Iodoacetic Acid

H301: Toxic if swallowed [Danger Acute toxicity, oral]

H314: Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]

P260, P264, P270, P280, P301+P316, P301+P330+P331, P302+P361+P354, P304+P340, P305+P354+P338, P316, P321, P330, P363, P405, and P501 (click each P-code to see the statement)

H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]

H314 (100%): Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]

Aggregated GHS information provided per 65 reports by companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

H310: Fatal in contact with skin [Danger Acute toxicity, dermal]

H318: Causes serious eye damage [Danger Serious eye damage/eye irritation]

H371: May cause damage to organs [Warning Specific target organ toxicity, single exposure]

H373: May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]

P260, P262, P264, P264+P265, P270, P280, P301+P316, P301+P330+P331, P302+P352, P302+P361+P354, P304+P340, P305+P354+P338, P308+P316, P316, P317, P319, P321, P330, P361+P364, P363, P405, and P501 (click each P-code to see the statement)

H317: May cause an allergic skin reaction [Warning Sensitization, Skin]

P260, P261, P264, P264+P265, P270, P272, P280, P301+P316, P301+P330+P331, P302+P352, P302+P361+P354, P304+P340, P305+P354+P338, P316, P317, P321, P330, P333+P317, P362+P364, P363, P405, and P501 (click each P-code to see the statement)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. IMMEDIATELY call a hospital or poison control center even if no symptoms (such as redness or irritation) develop. IMMEDIATELY transport the victim to a hospital for treatment after washing the affected areas.

INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. IMMEDIATELY call a physician and be prepared to transport the victim to a hospital even if no symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing.

INGESTION: DO NOT INDUCE VOMITING. Corrosive chemicals will destroy the membranes of the mouth, throat, and esophagus and, in addition, have a high risk of being aspirated into the victim's lungs during vomiting which increases the medical problems. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. IMMEDIATELY transport the victim to a hospital. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. Transport the victim IMMEDIATELY to a hospital. (NTP, 1992)

Fires involving this compound can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. (NTP, 1992)

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary.

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.

SPILL: Increase the immediate precautionary measure distance, in the downwind direction, as necessary.

FIRE: If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2024)

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

SRP: 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 air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Contaminated packaging: Dispose of as unused product.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Provide appropriate exhaust ventilation at places where dust is formed.

Appropriate engineering controls: Avoid contact with skin, eyes and clothing. Wash hands before breaks and immediately after handling the product.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

For more Preventive Measures (Complete) data for Iodoacetic acid (6 total), please visit the HSDB record page.

SMALL SPILLS AND LEAKAGE: If you spill this chemical, you should dampen the solid spill material with water, then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces with a strong soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

STORAGE PRECAUTIONS: You should store this material in a refrigerator. (NTP, 1992)

Keep container tightly closed in a dry and well-ventilated place. Recommended storage temperature: -20 °C.

MINIMUM PROTECTIVE CLOTHING: If Tyvek-type disposable protective clothing is not worn during handling of this chemical, wear disposable Tyvek-type sleeves taped to your gloves.

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with a combination filter cartridge, i.e. organic vapor/acid gas/HEPA (specific for organic vapors, HCl, acid gas, SO2 and a high efficiency particulate filter). Splash proof safety goggles should be worn while handling this chemical. Alternatively, a full face respirator, equipped as above, may be used to provide simultaneous eye and respiratory protection. (NTP, 1992)

Eye/face protection: Face shield and safety glasses. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166 (EU).

Handle with gloves.

Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Iodoacetic acid appears as colorless or white crystals. (NTP, 1992)

Colorless or white solid; [Merck Index] Pale yellow crystalline flakes; Soluble in water; [MSDSonline]

Colorless or white crystals

White to yellow powder or flakes

Decomposes (NTP, 1992)

Decomposes

181 °F (NTP, 1992)

82-83 °C

Colorless or white crystals. MP: 210 °C. Soluble in water, alcohol; very slightly soluble in ether. Hygroscopic in moist air /Iodoacetic acid, sodium salt/

greater than or equal to 100 mg/mL at 70.7 °F (NTP, 1992)

Soluble in water

Soluble in alcohol; very slightly soluble in ether

Soluble in ethanol, petroleum ether; slightly soluble in ether, chloroform

Stable under recommended storage conditions.

