterase (ChE) inhibition account for the acute toxicity of organophosphorus insecticide. Both the P = O type insecticide (direct ChE inhibitors: chlorfenvinphos and dichlorvos) and the P = S type insecticide (indirect ChE inhibitors: diazinon and fenthion) were employed. Rats treated with lethal doses of intravenous and oral P = O type insecticides and oral P = S type insecticides exhibited typical signs of anti-ChE poisoning along with marked inhibition of brain and erythrocyte ChE activity. In contrast, rats given lethal doses of intravenous P = S type insecticides exhibited tonic convulsions and opisthotonos, with only slight inhibition of ChE activities. When P = O type insecticides were intravenously administered to anesthetized and conscious rats, animals exhibited typical anti-ChE poisoning signs in cardiorespiration: hypertension and apnea which were antagonized by atropine. After administration of lethal doses of P = O type insecticides, breathing disappeared before the cessation of heart beats. Rats receiving lethal doses of intravenous P = S type insecticides did not show hypertension, but exhibited transient cessation of breathing and heart beats. Breathing was observed after the disappearance of heart beats. The electroencephalogram (EEG) was characterized by spike and wave complexes. The EEG and cardiorespiratory changes were not antagonized by atropine. It was concluded that lethality following intravenous P = S type insecticides may be independent of ChE inhibition.
Fresh water fish, Motsugo was reared in aquarium water tank containing about 1 ppm of 3 organophosphorus and 3 carbamate insecticides for about 30 days. The persistence of these insecticides in water and uptake and excretion of insecticides by fish were examined. Among organophosphorus insecticides, malathion is the most unstable in water, and degraded more than 99% for 7 days. Fenitrothion is moderately stable, and degraded 97% for 29 days. Diazinon is the most stable, and degraded 72% for 30 days. Among carbamates, carbaryl is the most unstable in water, and degraded more than 95% for 6 days. BPMC is moderately stable, and degraded 80% for 32 days. XMC is the most stable, and degraded 45% for 34 days. As for the uptake of the pesticides by fish, organophosphorus insecticides were generally higher than carbamate insecticides. The concentration of diazinon in fish reached to 211 ppm of the maximum level after 3 days, and that of fenitrothion reached to 162 ppm of the maximum level after 4 days. Afterwards, the concentration of both the insecticides decreased gradually due to the metabolism and excretion of the insecticides in fish. Uptake of malathion was very low and metabolized rapidly, and its concentration became to less than 0.01 ppm after 7 days. Among carbamate insecticides, the concentration of carbaryl in fish after one day reached to 7.5 ppm which was the maximum level of uptake. On the other hand, the concentration of BPMC in fish after 4 days became to 4.8 ppm, which was the maximum level, and decreased gradually. The concentration of XMC in fish was only 1.4 ppm after one day, but the metabolism rate of XMC in fish was fairly slow. Therefore, 0.55 ppm of XMC in fish remained even after 34 days. Moreover, in the test tank of diazinon, fenitrothion and BPMC, the appearance of deformed fish with spinal curvature of back bone came out at the rate of 10 to 30%.
