Male and female rats were treated with (14)C-bifenthrin labeled in the acid or alcohol moiety at single oral doses of 4 and 35 mg/kg. (14)C was rapidly excreted into feces and urine, and the excretion rates of the (14)C to feces and urine were 66-83% and 13-25%, respectively. ... The major fecal metabolites possessed intact ester linkage hydroxylated in the acid or alcohol moiety such as hydroxymethyl-bifenthrin, 4'-OH-bifenthrin, and 3'- or 4'-OH-hydroxymethyl bifenthrin. Ester-cleaved products derived from mono- and dihydroxylated parent compounds were also detected. On the other hand, the majority of urinary metabolites were ester-cleaved products such as 4'-OH-BPacid (4'-hydroxy-2-methyl-3-phenylbenzoic acid), BPacid (2-methyl-3-phenylbenzoic acid), 4'-OH-BPalcohol (4'-hydroxy-2-methyl-3-phenylbenzyl alcohol), dimethoxy-BPacid, 4'-methoxy BPacid, dimethoxy BPalcohol, BPalcohol, TFPacid [3-(2-chloro-3,3,3-trifluoro-1-propenyl-2,2-dimethyl-cyclopropanecarboxylic acid], cis- and trans-hydroxymethyl TFPacid. The major metabolic pathways are considered to be hydrolysis of ester linkage, oxidation at the methyl group of the acid moiety and at the 3'- and 4'-positions of the phenyl group, and O-methylation. The conjugation reactions are considered to take place; however, detailed information is not available.
Fastest breakdown is seen with primary alcohol esters of trans-substituted acids since they undergo rapid hydrolytic and oxidative attack. For all secondary alcohol esters and for primary alcohol cis-substituted cyclopropanecarboxylates, oxidative attack is predominant. /Pyrethroids/
Pyrethrins are reportedly inactivated in the GI tract following ingestion. In animals, pyrethrins are rapidly metabolized to water soluble, inactive compounds. /Pyrethrins/
Bifenthrin, a pyrethroid pesticide, is estrogenic in vivo in fishes. However, bifenthrin is documented to be anti-estrogenic in vitro, in the ER-CALUX (estrogen receptor) cell line. We investigated whether metabolite formation is the reason for this incongruity. We exposed Menidia beryllina (inland silversides) to 10 ng/L bifenthrin, 10 ng/L 4-hydroxy bifenthrin, and 10 ng/L bifenthrin with 25 ug/L piperonyl butoxide (PBO) - a P450 inhibitor. Metabolite-exposed juveniles had significantly higher estrogen-mediated protein levels (choriogenin) than bifenthrin/PBO-exposed, while bifenthrinalone was intermediate (not significantly different from either). This suggests that metabolites are the main contributors to bifenthrin's in vivo estrogenicity.
Synthetic pyrethroids are generally metabolized in mammals through ester hydrolysis, oxidation, and conjugation, and there is no tendency to accumulate in tissues. In the environment, synthetic pyrethroids are fairly rapidly degraded in soil and in plants. Ester hydrolysis and oxidation at various sites on the molecule are the major degradation processes. /Pyrethroids/
IDENTIFICATION AND USE: Bifenthrin is a light brown viscous oil. Bifenthrin is registered for use to control a variety of insects including aphids, worms, ants, gnats, moths, beetles, grasshoppers, mites, midges, spiders, ticks, yellow jackets, maggots, thrips, caterpillars, flies, fleas, and other pests in domestic, public health, agricultural, and industrial situations. HUMAN EXPOSURE AND TOXICITY: Neurological effects include symptoms such as dizziness, headache, tingling and numbness sensation, muscle spasms and tremors. Dermal effects include symptoms such as rash, hives, blisters, sores and itchiness. Respiratory effects include symptoms such as: shortness of breath, asthma, respiratory distress, respiratory irritation, coughing, difficulty in breathing, sinus problems, and chest pain. Most of the gastrointestinal symptoms were nausea, vomiting and few cases presented with abdominal pain and diarrhea. Ocular symptoms were redness, pain and swelling of eyes, itchy watery eyes and blurred vision. Few cases presented with cardiovascular symptoms such as high blood pressure, irregular heartbeat, and heart attack. Exposure to bifenthrin, even at "acceptable" limits, can increase the risk for and frequency of inflammatory responses and diseases such as asthma. ANIMAL STUDIES: Non-irritant to skin; virtually non-irritating to eyes (rabbits); no skin sensitization (guinea pigs). Bifenthrin Technical, 88.35% a.i., 98% cis, 2% trans; 200, 100, 