Thiacloprid

252.72

252.72

601-147-9

DSV3A944A4

DTXSID7034961

Yellowish crystalline powder|Crystals from ether

29349990

77.6

1.26 at 20 deg C

yellowish crystalline powder

1.46 g at 20 deg C

128-129 °C

decomp. >270 deg C

209.7±31.5 °C

1.691

In water, 185 mg/L at 20 deg C

0-6°C

6.0X10-12 mm Hg at 20 deg C (23X10-12 hPa at 20 deg C)

LD50 in male, female rats (mg/kg): 836, 444 orally; >2000, >2000 dermally; LC50 (4 hr) in male, female rats (mg/m3): >2535, 1223; LC50 (96 hr) in rainbow trout (mg/l): 30.5 (Elbert)

Odorless

pH = 7.4 at 20 °C

Henry's Law constant = 1.08X10-14 atm-cu m/mole at 20 °C (est)

154.84 Ų [M+H]+ [CCS Type: TW]|167.43 Ų [M+HCOO]-

Yellowish powder. Vapor pressure: 2.25X10-12 mm Hg (3X10-10 Pa) at 20 °C; solubility in water, 185 mg/L at 20 °C /Z-Thiacloprid/|Hydroxyl radical reaction rate constant = 8.9X10-13 cu cm/molecule-sec at 25 °C (est)

III

6.1(b)

2588

2

20/22-52/53

60

GS6093749

Xn

Stable for 2 weeks at 50 deg C.

Missing Phrase - N15.00950417-P201-P261-P280-P308 + P313

H301-H332-H336-H351-H360FD-H410

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.|Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber; Contaminated packaging: Dispose of as unused product.

Incompatible materials: Strong oxidizing agents.

|Danger|H301: Toxic if swallowed [Danger Acute toxicity, oral]|P201, P202, P261, P264, P270, P271, P273, P281, P301+P310, P304+P312, P304+P340, P308+P313, P312, P321, P330, P391, P403+P233, P405, and P501|H301 (82.97%): Toxic if swallowed [Danger Acute toxicity, oral]|P201, P202, P261, P264, P270, P271, P273, P281, P301+P310, P301+P312, P304+P312, P304+P340, P308+P313, P312, P321, P330, P391, P403+P233, P405, and P501|Aggregated GHS information provided by 229 companies from 5 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P201, P202, P260, P261, P264, P270, P271, P281, P301+P312, P304+P312, P304+P340, P307+P311, P308+P313, P312, P314, P321, P330, P405, and P501

Eye/face protection: Face shield and safety glasses. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).|Skin protection: Handle with gloves.|Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.|Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.|Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.|Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.|Appropriate engineering controls: Avoid contact with skin, eyes and clothing. Wash hands before breaks and immediately after handling the product.|Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.|SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

RURAL/REMOTE: Thiacloprid was not detected (detection limit 2.0 pg/cu m) in particulate phase atmospheric samples collected Jun-Sep 2013 from Osoyoos and Oliver, BC, Canada, in the Okanagan Valley, a southern agricultural region(1).

