Bromopropylate

428.12

428.12

242-070-7

3U468ZM257

DTXSID1034397

White crystalline solid

29181990

46.5

5.40

Yellowish crystals

1.49 g/cu cm at 20 deg C

77 °C

504°C (rough estimate)

>100 °C

1.6010 (estimate)

In water, 0.1 mg/L at 20 deg C

0-6°C

8.2X10-8 mm Hg at 20 deg C /Estimated/

Oral-Rat LD50: 5000 mg/kg; Oral-Mouse LD50: 8000 mg/kg

Combustion produces toxic bromide gas

Henry's Law constant = 4.6X10-7 atm cu m/mol at 25 °C /Estimated/

176.6 Ų [M+H]+

Hydroxyl radical reaction rate constant = 6.5X10-12 cu cm/molc sec at 25 °C /Estimated/

NONH for all modes of transport

2

38

DD2100000

Xi

The warehouse is ventilated, low temperature and dry; stored and transported separately from food materials

Fairly stable in neutral or slightly acidic media; DT50 34 days (pH 9).

P264, P273, P280, P302+P352, P321, P332+P313, P362, P391, P501

H315

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. 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 soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

|Warning|H315 (33.58%): Causes skin irritation [Warning Skin corrosion/irritation]|P264, P273, P280, P302+P352, P321, P332+P313, P362, P391, and P501|Aggregated GHS information provided by 134 companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

SOIL: A study in the Jordan Valley in 1998 found 1 of 5 sampled areas was contaminated with 0.22-0.34 ppm bromopropylate while no bromopropylate was detected at the other 4 test sites(1).

practically nontoxic

LD50 Rabbit dermal 10200 mg/kg|LD50 Mouse oral 8000 mg/kg|LD50 Rat oral 5000 mg/kg|LD50 Rat dermal >4000 mg/kg|LD50 Rabbit oral >6000 mg/kg bw /from table/

/BIRDS and MAMMALS/ Signs of intoxication /in mallard ducks from acute oral administration/: Tachypnea, ataxia, imbalance, & hyperexcitability. Signs appeared as soon as 15 min... /sample purity 97.5%/|/AQUATIC SPECIES/ It is highly toxic to fish...

Bromopropylate's former production and use in the US as an acaricide(1) may have resulted in its direct release to the environment(SRC).

TERRESTRIAL FATE: IN SOIL, THIS MATERIAL WAS CONVERTED TO CORRESPONDING PHENONE...|TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 21,000(SRC), determined from a log Kow of 5.40(2) and a regression-derived equation(3), indicates that bromopropylate is expected to be immobile in soil(SRC). Volatilization of bromopropylate from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 4.6X10-7 atm-cu m/mole(SRC), derived from its vapor pressure, 8.2X10-8 mm Hg(2), and water solubility, 0.10 mg/L(4). Bromopropylate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(2). Biodegradation half-lives in soil of 4-13 weeks have been reported(5).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 21,000(SRC), determined from a log Kow of 5.40(2) and a regression-derived equation(3), indicates that bromopropylate 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 4.6X10-7 atm-cu m/mole(SRC), derived from its vapor pressure, 8.2X10-8 mm Hg(2), and water solubility, 0.10 mg/L(4). According to a classification scheme(6), an estimated BCF of 2,900(SRC), from its log Kow(2) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is very high(SRC). Hydrolysis is not expected to be an important fate process based on estimated half-lives of >100 years(8). Biodegradation half-lives in soil of 4-13 weeks have been reported(9).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), bromopropylate, which has a vapor pressure of 8.2X10-8 mm Hg at 20 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase bromopropylate is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 2.5 days(SRC), calculated from its rate constant of 6.5X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase bromopropylate may be removed from the air by wet and dry deposition(SRC).

The rate constant for the vapor-phase reaction of bromopropylate with photochemically-produced hydroxyl radicals has been estimated as 6.5X10-12 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 2.5 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). A base-catalyzed second-order hydrolysis rate constant of 2.0X10-4 L/mole-sec(SRC) was estimated using a structure estimation method(2); this corresponds to half-lives of 110 and 1000 years at pH values of 7 and 8, respectively(2). Bromopropylate does not absorb sufficient energy from the environmental UV spectrum to directly photolyze.