When heated to decomposition it emits toxic fumes of /iodine/.

Corrosive

pKa = 3.18 at 25 °C

Light sensitive

Diamagnetic susceptibility

Magnetic susceptibility

Nuclear quadrupole resonance spectroscopy

Quadrupole coupling

Surface tension

Other Classes -> Organic Acids

Fatty Acyls [FA] -> Fatty Acids and Conjugates [FA01] -> Halogenated fatty acids [FA0109]

May be sensitive to heat, light, and air. Water soluble

Acids, Carboxylic

Halogenated Organic Compounds

IODOACETIC ACID reacts vigorously with bases and is corrosive. (NTP, 1992)

Incompatible materials: Strong bases, strong reducing agents.

IDENTIFICATION AND USE: Iodoacetic acid is a solid. It is used as a reagent. HUMAN STUDIES: Iodoacetic acid is toxic to essentially all parts of the eye, when either applied directly or administered systemically. Iodoacetate has been shown to be toxic to the cornea, iris, lens, ciliary body, and retina. Iodoacetic acid did not increase significantly the frequency of micronucleus in binucleated TK6 cells. Stable chromosome aberrations (translocations) were induced in human cells by sodium iodoacetate. ANIMAL STUDIES: Iodoacetate injected intravenously in rabbits or cats causes almost immediate drop in the electric action potentials of the retina, owing to injury of the visual cells. It also causes proteins and cells to appear in the aqueous humor and induces cellular exudation into the vitreous body in five days. Histologic changes are observable in the corneal endothelium and ciliary epithelium. When applied to eyes from which the corneal epithelium has been removed, or when injected into the corneal stroma, solutions from 0.001 M to 0.1 M cause severe to devastating injury. Addition of iodoacetate to the aqueous humor causes corneal edema. Injection into the anterior chamber caused severe damage to the cornea and iris as well as cataract. Excised or isolated rabbit retina has been shown by several investigators to be directly poisoned by iodoacetate, abolishing the ERG and causing selective destruction of rod cells at low concentrations. Iodoacetate is selectively more injurious to rods than cones. The intra-articular injection of iodoacetate into the knee joint of rats produced changes in the articular cartilage which resembled those of osteoarthritis. Iodoacetic acid transformed NIH3T3 cells in a cell-transformation assay that resulted in aggressive fibrosarcomas after injection into mice. Iodoacetic acid was significantly genotoxic to S. typhimurium.

Dermatotoxin - Skin burns.

Toxic Pneumonitis - Inflammation of the lungs induced by inhalation of metal fumes or toxic gases and vapors.

LCLo (rat) = 94,000 mg/m3/30min

LD50 Rat ip 75 mg/kg

LD50 Rat sc 60 mg/kg

LD50 Mouse oral 83 mg/kg

LD50 Dog iv 45 mg/kg

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/

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/

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

/GENOTOXICITY/ Stable /chromosome/ aberrations (translocations) were induced in human cells by sodium iodoacetate.

/GENOTOXICITY/ Chemical disinfection of water generates harmful chemical compounds, known as disinfection by-products (DBPs). One class of DBPs is constituted by haloacetic acids (HAAs), the second major group in prevalence (after trihalomethanes) detected in finished drinking water. In this article, we report the results obtained in the evaluation of the chromosome damage induced by three monohaloacetic acids, namely iodoacetic acid (IAA), bromoacetic acid (BAA) and chloroacetic acid (CAA). To evaluate the induction of chromosome damage, we used the cytokinesis-block micronucleus test that measures the ability of genotoxic agents to induce both clastogenic and/or aneugenic effects. ... We tested five doses of each HAA, in addition to the negative and positive controls. The highest dose tested for each HAA was that immediately lower than the dose producing total cytotoxicity. Our results show that none of the three HAAs tested was able to increase significantly the frequency of micronucleus in binucleated TK6 cells, the rank order in decreasing cytotoxicity was IAA > BAA >> CAA.

