2,3,5-Triiodobenzoic acid

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 64(SRC), determined from a structure estimation method(2), indicates that 2,3,5-triiodobenzoic acid is expected to have high mobility in soil(SRC). The pKa of 2,3,5-triiodobenzoic acid is approximately 1.5(3), indicating that this compound will primarily exist in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of 2,3,5-triiodobenzoic acid from moist soil surfaces is not expected to be an important fate process given that ions do not volatilize(SRC). 2,3,5-Triiodobenzoic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.3X10-7 mm Hg(SRC), determined from a fragment constant method(5). After 8 weeks incubation, soil microflora degraded this compound to 2,5- (15-20% peak concn) and 3,5-diiodobenzoic acid (14-15% peak concn) and one unknown metabolite(6), indicating that biodegradation may be an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 64(SRC), determined from a structure estimation method(2), indicates that 2,3,5-triiodobenzoic acid is not expected to adsorb to suspended solids and sediment(SRC). An approximate pKa of 1.5(3) indicates 2,3,5-triiodobenzoic acid will exist almost entirely in the anion form at pH values of 5 to 9 and therefore volatilization from water surfaces is not expected to be an important fate process(4). According to a classification scheme(5), an estimated BCF of 6(SRC), from an estimated log Kow of 5.03(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data for the compound in water were not available(SRC, 2008).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 2,3,5-triiodobenzoic acid, which has an estimated vapor pressure of 1.3X10-7 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase 2,3,5-triiodobenzoic acid 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 27 days(SRC), calculated from its rate constant of 6.0X10-13 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase 2,3,5-triiodobenzoic acid may be removed from the air by wet or dry deposition(SRC). UV radiation of 2,3,5-triiodobenzoic acid was shown to result in the formation of 2,5- and 3,5-diiodobenzoic acids(4); therefore, 2,3,5-triiodobenzoic acid may be susceptible to direct photolysis by sunlight(SRC).

The metabolites of 2,3,5-triiodobenzoic acid in cow's milk resulting from acute administration of the compound (1.197 g) were determined using electron capture gas-chromatograph procedures. The parent compound plus seven suspected metabolites were detected; of these, four were identified, and one quantitated. The primary metabolite was 2-OHI-3,5-diiodobenzoic acid. Occurring in trace amounts were mono-iodobenzoic acids, 2-0H-5 iodobenzoic acid, and 3,5-diiodobenzoic acid. The maximum concentration of 2,3,5-triiodobenzoic acid in raw milk was found in the 30-hr milk sample at the 0.79 mg/kilogram level and of 2-OH-3,5-diiodobenzoic acid in the 42-hr milk at the 0.27 mg/kilogram level.

Using a structure estimation method based on molecular connectivity indices(1), the Koc of 2,3,5-triiodobenzoic acid can be estimated to be 64(SRC). According to a classification scheme(2), this estimated Koc value suggests that 2,3,5-triiodobenzoic acid is expected to have high mobility in soil. The pKa of 2,3,5-triiodobenzoic acid is approximately 1.5(3), indicating that this compound will primarily exist in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

/SIGNS AND SYMPTOMS/ Harmful if swallowed

/SIGNS AND SYMPTOMS/ May cause skin irritation.

AEROBIC: Very little is known about biodegradation of 2,3,5-triiodobenzoic acid in soil(1). Soil microflora degraded this compound to 2,5- and 3,5-diiodobenzoic acid and one unknown metabolite; peak concns of 2,5- and 3,5-diiodobenzoic acid were 15-20% and 14-15%, respectively, after 8 weeks incubation(2).

ANAEROBIC: Using ruminal fluid as an inoculum, 2,3,5-triiodobenzoic acid was persistent, showing no evidence of dehalogenation(1).

An estimated BCF of 6 was calculated in fish for 2,3,5-triiodobenzoic acid(SRC), using an estimated log Kow of 5.03(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The pKa of 2,3,5-triiodobenzoic acid is approximately 1.5(1), indicating that this compound will primarily exist in the anion form in the environment and therefore volatilization from water surfaces is not expected to be an important fate process(2). 2,3,5-Triiodobenzoic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.3X10-7 mm Hg(SRC), determined from a fragment constant method(3).