IDENTIFICATION AND USE: Thiacloprid is an insecticide of the neonicotinoid class. It is used to control aphids, codling moth, leafhoppers, leafminers, psylla, and whiteflies in potatoes, oilseed rape, pome fruit, vegetables, and ornamentals. HUMAN STUDIES: There is a case report of thiacloprid poisoning resulting from deliberate ingestion in a 23-year-old man, manifesting with status epilepticus, respiratory paralysis, rhabdomyolysis, metabolic acidosis, and acute kidney injury, and ultimately giving rise to refractory shock and death. In human peripheral blood lymphocytes in vitro thiacloprid increased the chromosome aberrations and sister chromatid exchange significantly at all concentrations (75, 150, and 300 ug/mL) both in the absence and presence of the metabolic activation and induced a significant increase in micronucleus and nucleoplasmic bridge formations at all concentrations for 24 hr and at 75 and 150 ug/mL for 48-hr treatment periods in the absence of the metabolic activation. Thiacloprid was also found to significantly induce nuclear bud formation at 300 ug/mL for 24 hr and at 150 ug/mL for 48-hr treatment times in the absence of the metabolic activation and at the two highest concentrations (150 and 300 ug/mL) in the presence of the metabolic activation. ANIMAL STUDIES: Evidence of carcinogenicity reported in rats based on increased incidence of thyroid follicular cell adenomas in males and possibly also in females and increased incidence of uterine tumors (adenocarcinomas). Evidence of carcinogenicity reported in mice based on increased incidence of ovarian luteomas. Thiacloprid impairs development and quality of both mouse and rabbit preimplantation embryos, and shows embryotoxicity even at acute reference dose. Developmental neurotoxicity described in rats based on decreased pre-weaning and post-weaning body weights in both sexes and delayed sexual maturation in the males, and altered performance in passive avoidance testing. In rats treated with thiacloprid, statistically significant increases in free triiodothyronine and free thyroxine serum hormone levels were observed. The potential genotoxic effect of thiacloprid formulation on bovine peripheral lymphocytes was evaluated using the comet assay and the cytogenetic endpoints. Whole blood cultures were treated with the insecticide at concentrations of 30, 60, 120, 240 and 480 ug/mL for 24, 48 hr and/or 2 hr of incubation. A statistically significant increase in the frequency of DNA damage, as well as in unstable chromosome aberrations (% breaks) were found after exposure to the insecticide at concentrations ranging from 120 to 480 ug/mL. ECOTOXICITY STUDIES: Caenorhabditis elegans is less susceptible to neonicotinoids than target species of pest insect. Chronic thiacloprid exposure of early-life stages of carp affected ontogeny and growth rate, and inhibited antioxidant capacity. Pheromone production was altered in moth Cydia pomonella, with a reduction of the major compound, codlemone, and one minor component. In worker bees, thiacloprid (24 hr oral exposure, 200 ug/L or 2000 ug/L) reduced hemocyte density, encapsulation response, and antimicrobial activity even at field realistic concentrations. Thiacloprid, as active substance and as formulation, poses a substantial risk to honey bees by disrupting learning and memory functions. Honey bees (Apis mellifera carnica) were exposed chronically to thiacloprid in the field for several weeks at a sublethal concentration. Foraging behavior, homing success, navigation performance, and social communication were impaired, and thiacloprid residue levels increased both in the foragers and the nest mates over time. Thiacloprid exposed free-flying bumblebee colonies were more likely to die prematurely, and those that survived reached a lower final weight and produced 46% fewer reproductives than colonies placed at control farms. Earthworms were exposed to thiacloprid (1 and 3 mg/kg) for 7, 14, and 28 days and then transferred to the clean soil for 35, 42, and 56 days. Results showed that activities of molecular indicators are inhibited following the exposure to thiacloprid at one or more sample times and then increased during the recovery course compared with the control. Significant DNA damage to E. fetida was also observed by olive tail moments in comet assay.