An estimated BCF of 2,900 was calculated for bromopropylate(SRC), using a log Kow of 5.40(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is very high(SRC).

The Koc of bromopropylate is estimated as 21,000(SRC), using a log Kow of 5.40(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that bromopropylate is expected to be immobile in soil.

The Henry's Law constant for bromopropylate is estimated as 4.6X10-7 atm-cu m/mole(SRC) derived from its vapor pressure, 8.2X10-8 mm Hg(1), and water solubility, 0.1 mg/L(2). This Henry's Law constant indicates that bromopropylate is expected to be essentially nonvolatile from water surfaces(3). Bromopropylate's Henry's Law constant indicates that volatilization from moist soil surfaces may occur very slowly(SRC). Bromopropylate is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 8.2X10-8 mm Hg(1).

SURFACE WATER: Water samples from the southern edge of the Dead Sea basin (Jordan) were analyzed for bromopropylate content; 4 samples were taken with an average level of bromopropylate of 62.5 ppb in each sample(1). A study conducted in Spain on the Segre River found 2 of 6 samples contained approximately 0.01 ng/L of bromopropylate (detection limit was 0.01 ng/L)(2).

A 1994 study analyzed 11,348 US food samples for the presence of 329 pesticides(1). Bromopropylate was among the 94 pesticides listed as detected, not quantified(1).|From 1995 to 1999 a study conducted in Japan found 60 samples of oranges and grapefruit contained 4 samples with 0.05-0.1 micro gram/gram of acarol(1). The same study found 66 samples of Japanese pears contained 7 samples with 0.01-0.1 micrograms/gram of acarol(1). In a Belgian study from 1991 to 1993, 3064 food samples were analyzed for acarol residues, 8 food types (beans, radish, Lamb's lettuce, strawberries, apples, oranges, grapes and pears) were found to contain measurable quantities of acarol with concentrations ranging on average from 0.004-0.168 ppm and maximum measured quantities ranging from 0.08-2.0 ppm(2). A study from Egypt in 1996 reports that for 1579 food samples collected from open markets 2.02% of the samples contained acarol residues, the contaminated foods with average concentration in parentheses were cucumbers (0.12 mg/kg), eggplants (0.07 mg/kg ), peppers (0.13 mg/kg), apples (0.27 mg/kg), grapes (0.62 mg/kg), oranges (0.15 mg/kg), plums (0.22 mg/kg) and strawberries (0.89 mg/kg)(3).

Occupational exposure and general population exposure should be low or non-existent since bromopropylate is no longer used in the US. In the past, bromopropylate was applied directly to some fruit crops as an acaracide and exposure to this compound was primarily dermal and via inhalation for workers. However, recent monitoring data indicate that consumers may be exposed to bromopropylate via ingestion of some imported fruits and vegetables. (SRC)

2. 2= Slightly toxic: Probable oral lethal dose (human) 5-15 g/kg, between 1 pt & 1 qt for 70 kg person (150 Lb).

