Cobaltbis(2-ethylhexanoat)

Liquid material spills can be copiously flushed with water and channeled to a treatment system or holding tank for reclamation or proper disposal. Spills of dry material can be removed by vacuuming or wet mopping. Some spills can be removed by hosing, first with a mist of water to dampen the spilled material and then with a more forceful stream that flushes it into a holding tank or other facility for handling contaminated water. Work surfaces or contaminated clothing should never be cleaned by dry sweeping or blowing with pressurized hoses. Recovery systems used to reclaim waste metals should comply with federal, state, and local regulations. All waste materials generated in the handling of cobalt-containing substances should be disposed of in compliance with federal, state, and local regulations. /Cobalt and cobalt salts/

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.

Employers should institute programs that emphasize good personal hygiene to prevent skin and respiratory irritation caused by cobalt containing dusts. After working with cobalt products, workers should thoroughly wash their hands and face before drinking, eating, or smoking. If skin contact with cobalt solutions occurs, the worker should wash the affected skin promptly. The employer should provide showers if workers have substantial contact with cobalt. These workers should be encouraged to wash or shower after each workshift. Employers should prohibit smoking or carrying of tobacco products, and should prohibit eating, food handling, or food storage within the work area. /Cobalt and cobalt salts/

General plant maintenance must be conducted regularly to prevent cobalt containing dusts from accumulating in work areas. Cleaning should be performed with vacuum pickup or wet mopping to minimize the amount of dust dispersed into the air. A decontamination room should be available for cleaning equipment that is to receive major overhaul or maintenance. Spills of cobalt-containing material should be promptly cleaned up to minimize inhalation or dermal contact. /Cobalt and cobalt salts/

Special precautions are necessary when workers must enter tanks or vessels, such as reaction vessels containing cobalt catalysts or vessels used to prepare cobalt salts. Before any worker enters a vessel, all sources for transferring cobalt and other materials into or out of the vessel must be blanked to prevent their entry. The vessel interior must then be washed with water and purged with air. After purging the vessel's atmosphere with suitable instruments to ensure that no hazards from fire, explosion, oxygen deficiency, or dust inhalation exist. No one should enter a tank or vessel without first being equipped with an appropriate respirator and a secured lifeline or harness. Mechanical ventilation should be provided continuously when workers are inside the tank. At least one other worker similarly equipped with respiratory protection, lifeline, and harness should watch at all times from outside the vessel. Workers inside the tank must be able to communicate with those persons outside. Other workers must be available to assist in an emergency. Flame- or spark-generating operations, such as welding or cutting, should be performed only when an authorized representative of the employer has signed a permit based on a finding that all necessary safety precautions have been taken. /Cobalt and cobalt salts/

0.02 [mg/m3], as Co

8 hr Time Weighted Avg (TWA): 0.02 mg/cu m. /Cobalt and inorganic compounds, as Co/

Peak Exposure Recommendation: Transient increases in workers' exposure levels may exceed 3 times the value of the TLV-TWA level for no more than 15 minutes at a time, on no more than 4 occasions spaced 1 hour apart during a workday, and under no circumstances should they exceed 5 times the value of the TLV-TWA level. In addition, the 8-hour TWA is not to be exceeded for an 8-hour work period. /Cobalt and inorganic compounds, as Co/

A3: Confirmed animal carcinogen with unknown relevance to humans. /Cobalt and inorganic compounds, as Co/

Biological Exposure Index (BEI): Determinant: cobalt in urine; Sampling Time: end of shift at end of workweek; BEI: 15 ug/L. Notation: The determinant is nonspecific, since it is also observed after after exposure to other chemicals. /Cobalt and inorganic compounds, including cobalt oxides but not combined with tungsten carbide/

Biological Exposure Index (BEI): Determinant: cobalt in urine; Sampling Time: end of shift at end of workweek; BEI: None. Notation: The determinant is nonspecific, since it is also observed after exposure to other chemicals. Biological monitoring should be considered for this compound based on the review; however, a specific BEI could not be determined due to insufficient data. /Cobalt with tungsten carbide/

IDENTIFICATION AND USE: Cobalt bis(2-ethylhexanoate) is a blue liquid. It is used as paint drier, whitener, catalyst. HUMAN EXPOSURE AND TOXICITY: Case reports of occupational allergic contact dermatitis caused by cobalt-2-ethylhexoate have been published. ANIMAL STUDIES: The instillation of cobalt 2-ethylhexanoate into the eye of rabbits resulted in slight opacity of the cornea in the two female animals 24 hours after treatment and persisted until 72 hours after treatment. Cobalt 2-ethyl hexanoate was assayed for the ability to induce mutation at the hypoxanthine-guanine phosphoribosyl transferase (hprt) locus (6-thioguanine [6TG] resistance) in mouse lymphoma cells. The results of this study were negative.