Disturbance regimes determine communities' structure and functioning. Nonetheless, little effort has been undertaken to understand interactions of press and pulse disturbances. In this context, leaf-shredding macroinvertebrates can be chronically exposed to wastewater treatment plant effluents (i.e., press disturbance) before experiencing pesticide exposure following agricultural runoff (i.e., pulse disturbance). It is assumed that wastewater pre-exposure alters animals' sensitivity to pesticides. To test this hypothesis, we exposed model-populations of the shredder Gammarus fossarum to wastewater at three field-relevant dilution levels (i.e., 0%, 50%, and 100%). After 2, 4, and 6 weeks, survival, leaf consumption, dry weight, and energy reserves were monitored. Additionally, animals were assessed for their sensitivity toward the neonicotinoid insecticide thiacloprid using their feeding rate as response variable. Both wastewater treatments reduced gammarids' survival, leaf consumption, dry weight, and energy reserves. Moreover, both wastewater pre-exposure scenarios increased animals' sensitivity toward thiacloprid by up to 2.5 times compared to the control. Our results thus demonstrate that press disturbance as posed by wastewater pre-exposure can enhance susceptibility of key players in ecosystem functioning to further (pulse) disturbances. Therefore, applying mitigation measures such as advanced treatment technologies seems sensible to support functional integrity in the multiple-stress situation.|Microbial pathogens are thought to have a profound impact on insect populations. Honey bees are suffering from elevated colony losses in the northern hemisphere possibly because of a variety of emergent microbial pathogens, with which pesticides may interact to exacerbate their impacts. To reveal such potential interactions, we administered at sublethal and field realistic doses one neonicotinoid pesticide (thiacloprid) and two common microbial pathogens, the invasive microsporidian Nosema ceranae and black queen cell virus (BQCV), individually to larval and adult honey bees in the laboratory. Through fully crossed experiments in which treatments were administered singly or in combination, we found an additive interaction between BQCV and thiacloprid on host larval survival likely because the pesticide significantly elevated viral loads. In adult bees, two synergistic interactions increased individual mortality: between N. ceranae and BQCV, and between N. ceranae and thiacloprid. The combination of two pathogens had a more profound effect on elevating adult mortality than N. ceranae plus thiacloprid. Common microbial pathogens appear to be major threats to honey bees, while sublethal doses of pesticide may enhance their deleterious effects on honey bee larvae and adults. It remains an open question as to whether these interactions can affect colony survival.|Deltamethrin (DEL) and thiacloprid (THIA) are two insecticides that are widely used in agriculture either separately or in combination. Studies on genotoxicity and cytotoxicity of TIA and the mixture of DEL and THIA insecticides have not been reported so far. Therefore, we investigated the cytotoxic and genotoxic effects of commercial formulations DEL and/or THIA in rat bone marrow cells, using mitotic index (MI), micronucleus (MN) and chromosome aberrations (CA) assay. In vivo cytokinesis-block micronucleus (CBMN) assay using cytochalasin-B in bone marrow cells was performed ... . Rats were orally gavaged with a single dose of DEL (15 mg/kg), THIA (112.5 mg/kg) or DEL + THIA (15 + 112.5 mg/kg) for 24 hr (acute treatments), or DEL (3 mg/kg/day), THIA (22.5 mg/kg/day) or DEL + THIA (3 + 22.5 mg/kg/day) for 30 days (subacute treatments). A corn oil vehicle control group and cyclophosphamide (50 mg/kg) positive control group were also included. All DEL and/or THIA treatments significantly decreased MI and binucleated (BN) cell numbers, and significantly increased CA, as compared to the vehicle control group. The results of CBMN assay indicated that the combination of DEL and THIA for both treatment times and the 30-day treatment with THIA alone caused a significant increase in micronucleus formation in BN cells. The present findings indicated the combined exposure of DEL and THIA showed genotoxic and cytotoxic effects more than those of individual exposure of DEL or THIA in rat bone marrow cells.|BACKGROUND: The honeybee, Apis mellifera, is undergoing a worldwide decline whose origin is still in debate. Studies performed for twenty years suggest that this decline may involve both infectious diseases and exposure to pesticides. Joint action of pathogens and chemicals are known to threaten several organisms but the combined effects of these stressors were poorly investigated in honeybees. Our study was designed to explore the effect of Nosema ceranae infection on honeybee sensitivity to sublethal doses of the insecticides fipronil and thiacloprid. METHODOLOGY/FINDING: Five days after their emergence, honeybees were divided in 6 experimental groups: (i) uninfected controls, (ii) infected with N. ceranae, (iii) uninfected and exposed to fipronil, (iv) uninfected and exposed to thiacloprid, (v) infected with N. ceranae and exposed 10 days post-infection (p.i.) to fipronil, and (vi) infected with N. ceranae and exposed 10 days p.i. to thiacloprid. Honeybee mortality and insecticide consumption were analyzed daily and the intestinal spore content was evaluated 20 days after infection. A significant increase in honeybee mortality was observed when N. ceranae-infected honeybees were exposed to sublethal doses of insecticides. Surprisingly, exposures to fipronil and thiacloprid had opposite effects on microsporidian spore production. Analysis of the honeybee detoxification system 10 days p.i. showed that N. ceranae infection induced an increase in glutathione-S-transferase activity in midgut and fat body but not in 7-ethoxycoumarin-O-deethylase activity. CONCLUSIONS/SIGNIFICANCE: After exposure to sublethal doses of fipronil or thiacloprid a higher mortality was observed in N. ceranae-infected honeybees than in uninfected ones. The synergistic effect of N. ceranae and insecticide on honeybee mortality, however, did not appear strongly linked to a decrease of the insect detoxification system. These data support the hypothesis that the combination of the increasing prevalence of N. ceranae with high pesticide content in beehives may contribute to colony depopulation.|Deltamethrin (DEL) and thiacloprid (THIA) are the two commonly used synthetic insecticides applied either separately or as a mixture. The aim of this study was to assess thyroid stimulating hormone (TSH) and the serum levels of thyroid hormones exposure to these compounds in rats. The animals were orally gavaged with a single dose of DEL (15 mg/kg), THIA (112.5 mg/kg) or DEL + THIA (15 + 112.5 mg/kg) for 24 hr (acute treatments) or DEL (3 mg/kg per day), THIA (22.5 mg/kg per day) or DEL + THIA (3 + 22.5 mg/kg per day) for 30 days (subacute treatments). ... Statistically significant increases in free triiodothyronine (FT3) and free thyroxine (FT4) serum hormone levels were observed in the independent treatment with THIA and the combined treatment with DEL and THIA for 30 days. The results of this study suggest that in vivo exposure to subacute treatments of commercial formulations of THI and mixture of DEL + THIA increased serum FT3 and FT4 levels in rats. Further studies are required to determine the effects of endocrine disruptors and potential health risks of these insecticides in human, especially in children because of the importance of these hormones during growth and development.

LD50 Rat (female) oral 444 mg/kg|LD50 Rat (male) oral 836 mg/kg|LD50 Rat dermal >2000 mg/kg|LC50 Rat inhalation (female) 1223 mg/cu m/4 hr|For more Non-Human Toxicity Values (Complete) data for Thiacloprid (9 total), please visit the HSDB record page.