One cow received 0.33 mg/kg/day of 14C-labelled bromopropylate in the diet for five days. After a further 13 days without treatment the animal was killed. In the 20 days 94.9% of the administered activity was recovered, 0.96% in the milk, 20.5% in the urine and 73.4% in the feces. No activity was detectable in tissues other than adipose tissue which contained 0.06-0.17 ppm at the time of autopsy|Two male and two female rats were each administered by gavage 1.6 mg 14C-labelled bromopropylate. Expired CO2, urine and feces were collected for the next 120 hours in periods of 24 hours following which blood and other tissues were taken for analysis. Less than 0.2% of activity was found in respired CO2. In males, 90% of activity was found in feces and 6% in urine while in females 55% appeared in feces and 33% in urine. About 75% activity was eliminated in 48 hours but after 120 hours 2.6% (males) and 1.5% (females) of the administered dose remained in tissues, mainly kidneys, liver and fat.|Bromopropylate is rapidly and efficiently eliminated in animals.|Three groups of three beef calves were each fed diets containing 0, 5 and 50 ppm bromopropylate. Fat biopsies were taken after 2 and 8 weeks of feeding and 1 animal from each group was killed after 4 and 6 weeks. After 10 weeks feeding the remaining animal which had been fed on the 5 ppm diet was killed; the one on 50 ppm was maintained on control diet for a further 2 weeks before it was killed. After 4, 6 and 10 weeks the 5 ppm diet produced respectively levels of 1.5, 1.5 and 2.8 ppm of bromopropylate in the fat. The 50 ppm diet produced fat levels of 7.3 ppm after four, and 8.0 ppm after 6 weeks. After 2 weeks on control diet the concentration of bromopropylate in fat had fallen to 0.3 ppm. Muscle tissue contained low residues of unchanged bromopropylate while liver and kidneys also contained 4,4'-dibromobenzilic acid during the feeding period.|The absorption, distribution and elimination of bromopropylate were evaluated in rats. [U-14C]phenyl bromopropylate was given orally at single doses of 0.5 mg/kg bw (at a no-effect level) or 100 mg/kg bw (to produce some pharmacological/toxicological effect) to groups of 5 male and 5 female rats (Sprague-Dawley Crl: CD [SD] BR). At the low dose level an additional group received 14 consecutive daily doses of 0.5 mg/kg bw non-labelled compound (>95% pure) followed by a single dose with radiolabelled compound. Under all three dosing regimens the total recoveries of radioactivity within 168 hr past termination of dosing were 90% and higher. Most of the dose was eliminated in feces (males: 85.3-89.3%, females: 52.5- 63.7%). Lower amounts of radioactivity were excreted in the urine (males: 2.3-3%, females: 21.8-28.7%). Excretion of radioactivity was essentially complete within 96 hr independent of dose level or pretreatment. No radioactivity was expired in CO2. At the low-dose after 168 hr, tissue concentrations were low with highest values in liver (0.05 ug equivalents of bromopropylate/g tissue in male or female) and abdominal fat (0.02 or 0.03 ug equivalents of bromopropylate/g tissue in male or female). At the high dose, the tissue residue pattern was similar, with highest concentration of radioactivity in the abdominal fat (equivalent to 3.3 or 8.7 ug/g in male or female). Pre-treatment with the non-radiolabelled compound did not significantly alter tissue residues at 168 hr post-dose over those animals receiving a single administration. It was concluded that excretion rates were fast, and independent of dose level and pretreatment. The routes of elimination were sex-dependent. The low tissue residue levels were observed at 168 hr after administration.

When exposed to bromopropylate, spider mites (tetranychus urticae kock) & house flies (Musca domestica l) metabolized this material to bromine analogs of benzilic acid, benzhydrol, benzophenone, & benzoic acid.|Bromopropylate was metabolized by rat liver preparations, especially by the microsomal & the nuclear supernatant fractions. The limiting reaction was the cleavage of the ester linkage by carboxylesterases. The main metabolite was p-bromobenzoic acid.|Only the parent compound was detected in the adipose tissue and the milk of a cow which had received 0.33 mg/kg/day of 14C-labelled bromopropylate for 5 days. Most of the activity found in the feces was the parent compound as shown by analysis of the first post-treatment day sample which contained 92% parent compound, the remainder being unidentified metabolites. The majority of activity in urine consisted of 4,4'-dibromobenzilic acid and a more polar unidentified metabolite. Other possible metabolites, 4,4'-dibromobenzohydrol, 4,4'-dibromobenzophenone and 4-bromobenzoic acid were not found. In the feces of rats administered bromopropylate 60% of activity was parent compound and 20% 4,4'-dibromobenzilic acid.|The structures of 8 metabolites were identified from urine and feces, covering 80% and 72% of the dose for males and females, respectively. ...It is concluded that bromopropylate was metabolized preferentially by cleavage of the isopropyl ester and to a minor extent by oxidation reactions attacking the phenyl ring and the isopropyl group. The primary product formed after ester cleavage, the benzilic acid, was subject to subsequent conjugation reactions, leading to a variety of amino acid conjugates, or was excreted as such. Metabolites formed after oxidation were 3-hydroxy-benzilate and a propylene glycol derivative of the parent compound.|The metabolic profile of bromopropylate was investigated in urine, feces, and tissue extracts from male and female rats. The study involved single oral administration at a low (0.5 mg/kg bw) and high dose level (100 mg/kg bw), and repeated oral administration at the low dose level. ...In the urine pools, representing 1.7-26.4% of the administered dose, there were 7 distinct metabolite fractions. The metabolite pattern did not significantly differ between the dose levels or dose regimen. However, a pronounced sex difference was observed: the benzilic acid was a minor fraction (10-14%) in males but the major fraction (65-72%) in females. The metabolite pattern in feces did not significantly differ between dose levels, dose regimen and, in contrast to urine, between the sexes. The urinary and fecal metabolic patterns differed qualitatively: there was a non-polar fraction in the feces, corresponding to unchanged bromopropylate, which represented 14-54% of the total fecal radioactivity. The metabolite pattern in liver tissue was not sex-dependent and rather simple with the two major fractions corresponding to bromopropylate and the benzilic acid. The pattern in kidney tissue was also not sex-dependent. It contained only one major fraction accounting for at least 80% of the radioactivity in kidneys and corresponding to the benzilic acid. The benzilic acid accounted for at least 70% and 40% of the radioactivity in male and female lung tissue, respectively. The fat tissue contained unchanged bromopropylate as a major component representing 40% and 80% of the radioactivity for males and females, respectively. Thus, within the tested dose range the metabolism of bromopropylate in the rat was independent of dose level and dose regimen. However, a pronounced sex difference was observed in all groups. The benzilic acid was a minor metabolite in males (approximately 6% of the dose) and the major metabolite in females (approximately 23% of the dose). This parallels the sex difference observed for the route of excretion. The dominant compound in kidney and lung tissue was the benzilic acid, in fat tissue the unchanged bromopropylate, and in liver tissue both were present in substantial amounts.