In May 1983, granular formulations of carbofuran, chlorpyrifos, disulfoton, fonofos, isofenphos, phorate, and terbufos were applied in incorporated bands to duplicate 2 m2 field plots of clay loam. Insecticide concentrations were determined in the bands at 0,1,2,3,4,6,8,10,12,16, and 20 wk. Following spring cultivation, the insecticides were applied to the same plots in 1984 and 1985. In addition, carbofuran was applied to previously untreated plots in 1984 and all 7 materials were applied to previously untreated plots in 1985. Sampling and analysis were carried out as in 1983. Persistence was assessed on the basis of the disappearance rates measured for the 1st 8 wk and of a calculated Effectiveness Potential (the ratio of the average residue in the upper 5 cm of the band at 8, 10 and 12 wk and the published LC95 for western corn rootworm in clay loam soil). Soils treated with carbofuran and isofenphos in 1984 and all soils treated in 1985 were tested for anti-insecticide activity. Soil cores from some carbofuran, chlorpyrifos and terbufos treated plots were sectioned vertically to establish the distribution of the insecticides during 1985. In addition, granular and pure chemical forms of isofenphos and carbofuran were applied at 10 ppm to anti-isofenphos and anti-carbofuran active and control soils (from field plots) maintained at 10 and 20% moisture in the laboratory to assess the effect of formulation and moisture on persistence in active soils. Insecticide concentrations were determined at 0,1,3,7, 10,14,21,28, and 35 days. The persistence of chlorpyrifos, terbufos and phorate was relatively constant over the 3 years and between plots receiving single and multiple treatments. Disulfoton and fonofos behavior was more variable and that of carbofuran and isofenphos was extremely variable. Anti-insecticide activity against carbofuran and isofenphos was detectable 2 wk after an initial application and was still present the following spring. Anti-insecticide activity against fonofos, terbufos sulfoxide, phorate sulfone and disulfoton sulfone was also generated in this soil. Anti-insecticide activity against chlorpyrifos, disulfoton, terbufos and phorate was not present. Carbofuran, chlorpyrifos and terbufos (+ metabolites) present in the upper 5 cm of soil averaged 93, 94 and 94%, respectively, of the total core contents over 12 wk. Significant moisture dependent differences were observed between the behavior of granular carbofuran and granular isofenphos in anti-insecticide active soils.(ABSTRACT TRUNCATED AT 400 WORDS)
The effects of saturating concentrations of DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane] and the pyrethroid insecticides cismethrin and deltamethrin on alkaloid-dependent activation of the voltage-sensitive sodium channel were studied using measurements of 22Na+ uptake into mouse brain synaptosomes. In survey experiments, these compounds enhanced sodium uptake stimulated by veratridine and batrachotoxin, but inhibited uptake stimulated by aconitine. Concentration response curves for aconitine run in the absence and presence of 10 microM cismethrin demonstrated that the inhibition was noncompetitive. This unanticipated inhibitory effect of insecticides on aconitine-dependent sodium uptake suggests a possible overlap or negative allosteric coupling between the binding sites for insecticides and aconitine and reveals unique characteristics of the action of aconitine that are not shared by veratridine and batrachotoxin. More detailed studies of the effects of insecticides on veratridine- or batrachotoxin-stimulated uptake found small insecticide-dependent increases in the potency of these activators. In addition to this effect, DDT and deltamethrin also enhanced maximal uptake stimulated by veratridine. Possible mechanisms underlying these effects of insecticides on alkaloid-dependent uptake are discussed in light of a qualitative model formulated from these results and previous biochemical and electrophysiological studies. Additional experiments were designed to assess the interactions of insecticides and toxin II of the sea anemone Anemonia sulcata (ATX II) as modifiers of alkaloid-dependent uptake. DDT and ATX II acted synergistically to increase uptake stimulated by veratridine. Moreover, DDT shifted the potency of ATX II for enhancing veratridine-dependent uptake to 5-fold lower concentrations. In contrast, DDT and subsaturating concentrations of ATX II acted independently in their enhancement of sodium channel activation by batrachotoxin. Mutually exclusive effects on veratridine-dependent uptake were observed when cismethrin was co-applied with ATX II. However, independent effects of cismethrin and ATX II were found with aconitine-modified channels, in that cismethrin was able to inhibit ATX II-enhanced aconitine-dependent sodium flux. Thus, the interactions between insecticides and ATX II as modifiers of alkaloid-dependent uptake are complex and depend on the insecticide-activator combination under study.
