Page 2 of 18

EXECUTIVE SUMMARY

Sodium omadine is registered for use as an industrial preservative and as a dry film 

mildewcide. The industrial preservation uses include metal working fluids, adhesives, caulks, 

sealants, plastics, textile spin finishes, leather and paints and coatings. Additional preservation 

uses include carpet cleaners, surface cleaners, floor cleaners and sponges. The Registration 

Eligibility Decision (RED) for sodium omadine was completed in 1996 and the uses that existed 

at the time were found to be eligible for registration. 

There are twelve products that contain sodium omadine as the active ingredient (ai). Most of 

the labels have the statement “Do not use for applications involving direct or indirect 

food/drinking water contact”. Three labels (#1258-990, #1258-1205 and #39967-26) do not have 

this statement and label #39967-26 is approved for uses such as paper, cleaning solutions and 

detergents that might involve food contact. Sodium omadine is also approved by FDA as a 

preservative of adhesives in food contact packaging (21 CFR 175.105). 

Because it was thought that the low vapor pressure of sodium omadine and dilution during 

use would result in minimal exposure only two occupational exposure scenarios were assessed 

during the RED and no residential exposures scenarios were assessed. Because there is the 

potential for exposure to aerosols from certain occupational and residential uses and because the 

toxicological endpoints relating to residential exposures are fairly low, however, there are 

additional exposures that will need to be reassessed during registration review. The following 

exposure data will be needed to assess these exposures: 

• Indoor exposure studies (dermal and inhalation) during open pouring of liquids for 

material preservation and during the use of treated materials such as paints, metal 

working fluids, and household cleaners.

• Leaching studies on leather and textiles preserved with sodium omadine.

• Surface residue dissipation studies on dishes, household floors and carpets cleaned with 

sodium omadine preserved dish detergents, floor cleaners and carpet cleaners, 

respectively.

• Product use information

The toxicological database for sodium omadine is fairly robust and includes a 90 day oral 

toxicity study on rats, a 90 day dermal toxicity study on rats, a 90 day inhalation toxicity study

on rats, a developmental study on rabbits, a two generation reproduction study on rats and a 

carcinogenicity study on rats. No additional toxicology studies will be needed for registration 

review.
Page 3 of 18

1.0 BACKGROUND

1.1 Chemical Identity

The chemical identity of sodium omadine is listed in Table 1. Sodium omadine exists as mixture 

of two tautomers (A and B) that result from the resonance of the sodium ion between the sulfur 

and oxygen atoms. 

Table 1 - Chemical Identity of Sodium Omadine

Chemical Name A. 1-hydroxy-2 (1H)-pyridinethione, sodium salt 

B. 2-pyridinethion-1-oxide, sodium salt

Common Name Sodium Omadine

PC Code 088004

CAS Registry Number 15922-78-8 (A), 3811-73-2 (B)

Case No. 0209

Empirical Formula C5H4NOSNa

Structure

1.2 Chemical and Physical Properties

The physical and chemical properties of sodium omadine that are relevant for human health risk 

assessment are listed in Table 2. 

Table 2 - Physical and Chemical Properties of Sodium Omadine

Property Value Reference

Molecular Weight 149.2 Based on formula

Physical State Off White Powder US EPA, 1996

Melting Point >250 C US EPA, 1996

Water Solubility 121 grams per 100 ml @ 25 C US EPA, 1996

Vapor Pressure 7 x 10-8 mm Hg @ 22 C US EPA, 1996
Page 4 of 18

2.0 USE INFORMATION

2.1 Formulation Types and Percent Active Ingredient

There are twelve products that contain sodium omadine as the active ingredient (ai). These

products are formulated as ready to use solutions or soluble concentrates.

2.2 Summary of Registered Uses 

Sodium omadine is registered for use in the preservation of a wide variety of materials as 

listed in Table 3. Both in-can and dry film uses are included on the labels. The application rates

range from 33 to 5000 ppm with the lower rates being for products that contain other active 

ingredients such as HHT. 

Table 3 – Application Rates for Sodium Omadine

Use Application Rate Notes

Adhesives, Latexes, Urethane Foams, Caulks, Patching Compounds, Sealants, Pastes, 

and Grouts (Dry Film Preservation)

2000 – 5000 ppm 1

Air Freshener Gels (Carrageenan Based) 400 ppm

Aqueous Analytical and Diagnostic Reagents Used in Chemical and Clinical Analysis 33 – 500 ppm

Architectural Paints, Industrial Paints and Coatings, including Wood Coatings, (Dry 

Film Preservation)

