啶酰菌胺-安全技术说明书MSDS
啶酰菌胺
啶酰菌胺是由德国BASF公司发的新型酰胺类杀菌剂，英文名称为boscalid，目前在中国市场以商品名“凯泽”对黄瓜灰霉病进行了登记。
啶酰菌胺具有广谱、低毒、髙效和与市场上其它杀菌剂无交互抗性等优点。
啶酰菌胺对灰霉病、黑斑病和白粉病等病害有着非常优异的防效，特别是对多种作物如瓜类、葡萄、草毒和西红棉等的灰霉病有特效，同时它还具有吸收迅速、环境污染低、治疗效果明显、耐雨水冲刷、扩散速度快、对作物安全、和持效期长等特点。
2015年3月2日，陕西美邦农药有限公司获批登记国内企业第4个啶酰菌胺原药产品（97%含量）。
此前，河北省石家庄市兴柏生物工程有限公司、江苏省泰州百力化学股份有限公司和浙江禾本科技有限公司分别登记啶酰菌胺原药产品（含量分别为98%、98%和96%）。
boscalid epa data啶酰菌胺
United States Office of Prevention, PesticidesEnvironmental Protection and Toxic SubstancesAgency (7501C)PesticideFact SheetName of Chemical: BoscalidReason for Issuance: New ChemicalDate Issued: July 2003Description of ChemicalChemical Name:3-pyridinecarboxamide, 2-chloro-N-(4’chloro[1,1’biphenyl]-2-yl)Common Name: Boscalid (BAS 510)Trade Names: Emerald, Endura, and PristineChemical Class: Carboxamide aka anilideEPA Chemical Code: 128008Chemical Abstracts Service (CAS) Number: 188425-85-6Year of Initial Registration: 2003Pesticide Type: FungicideU.S. Producer: BASFUse Pattern and FormulationsBoscalid is a fungicide consisting of two formulated end-use products for use on food crops. The wettable granule (WG) Endura Fungicide contains 70% active ingredient, and the wettable granule (WG) Pristine contains a mixture of boscalid (25.2% active) and pyraclostrobin (12.8% active). Endura™ is intended for use on beans, berries, bulb vegetables, canola, carrots, fruiting vegetables, grapes, lettuce, peanuts, pistachios, potatoes, stone fruit, strawberries, tree nuts, Brassica vegetables (subgroups 5A and 5B), cucurbit vegetables, mint, edible peas, certain root vegetables, and sunflower. Pristine™ is intended for use on berries, bulb vegetables, carrots, grapes, pistachios, stone fruit, strawberries, and tree nuts. Application is via multiple, foliar, broadcast sprays at a seasonal rate of ca 0.9-1.8 lbs ai/A, depending on crop and target disease. Typically, retreatment intervals are 1-3 weeks and minimum PHIs are 0-30 days.1There is also a formulated 70% wettable granule end-use product named Boscalid Turf Fungicide for use on golf course turfgrass. No other residential uses have been proposed.Science FindingsSummary Science StatementThe Agency has completed its review of the product chemistry, toxicology, residue chemistry, occupational exposure, ecological effects and environmental fate data submitted in support of the registration of boscalid.The toxicology data base for boscalid is adequate to support the requested field use registrations and tolerances. There is high confidence in the hazard endpoints and dose-response assessments conducted for this chemical.Boscalid is classified as “suggestive evidence of carcinogenicity, but not sufficient to assess human carcinogenic potential”. Therefore, a cancer risk assessment is not required.The Agency has considered available information on boscalid’s toxicity, potential use areas, fate properties, and application methods in characterizing ecological risks related to labeled use. Boscalid is persistent, it has low mobility in soil; however, boscalid may move to surface water through spraydrift and runoff of soil and suspended sediments. The degree of surface water contamination is mitigated by the relatively low seasonal application rates (2.1 lbs ai/acre/season) and its tendency to sorb to soil and sediment. The compound does not bioaccumulate appreciably in fish (BCF 35X-105X).The fungicide is practically nontoxic to terrestrial animals and is moderately toxic to aquatic animals on an acute exposure basis. Boscalid acute risk quotients (RQs) do not exceed acute risk levels of concern and is not likely to pose an acute risk to animals at the maximum use rate. The RQ is not an absolute estimate of the likelihood, magnitude, or severity of risk. Inputs into this screening level assessment were designated to overestimate likely exposures and effects of boscalid. Given the slight exceedences of the RQs and the label limitations that will be imposed for boscalid, the Agency believes that potential ecological risks are low.Physical/Chemical PropertiesPhysical and Chemical Properties for Technical Grade Active IngredientResultRequirementWhite powder (TGAI); White crystalline (PAI)Color/Physical StateOdor TGAI - faint smokyPAI - odorlessThe test substance was found to be stable at RT and 54C for 14 days. The testStability substance was also found to be stable when exposed to metals like AI, & Fe, and tocorresponding acetate ions.It reacts very weakly with potassium permanganate but does not react with iron, Oxidation/Reduction water or the fire extinguishing agent monoammonium phosphate (MAP). It is a very2weak reducing agent..Not applicableFlammabilityNon-explosiveExplodabilityNot required for a TGAI. Accelerated storage at 54o C, in glass: day 0 -Storage Stability 98.16%, day 30 - 97.96..Not applicableMiscibilityThe test