Stictocephala bisonia is an important invasive agricultural pest. Due to the frequent application of insecticides in its habitat, this species is under intense selection pressure. Chemosensory proteins (CSPs) and odorant-binding proteins (OBPs) are known to play key roles in insecticide resistance, but their specific functions in S. bisonia remain unclear. In this study, we identified a total of 22 SbisCSPs and 16 SbisOBPs based on the S. bisonia genome. To screen for candidate genes potentially linked to insecticide resistance, we adopted a multi-criteria screening strategy that integrated phylogenetic analysis, molecular docking with three insecticides, and tissue-specific expression profiling. Phylogenetic analysis identified several SbisCSPs and SbisOBPs clustering with genes known to be involved in insecticide resistance, serving as an initial evolutionary filter. Molecular docking results indicated that λ-Cyhalothrin exhibited the strong predicted binding affinity with most of SbisCSPs and SbisOBPs. Subsequent qPCR validation of seven prioritized candidates revealed distinct expression patterns: SbisCSP22 was highly expressed in adults and demonstrated strong binding affinity to all three insecticides tested, suggesting a potential role in mediating multi-insecticide response. Conversely, SbisCSP17 was significantly upregulated in larvae, clustered with genes known to mediate imidacloprid resistance, and exhibited strong binding affinity to imidacloprid. Given its larval-specific expression and the soil-dwelling behavior of larvae, we hypothesize that SbisCSP17 is a key candidate gene for larvae coping with soil-treated insecticides.
Organophosphorus and carbamate insecticides are used commonly in agriculture to control pests of crops and animals. These compounds are toxic and livestock poisoning has occurred from mistaken addition of unused insecticide to feeds and animal access to improperly disposed of materials or "empty" containers. The morbidity rate approximates a third of animals exposed and about half of those affected die. Organophosphorus and carbamate insecticides generate their toxic effects by bonding to and inhibiting ChE enzymes (most importantly, AChE), which are responsible for breaking down the neurotransmitter ACh. The accumulation of ACh results in uninhibited impulse transmission at the cholinergic endings, including autonomic preganglionic junctions, certain neurons in the central nervous system, and motor nerves to the skeletal muscles. This eventually leads to fatigue of end organs; death usually is a result of respiratory failure. The "delayed neuropathy syndrome" is caused by some OP insecticides, but the pathophysiology of this syndrome does not involve the inhibition of ChE and accumulation of neurotransmitter. Over 100 anticholinesterase insecticides are in use. Variations in toxicity exist among these compounds, but larger diversities exist in the likelihood of poisoning because of differences in formulations, solvents, and conditions of use. Young animals usually are more sensitive than adults. Some of these agents are among the most toxic of manmade chemicals. These insecticides generally do not accumulate in tissues. The "chronic" effects depend on accrued physiological changes from frequent exposure to nonlethal doses. Clinical signs occur within minutes to a few hours and include the muscarinic signs of salivation, excessive lacrimation, frequent urination, and diarrhea. Concurrent nicotinic effects include muscular tremors followed by weakness and paralysis. Topical exposure results in similar poisoning but the onset of clinical signs may be delayed. Certain pour-on insecticides may cause a delayed (more than a week) syndrome in some breeds. Diagnosis of OP or carbamate insecticide poisoning is made by (1) interpretation of clinical signs and history that are consistent with this poisoning, (2) detection of the chemical compound in stomach or rumen contents and tissues, and (3) demonstration of the adverse biological effect, ChE inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)
A rapid analysis of Bacillus thuringiensis strains predictive of insecticidal activity was established by using polymerase chain reaction (PCR) technology. Primers specific to regions of high homology within genes encoding three major classes of B. thuringiensis crystal proteins were used to generate a PCR product profile characteristic of each insecticidal class. Predictions of insecticidal activity were made on the basis of the electrophoretic patterns of the PCR products. Included in the screen were PCR primers specific for cryI, cryIII, and cryIV genes, which are insecticidal for lepidopterans, coleopterans, and dipterans, respectively. Known B. thuringiensis strains as well as unidentified strains isolated from soil and insect cadavers were analyzed by PCR. Small amounts of crude sample lysates were assayed in a single PCR reaction containing 12 to 20 primers capable of distinguishing between the different insecticidal genes. Insecticidal activity predicted by the PCR screen was found to correspond with the insecticidal activity of insect bioassays. In addition to identifying strains with known insecticidal genes, the PCR screen can identify strains with altered electrophoretic patterns containing potentially novel genes.