2000 – 5000 ppm 1

Building Materials (gypsum, pearlite, plaster-like, mineral based or cellulose) used in 

the manufacture of ceilings, ceiling tile, walls and partitions

3840 ppm

Concrete Add-Mixtures (Water Based Chemical or Mineral) 500 ppm

Gypsum Wallboard 3840 ppm

Inks, Aqueous Based 328 - 512 ppm

Latex Emulsions Used in Adhesives, Caulks, Patching Compounds, Sealants, Pastes 

and Grouts 

98 - 410 ppm

Laundry Rinse Additives, Laundry Detergents, Carpet Cleaners, Surface Cleaners, 

Floor Cleaners 

640 ppm

Leather Preservation 4000 ppm

Metal Working Fluids 74 - 512 ppm

Spin Finishes - Aqueous Synthetic Fiber Lubricating 66 - 512 ppm

Paper Not Specified 2

Sponges, Zinc-chitosan modified 6000 ppm

1. The highest rate of 5000 ppm is from label 1258-843.

2. This use is only listed on one label (39967-26). The rates for this label are listed on a technical information sheet. 

The technical data sheet does not list a rate for paper.

The RED for sodium omadine was completed in 1996 and all of existing uses were found to 

be eligible for registration. Some additional uses such as leather preservation, paper and sponges 

were added after the completion of the RED. The sponge use was evaluated in a risk assessment 

(EPA, 1999) and it was determined that the risks were not of concern for either workers involved 

in the sponge treatment or residential users of the treated sponges. It should be noted that the 

worker risks were assessed for sodium omadine while the residential risks were assessed for zinc 

omadine because sodium omadine reacts with zinc that is impregnated within the sponge and 

forms zinc omadine. The leather and paper uses have not been evaluated.
Page 5 of 18

3.0 TOXICOLOGY

At the time of the RED, the toxicology database for sodium omadine was considered to be 

complete and no additional studies were required. No additional toxicity studies, other than a 

few acute toxicity studies, have been submitted since the RED.

3.1 Acute Toxicity

A summary of the acute toxicity findings is included in Table 4. Sodium omadine is of low

acute toxicity (toxicity category III) for oral, dermal and inhalation toxicity and it is a mild 

dermal irritant (toxicity category IV). It is not a dermal sensitizer. With respect to eye irritation,

the testing indicated sodium omadine belongs in Toxicity Category II, but this finding is 

confounded by the fact that 3 of the 6 animals died by day 2.

Table 4 - Acute Toxicity Values for Sodium Omadine 

Test (species) MRID Result Toxicity 

Category 81-1 Oral Toxicity (rat) 402478-01 LD50 (males) = 2000 mg/kg

LD50 (females) = 1100 mg/kg

LD50 (combined) = 1500 mg/kg

III

81-2 Dermal Toxicity (rabbit) 402478-02 LD50 (males) = 1900 mg/kg

LD50 (females) = 1800 mg/kg

LD50 (combined) = 1800 mg/kg

III

81-3 Inhalation Toxicity (rat) 403390-01 LC50 (males) = 1.26 mg/l 

LC50 (females) = 0.81 mg/l 

LC50 (combined) = 1.08 mg/l

III

81-4 Eye Irritation (rabbit) 44322901 No corneal opacity noted. Iritis cleared 

by day 2. Conjuctival irritation cleared 

by day 14. 

II*

81-5 Dermal Irritation (rabbit) 402478-03 Slight transient erythema and edema IV

81-6 Dermal sensitization (guinea pig) 402478-04 Not a sensitizer NA

81-6 Dermal sensitization (human) 403874-01 Not a sensitizer N/A

*Three of the six test animals died by day 2. Necropsy indicated abnormalities of the lung, peritoneal cavity and 

gastrointestinal tract. 

3.2 Subchronic and Chronic Toxicity 

The following is a summary of the currently available toxicology studies for sodium 

omadine. All of these studies were done using an aqueous solution of 40 to 41 percent sodium 

omadine.

3.2a Subchronic Toxicity

Oral Exposure Route

MRID 40756901 - In a subchronic toxicity/neurotoxicity study, sodium omadine was 

administered by oral gavage to groups of 20 male and 20 female rats for 13 weeks at doses of 0, 

0.5, 2.0, or 8.0 mg/kg/day. In-cage clinical observations for signs of neurotoxicity were made 
Page 6 of 18

prior to dosing, at 1 and 6 hours after dosing, and daily before dose administration throughout the

study. Prior to initiation and during weeks 5 and 13, all animals were given functional tests for 

potential neurotoxicity (hindlimb grip strength, hindlimb tactile placing response, and landing 

hindfoot spread test). 