Cobalt is believed to exhibit its toxicity through a oxidant-based and free radical-based processes. It produces oxygen radicals and may be oxidized to ionic cobalt, causing increased lipid peroxidation, DNA damage, and inducing certain enzymes that lead to cell apoptosis. Cobalt has also been shown to block inorganic calcium channels, possibly impairing neurotransmission. Cobalt can also chelate lipoic acids, impairing oxidation of pyruvate or fatty acids. In addition, cobalt may inhibit DNA repair by interacting with zinc finger DNA repair proteins, and has also been shown to inhibit heme synthesis and glucose metabolism. Cobalt may activate specific helper T-lymphocyte cells and interact directly with immunologic proteins, such as antibodies (IgA and IgE) or Fc receptors, resulting in immunosensitization. (L29)

/CASE REPORTS/ A 46-year-old woman, who worked as a laminator of spa baths, presented with hand dermatitis, which was suspected to be related to her occupation. Patch testing revealed strong reactions to both cobalt chloride and a polyester resin that the patient had been using at her workplace. She also reacted to latex and had been wearing cotton gloves underneath rubber gloves at work. It was later discovered that cobalt octoate (synonym: cobalt-2-ethylhexanoate), a compound not listed on the manufacturer's material safety data sheet, was included as an accelerator in the polyester resin. She was then tested to cobalt octoate, which was also strongly positive. Her successful treatment included protection of her hands at work with cotton lined PVC gloves. This case highlights the role of cobalt salts as sensitizers and their presence as accelerators used in polyester resins, and the importance of recognizing concomitant latex allergy that may complicate occupational dermatitis. ...

/CASE REPORTS/ A case report of occupational allergic contact dermatitis caused by cobalt-2-ethylhexoate was presented. A 52 year old man who worked as an offset printer for 35 years presented with hand eczema of a long duration. Patch testing performed 12 years ago elicited a positive reaction to bacitracin and negative reactions to the standard series, rubber chemical series, and plastics and glues series. Recently, his hand eczema worsened, and therefore, further patch testing was performed. Cobalt-chloride elicited an allergic reaction in the standard series. Two ink driers from work containing 5% and 2% cobalt-2-ethylhexoate, respectively, elicited allergic reactions in a dilution series. The author stressed the importance of patch testing dermatitis patients in contact with inks or paints and to regard with care the potential relevance of cobalt allergic reactions in these patients.

/ALTERNATIVE and IN VITRO TESTS/ CELL CULTURE:EST-1000 kits (Lot No.: EST 100329-001) were purchased ... . The EST-1000 tissue consisted of normal, human-derived epidermal keratinocytes which have been cultured to form a multilayered, highly differentiated model of the human epidermis. ... After exposure to the test item cobalt bis(2-ethylhexanoate) the relative absorbance values were unaltered at 106.9% after 3 minutes. After the 1 hour exposure relative absorbance values were reduced to 80.7%. Both values did not exceed the threshold for corrosivity of 50% for the 3 minutes exposure and 15% for the 1 hour exposure. Therefore, the test item was not considered to be corrosive.

/ALTERNATIVE and IN VITRO TESTS/ CELL CULTURE:EpiSkin kit (Lot No.: 10-EKIN-040) /were/ purchased ... . The EpiSkin tissue consists of normal, human-derived epidermal keratinocytes which have been cultured to form a multilayered, highly differentiated model of the human epidermis. After treatment with the test item cobalt 2-ethylhexanoate the relative absorbance values decreased to 88.0%. This value is above the threshold for irritancy of </= 50%. Therefore, the test item is not considered to possess an irritant potential.

For more Human Toxicity Excerpts (Complete) data for Cobalt bis(2-ethylhexanoate) (6 total), please visit the HSDB record page.

Cobalt bis(2-ethylhexanoate)'s production and use as a paint and varnish drier, adhesion additive, whitener and catalyst(1,2) may result in its release to the environment through various waste streams(SRC). Release to the environment of cobalt bis(2-ethylhexanoate) is likely to occur from: indoor use in long-life materials with low release rate (e.g. flooring, furniture, toys, construction materials, curtains, foot-wear, leather products, paper and cardboard products, electronic equipment), outdoor use in long-life materials with low release rate (e.g. metal, wooden and plastic construction and building materials), outdoor use and indoor use(3).

