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At least 19 recordsLinked to original sources
PubMed2004

A cross-sectional study of triallate exposure and neurological health among workers at a pesticide manufacturing and formulating facility.

AIMS: To evaluate the relation between an indicator of cumulative exposure to triallate and selected measures of neurological function, including nerve conduction, the prevalence of certain neurological deficits as determined by a medical examination, and vibration perception threshold testing in workers at a pesticide manufacturing plant. METHODS: Subjects were 50 workers with high estimated triallate exposure ("high triallate" group) and 50 workers with no or low triallate exposure ("no/low triallate" group). Industrial hygienists used existing work histories and personal knowledge of plant operations to develop a triallate score. In-person interviews elicited information on past medical history and on occupational and non-occupational exposures. A neurologist carried out nerve conduction tests of the sural and the peroneal nerves, a standardised neurological examination, and vibration sensation testing. RESULTS: Differences between the high and the no/low triallate groups were minimal for all but one of the six nerve conduction tests, for the prevalence of neurological abnormalities, and for vibration sensation perception. The high triallate group had lower mean sural nerve peak amplitude than the no/low triallate group (11.7 v 15.2 microV, p = 0.03). This difference was reduced when adjusted for other potential risk factors (12.5 v 14.5 microV, p = 0.25) and was not associated with cumulative triallate score. We also noted several associations between factors other than triallate and nerve conduction measures. CONCLUSION: The results were consistent with the absence of an association between triallate and measures of neurological function.

Adult↗
PubMed1984

Evaluation of diallate and triallate herbicides for genotoxic effects in a battery of in vitro and short-term in vivo tests.

Commercial-grade preparations of two thiocarbamate herbicides, diallate and triallate, were evaluated for their mutagenic potential in a battery of short-term bioassays. All in vitro bioassays were performed with and without mammalian metabolic activation, and all such tests were repeated after an interval of at least 1 week. Diallate and triallate were tested in the Salmonella/microsome assay over dose ranges of 0.59 to 118.0 micrograms/plate and 6.37 to 1273 micrograms/plate, respectively. Both diallate and triallate gave positive results in S. typhimurium strains TA1535, TA98, and TA100 only in the presence of a rat-liver metabolic activation system. In Saccharomyces cerevisiae strain D7, diallate was tested at concentrations from 1.18 to 29.50 micrograms/ml, and triallate was tested at 0.955 to 9.548 micrograms/ml. Both diallate and triallate gave negative results for mitotic gene conversion, mitotic crossing-over, and reverse mutation. In the mouse lymphoma L5178Y TK+/- assay, diallate was tested at concentrations ranging from 1 to 72 micrograms/ml, and triallate was tested at 0.5 to 60 micrograms/ml. Both herbicides produced mutagenic responses in the mouse lymphoma assay in the presence of metabolic activation. In the Drosophila sex-linked recessive lethal test, flies were exposed to 0.0004% diallate and 0.001% triallate. In this assay, diallate was considered mutagenic, whereas triallate did not produce a detectable mutagenic response.

Animals↗
PubMed1990

Absence of delayed neurotoxicity and increased plasma butyrylcholinesterase activity in triallate-treated hens.

Triallate (S-2,3,3-trichloroallyl diisopropylthiocarbamate) was tested for the potential to produce delayed neurotoxicity. Hens were given single oral doses ranging from 312.5 to 2500 mg/kg of triallate, 750 mg/kg tri-o-cresyl phosphate (TOCP), or empty gelatin capsules on Days 1 and 21 and were killed on Day 42. In a second experiment, animals were administered daily oral doses of 25-300 mg/kg triallate or 10 mg/kg TOCP for 90 days. In a third experiment, animals were given single oral doses of 2500 mg/kg triallate, 750 mg/kg TOCP, or empty gelatin capsules and killed after 24 hr. Delayed neurotoxicity was observed only in TOCP-treated animals. Animals given daily doses of 300 mg/kg triallate became moribund after 30 days; however, histological examination revealed no lesions characteristic of organophosphorus-induced delayed neurotoxicity. Neurotoxic esterase was not significantly altered in triallate-treated animals while it was 95% inhibited in TOCP-treated animals. Plasma butyrylcholinesterase increased significantly 24 hr after treatment with triallate in a dose-dependent manner. In summary, triallate, a thiocarbamate, did not produce neurotoxicity which has been previously reported for some dithiocarbamates.