At 2.0 mg/kg/day, slight atrophy of the hindlimb skeletal muscle was observed in 5/20 males 

and 5/20 females, and minimal atrophy was seen in one female. Atrophy of the panniculus 

muscle was observed in 3/20 females receiving 2.0 mg/kg/day; the atrophy was considered a 

neurotoxic effect (neurogenicatrophy). Both males and females dosed at 0, 0.5, and 2.0 

mg/kg/day had similar body weights throughout the study. The 8.0 mg/kg/day groups 

consistently gained less weight than the other groups, and weighed as much as 21% and 22% less 

than controls for males and females, respectively. Significant decreases in weight gains were 

seen for males (30%) and females (47%). 

The body weight and clinical observation data suggest a steep dose response. In the highdose groups, minimum to marked hindlimb atrophy was observed in 95-100% of the males and 

females (more severe in females), minimal paravertebral muscle atrophy was seen in 2/20 males 

and 17/20 females, and atrophy of the subcutaneous panniculus muscle was seen in 20/20 males 

and 17/20 females. Treatment-related neurotoxic signs observed in the high-dose animals 

consisted of slight hypoactivity, piloerection, ataxia (hindlimb), slight head searching, 

emaciation, hindlimb paralysis, and hunched posture. As a consequence of severe hindlimb 

motor dysfunction, 10 high-dose females were sacrificed in extremis. Effects on neuromuscular 

function included significant decreases in landing foot spread, hindlimb grip strength, and 

hindlimb tactile placing response.

The study Lowest Observed Effects Level (LOEL) was 2.0 mg/kg/day based on evidence of 

neurotoxicity in males and females (neurogenic skeletal muscle atrophy) and the No Observed 

Effects Level (NOEL) was 0.5 mg/kg/day.

The neurotoxicity portion of the study was classified as supplemental because cage 

observations were limited, many of the usual functional observation battery (FOB) parameters 

were not performed, grip strength measurements and motor activity were not quantified, 

guideline procedures for preparation of neural tissues (including perfusion) were not followed, 

and the histological examination of neural tissues was inadequate.

Dermal Exposure Route

MRID 40936201 - In a subchronic dermal toxicity study, rats were administered sodium 

omadine daily for 90 days at 0, 5, 15, or 50 mg/kg/day. There was no evidence of dose related

dermal irritation. Dose-related clinical signs seen in high-dose females included emaciation, 

hunched posture, stiff hindlimbs, incoordination, and tremors. Among the males, one high-dose 

rat was emaciated; there were no neurologic signs. The high dose (50 mg/kg/day) males and 

females consistently gained less weight than the other groups, and at termination, high-dose body 

weights were 9% and 17% less than controls for males and females, respectively. Food

consumption was not affected. There were no dose-related effects on eye health or clinical 
Page 7 of 18

pathology. Statistically significant increases in relative brain, pituitary, heart, lung, liver, kidney, 

and spleen weights in the high-dose males and females were attributed to retarded growth. There 

were no dose-related effects on absolute organ weights. The only dose-related gross lesion was 

wasting of the hindlimb skeletal muscle in 3/20 mid-dose females, and in 2/20 males and 19/20 

females in the high-dose. The gross findings were confirmed histopathologically as a reduction 

of muscle fiber diameter, fatty replacement, and an increase in the number of sarcolemmal 

nuclei. The subcutaneous panniculus muscle displayed atrophy in the mid-dose females and the 

high-dose males and females. In addition, degeneration of sciatic nerve fibers and minimal 

atrophy in the paravertebral muscles was seen in 10/20 high-dose females. Degenerated fibers 

showed a loss of myelin. 

The LOEL was 50 mg/kg/day in males and 15 mg/kg/day in females, based on atrophy of the 

hindlimb muscles and subcutaneous panniculus muscles. The NOEL was 15 mg/kg/day in 

males, and 5 mg/kg/day in females. At 50 mg/kg/day, both sexes had decreased weight gain 

compared to controls, and females showed minimal atrophy of the paravertebral muscle,

neurotoxic symptoms, and degeneration of some sciatic nerve fiber bundles.

Inhalation Exposure Route

MRID 41178201 - In the rat inhalation toxicity study, sodium omadine was administered by 

whole-body inhalation to male and female rats for 6 hours per day, 5 days per week, for 13 

weeks at analytical concentrations of 0.0, 0.00046, 0.0011, and 0.0038 mg/l. The high 

concentration of 0.0038 mg/l was increased to 0.0081 mg/l at week 6 because of the lack of signs 

of toxicity. The systemic NOEL(s) were 0.0081 mg/l in males and 0.0011 mg/l in females.

The systemic LOEL was 0.0081 mg/l in females, based on clinical signs of hindlimb 

dysfunction, histopathologic skeletal muscle regeneration, and decreases in female body weight

and body weight gain. 