/LABORATORY ANIMALS: Acute Exposure/ Intraperitoneal, Mouse LD50 = 562 mg/kg. Remarks: Behavioral:Rigidity (includes catalepsy). Behavioral:Muscle contraction or spasticity.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ The effects of some plant growth regulators (PGRs), 2,3,5-triiodobenzoic acid (TIBA), Naphthaleneacetic acid (NAA) and 2,4-Dichlorofenoxyacetic acid (2,4-D), at sublethal concentrations on antioxidant defense system [glutathione peroxidases (GPx), reduced glutathione (GSH), glutathione reductase (GR), glutathione-S-transferase (GST) and catalase (CAT)], immune potential enzymes [adenosine deaminase (ADA) and myeloperoxidase (MPO)], and lipid peroxidation content [Malondialdehyde, (MDA)] were investigated in lung and speen tissues of rats. Sprague-Dawley albino rats were exposed to 0, 50, or 100 ppm (parts per million) TIBA, NAA, or 2,4-D in drinking water ad libitum for 25 days continuously. According to the results, MDA concentration significantly increased in the tissues treated with 100 ppm dosage of NAA or 2,4-D without any change in the tissues of rats treated with either dosage of TIBA. The GSH depletion in the spleen tissue of rats treated with either the dosage of NAA and 2,4-D were found to be significant. Also, GSH level in the spleen was significantly reduced with 100 ppm of 2,4-D and NAA. The activity of antioxidant enzymes were also seriously affected by PGRs; GPx significantly decreased in the lung of rats treated with either dosages of the PGRs, whereas GPx activity in the spleen were significantly increased with 100 ppm dosage of 2,4-D and NAA. On the other hand, CAT activity significantly decreased in the lung of rats treated with both dosages of NAA, 100 ppm of 2,4-D and 50 ppm of TIBA, and also in the spleen treated with 50 ppm NAA and 2,4-D. The ancillary enzyme GR activity significantly decreased in the spleen with both doses of the PGRs, also in the lung treated with both dosages of 2,4-D, 50 ppm of NAA and 100 ppm of TIBA. The drug metabolizing enzyme GST activity significantly reduced in the lung of rats treated with either dosages of the PGRs and also in the spleen treated with 100 ppm dosage of 2,4-D and TIBA and 50 ppm of NAA. Meanwhile, immune potential enzyme MPO activity significantly increased in the spleen of rats treated with both doses of NAA and TIBA whereas ADA activity significantly decreased in the spleen of rats treated with 100 ppm dose of NAA and TIBA. The observations presented led us to conclude that the administrations of subacute NAA, 2,4-D, and TIBA promote MDA content, inhibit the antioxidative defense system and activate or inhibit immune potential enzymes in the rat's spleen and lung tissues. These data suggest that PGRs produced substantial organ toxicity in the lung and spleen during the period of a 25-day subacute exposure.