/AQUATIC SPECIES/ Neonicotinoid insecticides are frequently detected in surface waters near agricultural areas, leading to a potential for chronic exposure to sensitive aquatic species. The midge Chironomus dilutus and the mayfly Neocloeon triangulifer have been shown to be acutely sensitive to neonicotinoids. Previous studies have established chronic effects of some neonicotinoids on C. dilutus, but reproduction has not been studied. Toxic effects have not been assessed using N. triangulifer. ...The results of chronic, static-renewal tests for 6 neonicotinoids (acetamiprid, clothianidin, dinotefuran, imidacloprid, thiacloprid, and thiamethoxam) with C. dilutus (=56-day in length) and N. triangulifer (=32-day in length). Emergence was generally the most sensitive endpoint for both species across all neonicotinoids. Effect concentrations, 10% (EC10s; emergence) were 0.03 to 1.1 ug/L for acetamiprid, clothianidin, imidacloprid, and thiacloprid. Dinotefuran and thiamethoxam were less potent, with EC10s (C. dilutus) or median effect concentrations (EC50s; N. triangulifer) of 2.2 to 11.2 ug/L. Hazard was assessed through comparison of neonicotinoid environmental concentrations from agricultural surface waters in Ontario (Canada) with either the 5th percentile hazard concentration (for imidacloprid) or species-specific EC10s from the present study (for all remaining neonicotinoids). The resulting hazard quotients (HQs) indicated little to no hazard (HQ <1) in terms of chronic toxicity for acetamiprid, dinotefuran, thiacloprid, or thiamethoxam. A moderate hazard (HQ >1) was found for emergence of N. triangulifer for clothianidin, and a high hazard (HQ=74) was found for imidacloprid.|/AQUATIC SPECIES/ The present study assessed and compared the acute (48- or 96-hr) toxicity of 6 neonicotinoids (acetamiprid, clothianidin, dinotefuran, imidacloprid, thiacloprid, and thiamethoxam) to 21 laboratory-cultured and field-collected aquatic invertebrates spanning 10 aquatic arthropod orders. Test conditions mimicked species' habitat, with lentic taxa exposed under static conditions, and lotic taxa exposed under recirculating systems. Median lethal concentrations (LC50s) and median effect concentrations (EC50s; immobility) were calculated and used to construct separate lethal- and immobilization-derived species sensitivity distributions for each neonicotinoid, from which 5th percentile hazard concentrations (HC5s) were calculated. The results showed that the most sensitive invertebrates were insects from the orders Ephemeroptera (Neocloeon triangulifer) and Diptera (Chironomus dilutus), whereas cladocerans (Daphnia magna, Ceriodaphnia dubia) were the least sensitive. The HC5s were compared with neonicotinoid environmental concentrations from Ontario (Canada) monitoring studies. For all neonicotinoids except imidacloprid, the resulting hazard quotients indicated little to no hazard in terms of acute toxicity to aquatic communities in Ontario freshwater streams. For the neonicotinoid imidacloprid, a moderate hazard was found when only invertebrate immobilization, and not lethality, data were considered.|/AQUATIC SPECIES/ ... The aim of the present research was to assess effects of short-term (24-hr) exposure to the neonicotinoid insecticide thiacloprid, including a postexposure observation period. A comparison of several freshwater insect and crustacean species showed an increase of sensitivity by three orders of magnitude in the following order: Daphnia magna < Asellus aquaticus = Gammarus pulex < Simpetrum striolatum < Culex pipiens = Notidobia ciliaris = Simulium latigonium, with median lethal concentrations (LC50s) of 4,400, 153, 190, 31.2, 6.78, 5.47, and 5.76 ug/L, respectively (postexposure observation 11-30 days). Thiacloprid caused delayed lethal and sublethal effects, which were observed after 4 to 12 days following exposure. Reduction in LC50s found when postexposure observation was extended from 1 day to a longer period (11-30 days) was up to >50-fold. Hence, delayed effects occurring after short-term exposure should be considered in risk assessment. The 5% hazardous concentration (HC5) of thiacloprid obtained in the present study (0.72 ug/L) is more than one order of magnitude below the currently predicted worst-case environmental concentrations in surface water. Concerning the selection of test organisms, ...the widely employed test organism D. magna is least sensitive among the arthropods tested and that, for neonicotinoid insecticides, an insect like the mosquito C. pipiens would be more suitable for predicting effects on sensitive species.|/AQUATIC SPECIES/ Many studies show that neonicotinoid insecticides cause toxicity to aquatic invertebrates. Some studies report that insecticide toxicity may differ in combination with other agrochemicals under realistic field conditions. To explore such altered toxicity further, /this study/ aimed to determine the single and combined effects of environmentally relevant levels of the neonicotinoid thiacloprid and nutrients on different endpoints of 4 aquatic invertebrate species. Animals were exposed to these agrochemicals using a caged experiment within experimental ditches. ... Thiacloprid-induced toxicity /was observed/ for 2 crustaceans, Daphnia magna and Asellus aquaticus, and for 1 out of 2 tested insect species, Cloeon dipterum. ... For D. magna, the observed toxicity, expressed as the lowest-observed-effect concentration (LOEC), on growth and reproduction was present at thiacloprid concentrations that were 2456-fold lower than laboratory-derived LOEC values. This shows that these species, when exposed under natural conditions, may exhibit neonicotinoid-induced toxic stress. Contrary to the low nutrient treatment, such toxicity was often not observed under nutrient-enriched conditions. This was likely attributable to the increased primary production that allowed for compensatory feeding. These findings warrant the inclusion of different feeding regimes in laboratory experiments to retrieve the best estimates of neonicotinoid-induced toxicity in the natural environment.|For more Ecotoxicity Excerpts (Complete) data for Thiacloprid (17 total), please visit the HSDB record page.