3.2b. Chronic Toxicity

MRID 41178101 - Sodium omadine was administered by gavage to groups of 5 male and 5 

female Cynomolgus monkeys for 1 year at 0, 5, 25, or 150 mg/kg/day. The dose of 150 

mg/kg/day was lowered to 75 mg/kg/day at week 6 because of adverse effects on survival. No 

evidence of toxicity was seen at 5 mg/kg/day other than emesis in some monkeys. Emesis was 

observed in all monkeys at higher doses. Male body weights were un-affected by dosing, but 

female body weights were decreased as much as 8%, 17%, and 23% at the 5, 25, and both 75 and 

150 mg/kg/day, respectively. At 150 mg/kg/day, one female was sacrificed inextremis at week 6. 

At 75 mg/kg/day, one male and one female died at weeks 13 and 35, respectively; the cause of 

death was not apparent for either animal. Clinical signs noted prior to death in the dead and 

sacrificed females included prostration, decreased activity, emesis, thinness, weakness, and cold 

extremities. Emesis and ptyalism were seen in the male that died. Hematologic changes (i.e.,

decreases in erythrocyte count, hemoglobin, and hematocrit levels) were slight and considered of 

minor toxicological importance. 

The No Observed Adverse Effects Level (NOAEL) was 5 mg/kg/day. The Lowest Effects 

Level (LEL) was 25 mg/kg/day based on emesis and decreased female body weight.
Page 8 of 18

3.2c. Carcinogenicity

MRID 42100801 - In an 80-week dermal carcinogenicity study, sodium omadine 40%

aqueous solution was administered topically to groups of 50 male and 50 female mice at 0, 5, 15, 

or 40 mg/kg/day. At 40 mg/kg/day, an increase in the incidence of epidermal hyperplasia at the 

application site was seen in males (20% compared to 0% in controls, p <0.01) and in females 

(20% compared to 6% for controls; nonsignificant by pairwise comparison but a significant 

trend, p <0.05). No systemic toxicity was observed. Dermal application of sodium omadine did 

not induce any benign or malignant neoplasms. The NOEL for systemic effects was 40 

mg/kg/day, which was the highest dose tested, and was supported by the range-finding study. 

The NOEL for irritation was 15 mg/kg/day. The dermal LEL (lowest effect level) was 40 

mg/kg/day based on an increase in epidermal hyperplasia at the skin application site. The highdose was considered inadequate to assess carcinogenicity. 

MRID 42100901 - Sodium omadine was administered daily by oral gavage to groups of 70 

rats per sex at 0, 0.5, 1.5, or 5.0 mg/kg/day for 2 years. The highest dose was reduced to 3.5 

mg/kg/day after 12 weeks because of excessive weight loss in females. At the highest dose tested 

(5.0/3.5 mg/kg/day) there was a significant decrease in mean body weight (as much as 10%) and 

body weight gain in females throughout the study; a marked increase in nerve fiber degeneration 

in the sciatic nerve and spinal cord in both sexes; and an increased incidence of retinal atrophy in 

both sexes. An increase in neoplasia was not observed at any site. Dosing was considered 

adequate to assess carcinogenicity. The NOEL was 0.5 mg/kg/day. The LOEL was 1.5 

mg/kg/day, based on significant increases in the incidence of degeneration of the skeletal muscle 

of the hindlimbs in both sexes. 

The OPP RfD/Peer Review Committee met on 3/30/95 to discuss the adequacy of the 

carcinogenicity studies described above. The rat carcinogenicity study was found to be 

acceptable. The dermal carcinogenicity study in mice was found to be inadequate because the 

chemical was not tested at a sufficiently high dose level. However, the Agency concluded that a 

new study will not be required as long as the use patterns do not dramatically change and the 

potential for human exposure remains low. Sodium omadine was classified as a Group D 

carcinogen (insufficient weight of evidence).

3.2d. Developmental Toxicity

MRID 40487201 - In a developmental toxicity study, rabbits were given sodium omadine by 

daily dermal application for 6 hours at doses of 0, 1, 2.5, or 5 mg/kg/day on gestation days 6-19, 

inclusive. There was no evidence of maternal or fetal toxicity at any dose. The NOEL was 5 

mg/kg/day which was the highest dose tested. This NOEL was supported by the range-finding 

dose of 7.5 mg/kg/day that resulted in substantial toxicity.