50, 12 and 0 ppm /was given to rats in feed; 50/sex/dose for 2 years. No oncogenic effects reported. Effects included tremors, abrasions, alopecia, tail lacerations, reduced weight gain (females only), and reduced RBC 12% (males only). All effects were observed at 200 ppm. Technical (Bifenthrin), 89.7%, administered to 4 Beagles/sex/group at nominal concentrations of 0, 0.75, 1.50, 3.0, and 5.0 mg/kg/day in gelatin capsules for 52 weeks; Intermittent delayed onset of tremors occurring through week 29 at 3.0 and 5.0 mg/kg/day. Bifenthrin technical, 88.35% a.i., 98% cis, 2% trans; 100, 60, 30 and 0 ppm was given to rats in the feed for 8 weeks prior to F0 mating through F2b weaning; 25/sex/dose; no fertility or reproductive effects, other effects include tremors during lactation, ovary weight reduction in adults. Non-teratogenic in rats (> or = 2 mg/kg/day) & rabbits (8 mg/kg/day). Tremors were observed in 6 pups out of 40 examined (4 males on post-natal day (PND) 10 and 2 females on PND 28) at the highest dose (9 mg/kg/day). Bifenthrin was not mutagenic in the Ames assay, and did not produce chromosome aberrations in Chinese hamster ovary (CHO) cells. ECOTOXICITY STUDIES: Based on available data, bifenthrin has been classified as slightly toxic on an acute basis to birds. Bifenthrin showed no adverse effects to reproduction at the highest concentration tested for birds. Mammalian toxicity data suggest that this compound is moderately toxic to small mammals on an acute basis. Relative to steelhead, rainbow trout have different responses to bifenthrin acute toxicity as well as different rates of hepatic bifenthrin biotransformation. Bifenthrin is highly toxic on an acute and chronic basis to freshwater fish and aquatic-phase amphibians, and very highly toxic to freshwater aquatic invertebrates. Bifenthrin has also been classified as very highly toxic to estuarine/marine fish and invertebrates on an acute basis.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
癌症分类：C组可能的人类致癌物
Cancer Classification: Group C Possible Human Carcinogen
来源:Hazardous Substances Data Bank (HSDB)
毒理性
副作用
神经毒素 - 其他中枢神经系统神经毒素
Neurotoxin - Other CNS neurotoxin
来源:Haz-Map, Information on Hazardous Chemicals and Occupational Diseases
A novel two-tiered analytical approach was used to characterize and quantify interactions between Type I and Type II pyrethroids on Hyalella azteca using standardized water column toxicity tests. Bifenthrin, permethrin, cyfluthrin and lambda-cyhalothrin were tested in all possible binary combinations across six experiments. All mixtures were analyzed for 4 d lethality, and two of the six mixtures (permethrin-bifenthrin and permethrin-cyfluthrin) were tested for subchronic 10 d lethality and sublethal effects on swimming motility and growth. Mixtures were initially analyzed for interactions using regression analyses, and subsequently compared to the additive models of Concentration Addition (CA) and Independent Action (IA) to further characterize mixture responses. Negative interactions (antagonistic) were significant in two of the six mixtures tested, including cyfluthrin-bifenthrin and cyfluthrin-permethrin, but only on the acute 4d lethality endpoint. In both cases mixture responses fell between the additive models of CA and IA. All other mixtures were additive across 4 d lethality, and bifenthrin-permethrin and cyfluthrin-permethrin were also additive on subchronic 10 d lethality and sublethal responses.
Piperonyl butoxide ... potentiates /insecticidal activity/ of pyrethrins by inhibiting the hydrolytic enzymes responsible for pyrethrins' metabolism in arthropods. When piperonyl butoxide is combined with pyrethrins, the insecticidal activity of the latter drug is increased 2-12 times /Pyrethrins/
Male and female rats were treated with (14)C-bifenthrin labeled in the acid or alcohol moiety at single oral doses of 4 and 35 mg/kg. (14)C was rapidly excreted into feces and urine, and the excretion rates of the (14)C to feces and urine were 66-83% and 13-25%, respectively. Highest residues were found in the fat, with values of slightly more than 1 ppm after low-dose administration and 8 and 16 ppm in males and females, respectively, after application of the high dose. Residue levels in other organs were in most cases <0.2 ppm after low-dose administration and <1 ppm after high-dose administration.