Thiacloprid's production may result in its release to the environment through various waste streams; its former use as an insecticide in the US(1) resulted in its direct release to the environment(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1,100(SRC), determined from a structure estimation method(2), indicates that thiacloprid is expected to have low mobility in soil(SRC). Volatilization of thiacloprid from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.1X10-14 atm-cu m/mole(SRC), based upon its vapor pressure, 6.0X10-12 mm Hg(3), and water solubility, 185 mg/L(4). Thiacloprid is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). An aerobic half-life in soil ranging from 0.6 to 3.8 days(3) indicates that biodegradation may be an important environmental fate process in soil(SRC).|FIELD STUDIES: Thiocloprid was applied 3-4 times to cabbage crops in 2010 at the recommended maximum dose or at 1.5 times the recommended maximum dose in Beijing and Hubei Province, China, with climates of temperate monsoon and subtropical monsoon, respectively. Thiacloprid had a half-life of 1.3 days in cabbage and 2.1 days in soil in Beijing, and 1.6 days in cabbage and 3.1 days in Hubei(1). In the spring of 2007, Calypso SC 480, with the active ingredient thiacloprid, was applied to one orchard in the Ljubljana region and to one orchard in the Gorenjska region of Slovenia to determine if thiacloprid persists in pollen, which could result in honey bee exposure. Thiacloprid was detected 1 and 6 days following application in pollen loads, and was not detected above the 0.01 mg/kg detection limit in subsequent samples. No honey bee death was observed following application(2).|FIELD STUDIES: In East Sussex, United Kingdom, thiacloprid was reported in several soil, pollen, and nectar samples collected from 5 different farms, consisting of winter oilseed rape and winter-sown wheat crops. It was reported that thiacloprid had not been used on these crops in the previous 3 years(1).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1,100(SRC), determined from a structure estimation method(2), indicates that thiacloprid is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 1.1X10-14 atm-cu m/mole(SRC), derived from its vapor pressure, 6.0X10-12 mm Hg(4), and water solubility, 185 mg/L(5). According to a classification scheme(6), an estimated BCF of 3(SRC), from its log Kow of 1.26(4) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). The aquatic aerobic half-life for thiacloprid ranges from 10-63 days(4), suggesting that biodegradation may be an important environmental fate process in some water systems(SRC).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), thiacloprid, which has a measured vapor pressure of 6.0X10-12 mm Hg at 20 °C(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase thiacloprid may be removed from the air by wet and dry deposition. Thiacloprid in solution did not absorb UV above 290 nm(3) and, therefore, is not expected to be susceptible to direct photolysis since sunlight consists of wavelengths above 290 nm(SRC).

Thiacloprid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(1). Thiacloprid in solution did not absorb UV above 290 nm(2) and, therefore, is not expected to be susceptible to direct photolysis since sunlight consists of wavelengths above 290 nm(SRC). The dissipation of thiacloprid in sandy loam soil from New Delhi, India had a reported half-life of 12.8 days using UV-light treatment and 19.1 days using sunlight(2).

An estimated BCF of 3 was calculated for thiacloprid(SRC), using a measured log Kow of 1.26(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Reported Koc values for thiacloprid ranged from 408 to 1584(1) . According to a classification scheme(2), this Koc range suggests that thiacloprid is expected to have moderate to low mobility in soil.[Table#6877]

The Henry's Law constant for thiacloprid is estimated as 1.1X10-14 atm-cu m/mole(SRC) derived from its vapor pressure, 6.0X10-12 mm Hg(1), and water solubility, 185 mg/L(2). This Henry's Law constant indicates that thiacloprid is expected to be essentially nonvolatile from water surfaces(3). Thiacloprid is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

Thiacloprid was reported in 3 out of 17 fruit and vegetable samples collected from a grocery market in Boston, MA in 2012 and in 6 out of 13 pollen samples collected from New Zealand in 2011(1).