Two major classes of enzymes, i.e., hydrolases and transferases, comprise all the nonoxidative enzymes, and together these enzymes catalyze a wide variety of biotransformations of insecticides. The hydrolytic enzymes involved in insecticide metabolism are carboxylesterase (EC 3.1.1.1), arylesterase alkylamidase, and DFPase (EC 3.8.2.1). Recent experimental evidence suggests that carboxylesterase enzyme(s), formerly known to hydrolyze malathion-type insecticides, can also catalyze hydrolysis of a variety of diversified insecticidal esters such as benzilic acid derivatives, carbanilate compounds, and pyrethroids. These organophosphate-sensitive esterases, with the exception of the enzyme which hydrolyzes malathion, are all present in microsomes. Similarly, the action of amidases now extends to those insecticidal compounds of their intermediates which contain an aminoformyl (N-CHO) moiety. Arylesterase and DFPase catalyze the P-anhydride bond cleavage of the leaving group, a major hydrolytic pathyway for organophosphate insecticides. Transferal enzymes which are presently know to metabolize insecticidal organophosphates are GSH-S-alkyltransferase (EC 2.5.1.12) and GSH-S-aryltransferase (EC 2.5.1.13). These enzymes cleave P-O-R (R = alkyl) or P-0-X (X = aromatic), with subsequent transfer of the R or X group to glutathione. Regarding the other conjugating enzymes, UDP-glucuronyltransferase (EC 2.4.L.17), UDP-glucosyltransferase (EC 2.4.1.35), and arylamine acetyltransferase (EC 2.3.1.5), much work is needed to understand their interactions with insecticidal compounds. There is some evidence that arylsulfotransferase (EC 2.8.2.1) MAY PLAY A PROMINENT ROLE IN THE CONJUGATIVE MECHANISMS OF INSECTS.
Two major classes of enzymes, i.e., hydrolases and transferases, comprise all the nonoxidative enzymes, and together these enzymes catalyze a wide variety of biotransformations of insecticides. The hydrolytic enzymes involved in insecticide metabolism are carboxylesterase (EC 3.1.1.1), arylesterase (EC 3,1.1.2), alkylamidase, and DFPase (EC 3.8.2.1). Recent experimental evidence suggests that carboxylesterase enzymes(s), formerly known to hydrolyze malathion-type insecticides, can also catalyze hydrolysis of a variety of diversified insecticidal esters such as benzilic acid derivatives, carbanilate compounds, and pyrethroids. These organo-phosphate-sensitive esterases, with the exception of the enzyme which hydrolyzes malathion, are all present in microsomes. Similarly, the action of amidases now extends to those insecticidal compounds or their intermediates which contain an aminoformyl (N--CHO) moiety. Arylesterase and DFPase catalyze the P--anhydride bond cleavage of the leaving group, a major hydrolytic pathway for organophosphate insecticides. Transferal enzymes which are presently known to metabolize insecticidal organophosphates are GSH-S-alkyltransferase (EC 2.5.1.12) and GSH-S-aryltransferase (EC 2.5.1.13). These enzymes cleave P--O--R (R = alkyl) or P--O--X (X = aromatic), with subsequent transfer of the R or X group to glutathione. Regarding the other conjugating enzymes, UDP-glucuronyltransferase (EC 2.4.1.17), UDP-glucosyltransferase (EC 2.4.1.35), and arylamine acetyltransferase (EC 2.3.1.5), much work is needed to understand their interactions with insecticidal compounds. There is some evidence that arylsulfotransferase (EC 2.8.2.1) may play a prominent role in the conjugative mechanisms of insects.
The movement of chlorpyrifos and diazinon from cracks and crevices in empty dormitory rooms with and without forced air movement to houseflies and plates in non-target areas was studied. Aluminum pie plates in rooms with the high concentrations of an insecticide, no forced air movement, and at the earlier sampling interals contained more insecticide. Insecticides were not detectable at 48 hr. Increased housefly movement occurred simultaneously with the initiation of insecticide application in rooms with forced air and 1 min later in rooms with no forced air. Mortality of houseflies exposed during and at 5 hr after insecticide application was greater for males than females in all tests except one; at the high insecticide concentrations; and at successive time intervals through the 24-hr interval after their transfer from the treated rooms to holding rooms. Houseflies in cages near the ceiling, exposed to an insecticide, and forced air movement, exhibited greater mortality than those in cages on the floor, while the reverse was true for houseflies in rooms with no forced air movement.