The tissue residues /of rats/ were examined after oral administration of (14)C-bifenthrin at 0.5 mg/kg/day for 70 days. The peak (14)C concentrations on an average were 9.6 ppm in fat, 1.7 ppm in skin, 0.4 ppm in liver, 0.3 ppm in kidney, 1.7 ppm in ovaries, 3.2 ppm in sciatic nerve, 0.06 ppm in whole blood, and 0.06 ppm in plasma. Analyses were extended for an additional 85 days following cessation of dosing (depuration phase). Half-lives of 51 days (fat), 50 days (skin), 19 days (liver), 28 days (kidney), and 40 days (ovaries and sciatic nerve) were estimated from (14)C-depuration. Analysis of the fat revealed that the parent chemical accounted for a majority (65-85%) of the (14)C-residues in fat.
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
杀虫剂是透过完整皮肤被吸收的，当局部应用时。
Pyrethrins are absorbed through intact skin when applied topically. /Pyrethrins/
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
...在大鼠口服、吸入和静脉给药后，对双甲脒的药代动力学进行了描述。还介绍了通过口服和吸入途径的拟除虫菊酯类急性毒性。将雄性大鼠分组，通过口服灌胃给药3.1 mg/kg，用1 mL/kg的玉米油（临界、急性、口服基准剂量下限，BMDL）和等效剂量通过吸入（0.018 mg/L）4小时。在给药开始后2、4、6、8和12小时，测量血浆和大脑中双甲脒的浓度。血浆中双甲脒的最大浓度为361 ng/mL或0.853 uM（口服）和232 ng/mL或0.548 uM（吸入），在大脑中为83和73 ng/g。口服灌胃给药后，浓度-时间曲线下的面积（AUC）值为1969 h ng/mL（血浆）和763 h ng/mL（大脑），吸入后为1584 h ng/mL（血浆）和619 h ng/mL（大脑）。静脉给药导致明显的终末半衰期（t1/2）值为13.4 h（血浆）和11.1 h（大脑），血浆和大脑的AUC0-∞值为454和1566 h ng/mL。从血浆中清除的速率为37 mL/min/kg。口服给药后，血浆和大脑的峰浓度通常略高（约14%）。双甲脒的吸入给药没有因为避免肝脏的首过效应而在血浆或大脑中引起暴露增加。消除半衰期与其他拟除虫菊酯类相似，表明生物积累潜力很小。...
... The pharmacokinetics of bifenthrin in the rat after oral, inhalation and intravenous administration is described. Pyrethroid acute toxicity via oral and inhalation routes is also presented. Groups of male rats were dosed by oral gavage at 3.1 mg/kg in 1 mL/kg of corn oil (the critical, acute, oral benchmark dose lower limit, BMDL) and at an equivalent dose by inhalation (0.018 mg/L) for 4 hr. At 2, 4, 6, 8 and 12 hr after dosing initiation, blood plasma and brain bifenthrin concentrations were measured. The maximum concentrations of bifenthrin in plasma were 361 ng/mL or 0.853 uM (oral) and 232 ng/mL or 0.548 uM (inhalation), and in brain they were 83 and 73 ng/g. The area under the concentration versus time curve (AUC) values were 1969 h ng/mL (plasma) and 763 h ng/mL (brain) following oral gavage dosing, and 1584 h ng/mL (plasma) and 619 h ng/mL (brain) after inhalation. Intravenous dosing resulted in apparent terminal half-life (t1/2 ) values of 13.4 h (plasma) and 11.1 h (brain) and in AUC0-infinity values of 454 and 1566 h ng/mL for plasma and brain. Clearance from plasma was 37 mL/min/kg. Peak plasma and brain concentrations were generally a little higher after oral dosing (by ca 14%). Inhalation administration of bifenthrin did not cause increases in exposure in plasma or brain by avoiding first-pass effects in the liver. The elimination t1/2 was comparable with other pyrethroids and indicated little bioaccumulation potential. ...