Occupational exposure to thiacloprid may occur through inhalation and dermal contact with this compound at workplaces where thiacloprid is produced or used. Limited monitoring data indicate that the general population may be exposed to thiacloprid via consumption of food containing thiacloprid residues. (SRC)

Thiacloprid was not detected in urine samples collected in 1994 and 2000 from 20 women in Kyoto, Japan; in 2003, 2009 and 2011 the maximum concentration of thiacloprid in 20, 17 and 18 Japanese women was 3.09, 2.64 and 1.44 ug/g creatinine, respectively(1). Thiacloprid concentrations were 0.14-0.50 ug/L in 67% of urine samples collected from 52 (41 men, 11 women) adults from Aichi Prefecture, Japan(2). Thiacloprid was detected in <16% of urine samples collected from 223 three year old children (108 male, 115 female) from Japan(3).|Neonicotinoid insecticides that have been on the market since 1992 have been used globally including in Japan. Because they are sprayed over forests and agricultural areas, inadvertent toxicity in nontarget insects (especially honey bees) and humans is a matter of public concern. However, information on exposure levels and potential health impacts of neonicotinoids in children living around sprayed areas is scarce. Thus, we determined neonicotinoid exposure levels in children living in communities where thiacloprid was used to control pine wilt disease. A total of 46 children (23 males and 23 females) were recruited for the present study, and informed written consent was obtained from their guardians. Urine specimens were collected before, during, and after insecticide spraying events; and atmospheric particulate matter was also collected. Concentrations of thiacloprid and 6 other neonicotinoid compounds were determined in urine samples and in atmospheric particulate matter specimens using liquid chromatography-electrospray ionization-tandem mass spectrometry. In urine specimens, thiacloprid concentrations were <0.13 ug/L and were detectable in approximately 30% of all samples. Concentrations of the other neonicotinoids, N-dm-acetamiprid, thiamethoxam, dinotefuran, and clothianidin, were 18.7, 1.92, 72.3, and 6.02 ug/L, respectively. Estimated daily intakes of these neonicotinoids were then calculated from urinary levels; although the estimated daily intakes of the neonicotinoids were lower than current acceptable daily intake values, the children were found to be exposed to multiple neonicotinoids on a daily basis.

Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. (See all compounds classified as Insecticides.)

Thiacloprid is rapidly absorbed and is rapidly excreted after the following metabolic processes, with little remaining in the tissues.

Thiacloprid is rapidly absorbed and is rapidly excreted after the following metabolic processes, with little remaining in the tissues. The metabolic processes were summarized as: 1) hydroxylation of the thiazolidine ring and subsequent glucuronidation (as shown by metabolite PIZ 1270), 2) hydroxylation of the cyanamide moiety (metabolite KNO 1891), 3) opening of the thiazolidine ring (e.g., metabolites KNO2672, PIZ1297F/WAK 6935), 4) formation of an oxazole ring (metabolite PIZ 1253), 5) oxidation and subsequent methylation of the thiazolidine ring (e.g., PIZ 1297E and PIZ 1269X), and 6) oxidative cleavage of the methylene bridge (PIZ 1243). Only minor gender-related quantitative differences in metabolite profiles were observed.