substance is not expected to be corrosive to the commercial Corrosion Characteristics storage container5.5 at 23°C (1% solution)pH.Not applicableViscosity143.4-143.6E C (TGAI); 142.8-143.8E C (PAI)Melting Point/Melting RangeDensity1.394 g/cm3 (TGAI); 1.381 g/cm3 (PAI)Test substance does not dissociateDissociation Constant in Waterlog P o/w = 2.96; P o/w = 915 @ 21°CPartition Coefficient(Octanol/Water)PAI at 20°C in acetone (16-20 g/100 ml); acetonitrile (4-5 g/100ml); Solubility: methanol (4-5 g/100 ml); ethylacetate (6.7-8 g/100 ml); dichloromethane (20-25 g/100 ml); toluene (2-2.5 g/100 ml); 1-octanol (<1 g/100 ml; water, 6mg/L@20 C)Vapor Pressure7 x 10-9 hPa (PAI at 20°C); 2 x 10-8 hPa (PAI at 25°C) Toxicological Characteristics:Acute Toxicity Profile - Boscalid TechnicalTestMaterial GDLN Study TypeTechnical 870.1100 Acute Oral -ratTechnical 870.1200 Acute Dermal -ratTechnical 870.1300 AcuteInhalationTechnical 870.2400 Primary EyeIrritation 3Tox MRID Results Category45404814 LD50> 5000 mg/kg IV45404815 LD50> 2000 mg/kg III45404816 LC50(M & F): > 6.7 IVmg/L45404817 Not irritating to the eye IVTechnical 870.2500 Primary 45404818 Not irritating to the skin IVDermalIrritation4Technical870.2600Dermal45404819Study unacceptable as SensitizationN/Achallenge dose was Toxicity Profile of Boscalid Technical.Guideline No. Study Type 870.310090-Day oral toxicity rodents (rats)870.310090-Day oral toxicity rodents (mice)870.315090-Day oral toxicity in nonrodents (dogs)870.3200 21/28-Day dermal toxicity (rats)870.3700Prenatal developmental in rodents (rats)870.3700Prenatal developmental in nonrodents (rabbit)870.3800Reproduction and fertility effects (rat)5inadequateResultsNOAEL : 34/159 mg/kg/day (M/F)LOAEL : 137/395 mg/kg/day (M/F): M = increases in absolute and relative thyroid weights and increased incidence of thyroid hyperplasia as well as follicular epithelial hypertrophy; F = increases in absolute and relative thyroid weights.NOAEL : 197/2209 mg/kg/day (M/F)LOAEL : 788/2209 mg/kg/day (M/F): M = increased liver weights and increased incidence of marked fatty change in the liver; F = not attainedNOAEL : 7.6/8.1 mg/kg/day (M/F)LOAEL : 78.1/81.7 mg/kg/day (M/F): M = increased alkaline phosphatase activity and hepatic weights; F = increased alkaline phosphatase activity and hepatic weights.NOAEL : 1000 mg/kg/day (HDT) LOAEL : >1000 mg/kg/dayMaternal NOAEL : 1000 mg/kg/day Maternal LOAEL : cannot be established Developmental NOAEL : 1000 mg/kg/day Developmental LOAEL : cannot be established Maternal NOAEL : 300 mg/kg/dayMaternal LOAEL : 1000 mg/kg/day based on abortions or early delivery.Developmental NOAEL : 300 mg/kg/dayDevelopmental LOAEL : 1000 mg/kg/day based on abortions or early delivery.Parental systemic NOAEL :112.6/1180.8 mg/kg/day (M/F)Parental systemic LOAEL :1165.0/>1180.8Chronic toxicity rodents 870.4100a (rat)870.4100 Chronic toxicity dogs 870.4200Carcinogenicity rats 870.4200 Carcinogenicity mice870.4300 Chronicfeeding/Carcinogenicity ratGene Mutation bacterial 870.5100 reverse mutation assayIn vitro mammalian cell 870.5300 forward gene mutationassay (CHO cells/HGPRTlocus)In vitro mammalianChinese hamster V79 cells 870.5375 cytogenetics assay in6 mg/kg/day (M/F) decreased body weight and body weight gain (F1) as well as hepatocyte degenerationFand F1) in males only.Offspring systemic NOAEL:11.2/115.8 mg/kg/day (M/F)Offspring systemic LOAEL:112.6/1180.8mg/kg/day (M/F): decreased body weight for F2pups in males and females of both generations. Reproductive NOAEL:1165.0/1180.8 mg/kg/day (M/F)Reproductive LOAEL:>1165.0/1180.8 (M/F) NOAEL: 21.9/30.0 mg/kg/day (M/F)LOAEL: 110.0/150.3 mg/kg/day (M/F): M = thyroid toxicity (weights and microscopic changes); F = thyroid toxicity (weights and microscopic changes). Thyroid follicular cell adenomas: M = 0/20, 0/20,2/20,1/20; F = 0/20, 0/20, 1/20,0/20.NOAEL: 21.8/22.1mg/kg/day (M/F)LOAEL:57.4/58.3 mg/kg/day (M/F): M = elevated ALP activities and elevated hepatic weights; F = no effectsNOAEL: 23.0/29.7 mg/kg/day (M/F)LOAEL: 116.1/155.6 mg/kg/day (M/F): M = increased incidence of thyroid follicular cell hyperplasia and hypertrophy; F = decrease in body weight gain and increased incidence of thyroid follicular cell hyperplasia and hypertrophy. Thyroid follicular cell adenomas: M = 0/50, 0/50, 1/50, 4/50; F = 0/50, 1/50, 0/50, 3/50.NOAEL:65/443 mg/kg/day (M/F)LOAEL: 331/1804 mg/kg/day (M/F): M = decreases in body weight and body weight gains; F = decreases in body weight and body weight gains. No evidence of carcinogenicity.See 870.4100a and 870.4200.Negative without and with S-9 activation up to limit dose of 5000 µg/plate.Negative without and with S-9 activation up to the limit of solubility of 25 µg/mL.Negative without and with S-9 activation up to 3500 µg/mL with precipitation showing at