Propiconazole

342.22000

342.22

262-104-4

142KW8TBSR

DTXSID8024280

Yellowish, viscous liquid|White crystalline powder|Colorless solid

2934999025

49.17000

3.65340

Yellowish odorless liquid. Non corrosive. Used as a fungicide.

1.39 g/cm3

<25 °C

180 °C @ Press: 0.1 Torr

244.1ºC

1.623

In water, 100 mg/L at 25 deg C

APPROX 4ºC

5.6 x l0 -5 Pa (25 °C)

LD50 orally in rats: 1517 mg/kg (Urech)

Practically odorless

Henry's Law constant = 4.1X10-9 atm-cu m/mol at 25 °C (est)

The pKa of the conjugate acid of propiconazole is 1.09.

177.88 Ų [M+H]+

Hydroxyl radical reaction rate constant = 2.3X10-11 cu cm/molec-sec at 25 °C (est)

No rapid reaction with air. No rapid reaction with water.

Amines, Phosphines, and Pyridines

A triazole derivative.

Noncorrosive to metals.

UN3082

3

R22

36/37-46-60-61-45-16-7

XZ4620000

Xn; N; T; F

Stable. Incompatible with strong oxidizing agents.

P260-P280-P301 + P312 + P330-P304 + P340 + P310-P403 + P233

H302-H317-H330-H410

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

|Danger|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P201, P202, P261, P264, P270, P272, P273, P280, P281, P301+P312, P302+P352, P308+P313, P321, P330, P333+P313, P363, P391, P405, and P501|Warning|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|Aggregated GHS information provided by 462 companies from 11 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|P201, P202, P261, P264, P270, P272, P280, P281, P301+P312, P302+P352, P305+P351+P338, P308+P313, P321, P330, P333+P313, P337+P313, P363, P405, and P501

Non-irritating to skin and eyes. No /dermal/ sensitization (guinea pigs).

Propiconazole was detected in the effluent of an agricultural site in Sweden at a maximum concentration of 2 ug/L(1). Propiconazole was found in the runoff water of 4 out of 5 Costa Rican Banana plantations in concentrations ranging from 24.2-6.1 ug/L(2).

SEDIMENT: Propiconazole was detected in 4 out 4 mobile sediment samples in concentrations ranging from 5-10 ug/kg dry weight(1). The same study showed propiconizole in 3 out of 4 bed sediment samples with concentrations ranging from 20-30 ug/kg dry weight(1).

LD50 Rat oral 1,517 mg/kg|LD50 Rat percutaneous >4,000 mg/kg|LD50 Rabbit percutaneous >6,000 mg/kg|LC50 Rat inhalation >5,800 mg/cu m/4 hr|LD50 Mouse oral 1490 mg/kg

/AQUATIC SPECIES/ The fungicide propiconazole (1-(2-(2,4-dichlorophenyl)-4-propyl-1,3-dioxolan-2-ylmethyl) -1H-1,2,4-triazole) induced the hepatic cytochrome P4501A (CYP1A) activity towards ethoxyresorufin-O-deethylase (EROD), the content of CYP1A protein as quantified by enzyme-linked immunosorbent assay (ELISA) and the glutathione S-transferase (GST) activity towards the three commonly used substrates CDNB(1-chloro-2,4-dinitrobenzene), cumene hydroperoxide (CU) and ethachrynic acid (EA) in brown trout (Salmo trutta) depending on dose and body weight. An exponential dose response relationship existed between propiconazole exposure and CYP1A activity. A 2. order polynomial regression of the propiconazole concentration (square root transformed) on the data for CDNB, EU and CU revealed a bell-shaped pattern of the GST induction. Reverse-phase HPLC of the GSH-affinity chromatography purified GST isozymes in trout exposed to respectively 8.3, 23, 93, 313 and 606 microg l(-1) propiconazole in the water indicated that the propiconazole treatment may lead to changes in the composition of the subunits compared to the controls. Thus, propiconazole exposure through the water changed the properties of the brown trout hepatic CYP1A and GST, and these changes may be used as a bioindicator on the molecular level of exposure and effect of propiconazole in controlled experiments. The use in monitoring of propiconazole exposure under natural field conditions is possible, however needs further investigation.

Propiconazole's production may result in its release to the environment through various waste streams; it's use as a fungicide(1,2) will result in its direct release to the environment(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), measured Koc values ranging from 1,200-8,100(2), indicates that propiconazole is expected to have slight to no mobility in soil(SRC). Volatilization of propiconazole from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 9.1X10-10 atm-cu cm/mole derived from its vapor pressure, 4.2X10-7 mm Hg(3), and water solubility 100 mg/L(3). Propiconazole is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure. Propiconazole is expected to biodegrade in the environment(4-8). Based on monitoring data, field and laboratory tests, propiconazole has an estimated half-life of about 60-96 days in typical soils(4,8).|AQUATIC FATE: Based on a classification scheme(1), Koc values ranging from 1,200-1,800(2), indicates that propiconazole 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 9.1X10-10 atm-cu m/mole(SRC) derived from its vapor pressure, 4.2X10-7 mm Hg(4), and water solubility, 100 mg/L(4). According to a classification scheme(5), an estimated BCF of 146(SRC), from log Kow of 3.72(4) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is high(SRC). Propiconazole has been reported to be stable to hydrolysis(7). Propiconazole is expected to biodegrade in the environment and has and estimated half life of 25-85 days in aerobic water(4).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), propiconazole, which has a vapor pressure of 4.2X10-7 mm Hg at 25 °C(2), will exist solely in particulate phase in the ambient atmosphere. Particulate-phase propiconazole may be removed from the air by wet and dry deposition(SRC). Propiconazole does not absorb at wavelengths >290 nm(2) and has been shown to be resistant to direct photolysis from sunlight(3).