Provide supportive treatment, as there is no specific antidote for neonicotinoid poisoning. Patients with significant mental status changes should ideally be managed in the intensive care setting, at least initially. Use GI decontamination ... . Control extreme agitation with lorazepam or propofol. Consider cardiac monitoring, especially in patients with risk factors for coronary artery disease. In a severe poisoning, send patient to an intensive care setting for respiratory support. /Neonicotinoid insecticides/|/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W TKO /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam (Valium) or lorazepam (Ativan) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/CASE REPORTS/ ... Here we report a case of thiacloprid poisoning resulting from deliberate ingestion in a 23-year-old man, manifesting with status epilepticus, respiratory paralysis, rhabdomyolysis, metabolic acidosis, and acute kidney injury (AKI), and ultimately giving rise to refractory shock and death. Thiacloprid can cause fatal human toxicity when ingested heavily, and absence of an effective antidote raises concern in this regard.|/GENOTOXICITY/ Thiacloprid, a neonicotinoid insecticide, is widely used for controlling various species of pests on many crops. The potential genotoxic effects of thiacloprid on human peripheral blood lymphocytes (PBLs) were investigated in vitro by the chromosome aberrations (CAs), sister chromatid exchanges (SCEs), and cytokinesis-block micronucleus (MN) assays. The human PBLs were treated with 75, 150, and 300 ug/mL thiacloprid in the absence and presence of an exogenous metabolic activator (S9 mix). Thiacloprid increased the CAs and SCEs significantly at all concentrations (75, 150, and 300 ug/mL) both in the absence and presence of the S9 mix and induced a significant increase in MN and nucleoplasmic bridge formations at all concentrations for 24 hr and at 75 and 150 ug/mL for 48-hr treatment periods in the absence of the S9 mix; and at all concentrations in the presence of the S9 mix when compared with the control and solvent control. Thiacloprid was also found to significantly induce nuclear bud (NBUD) formation at 300 ug/mL for 24 hr and at 150 ug/mL for 48-hr treatment times in the absence of the S9 mix and at the two highest concentrations (150 and 300 ug/mL) in the presence of the S9 mix. Thiacloprid significantly decreased the mitotic index, proliferation index, and nuclear division index for all concentrations both in the absence and presence of the S9 mix.|/ALTERNATIVE and IN VITRO TESTS/ The enzyme aromatase (CYP19; cytochrome P450 19) in humans undergoes highly tissue- and promoter-specific regulation. In hormone-dependent breast cancer, aromatase is over-expressed via several normally inactive promoters (PII, I.3, I.7). Aromatase biosynthesizes estrogens, which stimulate breast cancer cell proliferation. The placenta produces estrogens required for healthy pregnancy and the major placental CYP19 promoter is I.1. Exposure to certain pesticides, such as atrazine, is associated with increased CYP19 expression, but little is known about the effects of neonicotinoid insecticides on CYP19. We developed sensitive and robust RT-qPCR methods to detect the promoter-specific expression of CYP19 in human adrenocortical carcinoma (H295R) and primary umbilical vein endothelial (HUVEC) cells, and determined the potential promoter-specific disruption of CYP19 expression by atrazine and the commonly used neonicotinoids imidacloprid, thiacloprid, and thiamethoxam. In H295R cells, atrazine concentration-dependently increased PII- and I.3-mediated CYP19 expression and aromatase catalytic activity. Thiacloprid and thiamethoxam induced PII- and I.3-mediated CYP19 expression and aromatase activity at relatively low concentrations (0.1-1.0 uM), exhibiting non-monotonic concentration-response curves with a decline in gene induction and catalytic activity at higher concentrations. In HUVEC cells, atrazine slightly induced overall (promoter-indistinct) CYP19 expression (30 uM) and aromatase activity (>/= 3 uM), without increasing I.1 promoter activity. None of the neonicotinoids increased CYP19 expression or aromatase activity in HUVEC cells. Considering the importance of promoter-specific (over)expression of CYP19 in disease (breast cancer) or during sensitive developmental periods (pregnancy), our newly developed RT-qPCR methods will be helpful tools in assessing the risk that neonicotinoids and other chemicals may pose to exposed women.

3-((6-chloro-3-pyridinyl)methyl)-2-thiazolidinylidene cyanamide

Granule, flowable concentrate, water dispersible granules.|Premix Partners: Flubendiamide; Spirotetramat.|Tradenames: Bariard; Calypso; Alanto.

The WHO Recommended Classification of Pesticides by Hazard identifies Thiacloprid (technical grade) as Class II: moderately hazardous; Main Use: insecticide.|Registration Notes: Outside USA: Brazil, Europe, Hungary, Israel, Japan, Korea, New Zealand, Romania, and Switzerland. Biscaya for use in United Kingdom on potatoes, oilseed rape. Lineout registration pending in Australia.