concentrationsof 100 µg/mL and higher.870.5395 Cytogenetics - mammalianerythrocyte micronucleustest in the mouseIn vitro unscheduled DNAhepatocytes)870.5500 synthesis (primary rat870.6200 Acute neurotoxicityscreening battery (rat)870.6200 Subchronic neurotoxicityscreening battery (rat)870.6300 Developmentalneurotoxicity (rat)870.7485 Metabolism andpharmacokinetics (rat)870.7600 Dermal Penetration (rat)SPECIAL STUDY:noneHepatic enzyme induction(rat)7 Negative at doses up to 2000 mg/kg.Negative response up to 50 µg/mL. Cytotoxicity at 100-500 µg/mL.NOAEL:2000/1000 mg/kg/day (M/F)LOAEL: >2000/2000 mg/kg/day (M/F): F = piloerectionNOAEL:1050.0/1272.5 mg/kg/day (M/F) LOAEL: >1050.0/1272.5 mg/kg/day(M/F)Maternal NOAEL:1442 mg/kg/dayMaternal LOAEL: >1442 mg/kg/dayOffspring NOAEL: 14 mg/kg/dayOffspring LOAEL: 147 mg/kg/day (decreased body weights on PND 4 and decreased body weight gain on PNDs 1-4)Boscalid was readily absorbed and excreted following single oral 50 mg/kg; at single 500 mg/kg or 15 doses of 500 mg/kg, absorption wassaturated. Excretion mainly byfeces (80-98%). Biliary excretion 40-50% of fecal activity at 50 mg/kg, 10% at 500 mg/kg. Urine, about 16% at 50 mg/kg, 3-5% at 500 mg/kg. Absorption about 56% at 50 mg/kg and 13-17% at 500 mg/kg. Excretory patterns similar by gender or radiolabel position. Metabolites (hydroxylation and conjugation products) were consistent with Phase I oxidation reactions followed by Phase II conjugation with glucuronic acid or sulfate, or by conjugation of the parent with glutathione with cleavage to sulfate metabolites.Maximum % absorption:0.01 mg/cm2 = 10.93 (24 hour exposure, 24 hour sacrifice)0.10 mg/cm2 = 3.76 (24 hour exposure, 24 hour sacrifice)1.00 mg/cm2 = 1.48 (10 hour exposure, 72 hour sacrifice)1. hypertrophy of zone III hepatocytes2. >20% increase in liver weight3. increase in CYP450 activity4. slight to extensive microscopic SER proliferation5. not a peroxisome proliferator6. enzymes in CYP450 subfamily not induced7. no notable microscopic increase in size or number of peroxisomesCONCLUSION: inducer of total CYP450 activitySPECIAL STUDY:noneHormone and enzymeinduction (rat)none SPECIAL STUDY:Reversibility study(dietary): 4-weekadministration followed by4 weeks recovery or 13weeks recovery (rat) Summary of Toxicology Findings. 1. slight (statistically significant) decrease in circulating T3and T4only in males2. increase in circulating TSH levels both sexes3. increase in all 3 liver microsomal glucuronyltransferasesCONCLUSION: disruption of thyroid homoeostasis by decreasing circulating T3and T4and increasing TSH; likely the result of hepatic microsomal glucuronyltransferase induction4 weeks dosing: at 2500 and 15000 ppm: increase in TSH (68% and 87%); increase in absolute and relative thyroid weights, hypertrophy of thyroid follicular epithelial cells and diffuse follicular hyperplasia, increase in absolute and relative liver weights and centrilobular hypertrophy as well as liver portal fatty changes.4 weeks dosing + 4 weeks recovery: no increases in TSH; increase in absolute and relative thyroid weights; thyroid hypertrophy and hyperplasia decreased to control values; all liver effects reversed to control.4 weeks dosing + 13 weeks recovery: no increases in TSH; increase in absolute and relative thyroid weights; thyroid hypertrophy and hyperplasia decreased to control values; all liver effects reversed to control.CONCLUSION: induction of liver microsomal enzyme system resulting in increased glucuronidation of thyroxine, resulting in an increase in TSH secretion as a compensatory response of the physiological negative feedback system; increased TSH resulted in increased thyroid weight.Boscalid has a low toxicity (toxicity categories III or IV for oral, dermal, inhalation, primary eye irritation and primary skin irritation). In a dermal sensitization study in guinea pigs, the study was unacceptable because the concentration used for the challenge was inadequate.In subchronic and chronic feeding studies in rats, mice and dogs, boscalid generally caused decreased 8body weights and body weight gains (primarily in mice) and effects on the liver (increase in weights, changes in enzyme levels and histopathological changes) as well as on the thyroid (increase in weights and histopathological changes).In a developmental toxicity study in rats, no developmental toxicity was observed in the fetuses at the highest dose tested (Limit Dose). No effects were noted in the dams in this study. In a developmental toxicity study in rabbits, an increased incidence of abortions or early delivery was observed at the Limit Dose. Since it could not be determined whether the abortions or early delivery were due to maternal toxicity or due to an effect on reproductive/developmental mechanisms, the LOAELs and NOAELs in