3.2e. Reproductive Toxicity

MRID 41097201 - In a two-generation reproduction study, rats received sodium omadine by 

gavage at dose levels of 0, 0.5, 1.5, or 3.5 mg/kg/day. The highest dose level was changed from 

4.5 mg/kg/day to 3.5 mg/kg/day after 3 weeks of dosing because of marked toxicity at 4.5 
Page 9 of 18

mg/kg/day. The parental NOEL was 0.5 mg/kg/day. The parental LOEL was 1.5 mg/kg/day in 

females, and 3.5 mg/kg/day in males, based on increased incidence of histologic atrophy in the 

upper hindlimb skeletal muscles (reduction in fiber diameter) in F1 females (3/25), F0 males 

(7/23), and F1 males (9/25). Additional parental effects seen at 3.5 mg/kg/day included increased 

histologic atrophy in the upper hindlimb skeletal muscles in F0 females (19/24), and F1 females 

(20/23); and significantly decreased body weight in F0 and F1 females.

The reproductive NOEL was 1.5 mg/kg/day. The reproductive LEL was 3.5 mg/kg/day, 

based on slightly decreased number of pups per litter born in both generations (possibly a 

consequence of reduced mating success due to hindlimb atrophy), delayed development in pups 

from both generations (including open ears and eyes and startle response), and decreased pup 

body weight and weight gain in both sexes. 

3.2f Mutagenicity

MRID 40411501 - Sodium omadine did not induce forward gene mutations at the HGPRT 

locus in cultured Chinese hamster ovary (CHO) cells at concentrations of up to 0.08 μg/ml 

without S9 activation or 27 μg/ml with S9 activation. These concentrations were found to be 

severely cytotoxic (i.e., <10% cell survival). 

MRID 40343701 - In the in vivo Micronucleus Assay, sodium omadine did not cause 

micronucleus induction in the bone marrow cells of male or female CD-1 mice at 30, 48, or 72 

hours after the intraperitoneal administration of 575 mg/kg (238 mg/kg/active ingredient). 

Clinical signs of toxicity (decreased body tone, body drop, abnormal gait, ptosis, lacrimation, 

and tremors) and target cell cytotoxicity were observed at this level. 

MRID 40387501 - Sodium omadine did not induce unscheduled DNA synthesis (UDS) in 

primary rat hepatocytes treated with doses up to 220 ng/ml (300 ng/ml, based on analytical 

determinations). Concentrations 71 ng/ml (80 ng/ml) were cytotoxic. 

3.2g Absorption, Distribution, Metabolism and Excretion (ADME)

MRID No. 41269001 - The ADME of sodium omadine was studied in groups of rats 

administered either: 1. A single oral dose of 0.5 mg/kg 14C-sodium omadine, 2. A single oral 

dose of 25 mg/kg 14C-sodium omadine, 3. Oral dosing of 0.5 mg/kg/day of unlabeled sodium 

omadine for 14 days followed by a single oral dose of 14C-sodium omadine (0.5 mg/kg), or 4. A

single (IV) dose of 0.5 mg/kg 14C-sodium omadine. Sodium omadine was rapidly absorbed, 

metabolized, and excreted at all dosing levels. Total recovery of administered radioactivity was 

85%-95% at 4 days postexposure. The urine is the major route of excretion of sodium omadine 

(73-85% of the dose); the feces are only a minor route of excretion (5-12% of the dose). Sodium 

omadine and its metabolites were not excreted in expired air. In the single oral low-dose group 

and the IV-dose group, most of the administered radioactivity was excreted within the first 12 

hours postdosing. In the repeated oral low-dose group and in the single oral high-dose group, the

majority of the administered radioactivity was excreted within 24 and 48 hours postdosing, 

respectively. There was no evidence of bioaccumulation of sodium omadine or its metabolites in 

the tissues. The metabolic profiles in the urine were similar in all dose groups; 12 urinary 
Page 10 of 18

metabolites (A-L) were characterized. The major metabolite in the urine, which was 41.4%-

67.2% of the recovered radioactivity, was 2-pyridinethiol-1-oxide-S-glucuronide (Metabolite K), 

while unchanged parent compound was not detected in the urine. 

3.2h Neurotoxicity

Results of a 13 week oral subchronic toxicity/neurotoxicity study were previously described

in section 3.2a. Although the neurotoxicity portion of this study was found to be supplemental 

due to reporting deficiencies, enough information was provided to derive a LOEL of 2.0 

mg/kg/day based on evidence of neurotoxicity in male and female rats (neurogenic skeletal 

muscle atrophy). The NOEL was found to be 0.5 mg/kg/day. In the subchronic dermal toxicity 

study, dose-related clinical signs seen in high-dose female rats included emaciation, hunched 

posture, stiff hindlimbs, incoordination, and tremors. Among the males, one high-dose rat was 

emaciated; there were no neurologic signs. The LOEL was 50 mg/kg/day in males and 15 

mg/kg/day in females, based on atrophy of the hindlimb muscles and subcutaneous panniculus 

muscles. The NOEL was 15 mg/kg/day in males, and 5 mg/kg/day in females.

