UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

WASHINGTON, D.C. 20460

OFFICE OF 

PREVENTION, PESTICIDES

AND TOXIC SUBSTANCES

January 26, 2006

MEMORANDUM

SUBJECT: Revised Inorganic Chlorates. HED Chapter of the Reregistration Eligibility

Decision Document (RED). Case #: 4049 DP Barcode: D303550

PC Codes: Sodium chlorate: 073301 (active) and 873301 (inert)

Calcium chlorate: 073302 (active) and 875606 (inert)

Potassium chlorate: 073303 (active) and 900583 (inert)

Magnesium chlorate: 530200 (active)

Regulatory Action: Phase 1 Reregistration Action

Risk Assessment Type: Multiple Chemicals/Aggregate

FROM: Susan V. Hummel, Branch Senior Scientist

Reregistration Branch 4

Health Effects Division (7509C)

THROUGH: Raymond Kent, Branch Chief

Reregistration Branch 4

Health Effects Division (7509C)

TO: Jacqueline Guerry, Chemical Review Manager

Reregistration Branch 3

Special Review and Reregistration Division (7508C)

This document provides a summary of the findings from the data evaluation and the subsequent assessment

of human health risk resulting from the uses of Inorganic Chlorates. The hazard characterization was

completed by Abdallah Khasawinah (HED/RRB4); the occupational and residential exposure assessment

was completed by Matthew Crowley (HED/RRB4); the residue chemistry data evaluation and dietary

(food) exposure estimates for the dietary risk assessment were completed by Bonnie Cropp-Kohlligian

(HED/RRB4); the dietary risk assessment analysis was completed by Thurston Morton (HED/RRB4); the

incident report was completed by Jerome Blondell (HED/CEB); the environmental fate characterization for

chlorate residues resulting from terrestrial food/feed uses was completed by Silvia Termes (EFED); the risk

assessment was compiled by Susan Hummel (HED/RRB4). The drinking water exposure characterization

and exposure estimate calculations for chlorate residues as a byproduct of the disinfection of drinking water

for the dietary (water) risk assessment analysis were provided by Patricia Fair of the Office of Ground

Water and Drinking Water Technical Support Center.
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Table of Contents

1.0 Executive Summary ...................................................1

2.0 Ingredient Profile . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

2.1 Summary of Registered/Proposed Uses of the Active Ingredient Sodium Chlorate

(073301) Under Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

2.2 Summary of Registered Conventional Uses of the Inert Ingredients Sodium

Chlorate (873301) and Potassium Chlorate (900583) Under Discussion . . . . . . 15