this study for both maternal and developmental toxicity were considered to be the same. The does (maternal toxicity) and fetuses (developmental toxicity) were considered to be equally sensitive to the test material. This study does not indicate an increased susceptibility of fetuses, as compared to does. In a 2-generation reproduction study in rats, the NOAEL for parental toxicity was based on decreased body weight and body weight gain as well as hepatocyte degeneration. The NOAEL for offspring toxicity was based on decreased body weights and body weight gains for the pups. No reproductive toxicity was observed in this study at the highest dose tested. There was no evidence of susceptibility in the developmental rat study. There was evidence of qualitative (not quantitative) susceptibility in the developmental rabbit study as characterized by an increased incidence of abortions or early delivery at the highest dose tested. There was quantitative evidence of increased susceptibility in the two-generation reproduction study in rats, where decreases in body weights and body weight gains in male offspring were seen at a dose that was lower than the dose that induced parental/systemic toxicity. There was quantitative evidence of increased susceptibility in the developmental neurotoxicity study in rats, where decreases in pup body weights (PND 4) and body weight gains (PND 1-4) were seen in the absence of any maternal toxicity.In a two-year chronic toxicity study and a two-year carcinogenicity study in male and female rats, the combined data showed that, for thyroid follicular cell adenomas, males had a significant increasing trend and significant differences in the pair-wise comparison of the highest dose group, when compared with controls. There was no treatment-related increase in thyroid follicular cell carcinomas. The increased incidence of the thyroid follicular cell adenomas exceeded the historical control mean and range. The increase in thyroid follicular cell adenomas appeared to be treatment-related in males. This was supported by thyroid hypertrophy and hyperplasia of follicular cells at the same dose as well as increased thyroid weights plus mechanistic data. Regarding females, combined data from the two rat studies indicated that there was an increasing trend for thyroid follicular cell adenomas which appeared to be treatment related. No carcinomas were observed in females. Boscalid is classified as, “suggestive evidence of carcinogenicity, but not sufficient to assess human carcinogenic potential”, according to the EPADraft Proposed Guidelines for Carcinogen Risk Assessment (July 2, 1999).Boscalid (BAS 510 F) was tested in five mutagenicity studies and was found to be negative in all of them.In neither an acute nor a subchronic neurotoxicity study in rats was there evidence of a neurotoxic effect at the Limit Dose. In a developmental neurotoxicity study in rats, there were no neurotoxic effects observed at the Limit Dose. No neurotoxic observations were noted in any of the other studies in any species.9In metabolism and pharmacokinetic studies, Boscalid was readily absorbed and excreted following a single oral dose of 50 mg/kg. At single 500 mg/kg or 15 doses of 500 mg/kg, absorption was saturated. Excretion was mainly by feces (80-98%). Biliary excretion was 40-50% of fecal activity at 50 mg/kg and 10% at 500 mg/kg. Urinary content was about 16% at 50 mg/kg and 3-5% at 500mg/kg. Absorption was about 56% at 50 mg/kg and 13-17% at 500 mg/kg. Excretory patterns were similar by gender or radiolabel position. Metabolites (hydroxylation and conjugation products) were consistent with Phase I oxidation reactions followed by Phase II conjugation with glucuronic acid or sulfate, or by conjugation of the parent with glutathione with cleavage to sulfate metabolites.A dermal absorption study in rats is available. Doses used were 0.01, 0.10 and 1.0 mg/cm2. The maximum percent absorptions were as follows: 0.01 = 10.93 (24 hour exposure, 24 hour sacrifice); 0.10 = 3.76 (24 hour exposure, 24 hour sacrifice); and 1.00 = 1.48 (10 hour exposure, 72 hour sacrifice). The total amount of absorption was 15% as represented by 11% being absorbed at 24 hours plus 4% found as bound residue on the skin.Occupational and Residential Exposure and Risk Characterization.All MOEs for the handlers performing agricultural crop uses were greater than the target of 100 at the baseline level (ranging from 460 to 31,000). All MOEs for the handlers performing golf course turfgrass uses were also greater than the target of 100 at the baseline level (ranging from 7,300 to 27,000).The handler exposure estimates in this assessment are based on a central tendency estimate of unit exposure and an upper-percentile assumption for the application rate, and are assumed to be