/ALTERNATIVE and IN VITRO TESTS/ Disinfection by-products (DBPs) are compounds produced in the raw water disinfection processes. Although increased cancer incidence has been associated with exposure to this complex mixture, the carcinogenic potential of individual DBPs remains not well known; thus, further studies are required. Haloacetic acids (HAAs) constitute an important group among DBPs. In this study, we have assessed the in vitro carcinogenic potential of three HAAs namely chloro-, bromo-, and iodoacetic acids. Using a long-term (8 weeks) and sub-toxic doses exposure scenario, different in vitro transformation markers were evaluated using a human urothelial cell line (T24). Our results indicate that long-term exposure to low doses of HAAs did not reproduce the genotoxic effects observed in acute treatments, where oxidative DNA damage was induced. No changes in the transformation endpoints analyzed were observed, as implied by the absence of significant morphological, cell growth rate and anchorage-independent cell growth pattern modifications. Interestingly, HAA-long-term exposed cells developed resistance to oxidative stress damage, what would explain the observed differences between acute and long-term exposure conditions. Accordingly, data obtained under long-term exposure to sub-toxic doses of HAAs could be more accurate, in terms of risk assessment, than under acute exposure scenarios.

/ALTERNATIVE and IN VITRO TESTS/ The process of disinfecting drinking water inadvertently leads to the formation of numerous disinfection byproducts (DBPs). Some of these are mutagenic, genotoxic, teratogenic, and cytotoxic, as well as potentially carcinogenic both in vivo and in vitro. We investigated the in vitro biological activity of five DBPs: three monohaloacetic acids (monoHAAs) [chloroacetic acid (CAA), bromoacetic acid (BAA), and iodoacetic acid (IAA)] and two novel halobenzoquinones (HBQs) [2,6-dichloro-p-benzoquinone (DCBQ) and 2,6-dibromo-p-benzoquinone]. We focused particularly on cytotoxicity and induction of two adaptive stress response pathways: the oxidative stress responsive Nrf2/ARE and DNA-damage responsive p53 pathways. All five DBPs were cytotoxic to the Caco-2 cell line after a 4 hr exposure, and all DBPs induced both of the adaptive stress response pathways, Nrf2/ARE and p53, in the micromolar range, as measured by two beta-lactamase-based reporter gene assays. The decreasing order of potency for all three endpoints for the five DBPs was IAA /approximately equal to/ BAA > DCBQ /approximately equal to/ DBBQ > CAA. Induction of oxidative stress was previously proposed to be the molecular initiating event (MIE) for both classes of DBPs. However, comparing the levels of activation of the two pathways uncovered that the Nrf2/ARE pathway was the more sensitive endpoint for HAAs, whereas the p53 pathway was more sensitive in the case of HBQs. Therefore, the DNA damage-responsive p53 pathway may be an important piece of information to fill in a gap in the adverse outcome pathway framework for the assessment of HBQs. Finally, we ... compared the potential risk of the two novel HBQs using a benchmarking approach to that of the well-studied CAA, which suggested that their relative risk may be lower than that of BAA and IAA.

For more Human Toxicity Excerpts (Complete) data for Iodoacetic acid (7 total), please visit the HSDB record page.

/LABORATORY ANIMALS: Acute Exposure/ Degenerative joint disease was induced in the knee joints of mice by intraarticular injection of ...iodoacetate... .

/LABORATORY ANIMALS: Acute Exposure/ Injection into the anterior chamber caused severe damage to the cornea and iris as well as cataract. Some have thought that iodoacetate acted directly on the lens. Others have thought that opacification in the lens was secondary to changes in the retina.

/LABORATORY ANIMALS: Acute Exposure/ Single doses of iodoacetate which cause severe damage in eyes of experimental animals often are lethal or cause severe systemic poisoning with widespread edema of skin.

/LABORATORY ANIMALS: Acute Exposure/ Excised or isolated rabbit retina has been shown by several investigators to be directly poisoned by iodoacetate, abolishing the ERG and causing selective destruction of rod cells at low concentrations.

For more Non-Human Toxicity Excerpts (Complete) data for Iodoacetic acid (37 total), please visit the HSDB record page.