Administration, Oral↗
PubMedDate not supplied

Two recessive gene inheritance for triallate resistance in Avena fatua L.

Extensive use of the preemergence herbicide triallate over the last three decades has selected for resistant (R) Avena fatua L. populations in several areas of the United States and Canada. R plants are also cross-resistant to the unrelated pyrazolium herbicide difenzoquat. We made reciprocal crosses between inbred R and susceptible (S) lines to determine the genetic basis of triallate resistance. Seeds from parental lines and F(2) populations were treated with soil applications of 0.275, 0.55, or 1.1 kg/ha triallate in the greenhouse and plant heights recorded after 37 days. Surviving F(2) plants were selfed and the resulting F(3) families were screened with 1.1 kg/ha triallate. In the F(2) populations, assortment of S and R phenotypes fit a 15:1 segregation ratio, suggesting that resistance was controlled by the two independently segregating recessive genes TRR1 and TRR2. None of the 912 F(3) progeny from 51 R F(2) individuals was susceptible to triallate treatment, further supporting a two-gene mode of inheritance. There was a possible maternal effect on susceptibility at the highest triallate rate tested.

Avena↗
PubMed1980

Influence of selected pesticides on the microbial degradation of 14C-triallate and 14C-diallate in soil.

Degradation in soil of [allyl-2-14C]triallate and [carbonyl-14C]diallate herbicides, as affected by other selected pesticides, was studied in an incubation system that allowed recovery of 95 to 100% of added 14C. The amount and sequence of pesticide additions simulated field use in the protection of wheat (triallate) and sugar beets (diallate). Neither the rate nor the pattern of triallate degradation in soil was influenced by the following sequence of formulated pesticides: dinoseb acetate, (bentazon + dichlorprop + 2,4,5-T), 2,4-D, (chlorcholinchloride + cholinchloride), tridemorph, and thiophanate. Similarly, diallate degradation was unaffected by pyrazon, dimethoate, and thiophanate. The effect of azinphosmethyl was unclear. In contrast, chlorpyrifos reduced diallate degradation by approximately 14% relative to the occurring in the insecticide's absence. This effect was caused by chlorpyrifos and not its formulation components. Chlorpyrifos was also found to partially inhibit degradation of triallate in soil. Inhibition of neither herbicide was considered to be of ecological significance. Triallate, diallate, and thiophanate were applied at 1 microgram/g; all others were at 2 microgram/g.

Biodegradation, Environmental↗
PubMed1981

Mutagenic activity of diallate and triallate determined by a battery of in vitro mammalian and microbial tests.

Diallate and Triallate are carbamate herbicides used mainly for the pre-emergence control of wild oats in various crops. The genetic activity of these compounds was studied using a battery of microbial and mammalian in vitro tests. In the Salmonella/mammalian-microsome assay, Diallate and Triallate show dose-related increases without metabolic activation in strains TA1535, TA100 and TA98, indicating that these compounds cause both frameshift and base-substitution mutations. Mutagenicity of both herbicides was enhanced greatly by incubation with Aroclor 1254 induced rat-liver S9. Genetic activity in mammalian cells was determined using a number of in vitro tests with Chinese hamster ovary (CHO) cells combined with metabolic activation as described above. Both Diallate and Triallate caused dose-related decreases in colony-forming ability, with concomitant dose-related increases in the frequencies of cells with chromosome damage and in the number of sister-chromatid exchanges. However, only Diallate caused a reduction in DNA molecular weight as determined by alkaline sucrose gradient (ASG) sedimentation. DNA damage was negligible even at concentrations of Triallate that reduced colony-forming ability to zero. This suggests that the lesions in DNA detected by the ASG technique are not necessarily related to those that produce chromosomal damage. These data, taken together, strongly implicate both Diallate and Triallate as capable of causing mutations in mammals. However the risk to man in terms of inherited disease or cancer remains to be established by appropriate in vivo methodology.

Animals↗
PubMed1998

Effects of the pesticides carbofuran, chlorpyrifos, dimethoate, lindane, triallate, trifluralin, 2,4-D, and pentachlorophenol on the metabolic endocrine and reproductive endocrine system in ewes.