representative of high-end exposures. The uncertainties associated with this assessment stem from the use of surrogate exposure data (e.g., differences in use scenario and data confidence), and assumptions regarding that amount of chemical handled. The estimated exposures are believed to be reasonable high-end estimates based on observations from field studies and professional judgement.The Agency uses the term “post-application” to describe exposures to individuals that occur as a result of being in an environment that has been previously treated with a pesticide. There are two recreational scenarios associated with boscalid that could lead to exposures for adults and children: 1.) golfing and 2.) picking their own fruit. These exposure durations are anticipated to be short-term (golfing) or acute (one day for picking fruit). Because “pick your own fruit” is considered a “one-time” event (duration <1 day) and oral studies indicated there were no toxicological endpoints appropriate to quantitate acute risk, this exposure scenario was not evaluated.The boscalid label specifies that this product is intended for golf course use only, and not for use on residential turfgrass or turfgrass being grown for sale or other commercial use such as sod production. Although the label does not indicate that the product is applied by licenced or commercial applicators, it is acknowledged that the homeowner will not be applying the product to golf courses.Therefore, a risk assessment for residential handler exposure is not required.FQPA CONSIDERATIONSThe special FQPA safety factor is reduced to 1X because the existing data indicate that there areno/low concerns and no residual uncertainties with regard to pre- and/or postnatal toxicity.10Conservative residue assumptions are used in the dietary risk assessments; there are no uses that will result in residential exposure except golf course and pick-your-own fruits; and the residue chemistry and environmental fate databases are relatively complete (evaluated by the risk assessment team). A 1X database factor is to be applied to all dietary and residential exposure endpoints as there are no data gaps. The Agency selected endpoints for chronic dietary exposure (all populations), incidental oral short- and intermediate-term residential only, dermal (all durations) and inhalation (all durations). As there were no toxic effects attributable to a single dose, an endpoint of concern was not identified to quantitate acute-dietary risk to the general population or to the subpopulation females 13-50 years old. Therefore, there is no acute reference dose (aRfD) or acute population-adjusted dose (aPAD). For all of the endpoints selected, liver and thyroid effects were chosen from the chronic toxicity study in rats, the carcinogenicity study in rats and the 1-year study in dogs. The NOAEL was 21.8 mg/kg/day. The uncertainty factor (UF) was 100. For the dermal route, the absorption rate was 15% relative to oral. For the inhalation route, the absorption rate was assumed to be 100%. The cPAD for the chronic dietary (all populations) exposure scenario = 0.218 mg/kg/day. The residential and occupational level of concern (LOC) is MOE = 100 for all routes (i.e., margins of exposure < 100 are of concern).DoseEndpoint Study/Effect Exposure ScenarioAcute dietaryNo appropriate endpoint none not applicable identified Chronic dietary (all populations)NOAEL = 21.8 mg/kg/day cRfD and cPAD = 0.218 mg/kg/day Chronic rat, carcinogenicity rat and 1-year dog studies based on liver and thyroid effects. Incidental oral (short- and intermediate-term Oral NOAEL = 21.8 mg/kg/day Target MOE = 100 (residential and occupational) Chronic rat, carcinogenicity rat and 1-year dog studies based on liver and thyroid effects. residential only)Oral NOAEL = Target MOE = Chronic rat, carcinogenicity rat and 1-year dog Dermal (all durations) Absorption: 15%21.8 mg/kg/day 100 (residential) , 100 (occupational studies based on liver and thyroid effects. ) Inhalation (all durations) Absorption: 100% Oral NOAEL = 21.8 mg/kg/day Target MOE = 100 (residential), 100 (occupational) Chronic rat, carcinogenicity rat and 1-year dog studies based on liver and thyroid effects. Aggregate Exposure And Risk CharacterizationAggregate exposure risk assessments were performed for short term and chronic aggregate exposure. Short term and chronic aggregate exposures take into account dietary (food + drinking water) and residential exposures. Since the Agency does not have ground and surface water monitoring data to calculate a quantitative aggregate exposure, drinking water levels of comparison (DWLOCs) were calculated. A DWLOC is a theoretical upper limit on a pesticide’s concentration in drinking water in light of total aggregate exposure to a pesticide in food, drinking