The behavior in the field and the transfer from olives to olive oil during the technological process of imidacloprid, thiacloprid, and spinosad were studied. The extraction method used was effective in extracting the analytes of interest, and no interfering peaks were detected in the chromatogram. The residue levels found in olives after treatment were 0.14, 0.04, and 0.30 mg/kg for imidacloprid, thiacloprid, and spinosad, respectively, far below the maximum residue levels (MRLs) set for these insecticides in EU. At the preharvest interval (PHI), no residue was detected for imidacloprid and thiacloprid, while spinosad showed a residue level of 0.04 mg/kg. The study of the effect of the technological process on pesticide transfer in olive oil showed that these insecticides tend to remain in the olive cake. The LC/DAD/ESI/MS method showed good performance with adequate recoveries ranging from 80 to 119% and good method limits of quantitation (LOQs) and of determination (LODs). No matrix effect was detected.|A validated analytical method to determine seven neonicotinoids (dinotefuran, nitenpyram, thiamethoxam, clothianidin, imidacloprid, acetamiprid and thiacloprid) in sunflower seeds (hull and kernel) using HPLC coupled to electrospray ionization mass spectrometry (ESI-MS) is presented. Sample clean-up based on a solid-liquid extraction, and the removal of lipid fraction, in the case of kernels, is proposed and optimized. Low limits of detection and quantification were obtained, ranging from 0.3 x 10(-3) to 1.2 x 10(-3) ug/g and from 1.0 x 10(-3) to 4.0 x 10(-3) ug/g, with good precision, and recovery values ranged from 90% to 104% for hulls and kernels. The method was applied for the analysis of five thiamethoxam-dressed sunflower seeds and four non-treated seeds, where, besides thiamethoxam, residues of the other neonicotinoid, clothianidin, were also detected and confirmed via tandem mass spectrometry (LC-ESI-MS/MS). Finally, the presence of residues of thiamethoxam and clothianidin in collected sunflower seeds (hulls) coming from coated seeds confirmed the translocation of these neonicotinoids through the plant up to these seeds.|A novel and sensitive enhanced chemiluminescence enzyme-linked immunosorbent assay (ECL-ELISA) for the simultaneous analysis of imidaclothiz and thiacloprid is described. The concentrations of coating antibodies and enzyme tracers were optimized by three different ECL-ELISA formats. Under the optimized conditions, when anti-imidaclothiz polyclonal and anti-thiacloprid polyclonal antibodies were immobilized in a single well, single-enzyme tracer ECL-ELISA was used to screen the corresponding pesticide residue, and multi-enzyme tracer ECL-ELISA was used for the analysis of imidaclothiz and thiacloprid residue mixtures. The average recoveries of the two pesticides from spiked tomato, cabbage, and rice samples were in the range of 83.7-117%. Meanwhile, the results showed that the multi-enzyme tracer ECL-ELISA could be applied to the accurate analysis of different proportions of imidaclothiz and thiacloprid (1 : 4 to 4 : 1, m/m) when the gross residues ranged from 20 to 250 ug/kg. The results of the multi-enzyme tracer ECL-ELISA in the real tomato samples correlated well with those of high-performance liquid chromatography, with a correlation coefficient of 0.996. Therefore, this new strategy for developing immunoassays is suitable for the simultaneous quantitative detection of imidaclothiz and thiacloprid residues in agricultural samples.|Two liquid chromatography-tandem mass spectrometric methods were developed and validated to determine spinosyn A and D, thiacloprid and pyridalyl in spring onions cultivated under Egyptian field conditions. The degradation rates, the pre-harvest interval (PHI) values and the half-life values of the three pesticides were estimated. QuEChERS was used for sample preparation and the separation was performed on an X-Bridge C18 column with ACN-formic acid 0.1% as the mobile phase. Linear range, method detection limits (MDLs), precision, recovery and matrix effects were estimated. The multi-residue MDLs ranged from 0.02 ug/kg (spinosyn A & D) to 0.05 ug/kg for pyridalyl. All the investigated pesticides showed high degradation rates. For spinosad the half-life value was 1.2 days, for thiacloprid it reached 2.2 days and for pyridalyl 4.4 days. Furthermore, the calculated PHI values, according to the maximum residue levels set by the EU, were 0days for spinosad, 9.8 days for thiacloprid and 39.4 days for pyridalyl.|For more Analytic Laboratory Methods (Complete) data for Thiacloprid (7 total), please visit the HSDB record page.

A semiautomated method based on ultra-high performance liquid chromatography (UHPLC) coupled to Orbitrap high resolution mass spectrometry has been developed for the determination of neonicotinoids (imidacloprid, acetamiprid, clothianidin, dinotefuran, nitenpyram, thiacloprid and thiamethoxam) and the metabolite acetamiprid-n-desmethyl in urine samples. Two automated methods were tested (solid-phase extraction "SPE" and turbulent flow chromatography "TurboFlow"), obtaining the best results when TurboFlow was applied. The total analysis time for the developed method was 14 min. The optimized method was validated, obtaining suitable results for all validation parameters. Recoveries ranged from 78% to 116% meanwhile repeatability and reproducibility were evaluated obtaining values lower than 10% and 20% respectively (except for dinotefuran and nitenpyram at 0.2 ug/L). The limit of quantification (LOQ) for all compounds was established at 0.2 ug/L. The proposed analytical methodology was applied to analyze the target compounds in thirty six urine samples from pregnant women living in agricultural areas of Almeria (Spain). Imidacloprid, acetamiprid and acetamiprid-n-desmethyl were detected in some of the samples at concentrations ranging from 0.23 to 1.57 ug/L. Furthermore, dinotefuran was identified in two samples at trace levels.

Agrochemicals -> Insecticides|Insecticides, Molluscicides|Pesticides -> Insecticides|Environmental transformation -> Pesticides (parent, predecessor)

Thiacloprid has known environmental transformation products that include Thiacloprid-amide.|Thiacloprid has known environmental transformation products that include thiacloprid sulfonic acid and thiacloprid-amide.