Many pesticides are used in the agricultural environment, and some may have the potential to disrupt reproductive or endocrine function. Ewes, in separate groups of 6, received orally into their rumen either empty gelatin capsules or capsules containing chlorpyrifos (12.5 mg/kg), trifluralin (17.5 mg/kg), lindane (2.5 mg/kg), or pentachlorophenol (2 mg/kg) 2 times per week for 43 d. Dimethoate (0.2 mg/kg), carbofuran (0.30 mg/kg), 2,4-dichlorophenoxyacetic acid (10 mg/kg), or triallate (5 mg/kg) was given 3 times per week. After 36 d of treatment, blood samples were taken every 12 min for 6 h for hormone analysis. Ewes were euthanized at the end of the study for necropsy and histopathology. No overt signs of toxicity were seen, and body weight was not affected by treatment. Carbofuran caused a significant increase in serum concentrations of thyroxine compared to control ewes, but all other pesticides, except trifluralin, resulted in a marked decrease in thyroxine concentrations. Serum concentrations of cortisol were significantly increased by trifluralin and chlorpyrifos. Concentrations of insulin in serum were markedly increased in ewes given dimethoate, lindane, trifluralin, triallate, and pentachlorophenol, and concentrations of estradiol were also significantly increased in ewes given lindane and trifluralin. Mean serum concentrations of LH were markedly decreased by trifluralin, and basal LH concentrations were significantly decreased by lindane, dimethoate, and trifluralin but increased by triallate. Both pentachlorophenol and triallate caused a significant increase in severity of oviductal intraepithelial cysts in ewes. Data suggest that several currently used pesticides could influence serum concentrations of reproductive and metabolic hormones, particularly thyroxine, the major secretory product of the thyroid and a principal regulator of metabolism.

Agriculture↗
PubMedDate not supplied

A review of the genotoxicity of triallate.

Triallate is a selective herbicidal chemical used for control of wild oats in wheat. It has an extensive genotoxicity database that includes a variety of in vitro and in vivo studies. The chemical has produced mixed results in in vitro assay systems. It was genotoxic in bacterial mutation Ames assays, predominantly in Salmonella typhimurium strains TA100 and TA1535 in the presence of S9. Weaker responses have been observed in TA100 and TA1535 in the absence of S9. Mixed results have been observed in strain TA98, whereas no genotoxicity has been observed in strains TA1537 and TA1538. The presence and absence of S9 and its source seem to play a role in the bacterial response to the chemical. There have also been conflicting results in other test systems using other bacterial genera, yeast, and mammalian cells. Chromosome effects assays (sister-chromatid exchange and cytogenetics assays) have produced mixed results with S9 but no genotoxicity without S9. Triallate has not produced any genotoxicity in in vitro DNA damage or unscheduled DNA synthesis assays using EUE cells, human lymphocytes, and rat and mouse hepatocytes. In a series of in vivo genotoxicity assays (cytogenetics, micronucleus, dominant lethal, and unscheduled DNA synthesis), there has been no indication of any adverse genotoxic effect. Metabolism data indicate that the probable explanation for the differences observed between the in vitro studies with S9 and without S9 and between the in vitro and the in vivo studies is the production of a mutagenic intermediate in vitro at high doses of triallate is expected to be at most only transiently present in in vivo studies. The weight of evidence strongly suggests that triallate is not likely to exert mutagenic activity in vivo due to toxicokinetics and metabolic processes leading to detoxification.

Animals↗
PubMedDate not supplied

Environmental concentrations of agricultural herbicides: 2,4-d and triallate.

The herbicides 2,4-D (2,4-dichlorophenoxyacetic acid) and triallate [S-2,3,3-trichloroallyl di-isopropyl(thiocarbamate)] are extensively used to control broadleaf and wild oat (respectively) weed infestations in Canadian cereal crops. In 1990, for example, more than 3.8 million kg of 2,4-D and 2.7 million kg of triallate were applied in the three prairie provinces (Alberta, Saskatchewan, and Manitoba). Maximum air concentrations of these two herbicides during the summers of 1989 and 1990 near Regina, Saskatchewan, were 3.90 ng m(-3) (2,4-D) and 60.04 ng m(-3) (triallate). Concentrations of these two herbicides were also measured in bulk atmospheric deposition (wet plus dry) and in farm pond water and associated surface film. Maximum measured levels of 2,4-D were 3550 ng m(-2) d(-1) (bulk deposition), 332 ng m(-2) (surface film), and 290 ng L(-1) (pond water). Maximum levels of triallate were 2300 ng m(-2) d(-1) (bulk deposition), 212 ng m(-2) (surface film), and 500 ng L(-1) (pond water). The highest quantities of the herbicides tended to be found during or immediately after the time of regional application. The movement of the herbicides in the environment will be discussed in relation to the four matrices studied.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1985

Metabolic activation of 3-(2-chloroethoxy)-1,2-dichloropropene: a mutagen structurally related to diallate, triallate, and sulfallate.