water, and through residential uses. A DWLOC will vary depending on the toxic endpoint, drinking water consumption, body weights, and pesticide uses. Different populations will have different DWLOCs. The Agency uses DWLOCs in the risk assessment process to assess potential concern for exposure associated with pesticides in drinking water. DWLOC values are not regulatory standards for drinking water.11To calculate chronic DWLOCs, the dietary food estimates (from DEEM™) were subtracted from the chronic PAD value to obtain the maximum water exposure level. DWLOCs were then calculated using the standard body weights and drinking water consumption figures: 70kg/2L (adult male and US Population), 60 kg/2L (adult female), and 10kg/1L (infant & children).As there were no toxic effects attributable to a single dose, an endpoint of concern was not identified to quantitate acute-dietary risk to the general population or to the subpopulation females 13-50 years old. Therefore, there is no acute reference dose (aRfD) or acute population-adjusted dose (aPAD) for the general population or females 13-50 years old. An acute aggregate risk assessment is not needed. The chronic aggregate risk assessment takes into account average exposures estimates from dietary consumption of boscalid (food and drinking water) and residential uses. Since there are no chronic residential exposures associated with uses of boscalid, the chronic aggregate included food and drinking water only. The calculated chronic DWLOCs for chronic exposure to Boscalid in drinking water range from 1400 to 7000 µg/L (ppb). EECs generated are less than the calculated chronic DWLOCs . Therefore, the chronic aggregate risk associated with the proposed use of BAS 510 does not exceed the Agency’s level of concern for the general U.S. population or any population subgroups. Post application exposures from the sue oon golf couse is considered short term and applies to adults and youth. Although, a shourt term dermal risk assessment was conducted for the adult only, the adult MOEs are also considered representative for youths playing golf since the body surface area to weight ratios for adolescents do not vary significantly from those for adults. Since all endpoints are from the same study, exposure from different routes can be aggregated . The short term aggregate risk assessment takes into account average exposures from dietary consumption of boscalid (food and drinking water) and exposures from non-occupational sources (golf course). The calculated MOE from food and non-occupational exposure is 1200, and the calculated short term DWLOC is 6000 ppb. Compared to the surface water and ground waer EECs the short-term DWLOC is considerably larger and therefore the short term aggregate risk does not exceed the Agency’s level of concern.Cancer AssessmentThe Agency classified Boscalid (BAS 510 F) as, “suggestive evidence of carcinogenicity, but not sufficient to assess human carcinogenic potential”, and, therefore, the quantification of human cancer risk is not recommended. The cancer classification was based on the following weight of evidence considerations. First, in male Wistar rats, there was a significant trend (but not pair wise comparison) for the combined thyroid adenomas and carcinomas. This trend was driven by the increase in adenomas. Second, in the female rats, there was only a borderline significant trend for thyroid adenomas (there were no carcinomas). Third, the mouse study was negative as were all of the mutagenic tests. Consistent with this weak evidence of carcinogenic effects, the Agency concluded that a dose-response assessment for cancer (either linear low-dose extrapolation or margin of exposure calculation) was not needed.Ecological Effects/Environmental Fate Characteristics:1. Environmental Fate Summary:Boscalid is a slowly degradable compound with low mobility in most soils. The primary degradation12。
新型烟酰胺类杀菌剂啶酰菌胺的研究进展_于乐祥
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专 利 与 登 记 : 陡 酸 菌胺 为 德 国 巴斯 夫 公 司 于
巴斯夫凯泽Cantus
安全技术说明书页: 1/12 巴斯夫安全技术说明书按照GB/T 16483编制日期 / 本次修订: 17.12.2021版本: 14.1日期/上次修订: 08.06.2021上次版本: 14.0日期 / 首次编制: 16.01.2006产品: 凯泽 Cantus®Product: Cantus(30174304/SDS_CPA_CN/ZH)印刷日期 11.09.20231. 化学品及企业标识凯泽 Cantus®Cantus推荐用途和限制用途: 植物保护产品, 杀真菌剂公司:巴斯夫(中国)有限公司中国上海浦东江心沙路300号邮政编码 200137电话: +86 21 20391000传真号: +86 21 20394800E-mail地址: **********************紧急联络信息:巴斯夫紧急热线中心（中国）+86 21 5861-1199巴斯夫紧急热线中心（国际）:电话: +49 180 2273-112Company:BASF (China) Co., Ltd.300 Jiang Xin Sha RoadPu Dong Shanghai 200137, CHINA Telephone: +86 21 20391000Telefax number: +86 21 20394800E-mail address: ********************** Emergency information:Emergency Call Center (China):+86 21 5861-1199International emergency number: Telephone: +49 180 2273-1122. 危险性概述纯物质和混合物的分类:对水环境的急性危害: 分类2巴斯夫安全技术说明书日期 / 本次修订: 17.12.2021版本: 14.1产品: 凯泽 Cantus®Product: Cantus(30174304/SDS_CPA_CN/ZH)印刷日期 11.09.2023标签要素和警示性说明:危险性说明:H401对水生生物有毒。