3.3 Toxicology Endpoints 

The following endpoints were used for assessing risks for the RED.

• Dermal Exposure, Short-term - NOEL of 5 mg/kg/day based on the dermal

developmental toxicity study in rabbits. The target Margin of Exposure (MOE) is 100.

• Dermal Exposure, Intermediate term - NOEL of 5 mg/kg/day based on the 90-day dermal 

toxicity study in rats. The target MOE is 100.

• Inhalation Exposure, Intermediate term - systemic NOEL of 0.0011 mg/l, based on the 

90-day inhalation study in rats. The target MOE is 100.

• RfD - 0.005 mg/kg/day based on a NOEL of 0.5 mg/kg/day from the chronic rat study 

and an uncertainty factor of 100. The rat reproduction study with a parental NOEL of 0.5 

mg/kg/day supports the RfD as a co-critical study. 

No additional toxicology data were required in the RED and no additional data will be needed 

for registration review. Additional PBPK data are currently being reviewed for a related 

chemical, zinc omadine, and if appropriate, this data will be used for sodium omadine. 

4.0 DIETARY ASSESSMENT

4.1 Dietary Exposure

Most of the labels have the statement “Do not use for applications involving direct or indirect 

food/drinking water contact.” Three labels (#1258-990, #1258-1205 and #39967-26) do not have 

this statement; however, and label #39967-26 is approved for uses such as paper, cleaning 
Page 11 of 18

solutions and detergents that might involve food contact. Sodium omadine is also approved by 

FDA as a preservative of adhesives in food contact packaging (21 CFR 175.105). Given these 

approvals, it will be necessary to assess indirect food contact exposures from these uses and 

residue data will be needed as listed in Table 5. 

4.2 Drinking Water Exposure 

The registered uses of sodium omadine might result in contamination of surface and ground 

water as a result of discharges of treated water from industries using this antimicrobial as a 

material preservative. Therefore, drinking water exposure might occur. However, the need for a 

drinking water exposure assessment will be determined upon review of the environmental fate 

data that the Agency anticipates requiring. These data will be used to determine if sodium 

omadine can pass through wastewater treatment plants into drinking water. Therefore, the need 

for a drinking water assessment will be revisited upon submission and review of the 

environmental fate data

5.0 OCCUPATIONAL AND RESIDENTIAL EXPOSURES

5.1 Occupational Exposures

Occupational handler exposures were assessed in the RED for the mixing and loading for the 

general preservation and metal working fluid uses. The exposures were calculated based on the 

combined dermal and inhalation unit exposures from the Chemical Manufacturer’s Association 

study along with a daily treatment volume of 10,000 gallons for both scenarios and application 

rates of 46 ppm for general preservation and 500 ppm for MWF. The MOEs were calculated 

from these exposures using the dermal NOEL of 5 mg/kg/day. The MOEs of 4700 for general 

preservation and 450 for MWFs were greater than the target MOE of 100 and were not 

considered to be of concern. 

Occupational post application exposures that occur during the use of treated materials were 

not assessed for the RED because it was believed at the time that these exposures would be 

minimal because of low application rates and because sodium omadine has low vapor pressure. 

Although it is true that vapor exposures to sodium omadine will be minimal as stated in the RED, 

there is the potential for dermal and inhalation exposures to aerosols during the use of materials 

such as paints, metal working fluids, surface cleaners and floor cleaners treated with sodium 

omadine. The exposures that will need to be assessed and the data that will be needed are listed 

in Table 5. In addition, it will be necessary to reassess the general preservative uses because 

some materials have application rates of up to 5000 ppm which is much greater than the rate of 

46 ppm that was assessed in the RED.

5.2 Residential Exposures

Sodium omadine residential exposure may occur during the use of treated products such as 

paints and coatings, surface cleaners, floor cleaners, carpet cleaners, textiles and leather. 
Page 12 of 18

Residential exposures were not assessed in the RED because it was believed at the time that the

exposures would be very low due to dilution. While it is true that the use rates are fairly low, the 

toxicological endpoints are also fairly low and therefore it will be necessary to assess these 

exposures during registration review. These exposures and the data that will be needed to assess 

them are listed in Table 5.

6.0 AGGREGATE AND CUMULATIVE EXPOSURE

In examining aggregate exposure, EPA takes into account the available and reliable 

information concerning exposures to pesticide residues in food and drinking water, as well as

non-occupational (i.e. residential) pesticide exposures. In the case of sodium omadine, an 

aggregate risk assessment will likely be needed because of the use pattern which is likely to 

result in dietary, drinking water and residential exposures. 

With respect to cumulative exposure, sodium omadine is toxicologically very similar to zinc 

omadine and it may be necessary to conduct a cumulative risk assessment based on these two 

chemicals. This determination will be made during registration review.