3-(2-Chloroethoxy)-1,2-dichloropropene (CP), a Salmonella promutagen that was recently isolated from a sample of residue organics previously concentrated from drinking water, is structurally related to three other chlorinated promutagens, the S-chloroallyl thiocarbamate herbicides diallate, triallate, and sulfallate. These four chloroallyl ether compounds were found to be similar with respect to strain specificity, potency, and requirement for specific metabolic activation. The 9,000g supernatant (S9) fractions from polychlorinated biphenyl Aroclor 1254- or phenobarbital-induced rats metabolized the four chloroallyl ethers to mutagenic products, whereas S9 from 3-methylcholanthrene-induced or uninduced rats did not. The metabolic activation of CP, diallate, and triallate to mutagens was catalyzed by the 100,000g microsomal pellet of S9 alone, but the activation of sulfallate to mutagenic metabolites required both microsomal and cytosolic fractions of S9. Direct-acting (minus S9) mutagenic metabolites of diallate and triallate could be extracted into methylene chloride from S9 incubation mixtures. Incubations containing S9 and either sulfallate or CP did not yield methylene chloride-extractable metabolites with direct-acting mutagenic activity. On the basis of these results and those from previous studies on the metabolism of diallate, triallate, and sulfallate, a tentative model for the metabolic activation of CP is proposed in which this chloroallyl ether undergoes alpha-carbon hydroxylation to form multiple mutagenic products.

Allyl Compounds↗
PubMed1991

Analysis of triallate residues in cereals and soil by gas chromatography with ion-trap detection.

Triallate residues in barley seedlings and soil samples were determined by gas chromatography with ion-trap detection. Soil was extracted with methanol on a mechanical shaker, and plants were extracted with acetonitrile in a Sorvall homogenizer. After evaporation of the organic solvents, the residue was dissolved in hexane, and plants extracts were cleaned-up on an alumina column. Gas chromatographic analysis was carried out using a BP-1 fused-silica capillary column with helium as carrier gas. To quantitate residues the total-ion chromatogram was obtained and then the selected-ion monitoring chromatograms were displayed at m/z 86 for triallate and at m/z 154 for the internal standard, methyl-(4-amino-2-chloro)-benzoate. The average recovery through the method from barley and soil samples was always higher than 80%. The limit of detection in the selected-ion mode was 0.01 mg/kg. Barley and soil samples treated with triallate were also analysed. A good agreement was observed between results obtained by this method and by gas chromatography with nitrogen-phosphorus detection.

Chromatography, Gas↗
PubMed2004

Chlorinated herbicide (triallate) dehalogenation by iron powder.

The reductive degradation of a chlorinated herbicide by iron powder was investigated at lab scale. The studied substrate was triallate (S-2,3,3-trichloroallyl di-isopropyl thiocarbamate) which contains a trichloroethylene moiety potentially reducible by zero-valent iron. Degradation reactions were carried out in batch, at 25 degrees C, in the absence of oxygen, by contacting electrolytic iron powder (size range: 20-50 microm) with a triallate aqueous solution (2.5 mgl(-1)). Herbicide decay, corresponding evolutions of TOC, TOX and chloride ion release were regularly monitored throughout the reactions. Furthermore, the main degradation by-products were identified by HPLC/MS. The results showed that, after 5 days, herbicide degradation extent was about 97% and that the reaction proceeded through the formation of a dechlorinated alkyne by-product (S-2-propinyl di-isopropyl thiocarbamate) resulting from the complete dechlorination of triallate. The subsequent reduction of such an alkyne intermediate gave S-allyl di-isopropyl thiocarbamate as main end by-product. The identified by-products suggested that dechlorination took place mainly via reductive beta-elimination. However, as traces of dichloroallyl di-isopropyl thiocarbamate were also detected, a role, although minor, was assigned even to hydrogenolysis in the overall dechlorination process.

Chromatography, High Pressure Liquid↗
PubMed1985

Neurotoxicity of diallate and triallate when administered orally or topically to hens.