No hydrolysis of propiconazole at environmentally relevant pH has been observed(1,3). Propiconazole does not absorb at wavelengths >290 nm(1) and has been shown to be resistant to direct photolysis from direct sunlight(2).

An estimated BCF of 146 was calculated for propiconazole(SRC), using a log Kow of 3.72 and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is high(SRC).

2.45e+03 L/kg|Measured Koc values of propiconazole ranged from 1,200-8,100(SRC). According to a classification scheme(2), these Koc values suggest that propiconazole is expected to have slight to no mobility in soil.

The Henry's Law constant for propiconazole is estimated as 9.1X10-10 atm-cu m/mole(SRC) derived from its vapor pressure, 4.2X10-7 mm Hg(1), and water solubility, 100 mg/L(1). This Henry's Law constant indicates that propiconazole is expected to be essentially nonvolatile from moist soil and water surfaces(2). Propiconazole is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

GROUNDWATER: Propiconazole was detected but not quantified in ground water samples taken from various golf courses around the United States(1) and detected in 1 out of 46 shallow ground water samples in Denmark at a concentration <1 ug/L(2).|DRINKING WATER: Propiconazole was detected at 5 drinking water sites in Australia at concentrations of 0.6-5.0 ug/L(1).|SURFACE WATER: Propiconazole was detected in 6 out of 7 surface water samples taken from golf courses around the United State with a maximum detection of 0.85 ug/L(1). Propiconazole was not detected in 22 samples from shallow Danish ground water(2). Propiconazole was detected in streams in southern Sweden at a maximum concentration of 1.2 ug/L(3).|RAIN/SNOW: Propiconazole was detected in the rainfall in Germany at concentrations of less than 30 ng/L to 53 ng/L(1). Propiconazole was identified, not quantified in the rainfall in Norway(2).

Propiconazole was detected in celery with a mean concentration of 0.034 ppm(1). Propiconazole was detected in wine with a mean concentration of 0.0009 ppm(1). Propiconazole was detected in must (0.01 mg/L), white wine (0.01 mg/L) and red wine 0.70 mg/L(2). Propiconazole was found in 1/13 apple samples from an Egyptian market with a concentration of 0.39 mg/kg(3).

Occupational exposure to propiconazole may occur through dermal contact with this compound at workplaces where propiconazole is produced or used. Monitoring data indicate that the general population may be exposed to propiconazole via ingestion or dermal contact with contaminated food and water. (SRC)

After oral administration to rats, propiconazole is rapidly absorbed and also rapidly and almost completely eliminated with urine and feces. Residues in tissues were generally low and there was no evidence for accumulation or retention of propiconazole or its metabolites.|Male and female mice were fed a diet containing 5, 100 and 2500 ppm propiconazole for 21 days, followed by a single oral dose of (14C)-phenyl propiconazole at a mean corresponding dose level (0.8/1.0, 16.8/21.5 and 434/475 mg/kg bw for males/females). Urinary excretion accounted for 45-81% of the administered dose after 96 hours and tended to be higher by males than by females. In the feces 22-43% was excreted. At the lowest dose level (5 ppm propiconazole) the residual radioactivity in blood, liver, kidneys, lungs and in the remaining carcass was below 0.02 mg/kg propiconazole equivalents and accordingly higher at the 100 and 2500 ppm dose level. Residues in female mice were higher than in male mice, except in the kidneys where the males showed higher or equal values. Independent of the dose level and sex of the animals, the highest residues were found in the liver, up to 2.3 and 3.0 mg/kg in males and females of the highest dose level, respectively.|Orally administered single doses (0.5 and 25 mg/kg bw) of triazole labelled (3,5-14C)-propiconazole to rats were rapidly excreted within 24 hours (74-84%). After 6 days, 0.04-0.15%, 28-46% and 53-67% had been recovered from expired air, feces and urine respectively. Only about 0.4% of the administered dose remained in the tissues. Highest tissue residues were found in liver, blood and kidneys. No unchanged propiconazole was excreted in the urine. Within 3 days after treatment of male rats with a single oral dose of about 32 mg/kg bw of triazole labelled (3,5-14C)-propiconazole or a phenyl-(U-14C) labelled propiconazole, more than 95% of the dose was excreted. Of this, 52% was found in the urine and 43-48% in the feces. The excretion pattern for both compounds was identical with no administered compound being found in the urine.|Single doses of triazole-14C-propiconazole (1.0 and 10.0 mg/kg bw) applied dermally to rats were absorbed through the skin following first order kinetics with half-lives averaging 24-31 hours for low and high dosed rats, respectively. Equal amounts of the dose were excreted within 72 hours in urine and feces. The amount of residual radioactivity on the skin averaged 20% of the applied dose.|Feed consumption, milk production or the general health of a lactating goat were not affected after the daily oral administration of 5 mg triazole-14C-propiconazole for 10 consecutive days (which would correspond to 4.5 ppm in the feed). Of the total dose, 89% was excreted within 24 hours after the last administration (68% and 21% in urine and feces, respectively). All tissues contained less than 0.02 mg/kg propiconazole equivalents, except liver (0.096 mg/kg) and kidney (0.029 mg/kg). The total radioactivity secreted with the milk reached a plateau at day three of 0.013-0.016 mg/kg, representing 0.18% of the total dose.