/OTHER TOXICITY INFORMATION/ This study aims to investigate the effects of the plant growth regulators (PGRs) (2,3,5-triiodobenzoic acid (TIBA), Naphthaleneacetic acid (NAA), and 2,4-dichlorofenoxyacetic acid (2,4-D)) on serum marker enzymes (aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatine phosphokinase (CPK), and lactate dehydrogenase (LDH)), antioxidant defense systems (reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase (GST), and catalase (CAT)), and lipid peroxidation content (malondialdehyde = MDA) in various tissues of rats. 50 and 100 ppm of PGRs as drinking water were administered orally to rats (Sprague-Dawley albino) ad libitum for 25 days continuously. The PGRs treatment caused different effects on the serum marker enzymes, antioxidant defense systems, and the MDA content in experimented rats compared to controls. Results showed that TIBA caused a significant decrease in serum AST activity with both the dosage whereas serum CPK was significantly increased with 100 ppm dosage of TIBA. Meanwhile, serum AST, CPK, and LDH activities were significantly increased with both dosage of NAA and 2,4-D. The lipid peroxidation end-product MDA significantly increased in the all tissues treated with both dosages of PGRs without any change in the brain and erythrocyte of rats treated with both the dosages of 2,4-D. The GSH depletion in the kidney and brain tissues of rats treated with both dosages of PGRs was found to be significant. Furthermore, the GSH depletion in the erythrocyte of rats treated with both dosages of PGRs except 50 ppm dosage of 2,4-D was significant too. Also, the GSH level in the liver was significantly depleted with 50 ppm of 2,4-D and NAA, whereas the GSH depletion in the same tissue did not significantly change with the treatment. The activity of antioxidant enzymes was also seriously affected by PGRs; SOD significantly decreased in the liver, heart, kidney, and brain of rats treated with both dosages of NAA, whereas the SOD activity in the erythrocytes, liver, and heart was either significantly decreased or not changed with two doses of 2,4-D and TIBA. Although the CAT activity significantly increased in the erythrocyte and brain of rats treated with both doses of PGRs, it was not changed in the liver, heart, and kidney. Meanwhile, the ancillary enzyme GR activity significantly increased in the brain, heart, and liver but decreased in the erythrocyte and kidney of rats treated with both doses of PGRs. The drug-metabolizing enzyme GST activity significantly increased in the heart and kidney but decreased in the brain and erythrocytes of rats treated with both dosages of PGRs. As a conclusion, the results indicate that PGRs might affect antioxidant potential enzymes, the activity of hepatic damage enzymes, and lipid peroxidation dose independently. Also, the rats resisted to oxidative stress via antioxidant mechanism but the antioxidant mechanism could not prevent the increases in lipid peroxidation in rat's tissues. These data, along with the determined changes, suggest that PGRs produced substantial systemic organ toxicity in the erythrocyte, liver, brain, heart, and kidney during the period of a 25-day subacute exposure.

The rate constant for the vapor-phase reaction of 2,3,5-triiodobenzoic acid with photochemically-produced hydroxyl radicals has been estimated as 6.0X10-13 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 27 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). 2,3,5-Triiodobenzoic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). UV radiation of foliar-applied 2,3,5-triiodobenzoic acid to soybean plants was shown to result in the formation of 2,5- and 3,5-diiodobenzoic acids(4); therefore, 2,3,5-triiodobenzoic acid may be susceptible to direct photolysis by sunlight(SRC).

2,3,5-Triiodobenzoic acid's production may result in its release to the environment through various waste streams; its use as a plant growth regulator will result in its direct release to the environment. If released to air, an estimated vapor pressure of 1.3X10-7 mm Hg at 25 °C indicates 2,3,5-triiodobenzoic acid will exist in both the vapor and particulate phases in the atmosphere. Vapor-phase 2,3,5-triiodobenzoic acid will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 27 days. Particulate-phase 2,3,5-triiodobenzoic acid will be removed from the atmosphere by wet or dry deposition. UV radiation of 2,3,5-triiodobenzoic acid was shown to result in the formation of 2,5- and 3,5-diiodobenzoic acids and therefore, 2,3,5-triiodobenzoic acid may be susceptible to direct photolysis by sunlight. If released to soil, 2,3,5-triiodobenzoic acid is expected to have high mobility based upon an estimated Koc of 64. The pKa of 2,3,5-triiodobenzoic acid is approximately 1.5, indicating that this compound will exist almost entirely in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts. Volatilization from moist soil surfaces is not expected to be an important fate process based upon its ionic form. After 8 weeks incubation, soil microflora degraded this compound to 2,5- (15-20% peak concn) and 3,5-diiodobenzoic acid (14-15% peak concn) and one unknown metabolite, indicating that biodegradation may be an important environmental fate process in soil. If released into water, 2,3,5-triiodobenzoic acid is not expected to adsorb to suspended solids and sediment based upon the estimated Koc. Biodegradation data in water were not available. The estimated pKa indicates 2,3,5-triiodobenzoic acid will exist almost entirely in the anion form at pH values of 5 to 9 and therefore volatilization from water surfaces is not expected to be an important fate process. An estimated BCF of 6 suggests the potential for bioconcentration in aquatic organisms is low. Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. Occupational exposure to 2,3,5-triiodobenzoic acid may occur through inhalation and dermal contact with this compound at workplaces where 2,3,5-triiodobenzoic acid is produced or used. (SRC)

A plant growth regulator used as a growth retardant

Plant growth regulator synthesis and function inhibitor

Plant growth regulator and defoliant with the properties of an antiauxin