The following link will take the user to the National Toxicology Program (NTP) Test Status of Agents Search page, which tabulates the results and current status of tests such as "Short-Term Toxicity Studies", "Long-term Carcinogenicity Studies", "Developmental Studies", "Genetic Toxicology Studies", etc., performed with this chemical. Testing status for iodoacetic acid is available.[Available from, as of February 1, 2019: https://ntpsearch.niehs.nih.gov/?e=True&ContentType=Testing+Status]

/AQUATIC SPECIES/ Using seawater for toilet flushing may introduce high levels of bromide and iodide into a city's sewage treatment works, and result in the formation of brominated and iodinated disinfection byproducts (DBPs) during chlorination to disinfect sewage effluents. In a previous study, the authors' group has detected the presence of many brominated DBPs and identified five new aromatic brominated DBPs in chlorinated saline sewage effluents. The presence of brominated DBPs in chlorinated saline effluents may pose adverse implications for marine ecology. In this study, besides the detection and identification of another seven new aromatic halogenated DBPs in a chlorinated saline sewage effluent, their developmental toxicity was evaluated using the marine polychaete Platynereis dumerilii. For comparison, the developmental toxicity of some commonly known halogenated DBPs was also examined. The rank order of the developmental toxicity of 20 halogenated DBPs was 2,5-dibromohydroquinone > 2,6-diiodo-4-nitrophenol >/= 2,4,6-triiodophenol > 4-bromo-2-chlorophenol >/= 4-bromophenol > 2,4-dibromophenol >/= 2,6-dibromo-4-nitrophenol > 2-bromo-4-chlorophenol > 2,6-dichloro-4-nitrophenol > 2,4-dichlorophenol > 2,4,6-tribromophenol > 3,5-dibromo-4-hydroxybenzaldehyde > bromoform >/= 2,4,6-trichlorophenol > 2,6-dibromophenol > 2,6-dichlorophenol > iodoacetic acid ? tribromoacetic acid > bromoacetic acid > chloroacetic acid. On the basis of developmental toxicity data, a quantitative structure-activity relationship (QSAR) was established. The QSAR involved two physical-chemical property descriptors (log P and pKa) and two electronic descriptors (the lowest unoccupied molecular orbital energy and the highest occupied molecular orbital energy) to indicate the transport, biouptake, and biointeraction of these DBPs. It can well predict the developmental toxicity of most of the DBPs tested.

Iodoacetic acid's production and use as an analytical reagent, presence in iodinated x-ray contrast media and formation as a chemical by-product of chlorination and chloramination of drinking water may result in the release of iodoacetic acid to the environment through various waste streams. If released to air, an estimated vapor pressure of 3.2X10-2 mm Hg at 25 °C indicates iodoacetic acid will exist solely as a vapor in the atmosphere. Vapor-phase iodoacetic 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 18 days. Iodoacetic acid absorbs UV light at wavelength 260 nm and, therefore, is not expected to be susceptible to direct photolysis since sunlight consists of wavelengths above 290 nm. If released to soil, iodoacetic acid is expected to have very high mobility based upon an estimated Koc of 1.4. The pKa of iodoacetic acid is 3.18, 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 is not expected because the compound exists as an anion and anions do not volatilize. Iodoacetic acid is not expected to volatilize from dry soil surfaces based upon its vapor pressure. Biodegradation data in soil were not available; however, iodoacetic acid was susceptible to biodegradation by a Norcadia sp isolated from soil. If released into water, iodoacetic acid is not expected to adsorb to suspended solids and sediment based upon the estimated Koc. Biodegradation data in water were not available. However, iodoacetic acid was biodegraded 95-100% by Afipia spps isolated from drinking water enrichment cultures developed through acclimation to chloroacetic acids. A pKa of 3.18 indicates iodoacetic 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 3 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 (pH 5 to 9). Occupational exposure to iodoacetic acid may occur through inhalation and dermal contact with this compound at workplaces where iodoacetic acid is produced or used. Limited monitoring data indicate that the general population may be exposed to iodoacetic acid via ingestion of chlorinated drinking water. A segment of the general population may also be exposed via medical imagining procedures using iodinated x-ray contrast media. (SRC)