Basic treatment: Establish a patent airway. 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 normal saline 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 ... . /Poison A and B/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in respiratory arrest. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. Watch for signs of fluid overload. Consider drug therapy for pulmonary edema ... . For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam (Valium) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poison A and B/|Basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist respirations if necessary. 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 ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline 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. Activated charcoal is not effective ... . Do not attempt to neutralize because of exothermic reaction. Cover skin burns with dry, sterile dressings after decontamination ... . /Organic acids and related compounds/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in respiratory arrest. Early intubation, at the first sign of upper airway obstruction, may be necessary. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. Watch for signs of fluid overload. Consider drug therapy for pulmonary edema ... . For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Organic acids and related compounds/

bromopropylate

An emusifiable concentrate: 'Neoron 250'/'Acarol 250' & 'Neoron 500'/'Acarol 500' (250 & 500 ai, respectively)|Purity: (technical material) Minimum 88% isopropyl-4,4' dibromobenzilate. Maximum 12% by-products of manufacture: isopropyl-4-bromobenzoate; isopropyl ether of isopropyl-4,4' dibromobenzilate; isopropyl-4-bromobenzilate; isopropyl-alpha,alpha-bis (4-bromophenyl); acetate; toluene.

It was introduced in 1966 by JR Geigy SA (now Ciba-Geigy AG) as exptl acaricide under code number 'gs 19851', trade marks 'Neoron' & 'Acarol' & protection of Belgian patent 691105; Swiss patent 471065. It was described by H Grob et al, Abstr Int Plant Prot Congr, 6th, 1967, page 198.|Contact acaricide having considerable residual action. Effective against mites which have developed resistance to certain other acaricides. Recommended on pome & stone fruit, citrus, hops, strawberries, cucumbers, melons, beans, tomatoes, cotton and ornamentals at 37.5 to 60 g ai/100 L; field crops 500 to 1000 g ai/ha.

ANALYSIS OF ACTIVE INGREDIENT: DETERMINATION OF ESTER GROUP BY SAPONIFICATION; DETERMINATION OF TOTAL BROMINE; DETERMINATION OF OH GROUP BY INFRARED ABSORPTION. TLC.|RESIDUE ANALYSIS IS BY GLC AFTER COLUMN CHROMATOGRAPHIC CLEAN-UP. PARTICULARS FROM CIBA-GEIGY AG.|Residues of bromopropylate were determined in honey by gas chromatography. The method is sensitive to 0.02 mg bromopropylate.

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

Bromopropylate has known environmental transformation products that include 4,4-dibromobenzilic acid.