... This study evaluated the oral disposition and bioavailability of bifenthrin in the adult male Long-Evans rat. In the disposition study, rats were administered bifenthrin (0.3 or 3 mg/kg) by oral gavage and serially sacrificed (0.25 hr to 21 days). Blood, liver, brain and adipose tissue were removed. In the bioavailability study, blood was collected serially from jugular vein cannulated rats (0.25 to 24 hr) following oral (0.3 or 3 mg/kg) or intravenous (0.3 mg/kg) administration of bifenthrin. Tissues were extracted and analyzed for bifenthrin by high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Bifenthrin concentration in blood and liver peaked 1-2-hr post-oral administration and were approximately 90 ng/mL (or g) and 1000 ng/mL (or g) for both tissues at 0.3 and 3 mg/kg, respectively. Bifenthrin was rapidly cleared from both blood and liver. Brain concentrations peaked at 4-6 hr and were lower than in blood at both doses (12 and 143 ng/g). Bifenthrin in adipose tissue peaked at the collected time points of 8 (157 ng/g) and 24 (1145 ng/g) hr for the 0.3 and 3 mg/kg doses, respectively and was retained 21 days post-oral administration. Following intravenous administration, the blood bifenthrin concentration decreased bi-exponentially, with a distribution half-life of 0.2 hr and an elimination half-life of 8 hr. Bifenthrin bioavailability was approximately 30%. These disposition and kinetic bifenthrin data may decrease uncertainties in the risk assessment for this pyrethroid insecticide.
Novel ether-amide compounds are described. Uses of the compounds, in particular as solvents, for example in phytosanitary formulations are also described.
描述了新型醚酰胺化合物。还描述了该化合物的用途，特别是作为溶剂，例如在植物保护制剂中的用途。
NOVEL USES OF ESTERAMIDE COMPOUNDS
申请人：Guglieri Massimo
公开号：US20130210933A1
公开（公告）日：2013-08-15
The use of an esteramide compound, alone or as a mixture of the following formula (I):
R
1
OOC-A-CONR
2
R
3
(I)
is described, wherein:
A is a covalent bond or a methylene group —CH
2
—,
R
1
is an optionally substituted hydrocarbon group having from 1 to 36 carbon atoms,
R
2
and R
3
, either identical or different, are groups selected from a hydrogen atom and optionally substituted hydrocarbon groups comprising from 1 to 36 carbon atoms,
R
2
and R
3
may form together a ring having the nitrogen atom to which they are bound, said ring being, if need be, substituted and/or having an additional heteroatom and
R
2
and R
3
not being simultaneously hydrogens.
Also described, are applications for using the esteramide compound as a solvent, a co-solvent, a coalescence agent, a crystallization inhibitor, a plasticizer or an agent for increasing biological activity.
The present invention concerns the use of a furfural derivative of formula (I)
in which R represents (i) a —CH═CR′
1
—COR
1
group, a group
a group
a group
or a —CHO and R′ represents a hydrogen atom or a (C
1
-C
4
)alkyl group, as a chemical vehicle, as a solvent, co-solvent, coalescing agent, crystallization inhibitor, plasticising agent, degreasing agent, etchant, cleaning agent or agent for increasing biological activity, and more particularly as a solvent.
It also concerns phytosanitary formulations or resin-solubilising formulations comprising at least one such furfural derivative of formula (I).
ESTERAMIDE SOLVENTS/COALESCING AGENTS IN PHYTOSANITARY, CLEANING, DEGREASING, STRIPPING, LUBRICATING, COATING, AND PIGMENT/INK COMPOSITIONS
申请人：Jentzer Olivier
公开号：US20110166025A1
公开（公告）日：2011-07-07
Esteramide compounds are useful solvents/coalescing agents for a variety of phytosanitary, cleaning, degreasing, stripping, lubricating, coating and pigment/ink compositions.
Photochemical Degradation of Bifenthrin in Water Solution
作者：Yan-Ru Liang、Zhen-Bin Gong、Wen-Quan Li
DOI：10.14233/ajchem.2013.15019
日期：——
The mechanism of photochemical degradation of bifenthrin in water solution has been investigated using a laboratory-built photochemical degradation device hyphenated with commercial high performance liquid chromatography and UV-visible photo-spectrometric, fluorescent and mass spectrometric detector. Spectrometric characteristics of bifenthrin and its main degradation products suggest that bifenthrin could be photo-degraded under UV irradiation. The kinetics of the photochemical reaction demonstrates that laboratory-built photochemical degradation is of high efficiency for off-line degradation of interested organics. The photo-degradation reaction of bifenthrin in water solution is approximately the pseudo-first-order reaction. Mass spectrometric results show that bifenthrin is first converted into its space isomerism and then further degraded and converted to the final products under a series of molecular rearrangement, oxidation reduction and de-chlorination reaction.