Iodoacetic acid's production and use as an analytical reagent(1), presence in iodinated x-ray contrast media and formation as a chemical by-product of chlorination and chloramination of drinking water(2) may result in the release of iodoacetic acid to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1.4(SRC), determined from a structure estimation method(2), indicates that iodoacetic acid is expected to have very high mobility in soil(SRC). The pKa of iodoacetic acid is 3.18(3), 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(4). Volatilization from moist soil is not expected because the compound exists as an anion and anions do not volatilize. Iodoacetic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.2X10-2 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2018); however, iodoacetic acid was susceptible to biodegradation by a Norcadia sp isolated from soil(5).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1.4(SRC), determined from a structure estimation method(2), indicates that iodoacetic acid is not expected to adsorb to suspended solids and sediment(SRC). A pKa of 3.18(3) indicates iodoacetic 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(SRC). According to a classification scheme(4), an estimated BCF of 3(SRC), from an estimated log Kow of 0.85(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Iodoacetic acid is degraded in natural water by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in natural water is estimated to be about 41 minutes(SRC), calculated from a measured rate constant of 5.7X10-9 L/mol-sec(5). Biodegradation data in water were not available(SRC, 2018). However, iodoacetic acid was biodegraded 95-100% by Afipia spps isolated from drinking water enrichment cultures developed through acclimation to chloroacetic acids(6).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), iodoacetic acid, which has an estimated vapor pressure of 3.2X10-2 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase iodoacetic 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 18 days(SRC), calculated from its rate constant of 8.9X10-13 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). Iodoacetic acid absorbs UV light at wavelength 260 nm(3) and, therefore, is not expected to be susceptible to direct photolysis since sunlight consists of wavelengths above 290 nm(SRC).

PURE CULTURE: A single bacteria strain of Nocardia, isolated from soil, was able to readily bio-metabolize iodoacetic acid in a 20-day laboratory incubation study(1); in contrast, a single strain of Pseudomonas was unable to metabolize iodoacetic acid(1). Biodegradation of iodoacetic acid by Afipia spp and Methylobacterium sp (phylum Proteobacteria) was reported, isolated from drinking water system cultures enriched by previous exposures to mono-, di- and trichlioroacetic acids. Iodoacetic acid, present at 30 mg/L was approximately 95% biodegraded in 5 days by Afipia felis strain EMDA2 and 100% biodegraded in less than 2 days by A. broomeae strain GTs(2).

The rate constant for the vapor-phase reaction of iodoacetic acid with photochemically-produced hydroxyl radicals has been estimated as 8.9X10-13 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 18 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The rate constant for the estimated OH radical reaction of iodoacetic acid with hydroxyl radicals in aqueous solutions at pH 1 is 5.7X10+9 L/mol-sec(2); this corresponds to an aquatic half-life of 140 days at an aquatic concentration of 1X10-17 hydroxyl radicals per liter(3). Iodoacetic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(4). Iodoacetic acid absorbs UV light at wavelength 260 nm(5) and, therefore, is not expected to be susceptible to direct photolysis since sunlight consists of wavelengths above 290 nm(SRC).

An estimated BCF of 3 was calculated for iodoacetic acid (SRC), using an estimated log Kow of 0.85(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).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of iodoacetic acid can be estimated to be 1.4(SRC). According to a classification scheme(2), this estimated Koc value suggests that iodoacetic acid is expected to have very high mobility in soil. The pKa of iodoacetic acid is 3.18(3), 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(4).

A pKa of 3.18(1) indicates iodoacetic 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(SRC). Iodoacetic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.2X10-2 mm Hg(SRC), determined from a fragment constant method(1).

DRINKING WATER: Iodoacetic acid concentrations of up to 1.7 ug/L have been reported in tap water, finished drinking water and other similar sources(1). Iodoacetic acid concentrations ranged from <0.0002 to 0.67 ug/L in chloraminated and chlorinated drinking water samples from one city in Canada and 22 cities in the United States, collected from full-scale water treatment plants in 2005 and 2006(2).

Iodoacetic acid's presence in raw waste water has been traced in some cases to use of iodinated x-ray contrast media used in medical imaging. Concentrations ranging from 3,880-4,100 ug/L have been reported for various iodinated contrast media, with a resulting iodoacetic acid concentration range of 0.09-1.8 ug/L formed as a disinfectant byproduct. By-product formation levels of 1.8-4.3 yg/L have been reported from use of tincture of iodine(1).

Iodoacetic acid concentrations of 1.8 to 4.3 ug/L have been reported in water treated with iodine tincture as a point-of-use disinfection(1).