新颖杀菌剂——啶酰菌胺
有悬浮剂（ＳＣ）、悬乳剂（ｓＥ）、水分散粒剂 （ｗＧ）、可湿性粉剂。 ３．安全性
对雄雌大、小鼠急性经口Ⅱｋ均＞５０００Ⅱ∥ｋｇ。 对雄、雌大鼠急性经皮ｕ‰均＞２０００ Ｈ∥ｋｇ。对雄、
雌小鼠急性吸入Ⅱ‰＞６．７ ｍｇ／ｋ。对兔眼睛和皮
肤试验无刺激陛。豚鼠试验无致敏性。
对鲤鱼ＬＣ５０（９６ ｈ）＞１０００ Ｉ哕Ｌ，大型水蚤Ｅｃ５０
原菌的能量源Ａ皿的合成，以使菌体死亡。
５．２作用点： 在灰霉病生活环境中，啶酰菌胺对孢子的萌发
具有极强的抑制作用。另外，它能有效地阻止芽管 伸长、附着器形成，故呈现了优异的预防效果。由于 抑制了灰霉病菌的菌丝伸长及孢子形成，故能防止 发病后的二次感染（图２）。
图１线粒体的电子传递系统 ５．３啶酰茵胺在植物体内的移行：
图６扁豆灰霉病耐雨性试验 ５．７对其他药剂抗性菌的效果：
啶酰菌胺属苯胺类（也可归为吡啶酰胺类）杀菌 剂。由于其与苯并咪唑类及二羧酰亚胺类杀菌剂的
６．使用方法 啶酰菌胺可用于油菜、豆类、球茎蔬菜、芥菜、胡
萝卜、菜果、莴苣、花生、马铃薯、草莓、核果、坚果、甘 蓝、黄瓜、薄荷、豌豆、根类蔬菜、向日葵、葡萄、草坪 及其他果树、蔬菜及大田作物，防治白粉病、灰霉病、 菌核病及各种腐烂病。使用剂量为ｏ．２５ ｋｇ（ａ．ｉ）／ １１１１１２，或将５０％制剂稀释１０００～１５００倍。 ７．结 语
近十年全球开发的杀菌剂
近10年全球开发的杀菌剂作者：刘长令更新时间：2015-04-15近10年开发的杀菌剂61个，其中包括酰胺类杀菌剂（27个）、三唑类（1个）、甲氧基丙烯酸酯类化合物（13个）、氨基酸衍生物（3个）、磺酰胺类化合物（3个）、二芳酮类化合物（2个）、肟醚类化合物（4个）、异噁唑啉类化合物（2个）及其它类化合物（6个）。
1.1 啶酰菌胺(boscalid)啶酰菌胺（boscalid，试验代号：BJL-994）是德国巴斯夫公司开发的线粒体呼吸链中琥珀酸辅酶Q还原酶抑制剂（SDHI），主要防治白粉病、灰霉病、各种腐烂病、褐腐病和根腐病等，与其它杀菌剂无交互抗性，于2004年在英国、德国和瑞士首次登记。
使用剂量为285～770 g/hm2。
2012年销售额为3.55亿美元。
1.2 氟吡菌胺(fluopicolide)氟吡菌胺（fluopicolide，试验代号：AVF-002）由拜耳公司开发，主要用于防治卵菌纲病害，如霜霉病、疫病等，与其它类化合物无交互抗性。
田间试验结果表明，叶面施药不仅具有很好的防效，且持效期长。
使用剂量为70～100g/hm2。
2012年销售额为0.60亿美元。
1.3 氟吡菌酰胺(fluopyram)氟吡菌酰胺由拜耳公司开发的琥珀酸脱氢酶抑制剂（SDHI）类杀菌剂。
主要用于防治白菜黑斑病、葡萄灰霉病以及大麦网斑病等病害。
使用剂量为200～250g/hm2。
2012年销售额＜0.1亿美元。
1.4 呋吡菌胺(furametpyr)呋吡菌胺（furametpyr，试验代号：S-82658）是由日本住友化学株式会社开发的SDHI类杀菌剂。
具有内吸活性，且传导性能优良，因此具有优异的预防和治疗效果。
对水稻纹枯病具有适度的长持效活性。
使用剂量为300～400g/hm2。
2012年销售额＜0.10亿美元。
1.5 吡噻菌胺(penthiopyrad)吡噻菌胺（penthiopyrad，试验代号：MTF-753）是日本三井化学株式会社开发的SDHI类杀菌剂。
SDHI类杀菌剂啶酰菌胺
第40卷第5期 世 界 农 药2018年10月 World Pesticides ·9·作者简介：华乃震(1939—)，男，高级工程师，主要从事农药新剂型和助剂的研究和开发。
E-mail ：nzhua88@ 。
收稿日期：2018-08-08。
SDHI 类杀菌剂啶酰菌胺华乃震摘要：啶酰菌胺是2003年上市的第一个广谱性SDHI 类杀菌剂，之后迅速成为上亿美元的产品，这对于整个SDHI 类杀菌剂的发展功不可没。
较详细论述了啶酰菌胺的发展、作用机理、市场、合成、剂型和应用。
同时指出啶酰菌胺归类为中等抗性风险杀菌剂，应杜绝滥用，合理混配使用，特别是与其他类杀菌剂混配使用，可以提供好的药效，同时能有效地延缓抗性的发生。
关键词：琥珀酸脱氢酶抑制剂；作用机理；市场；剂型；应用 DOI ：10.16201/31-1827/tq.2018.05.02中图分类号：TQ455 文献标志码：A 文章编号：1009-6485(2018)05-0009-07A Review of SDHI Fungicide DinotrimideHUA NaizhenAbstract : Boscalid is the first broad-spectrum SDHI class fungicide to be marketed in 2003. Soon the product has a sale of more than 100 million dollar a year. This has promoted the development of entire SDHI class fungicides. Since then, its has also brought a new era of SDHI class fungicides in the world. In this paper, progress, action mechanism, synthetic ，market, formulation and application of boscalid were discussed in detail. At same time, it is pointed out that boscalid is considered as a medium resistance risk fungicide, and should be reasonably used, and mixed rationally with other fungicides, especially with other classes of fungicides except SDHIs, which can provide good efficacy and effectively delay the occurrence of resistance.Keywords : SDHI; action mechanism; market; formulation; application啶酰菌胺(boscalid)是巴斯夫公司开发的第一个广谱性SDHI(琥珀酸脱氢酶抑制剂)类杀菌剂。
啶酰菌胺类的制备方法[发明专利]
![啶酰菌胺类的制备方法[发明专利]](https://img.taocdn.com/s3/m/45097d6276232f60ddccda38376baf1ffc4fe3c5.png)
(10)申请公布号(43)申请公布日 (21)申请号 201510476648.0(22)申请日 2015.08.07C07D 213/82(2006.01)(71)申请人陆月霞地址安徽省安庆市宜秀区杨桥镇宣店村大岭组28号(72)发明人陆月霞(74)专利代理机构北京卓恒知识产权代理事务所(特殊普通合伙) 11394代理人尹锋(54)发明名称啶酰菌胺类的制备方法(57)摘要本发明公开了一种啶酰菌胺类的制备方法,涉及化工技术域，包括预处理、MS-Pd 催化、氢还原和分层处理四个步骤。
本发明通过以邻氯硝基苯和对氯苯硼酸为原料，在催化剂MS-Pd、无水碳酸钾及DMF 溶液存在下制备啶酰菌胺。
本发明采用催化剂MS-Pd、无水碳酸钾及DMF 溶液合成啶酰菌胺的方法，具有工艺简单、反应条件温和、生产成本低等优点，具有很好的工业应用前景。
(51)Int.Cl.(19)中华人民共和国国家知识产权局(12)发明专利申请权利要求书1页 说明书3页CN 105061306 A 2015.11.18C N 105061306A1.一种啶酰菌胺类的制备方法，其特征在于：包括如下步骤：预处理：将45%-55%邻氯硝基苯和55%-45%对氯苯硼酸原料加入到无水碳酸钾及TBAB 的DMF溶液溶剂中，搅拌10-30min，使充分溶解；MS-Pd催化：将催化剂MS-Pd添加到步骤（1）后溶液中，加热到115-120℃，保温10-30min，使充分反应；氢还原：将步骤（2）后溶液降至室温，缓慢添加蒸馏水，再利用氢催化还原，使充分反应；分层处理：利用2-氯烟酰氯对步骤（3）溶液进行缩合，分层，脱溶，即可得啶酰菌胺。
2.根据权利要求1所述的啶酰菌胺类的制备方法，其特征在于，所述步骤（1）原料包括以下组分（质量分数）：邻氯硝基45%，苯氯苯硼酸55%。
3.根据权利要求1所述的啶酰菌胺类的制备方法，其特征在于，所述步骤（1）原料中邻氯硝基苯和对氯苯硼酸的充分溶解的温度为25℃。
丁酰胺安全技术说明书(msds)
有害燃烧产物：
一氧化碳、二氧化碳、氧化氮。
灭火方法：
雾状水、泡沫、二氧化碳、干粉、砂土。
第六部分：泄漏应急处理
应急处理：
雾状水、泡沫、二氧化碳、干粉、砂土。第七部分Βιβλιοθήκη 操作处置与储存操作注意事项：
无资料
储存注意事项：
储存于阴凉、通风仓间内。远离火种、热源。防止阳光直射。保持容器密封。应与氧化剂、酸类、碱类分开存放。搬运时要轻装轻卸，防止包装及容器损坏。
眼睛防护：
戴化学安全防护眼镜。
身体防护：
穿工作服。
手防护：
可能接触毒物时，戴橡皮胶手套。
其他防护：
无资料
第九部分：理化特性
pH：
无资料
熔点(℃)：
116
沸点(℃)：
216
分子式：
C4H9NO
主要成分：
无资料
临界温度(℃)：
无资料
辛醇/水分配系数的对数值：
无资料
饱和蒸气压(kPa)：
无资料
闪点(℃)：
第四部分：急救措施
皮肤接触：
脱去污染的衣着，用流动清水冲洗。
眼睛接触：
立即翻开上下眼睑，用流动清水冲洗15分钟。就医。
吸入：
脱离现场至空气新鲜处。就医。
食入：
误服者。漱口，饮牛奶或蛋清，就医。
第五部分：消防措施
危险特性：
遇高热、明火或与氧化剂接触，有引起燃烧的危险。燃烧分解时，放出有毒的氮氧化物。
建规火险分级：
废弃处置方法：
无资料
废弃注意事项：
无资料
第十四部分：运输信息
危险货物编号：
无资料
UN编号：
无资料
IMDG规则页码：
啶酰菌胺
啶酰菌胺是由德国BASF公司发的新型酰胺类杀菌剂，英文名称为boscalid，目前在中国市场以商品名“凯泽”对黄瓜灰霉病进行了登记。
啶酰菌胺具有广谱、低毒、髙效和与市场上其它杀菌剂无交互抗性等优点。
啶酰菌胺对灰霉病、黑斑病和白粉病等病害有着非常优异的防效，特别是对多种作物如瓜类、葡萄、草毒和西红棉等的灰霉病有特效，同时它还具有吸收迅速、环境污染低、治疗效果明显、耐雨水冲刷、扩散速度快、对作物安全、和持效期长等特点。
2015年3月2日，陕西美邦农药有限公司获批登记国内企业第4个啶酰菌胺原药产品（97%含量）。
此前，河北省石家庄市兴柏生物工程有限公司、江苏省泰州百力化学股份有限公司和浙江禾本科技有限公司分别登记啶酰菌胺原药产品（含量分别为98%、98%和96%）。