Using OECD Guideline 301 B (Ready Biodegradability: CO2 Evolution Test) and an activated sludge inoculum, cobalt bis(2-ethylhexanoate), at an initial concentration of 10 mg/L, reached 60% of its theoretical CO2 evolution within 10 days of incubation which classified the compound as readily biodegradabale(1).

/LABORATORY ANIMALS: Acute Exposure/ The instillation of cobalt 2-ethylhexanoate into the eye /of rabbits/ resulted in slight opacity of the cornea in the two female animals 24 hours after treatment and persisted until 72 hours after treatment. Marked reddening of the conjunctivae was observed in the two female animals 1 hour after treatment and slight reddening was observed in the male animal 24 hours after treatment. Conjunctival reddening persisted as slight to marked until 72 hours (male), 7 days (one female) or 10 days (second female) after treatment. Slight to moderate chemosis of the conjunctivae was observed in the two female animals 1 hour after treatment and persisted until 72 hours after treatment. Moderate reddening of the sclerae was observed in the two female animals 1 hour after treatment and persisted as slight to marked reddening until 7 days after treatment. Slight to moderate ocular discharge was observed in the two female animals 1 hour after treatment and persisted until 72 hours after treatment. All eye reactions were reversible and were no longer evident 7 days (male), 10 days (one female) or 14 days (second female) after treatment. No abnormal findings were observed for the iris light reflex. No corrosion was observed. No staining of the treated eyes by the test item was observed. Test item remnants were observed in the treated eyes of all animals 1 hour after treatment and persisted in one animal (male) until 24 hours after treatment. Thus, the test item did not induce significant or irreversible damage to the rabbit eye.

/GENOTOXICITY/ Cobalt 2-ethyl hexanoate was assayed for the ability to induce mutation at the hypoxanthine-guanine phosphoribosyl transferase (hprt) locus (6-thioguanine [6TG] resistance) in mouse lymphoma cells using a fluctuation protocol. The study consisted of a cytotoxicity Range-Finder Experiment followed by two independent experiments, each conducted in the absence and presence of metabolic activation (S9). A 3-hour treatment incubation period was used for all experiments. In the cytotoxicity Range-Finder Experiment, six concentrations were tested in the absence and presence of S9, ranging from 6.25 to 2000 ug/mL (limited by solubility in culture medium). The highest concentration to provide >10% RTG was 125 ug/mL, which gave 10% and 18% RS in the absence and presence of S9, respectively. Accordingly, for Experiment I ten concentrations, ranging from 15 to 200 ug/mL, were tested in the absence and presence of S9. Seven days after treatment, the highest concentration selected to determine viability and 6TG resistance was 95 ug/mL in the absence and presence of S9, which gave 11% and 13% RS, respectively. In Experiment II ten concentrations, ranging from 10 to 150 ug/mL ug/mL, were tested in the absence and presence of S9. Seven days after treatment, the highest concentrations selected to determine viability and 6TG resistance were 100 ug/mL in the absence of S9 and 120 ug/mL in the presence of S9, which gave 14% and 13% RS, respectively. Negative (vehicle) and positive control treatments were included in each Mutation Experiment in the absence and presence of S9. Mutant frequencies in negative control cultures fell within acceptable ranges and clear increases in mutation were induced by the positive control chemicals. In Experiments I and II, no statistically significant increases in mutant frequency were observed following treatment with Cobalt 2-ethyl hexanoate at any concentration analyzed in the absence and presence of S9 and there were no significant linear trends.

Cobalt and cobalt compounds that release cobalt ions in vivo, /including cobalt 2-ethylhexanoate/, are reasonably anticipated to be human carcinogens based on sufficient evidence of carcinogenicity from studies in experimental animals and supporting data from studies on mechanisms of carcinogenesis. /Cobalt and Cobalt Compounds That Release Cobalt Ions In Vivo/

There is inadequate evidence for the carcinogenicity of cobalt and cobalt compounds in humans. There is sufficient evidence for the carcinogenicity of cobalt metal powder in experimental animals. There is limited evidence for the carcinogenicity of metal alloys containing cobalt, chromium and molybdenum in experimental animals. ... Overall Evaluation: Cobalt and cobalt compounds are possibly carcinogenic to humans (Group 2B). /Cobalt and cobalt compounds/

A3: Confirmed animal carcinogen with unknown relevance to humans. /Cobalt and inorganic compounds, as Co/

Cobalt and cobalt compounds that release cobalt ions in vivo are reasonably anticipated to be human carcinogens based on sufficient evidence of carcinogenicity from studies in experimental animals and supporting data from studies on mechanisms of carcinogenesis. /Cobalt and cobalt compounds/

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Cobalt bis(2-ethylhexanoate) is included on this list.