Occupational exposure to iodoacetic acid may occur through inhalation and dermal contact with this compound at workplaces where iodoacetic acid is produced or used. Limited monitoring data indicate that the general population may be exposed to iodoacetic acid via ingestion of chlorinated drinking water. A segment of the general population may also be exposed via medical imagining procedures using iodinated x-ray contrast media. (SRC)

/AQUATIC SPECIES/ Using seawater for toilet flushing may introduce high levels of bromide and iodide into a city's sewage treatment works, and result in the formation of brominated and iodinated disinfection byproducts (DBPs) during chlorination to disinfect sewage effluents. In a previous study, the authors' group has detected the presence of many brominated DBPs and identified five new aromatic brominated DBPs in chlorinated saline sewage effluents. The presence of brominated DBPs in chlorinated saline effluents may pose adverse implications for marine ecology. In this study, besides the detection and identification of another seven new aromatic halogenated DBPs in a chlorinated saline sewage effluent, their developmental toxicity was evaluated using the marine polychaete Platynereis dumerilii. For comparison, the developmental toxicity of some commonly known halogenated DBPs was also examined. The rank order of the developmental toxicity of 20 halogenated DBPs was 2,5-dibromohydroquinone > 2,6-diiodo-4-nitrophenol >/= 2,4,6-triiodophenol > 4-bromo-2-chlorophenol >/= 4-bromophenol > 2,4-dibromophenol >/= 2,6-dibromo-4-nitrophenol > 2-bromo-4-chlorophenol > 2,6-dichloro-4-nitrophenol > 2,4-dichlorophenol > 2,4,6-tribromophenol > 3,5-dibromo-4-hydroxybenzaldehyde > bromoform >/= 2,4,6-trichlorophenol > 2,6-dibromophenol > 2,6-dichlorophenol > iodoacetic acid ? tribromoacetic acid > bromoacetic acid > chloroacetic acid. On the basis of developmental toxicity data, a quantitative structure-activity relationship (QSAR) was established. The QSAR involved two physical-chemical property descriptors (log P and pKa) and two electronic descriptors (the lowest unoccupied molecular orbital energy and the highest occupied molecular orbital energy) to indicate the transport, biouptake, and biointeraction of these DBPs. It can well predict the developmental toxicity of most of the DBPs tested.

Iodoacetic acid's production and use as an analytical reagent, presence in iodinated x-ray contrast media and formation as a chemical by-product of chlorination and chloramination of drinking water may result in the release of iodoacetic acid to the environment through various waste streams. If released to air, an estimated vapor pressure of 3.2X10-2 mm Hg at 25 °C indicates iodoacetic acid will exist solely as a vapor in the atmosphere. Vapor-phase iodoacetic 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 18 days. Iodoacetic acid absorbs UV light at wavelength 260 nm and, therefore, is not expected to be susceptible to direct photolysis since sunlight consists of wavelengths above 290 nm. If released to soil, iodoacetic acid is expected to have very high mobility based upon an estimated Koc of 1.4. The pKa of iodoacetic acid is 3.18, 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 is not expected because the compound exists as an anion and anions do not volatilize. Iodoacetic acid is not expected to volatilize from dry soil surfaces based upon its vapor pressure. Biodegradation data in soil were not available; however, iodoacetic acid was susceptible to biodegradation by a Norcadia sp isolated from soil. If released into water, iodoacetic acid is not expected to adsorb to suspended solids and sediment based upon the estimated Koc. Biodegradation data in water were not available. However, iodoacetic acid was biodegraded 95-100% by Afipia spps isolated from drinking water enrichment cultures developed through acclimation to chloroacetic acids. A pKa of 3.18 indicates iodoacetic 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 3 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 (pH 5 to 9). Occupational exposure to iodoacetic acid may occur through inhalation and dermal contact with this compound at workplaces where iodoacetic acid is produced or used. Limited monitoring data indicate that the general population may be exposed to iodoacetic acid via ingestion of chlorinated drinking water. A segment of the general population may also be exposed via medical imagining procedures using iodinated x-ray contrast media. (SRC)