The metabolism of orally administered (14C)-phenyl propiconazole was studied in mice pretreated with unlabeled propiconazole followed by a single oral dose of (14C)-phenyl propiconazole at a corresponding dose level. The urinary metabolite pattern of propiconazole demonstrated a marked sex dependency. In male mice, 60% of the radioactivity in 0-24 hour urine was represented by one metabolite, this metabolite accounted for 30% in the 0-24 hour urine in female mice. This metabolite was identified by spectroscopy as the glucuronic acid conjugate of 1-(2,4-dichlorophenyl)-2-(1 H-1,2,4-triazol-1-yl) ethanol. This demonstrates that the major metabolic pathway in mice involves dioxolane ring cleavage.|The metabolism of propiconazole was investigated in male rats administered a single oral dose of 31.4 mg/kg triazole-(3,5-14C-propiconazole). Metabolites were isolated from first day urine and feces excretion representing 44.5% and 36.2% of the applied dose, respectively. A wide array of biotransformations occurred leading to numerous metabolites. The major site of enzymatic attack oxidation of the propyl side chain leading via alcohols and diols to carboxy acids and alpha-hydroxy carboxy acid or cleavage of the dioxolane ring. The majority of the alcoholic and phenolic metabolites are renally excreted as sulfuric acid and glucuronic acid conjugates. In the rat the main metabolite is the alpha hydroxyl carboxylic acid of propiconazole.|/In rats/...the major sites of enzymic attack are the propyl side-chain and the cleavage of the dioxolane ring, together with some attack at the 2,4-dichlorophenyl and 1,2,4-triazole rings. In mice, the major metabolic pathway is via cleavage of the dioxolane ring.

5.01 Days|Half-live averages 24-31 hours /in rats/.

A first version cDNA microarray of the cladoceran Daphnia magna /was developed/. Through Suppression Subtractive Hybridization PCR (SSH-PCR) 855 life stage-specific cDNAs were collected and used to document the toxicological mode of action of the pesticide propiconazole. DNA sequencing analysis revealed gene fragments related to important functional classes such as embryo development, energy metabolism, molting and cell cycle. Major changes in transcription were observed in organisms exposed for 4 and 8 days to 1 microg/mL. After 4 days a 3-fold down-regulation of the gene encoding the yolk protein, vitellogenin, was observed indicating impaired oocyte maturation. Moreover, genes such as a larval-specific gene and chaperonin were repressed, whereas the heat shock 90 protein and ATP synthase were induced. Organismal effects clearly confirmed the major molecular findings: at the highest concentration (1 ug/mL) adult growth was significantly (p < 0.05) impaired and increased developmental effects in the offspring could be noted. We have demonstrated the potential of microarray analysis in toxicity screening with D. magna. The use of vitellogenin mRNA as a rapid biomarker of reproductive effects in chronic toxicity studies with cladocerans is suggested.

/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 /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's 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 or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

1-((2-(2,4-dichlorophenyl)-4-propyl-1,3-dioxolan-2-yl)methyl)-1H-1,2,4-triazole

Formulation types: emulsifiable concentrate; emulsifiable get; suspension (flowable) concentrate.|Trade name: Tilt (Novartis); Radar (Zeneca).|Wettable powder

Method: USGS-NWQL O-2060-10; Procedure: graphitized carbon-based solid-phase extraction and high performance liquid chromatography-mass spectrometry; Analyte: propiconazole; Matrix: water; Detection Limit: 0.0105 ug/L.|Analyte: propiconazole; matrix: water (river); procedure: high-performance liquid chromatography with mass spectrometry detection; limit of detection: 100 ng/L

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

Propiconazole has known environmental transformation products that include (2S,4S-2R,4R)-2-(2,4-dichlorophenyl)-2-(1H-1,2,4-triazol-1-ylmethyl)-1,3-dioxolane-4-carboxylic acid and 1H-1,2,4-triazole-1-ethanol, alpha-(2,4-dichlorophenyl)- 2-(1,2,4) triazol-1-yl-ethanol.|Propiconazole has known environmental transformation products that include 1,2,4-triazole and 3-(2-((1H-1,2,4-triazol-1-yl)methyl)-2-(2,4-dichlorophenyl)-1,3-dioxolan-4-yl)propan-1-ol.