Most childhood exposures to insecticides and herbicides do not result in poisonings. Decontamination and observation are usually adequate treatments. The most frequent exposures involve carbamate and organophosphate insecticides. These compounds inhibit acetylcholinesterase, resulting in cholinergic signs that are reversible with atropine administration. Recent reports from poison control centers indicate that organophosphates have been associated with most of the serious childhood poisonings. Pralidoxime, a cholinesterase reactivator, must be administered along with atropine to patients with serious organophosphate poisoning, to reverse nicotinic receptor effects--in particular, respiratory paralysis. Although carbamates and organophosphates may cause clinically indistinguishable physical signs, pralidoxime therapy may be contraindicated for carbamate intoxications. In the event of a serious poisoning caused by a combination of organophosphate and carbamate insecticides, or by an unknown cholinergic agent, pralidoxime should not be withheld. Many organochlorine insecticides are restricted or are no longer available in the United States. CNS excitation and seizures, manifestations of organochlorine intoxication, can occur following ingestion or inappropriate application of the 1 per cent topical formulation of lindane used to treat scabies and lice. Treatment of such intoxication consists of decontamination measures and anticonvulsant administration. Pyrethrins are generally nontoxic in doses commonly ingested. Individuals with an allergic history may be at greatest risk for the most common adverse effects, contact dermatitis and hypersensitivity reactions. Of all insecticides or herbicides, paraquat is the most toxic. Any exposure to paraquat must be evaluated, even if several days have passed since the herbicide was ingested. Signs of pulmonary status deterioration usually portend a grave prognosis in paraquat poisoning. Despite in vitro toxicity similar to paraquat, diquat does not cause lung effects in human poisonings, and reported deaths have been from other causes. Poisoned patients who receive appropriate and timely treatment are virtually assured of complete recovery from most insecticide and herbicide poisonings. Deaths and long-term sequelae most often result from respiratory complications, which may occur as complications of the intoxication or from other constituents in the insecticide or herbicide formulation. Good supportive care with meticulous attention to, and anticipation of, respiratory complications is absolutely essential to prevent long-term sequelae or death from hypoxia.(ABSTRACT TRUNCATED AT 400 WORDS)
Assays of five commercial insecticides applied as residual sprays at label rates to plywood indicated the most toxic insecticide overall for pteromalid parasitoids of house flies, Musca domestica L., was Atroban (permethrin), followed by Ciodrin (crotoxyphos), Rabon (tetrachlorvinphos), Ectrin (fenvalerate), and Cygon (dimethoate). Insecticide-susceptible house flies were susceptible to all five insecticides (mortality, 62-100%). Flies that were recently colonized from populations on dairy farms in New York were susceptible only to Rabon. Urolepis rufipes (Ashmead) was the most susceptible parasitoid species overall to these insecticides, followed by Muscidifurax raptor Girault & Sanders, Nasonia vitripennis Walker, Pachycrepoideus vindemmiae (Rondani), and Spalangia cameroni Perkins. Compared with susceptible flies, newly colonized flies showed moderate resistance to avermectin B1a (abamectin). Abamectin was more toxic to all of the parasitoids except N. vitripennis and S. cameroni than to newly colonized house flies when exposed for 90 min to plywood boards treated with 0.001-0.1% abamectin. Space sprays with Vapona (dichlorvos) killed all of the parasitoids and susceptible flies and 64% of the newly colonized flies when insects were placed directly in the path of the spray; mortality was substantially lower among flies and parasitoids protected under 5 cm of wheat straw. Space sprays with Pyrenone (pyrethrins) killed greater than 86% of all insects exposed to the spray path except for the newly colonized flies (1% mortality); mortality of insects protected under straw was low (less than 12%) except for S. cameroni (76%). Because responses of the five parasitoids to the different insecticides varied considerably, general conclusions about parasitoid susceptibility to active ingredients, insecticide class, or method of application were not possible.