7.0 INCIDENTS

There are no human incidents reported in the OPP incident database that are associated with 

sodium omadine exposure. However, there are literature reports of allergic contact dermatitis

(Le Coz, 2001) and contact dermatitis (Totsi et al., 1990) associated with occupational exposure 

to sodium omadine in metal working fluids. 

8.0 TOLERANCES

There are no tolerances or exemptions from tolerances established by the EPA for sodium 

omadine. Sodium omadine is approved by FDA as a preservative of adhesives in food contact 

packaging (21 CFR 175.105). 

9.0 ENDOCRINE DISRUPTION EFFECTS

As required under FFDCA section 408(p), EPA has developed the Endocrine Disruptor 

Screening Program (EDSP) to determine whether certain substances (including pesticide active 

and other ingredients) may have an effect in humans or wildlife similar to an effect produced by 

a “naturally occurring estrogen, or other such endocrine effects as the Administrator may 

designate.” The EDSP employs a two-tiered approach to making the statutorily required 

determinations. Tier 1 consists of a battery of 11 screening assays to identify the potential of a 

chemical substance to interact with the estrogen, androgen, or thyroid (E, A, or T) hormonal 

systems. Chemicals that go through Tier 1 screening and are found to have the potential to 

interact with E, A, or T hormonal systems will proceed to the next stage of the EDSP where EPA 

will determine which, if any, of the Tier 2 tests are necessary based on the available data. Tier 2 

testing is designed to identify any adverse endocrine related effects caused by the substance, and 

establish a dose-response relationship between the dose and the E, A, or T effect.
Page 13 of 18

Between October 2009 and February 2010, EPA issued test orders/data call-ins for the first 

group of 67 chemicals, which contains 58 pesticide active ingredients and 9 inert ingredients. 

This list of chemicals was selected based on the potential for human exposure through pathways 

such as food and water, residential activity, and certain post-application agricultural scenarios. 

This list should not be construed as a list of known or likely endocrine disruptors. Sodium 

omadine is not among the group of 58 pesticide active ingredients on the initial list to be 

screened under the EDSP. Under FFDCA Section 408 (p), the Agency must screen all pesticidal 

chemicals. Accordingly, EPA anticipates issuing future EDSP test orders/data call-ins for all 

pesticide active ingredients. Further information on the status of the EDSP, the policies and 

procedures, the list of 67 chemicals, the test guidelines and the Tier 1 screening battery, is 

available on the website: http://www.epa.gov/endo/.

10.0 ANTICIPATED DATA NEEDS

10.1 Toxicology Studies

No new toxicology studies are needed for the registration review of sodium omadine.

10.2 Exposure Studies

There are three exposures studies that are needed to assess dietary and 

occupational/residential exposure scenarios. These studies are listed in Table 5 and detailed 

justifications are provided in Appendix A.

Table 5 –Exposure Studies Needed for Sodium Omadine Registration Review

Study Needed Guideline Applicable Exposure Scenarios

Indoor Exposure, Dermal

Indoor Exposure, Inhalation

Data Reporting/Calculations

875.1100 

875.1300 

875.1600 

Open pour liquids during material preservation

Brush/roller application of preserved paints

A,B

Airless sprayer application of preserved paints

B

Use of treated metal working fluids

B

Trigger sprayer and mop application of preserved cleaners

B

B

Surface Residue Dissipation 875.2300 Dishes washed with preserved dish detergents.

Floors and carpets cleaned with preserved household cleaners. 

Textiles and leather preserved with sodium omadine.

Product Use Information 875.1700 All above scenarios

A. If the labels are amended to require closed mixing/loading, then the exposure study for this scenario can be waived.

B. It may be possible to use proprietary surrogate exposure data if data compensation issues can be addressed.
Page 14 of 18

11.0 REFERENCES

Le Coz, C.J. 2001. Allergic Contact Dermatitis from Sodium Pyrithione in Metalworking Fluid. 

Contact dermatitis. Volume 45, pages 58-59.

Tosti, A.; Piraccini, B.; and Brasile, G.P. 1990. Occupational Contact Dermatitis due to Sodium 

Pyrithione. Contact Dermatitis. Volume 22, pages 118-119

US EPA, 1996. Reregistration Eligibility Decision (RED) for Sodium Omadine, January 1996,

http://www.epa.gov/pesticides/reregistration/status.htm

US EPA, 1999. Zinc 2-pyridinethiol-1-oxide (Zinc Omadine): Assessment of New Use. 