Two allylthiocarbamate herbicides, diallate and triallate, were evaluated for neurotoxicity by oral and topical dosing studies with mature white leghorn hens. Diallate was tolerated for 90 days at topical doses of 40 mg/kg/day and oral doses of 20 mg/kg/day. Reversible ataxia and narcosis occurred at diallate doses of 80 mg/kg/day and higher by either route of administration. Triallate did not elicit signs of neurotoxicity at 300 mg/kg/day topically or 400 mg/kg/day orally. The oral dose, however, resulted in gastrointestinal irritation and severe weight loss, such that dosing was terminated after 25 days. Triallate was tolerated at oral dosages of 90 mg/kg/day and topical doses up to 330 mg/kg/day.

Administration, Oral↗
PubMed1998

Effect of 2,4-dicholorophenoxyacetic acid, trifluralin and triallate herbicides on immune function.

The commercial formulations of 3 commonly used herbicides (the amine salt of 2,4-dichlorophenoxyacetic acid, trifluralin and triallate) were evaluated for effects on immune function in male Fisher 344 rats. The herbicides were prepared in an olive oil vehicle and administered by oral gavage twice weekly for 28 d at the following doses: 10.0 mg 2,4-D/kg; 17.5 mg trifluralin/kg; 5.0 mg triallate/kg/treatment. Normal body weight and organ/body weight ratios indicated the rats tolerated the herbicide treatments without difficulty. Exposure to 2,4-D did not alter lymphocyte blastogenesis, 1 gm antibody production (anti-sheep red blood cell), lymphocyte cell surface marker expression or phagocytic function of peritoneal macrophages. Trifluralin acted as a weak mitogen, but impaired T-lymphocyte blastogenesis induced by phytohemagglutinin and concanavalin A. Other immunological measurements were unaffected by trifluralin exposure. Triallate exposure reduced peritoneal macrophage phagocytosis by 33%, showed weak mitogenic properties and impaired T-lymphocyte blastogenesis in the presence of phytohemagglutin. Triallate also increased the anti-sheep red blood cell response expressed/spleen by 43%, a phenomenon suggestive of a compensatory response to minimize the impact on overall immune function. The changes in lymphocyte or macrophage function due to the herbicide treatments were not associated with changes in lymphocyte cell surface antigen expression.

2,4-Dichlorophenoxyacetic Acid↗
PubMed2001

Volatilisation of triallate as affected by soil texture and air velocity.

The rate of volatilisation of the formulated herbicide triallate was investigated in a wind tunnel under controlled wind-speed conditions. An experimental set-up is described which allows the monitoring of wind speed (w.s.), soil-water content, and the temperature of air and soil. A system controlling soil-water content is also described. The influence of air velocity and soil texture was investigated measuring the cumulative volatilisation losses of triallate from soil. The herbicide volatilisation losses after application ranged from 40% at 3 m/s to 53% at 9 m/s for loam soil and from 60% at 3 m/s to 73% at 9 m/s for sandy soil.

Air↗
PubMed1982

Steam distillation and gas-liquid chromatographic determination of triallate and diallate in milk and plant tissue.

A procedure based on steam distillation is described for the determination of residues of the thiocarbamate herbicides diallate and triallate. The herbicides are steam-distilled directly from aqueous suspensions of milk and plant samples and trapped in hexane. After column cleanup on either activated Florisil or silica cartridges, samples are quantitated by gas-liquid chromatography. Recoveries of diallate and triallate from milk, lettuce, peas, corn, canarygrass seed and straw, and flax straw ranged from 77 to 96%.

Animals↗
PubMed1978

Mutagenicity of diallate, sulfallate, and triallate and relationship between structure and mutagenic effects of carbamates used widely in agriculture.

In an investigation of the mutagenic properties of 20 carbamate herbicides and fungicides by use of the Salmonella/microsome mutagenicity test as developed by Ames et al. (Mutation Res., 31: 347-364, 1975), we have found that three thiocarbamate compounds, diallate, sulfallate and triallate, are mutagenic in the presence of a liver microsomal fraction on strains TA1535 and TA100. This indicates that the metabolic products of these thiocarbamates are causing base-pair substitutions. Since the 2-chloro-allyl group is common to the three mutagenic compounds but is not common to the 17 nonmutagenic compounds, a metabolic derivative of this group is probably responsible for the mutagenic activity.

Animals↗