The clinical study of 13 patients with chronic neurological manifestation induced by insecticides (organophosphorades and organochlorades compounds) is reported. Twelve patients were male and farmers and one was a saleslady. The authors adopted five conditions for diagnosis: frequent contact with insecticides, synaptomatology directly related to the compounds exposition, clinical and laboratorial exclusion of others pathologies, quickly improvement of the symptoms when the patients were away from their original environment and high levels of insecticides in blood and urine determination. The clinical data was not uniform and the manifestation include pure motor neuropathy, mixed sensory-motor neuropathy, mielopathy and cranial nerves palsies. No relationship could be established between the insecticides (type, frequency of number of exposition) to the clinical picture. The insecticides determination was positive (moderated or elevated levels) in all patients and in 40% of controls (traces). Eletromyographic studies showed a neuropathic pattern in the majority of cases and reduced motor nerve conduction velocities. The authors believe that insecticides determination has a relative value and others criterion must be used in the diagnosis of chronic illness caused by insecticides. They think that others factors can be related with the symptomatology (hypersensibility, malnutrition, previous sensibilization or cumulative effect).
Insecticide resistance is an inherent characteristic dependent on relatively simple genetic mechanisms. This seems to be especially true of dieldrin resistance in anopheline mosquitos, though less obvious in DDT resistance among these species; little is known as yet about the inheritance of organophosphate and carbamate resistance as it occurs in Anopheles albimanus. The speed of selection of resistance depends on the original frequency of the gene or genes involved, the nature of the resistance imparted, and the selection pressure of the insecticide. This in turn depends on the inherent toxicity of the chemical, the efficiency with which it is applied, the proportion of the mosquito population coming under its influence, and the behaviour of the mosquito. In the past, too much reliance has been placed on the determination of the LD(50) in assessing the presence or absence of insecticide resistance. Quite high incidences of resistant individuals can result in such small changes in the LD(50) that resistance may be overlooked. The use of single discriminating dosages is advocated, based on concentrations of insecticides that normally kill all susceptible individuals. The authors discuss such dosages in respect of dieldrin and DDT, and put forward newly-established tentative discriminating dosages for organophosphorus and carbamate insecticides, which await field confirmation.From a practical standpoint, an insecticide should not be abandoned or replaced by another as soon as resistance is confirmed. This may not be necessary where the degree of resistance is not high and the vector is not highly efficient. Certain procedures are proposed in order to assess the epidemiological and entomological implications of resistance before the insecticide concerned is abandoned.
The effects of aerial spraying of an insecticide were investigated in a mountain stream using a drift net. The concentration of fenitrothion (organophosphorus insecticide) in the river water increased to ca. 20 micrograms liter-1 3 hr after the spraying and decreased exponentially to half the peak value after 2 hr. A large number of aquatic insects were found drifting after the spraying. The total number of individuals which drifted in the daytime after spraying reached nine times the number found the previous night. The total number of species which drifted during the 24 hr following the spray increased to 43 from 17 on the previous day. Before the insecticide spraying, the drifting benthos were almost entirely made up of three species of Baetis (Ephemeroptera). However, many individuals of several species of Heptageniidae (Ephemeroptera), Apsilochorema sutshanum (Trichoptera), and Chironomidae (Diptera) drifted in addition to Baetis after the spray. A large number of young Baetis, which had not been seen in the natural night drift samples, were found drifting due to the insecticide. Natural night drift almost disappeared from the day following insecticide spraying. At the second insecticide spraying, conducted 20 days after the first, the number of individuals which drifted during the 24 hr following spraying decreased to only 0.85% of that in the first spraying although changes in insecticide concentration showed a similar pattern. Several species of Ephemeroptera were dominant among the fauna in the studied stream, and the causal relationships of this are discussed.