D249404, February 16, 1999.
Page 15 of 18

Appendix A – Justification for the 

Studies Needed for the Human Health

Registration Review of Sodium Omadine
Page 16 of 18

Study Title: Indoor Exposure Dermal, Indoor Exposure Inhalation, Data Reporting and Calculations

Guideline Numbers: 875.1100, 875.1300, 875.1600

Rationale for Requiring the Data 

 

Dermal and inhalation exposures to sodium omadine are expected during the open pour additionA of 

liquids during materials preservation. Although dermal exposures were assessed in the RED, it will 

be necessary to reassess dermal exposures because some materials have application rates of up to 

5000 ppm which is much greater than the rate of 46 ppm that was assessed in the RED. It will also be 

necessary to assess inhalation exposures because these exposures were not assessed in the RED.

Dermal and inhalation exposures are also expected during the use of preserved products such as 

paints, metal working fluids and household surface cleaners. These exposures were not assessed in 

the RED because it was believed at the time that the exposures would be very low due to dilution. 

While it is true that the use rates are fairly low, the toxicological endpoints are also fairly low and 

therefore it will be necessary to assess these exposures during registration review.

Dermal and inhalation exposures from these scenarios are evident in exposure studies in the Pesticide 

Handlers Exposure Database (PHED). The existing Chemical Manufacturer Association (CMA) data 

base and PHED for these scenarios are limited in scope for QA/QC and the number of replicates (i.e., 

number of times a worker is monitored for a specific activity). EPA presented the need for additional 

handler exposure data to the January 2007 Science Advisory Panel (SAP) as well as to the April 2007 

Human Studies Review Board (HSRB) and both groups agreed that additional data are warranted. 

 

Practical Utility of the Data 

 

1) How would the data be used?

The data would be used to assess dermal and inhalation exposures that result from the open pour 

additionA of liquids during materials preservation and during the use of treated materials including 

paintsB

, metal working fluids and household surface cleanersB.

2) How could the data impact the Agency’s future decision making?

The exposure data would be used to assess the risks of exposure and to determine if mitigation 

measures, such as closed system loading, decreased application rates or use of PPE are needed to 

reduce these risks. If exposure data are not available, these assessments will have to be made using 

models which might lead to the overestimation of risk and the requirement for excessive and onerous 

mitigation measures.

A. If the labels are amended to require closed mixing/loading, the study for the open pour scenario can be waived.

B. There are proprietary studies that can be used as surrogate data for these exposure scenarios if data compensation 

issues are addressed
Page 17 of 18

Study Title: Surface Residue Dissipation

Guideline Numbers: 875.2300

Rationale for Requiring the Data 

 

Dermal and incidental oral exposures to sodium omadine are expected for toddlers who sit or play on 

household floors and carpets after they are cleaned with floor or carpet cleaners that are preserved 

with sodium omadine, during use of consumer goods such as clothing, towels and blankets made from 

textiles that are treated with spin finishes that are preserved with sodium omadine and during the use 

of consumer goods made from sodium omadine preserved leather. In addition, indirect dietary 

exposures to sodium omadine are expected during the use of dish detergents that are preserved with 

sodium omadine. Surface residue dissipation data are needed to accurately assess these exposures. 

These exposures were not assessed in the RED.

 

Practical Utility of the Data 

 

1) How would the data be used?

The surface residue data would be used to assess sodium omadine exposures that result from the use 

of floor and carpet cleaners preserved with sodium omadine, the use of clothing, towels and blankets 

made from textiles that are treated with spin finishes that are preserved with sodium omadine, the use 

of consumer goods made from sodium omadine preserved leather and the use of dish detergents 

preserved with sodium omadine. 

2) How could the data impact the Agency’s future decision making?

The surface residue data will be used during registration review to decide if the exposures to sodium 

omadine from it’s use in household cleaners, textiles, leathers and dish detergents generates a risk of 

concern that requires mitigation. This mitigation could include reduction of the application rate or 

elimination of the use. If surface residue data are not available, then the standard assumption of 100 

percent transferable surface residue will be used which might overestimate the risk and require 

excessive mitigation. 
Page 18 of 18

Study Title: Product Use Information

Guideline Numbers: 875.1700

Rationale for Requiring the Data 

 

Product use information serves as the basis for determining what exposure scenarios should be 

assessed and what assumptions and exposure data are needed to perform these assessments in a 

manner that does not over- or underestimate the actual risk.

 

Practical Utility of the Data 

 

1) How would the data be used?

The product use information will be used to define and characterize the exposure scenarios that will be 

assessed in the risk assessment.

2) How could the data impact the Agency’s future decision making?

A complete description of product use would ensure that the risk assessment is inclusive of the types 

of exposures occurring during and after use and that these exposures are accurately assessed. 

Without product use information the Agency will have to use default assumptions that might overestimate the actual risk.