啶酰菌胺，专治抗性灰霉病、白粉病、根腐病等病害
啶酰菌胺，专治抗性灰霉病、白粉病、根腐病等病害棚室蔬菜由于温度高，湿度大，很容易发生病虫害，尤其是灰霉病，危害逐年加重，已经成为棚室蔬菜栽培中最难根除的病害之一。
今天，小编就给大家推荐一个防治灰霉病的优秀药剂--啶酰菌胺。
对灰霉病具有预防、治疗和铲除作用。
1、作用机理啶酰菌胺是由德国巴斯夫公司开发的新型酰胺类杀菌剂，商品名：“凯泽”。
主要通过抑制病菌的线粒体内的能量物质琥珀酸脱氢酶合成，使氨基酸、糖等物质无法合成，干扰细胞的分裂和生长，达到杀灭病菌的目的。
对灰霉病、菌核病、白粉病等多种病害具有预防、保护和治疗作用。
2、主要特点（1）杀菌谱广：啶酰菌胺是一种广谱性杀菌剂，能有效防治灰霉病、菌核病、白粉病、根腐病、早疫病等10多种病害都具有很好的保护和治疗作用，尤其对灰霉病特效。
（2）无交互抗性：啶酰菌胺是最新一代酰胺类杀菌剂，与传统的异菌脲、腐霉利、嘧霉胺等杀菌剂无交互抗性，是抗性灰霉病治理的首选药剂。
（3）渗透性强：啶酰菌胺具有很好的渗透性，还具有垂直渗透作用，可以通过叶部组织渗透到叶子的背面，达到隔叶治病的效果。
（4）治病更彻底：啶酰菌胺主要是通过抑制病菌线粒体内的物质合成，达到杀灭病菌的作用，对病菌的各个阶段都有很好的杀灭作用。
治病更彻底。
（5）内吸传导性好：啶酰菌胺可通过木质部向顶传输至植株的叶尖和叶缘，可以较好的防治各个部位发生的病害。
（6）混配性好：啶酰菌胺能与嘧菌酯、吡唑醚菌酯、腐霉利、咯菌腈等多种杀菌剂，混合使用，不但扩大了杀菌谱，还降低了病菌的抗药性。
3、适用作物主要用于油菜、黄瓜、番茄、辣椒、茄子、葡萄等作物病害的防治。
4、防治对象主要防治灰霉病、白粉病、腐烂病、根腐病、早疫病、菌核病等多种病害。
尤其对番茄、黄瓜、草莓灰霉病、油菜、茄子菌核病等病害有特效。
5、使用技术（1）防治黄瓜、番茄、辣椒、草莓、茄子等棚室蔬菜灰霉病，可在发病初期，用38%唑醚·啶酰菌悬浮剂30～60毫升，兑水30公斤均匀喷雾，可快速控制住灰霉病的危害和蔓延。
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第一部分化学品及企业标识化学品中文名： (2S,4S)-N-Boc-顺式-4-氟-L-脯氨酸化学品英文名： (2S,4S)-1-(tert-Butoxycarbonyl)-4-fluoro-2-pyrrolidinecarboxylic AcidCAS No.：203866-13-1分子式：C10H16FNO4产品推荐及限制用途：工业及科研用途。
第二部分危险性概述紧急情况概述造成皮肤刺激。
造成严重眼刺激。
可引起呼吸道刺激。
GHS危险性类别皮肤腐蚀 / 刺激类别 2严重眼损伤 / 眼刺激类别 2特异性靶器官毒性一次接触类别 3标签要素：象形图：警示词：警告危险性说明：H315 造成皮肤刺激H319 造成严重眼刺激H335 可引起呼吸道刺激●预防措施：—— P264 作业后彻底清洗。
—— P280 戴防护手套/穿防护服/戴防护眼罩/戴防护面具。
—— P261 避免吸入粉尘/烟/气体/烟雾/蒸气/喷雾。
—— P271 只能在室外或通风良好处使用。
●事故响应：—— P302+P352 如皮肤沾染：用水充分清洗。
—— P332+P313 如发生皮肤刺激：求医/就诊。
—— P362+P364 脱掉沾染的衣服，清洗后方可重新使用—— P305+P351+P338 如进入眼睛：用水小心冲洗几分钟。
如戴隐形眼镜并可方便地取出，取出隐形眼镜。
继续冲洗。
—— P337+P313 如仍觉眼刺激：求医/就诊。
—— P304+P340 如误吸入：将人转移到空气新鲜处，保持呼吸舒适体位。
—— P312 如感觉不适，呼叫解毒中心/医生●安全储存：—— P403+P233 存放在通风良好的地方。
保持容器密闭。
—— P405 存放处须加锁。
●废弃处置：—— P501 按当地法规处置内装物/容器。
物理和化学危险：无资料。
健康危害：造成皮肤刺激。
造成严重眼刺激。
可引起呼吸道刺激。
环境危害：无资料。
第三部分成分/组成信息√物质混合物第四部分急救措施急救：吸入：如果吸入，请将患者移到新鲜空气处。
皮肤接触：脱去污染的衣着，用肥皂水和清水彻底冲洗皮肤。
如有4不适感，就医。
眼晴接触：分开眼睑，用流动清水或生理盐水冲洗。
如有不适感，就医。
食入：饮水，禁止催吐。
如有不适感，就医。
对保护施救者的忠告：将患者转移到安全的场所。
咨询医生。
出示此化学品安全技术说明书给到现场的医生看。
对医生的特别提示：无资料。
第五部分消防措施灭火剂：用水雾、干粉、泡沫或二氧化碳灭火剂灭火。
避免使用直流水灭火，直流水可能导致可燃性液体的飞溅，使火势扩散。
特别危险性：无资料。
灭火注意事项及防护措施：消防人员须佩戴携气式呼吸器，穿全身消防服，在上风向灭火。
尽可能将容器从火场移至空旷处。
处在火场中的容器若已变色或从安全泄压装置中发出声音，必须马上撤离。
隔离事故现场，禁止无关人员进入。
收容和处理消防水，防止污染环境。
第六部分泄漏应急处理作业人员防护措施、防护装备和应急处置程序：建议应急处理人员戴携气式呼吸器，穿防静电服，戴橡胶耐油手套。
禁止接触或跨越泄漏物。
作业时使用的所有设备应接地。
尽可能切断泄漏源。
消除所有点火源。
根据液体流动、蒸汽或粉尘扩散的影响区域划定警戒区，无关人员从侧风、上风向撤离至安全区。
环境保护措施：收容泄漏物，避免污染环境。
防止泄漏物进入下水道、地表水和地下水。
泄漏化学品的收容、清除方法及所使用的处置材料：小量泄漏：尽可能将泄漏液体收集在可密闭的容器中。
用沙土、活性炭或其它惰性材料吸收，并转移至安全场所。
禁止冲入下水道。
大量泄漏：构筑围堤或挖坑收容。
封闭排水管道。
用泡沫覆盖，抑制蒸发。
用防爆泵转移至槽车或专用收集器内，回收或运至废物处理场所处置。
第七部分操作处置与储存操作注意事项：操作人员应经过专门培训，严格遵守操作规程。
操作处置应在具备局部通风或全面通风换气设施的场所进行。
避免眼和皮肤的接触，避免吸入蒸汽。
个体防护措施参见第8部分。
远离火种、热源，工作场所严禁吸烟。
使用防爆型的通风系统和设备。
如需罐装，应控制流速，且有接地装置，防止静电积聚。
避免与氧化剂等禁配物接触（禁配物参见第10部分）。
搬运时要轻装轻卸，防止包装及容器损坏。
倒空的容器可能残留有害物。
使用后洗手，禁止在工作场所进饮食。
配备相应品种和数量的消防器材及泄漏应急处理设备。
储存注意事项：储存于阴凉、通风的库房。
库温不宜超过37°C。
应与氧化剂、食用化学品分开存放，切忌混储（禁配物参见第10部分）。
保持容器密封。
远离火种、热源。
库房必须安装避雷设备。
排风系统应设有导除静电的接地装置。
采用防爆型照明、通风设置。
禁止使用易产生火花的设备和工具。
储区应备有泄漏应急处理设备和合适的收容材料。
第八部分接触控制/个体防护职业接触限值无资料。
生物限值无资料。
监测方法GBZ/T160.1~GBZ/T160.81-2004工作场所空气有毒物质测定（系列标准）。
工程控制作业场所建议与其它作业场所分开。
密闭操作，防止泄漏。
加强通风。
设置自动报警装置和事故通风设施。
设置应急撤离通道和必要的泻险区。
设置红色区域警示线、警示标识和中文警示说明，并设置通讯报警系统。
提供安全淋浴和洗眼设备。
呼吸系统防护呼吸系统防护：空气中浓度超标时，佩戴过滤式防毒面具（半面罩）。
紧急事态抢救或撤离时，应该佩戴携气式呼吸器。
手防护：戴橡胶耐油手套。
眼睛防护：戴化学安全防护眼睛。
皮肤和身体防护：穿防毒物渗透工作服。
第九部分理化特性第十部分稳定性和反应性稳定性：正常环境温度下储存和使用，本品稳定。
危险反应：无资料。
避免接触的条件：静电放电、热、潮湿等。
禁配物：无资料。
危险的分解产物：无资料。
第十一部分毒理学信息急性毒性：无资料。
致癌性：无资料。
皮肤刺激性或腐蚀性：根据现有资料，不符合分类标准。
眼睛刺激或腐蚀：根据现有资料，不符合分类标准。
皮肤致敏：根据现有资料，不符合分类标准。
呼吸致敏：根据现有资料，不符合分类标准。
生殖细胞突变性：根据现有资料，不符合分类标准。
生殖毒性：根据现有资料，不符合分类标准。
特异性靶器官系统毒性--一次接触可能：根据现有资料，不符合分类标准。
特异性靶器官系统毒性--反复接触：根据现有资料，不符合分类标准。
吸入危害：根据现有资料，不符合分类标准。
第十二部分生态学信息急性水生毒性：无资料。
慢性水生毒性：无资料。
持久性和降解性：无资料。
潜在的生物累积性：无资料。
土壤中的迁移性：无资料。
其他有害作用：无资料。
第十三部分废弃处置废弃化学品：尽可能回收利用。
如果不能回收利用，采用焚烧方法进行处置。
不得采用排放到下水道的方式废弃处置本品。
污染包装物：将容器返还生产商或按照国家和地方法规处置。
废弃注意事项：废弃处置前应参阅国家和地方有关法规。
处置人员的安全防范措施参见第8部分。
第十四部分运输信息联合国危险货物编号（UN）：UN2430（仅供参考，请核实）。
联合国运输名称：固态烷基苯酚，未另作规定的（包括C2~C12的同系物）（仅供参考，请核实）。
联合国危险性分类：8（仅供参考，请核实）。
包装类别：Ⅰ（仅供参考，请核实）。
包装标签：海洋污染物（是/否）：否。
包装方法按照生产商推荐的方法进行包装，例如：开口钢桶。
安瓿瓶外普通木箱。
螺纹口玻璃瓶、铁盖压口玻璃瓶、塑料瓶或金属桶（罐）外普通木箱等。
运输注意事项运输车辆应配备相应品种和数量的消防器材及泄漏应急处理设备。
严禁与氧化剂、食用化学品等混装混运。
装运该物品的车辆排气管必须配备阻火装置。
使用槽（罐）车运输时应有接地链，槽内可设孔隔板以减少震荡产生静电。
禁止使用易产生火花的机械设备和工具装卸。
夏季最好早晚运输。
运输途中应防暴晒、雨淋，防高温。
中途停留时应远离火种、热源、高温区。
公路运输时要按规定路线行驶，勿在居民区和人口稠密区停留。
铁路运输时要禁止溜放。
严禁用木船、水泥船散装运输。
运输工具上应根据相关运输要求张贴危险标志、公告。
第十五部分法规信息中国化学品管理名录【B】《重点环境管理危险化学品目录》，环保部办公厅2014年第33号文【C】《中国严格限制的有毒化学品名录》，环保部2017年第74号公告【D】《麻醉药品和精神药品品种目录（2013年版）》，食药总局2013年第230号通知【E】《重点监管的危险化学品名录（第1和第2批）》，安监总局2011年第95号和2013年第12号通知【F】《中国进出口受控消耗臭氧层物质名录（第1到6批）》，环保部2000年至2012系列公告【G】《易制爆危险化学品名录（2017年版）》，公安部2017年5月11日公告【H】《高毒物品目录》，卫生部2003年第142号通知第十六部分其他信息最新修订版日期：2023/03/22修改说明本SDS按照《化学品安全技术说明书内容和项目顺序》（GB/T16483-2008）和《化学品安全技术说明书编写指南》（GB/T17519-2013）等标准修订。
其中，化学品GHS分类结果依据《危险化学品目录（2015版）实施指南（试行）》及《化学品分类和标签规范》（GB30000.2-2013~GB30000.29-2013）系列标准。