Iodoacetic acid's production and use as an analytical reagent(1), presence in iodinated x-ray contrast media and formation as a chemical by-product of chlorination and chloramination of drinking water(2) may result in the release of iodoacetic acid to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1.4(SRC), determined from a structure estimation method(2), indicates that iodoacetic acid is expected to have very high mobility in soil(SRC). The pKa of iodoacetic acid is 3.18(3), 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(4). Volatilization from moist soil is not expected because the compound exists as an anion and anions do not volatilize. Iodoacetic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.2X10-2 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2018); however, iodoacetic acid was susceptible to biodegradation by a Norcadia sp isolated from soil(5).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1.4(SRC), determined from a structure estimation method(2), indicates that iodoacetic acid is not expected to adsorb to suspended solids and sediment(SRC). A pKa of 3.18(3) indicates iodoacetic 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(SRC). According to a classification scheme(4), an estimated BCF of 3(SRC), from an estimated log Kow of 0.85(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Iodoacetic acid is degraded in natural water by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in natural water is estimated to be about 41 minutes(SRC), calculated from a measured rate constant of 5.7X10-9 L/mol-sec(5). Biodegradation data in water were not available(SRC, 2018). However, iodoacetic acid was biodegraded 95-100% by Afipia spps isolated from drinking water enrichment cultures developed through acclimation to chloroacetic acids(6).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), iodoacetic acid, which has an estimated vapor pressure of 3.2X10-2 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase iodoacetic 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 18 days(SRC), calculated from its rate constant of 8.9X10-13 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). Iodoacetic acid absorbs UV light at wavelength 260 nm(3) and, therefore, is not expected to be susceptible to direct photolysis since sunlight consists of wavelengths above 290 nm(SRC).

PURE CULTURE: A single bacteria strain of Nocardia, isolated from soil, was able to readily bio-metabolize iodoacetic acid in a 20-day laboratory incubation study(1); in contrast, a single strain of Pseudomonas was unable to metabolize iodoacetic acid(1). Biodegradation of iodoacetic acid by Afipia spp and Methylobacterium sp (phylum Proteobacteria) was reported, isolated from drinking water system cultures enriched by previous exposures to mono-, di- and trichlioroacetic acids. Iodoacetic acid, present at 30 mg/L was approximately 95% biodegraded in 5 days by Afipia felis strain EMDA2 and 100% biodegraded in less than 2 days by A. broomeae strain GTs(2).

The rate constant for the vapor-phase reaction of iodoacetic acid with photochemically-produced hydroxyl radicals has been estimated as 8.9X10-13 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 18 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The rate constant for the estimated OH radical reaction of iodoacetic acid with hydroxyl radicals in aqueous solutions at pH 1 is 5.7X10+9 L/mol-sec(2); this corresponds to an aquatic half-life of 140 days at an aquatic concentration of 1X10-17 hydroxyl radicals per liter(3). Iodoacetic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(4). Iodoacetic acid absorbs UV light at wavelength 260 nm(5) and, therefore, is not expected to be susceptible to direct photolysis since sunlight consists of wavelengths above 290 nm(SRC).

An estimated BCF of 3 was calculated for iodoacetic acid (SRC), using an estimated log Kow of 0.85(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).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of iodoacetic acid can be estimated to be 1.4(SRC). According to a classification scheme(2), this estimated Koc value suggests that iodoacetic acid is expected to have very high mobility in soil. The pKa of iodoacetic acid is 3.18(3), 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(4).

A pKa of 3.18(1) indicates iodoacetic 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(SRC). Iodoacetic acid is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 3.2X10-2 mm Hg(SRC), determined from a fragment constant method(1).

DRINKING WATER: Iodoacetic acid concentrations of up to 1.7 ug/L have been reported in tap water, finished drinking water and other similar sources(1). Iodoacetic acid concentrations ranged from <0.0002 to 0.67 ug/L in chloraminated and chlorinated drinking water samples from one city in Canada and 22 cities in the United States, collected from full-scale water treatment plants in 2005 and 2006(2).

Iodoacetic acid's presence in raw waste water has been traced in some cases to use of iodinated x-ray contrast media used in medical imaging. Concentrations ranging from 3,880-4,100 ug/L have been reported for various iodinated contrast media, with a resulting iodoacetic acid concentration range of 0.09-1.8 ug/L formed as a disinfectant byproduct. By-product formation levels of 1.8-4.3 yg/L have been reported from use of tincture of iodine(1).

Iodoacetic acid concentrations of 1.8 to 4.3 ug/L have been reported in water treated with iodine tincture as a point-of-use disinfection(1).

Occupational exposure to iodoacetic acid may occur through inhalation and dermal contact with this compound at workplaces where iodoacetic acid is produced or used. Limited monitoring data indicate that the general population may be exposed to iodoacetic acid via ingestion of chlorinated drinking water. A segment of the general population may also be exposed via medical imagining procedures using iodinated x-ray contrast media. (SRC)

SRP: 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 air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Contaminated packaging: Dispose of as unused product.

Corrosive