2.3 Summary of Uses of the Inert Ingredients Sodium Chlorate (873301) and Calcium

Chlorate (875606) in Antimicrobial Agents Under Discussion Due to Dietary

Concerns Only . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

2.4 Chemical Formula and Nomenclature . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16

2.5 Physical and Chemical Properties . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

3.0 Metabolism Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

3.1 Comparative Metabolic Profile . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

3.2 Nature of the Residue in Foods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

3.2.1 Description of Primary Crop Metabolism . . . . . . . . . . . . . . . . . . . . . . . 17

3.2.2 Description of Livestock Metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . 18

3.2.3 Description of Rotational Crop Metabolism . . . . . . . . . . . . . . . . . . . . . 18

3.3 Environmental Degradation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

4.0 Hazard Characterization/Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

4.1 Hazard Characterization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

4.1.1 Database Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

4.1.1.1 Studies available and considered (animal, human, general

literature) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

4.1.1.2 Mode of action, metabolism and toxicokinetic data . . . . 19

4.1.1.3 Sufficiency of studies/data . . . . . . . . . . . . . . . . . . . . . . . 19

4.1.2 Toxicological Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

4.1.3 Dose-response . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

4.2 FQPA Hazard Considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

4.2.1 Adequacy of the Toxicity Data Base . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

4.2.2 Evidence of Neurotoxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

4.2.3 Developmental Toxicity Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

4.2.4 Reproductive Toxicity Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

4.2.5 Additional Information from Literature Sources . . . . . . . . . . . . . . . . . . 34

4.2.6 Pre-and/or Postnatal Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34

4.2.6.1 Determination of Susceptibility . . . . . . . . . . . . . . . . . . . 34

4.2.6.2 Degree of Concern Analysis and Residual Uncertainties for

Pre and/or Post-natal Susceptibility . . . . . . . . . . . . . . . . 34
iii

4.3 Safety Factor for Infants and Children . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34

4.4 Hazard Identification and Toxicity Endpoint Selection . . . . . . . . . . . . . . . . . . . 35

4.4.1 Acute Reference Dose (aRfD) - Females age 13-49 . . . . . . . . . . . . . . . . 35

4.4.2 Acute Reference Dose (aRfD) - General Population . . . . . . . . . . . . . . . 35

4.4.3 Chronic Reference Dose (cRfD) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

4.4.4 Incidental Oral Exposure (Short and Intermediate Term) . . . . . . . . . . . . 37

4.4.5 Dermal Absorption . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

4.4.6 Dermal Exposure (Short, Intermediate and Long Term) . . . . . . . . . . . . 38

4.4.7 Inhalation Exposure (Short and Intermediate Term) . . . . . . . . . . . . . . . 38

4.4.8 Margins of Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

4.4.9 Recommendation for Aggregate Exposure Risk Assessments . . . . . . . . 38

4.4.10 Classification of Carcinogenic Potential . . . . . . . . . . . . . . . . . . . . . . . . . 38

4.5 Endocrine disruption . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

5.0 Public Health Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

5.1 Incident Reports . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

5.2 Other . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

6.0 Exposure Characterization/Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

6.1 Dietary Exposure/Risk Pathway . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

6.1.1 Residue Profile . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

6.1.2 Chronic (non-cancer) Dietary (food only) Exposure and Risk . . . . . . . . 50

6.1.3 Cancer Dietary (food only) Exposure and Risk . . . . . . . . . . . . . . . . . . . 50

6.2 Water Exposure/Risk Pathway . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52

6.2.1 Environmental Fate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50

6.2.2 Drinking Water . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50

6.2.2.1 Sources and Control of Chlorate Ion . . . . . . . . . . . . . . . 50

6.2.2.2 Chlorate Ion Occurrence Data . . . . . . . . . . . . . . . . . . . . 50

6.2.2.3 Chronic Exposure to Chlorate Ion . . . . . . . . . . . . . . . . . 50

6.2.2.4 Estimated Concentrations for Chlorate Ion Deemed

Appropriate for Inclusion in the Dietary Risk Assessment(s)50

6.3 Residential (Non-Occupational) Exposure/Risk Pathway - Conventional Pesticides57

6.3.1 Home Uses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57

6.3.1.1 Sodium Chlorate (073301) as an active ingredient in

conventional pesticide products - Short-Term Residential

Handler Exposure via Inhalation Route only . . . . . . . . . 57

6.3.1.2 Sodium Chlorate (873301) as an inert ingredient in

conventional pesticide products - Short-Term Residential

Postapplication Exposure via Incidental Oral Route only 60

6.3.2 Recreational Uses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61

6.3.3 Other (Spray Drift, etc.) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61

7.0 Aggregate Risk Assessments and Risk Characterization . . . . . . . . . . . . . . . . . . . . . 62
iv

7.1 Short-Term Aggregate Risk - Residential Handler via Inhalation plus background

(chronic dietary (food + water)) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62

7.2 Chronic (non-cancer) Dietary Risk - Food + Water . . . . . . . . . . . . . . . . . . . . . . 62

7.3 Cancer Dietary Risk - Food + Water . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62

8.0 Cumulative Risk Characterization/Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

9.0 Occupational Exposure/Risk Pathway - Conventional Pesticide Products Only . . 63

9.1 Short/Intermediate/Long-Term Handler Risk . . . . . . . . . . . . . . . . . . . . . . . . . . 63

9.1.1 Sodium chlorate (073301) as the active ingredient in conventional pesticide

products - Short-/Intermediate-Term Occupational Handler Exposure via

Inhalation Route only . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

9.1.2 Sodium chlorate (873301) as an inert ingredient in conventional pesticide

products - Short-/Intermediate-Term Occupational Handler Exposure via

Inhalation Route only . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69

9.1.3 Potassium chlorate (900583) as an inert ingredient in conventional

pesticide products - Short-/Intermediate-Term Occupational Handler

Exposure via Inhalation Route only . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71

9.2 Short/Intermediate/Long-Term Postapplication Risk . . . . . . . . . . . . . . . . . . . . . 72

10.0 Data Needs and Label Requirements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72

10.1 Toxicology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72

10.2 Residue Chemistry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72

10.3 Occupational and Residential Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72

References: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 72

Appendix A Toxicology Data Requirements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 74

Appendix B Toxicology Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75

Appendix C Residue Chemistry Considerations for Sodium Chlorate (073301) as an active

ingredient in conventional (agricultural) pesticides . . . . . . . . . . . . . . . . . . . 95

Appendix D Tolerance Reassessment Summary For Inorganic Chlorates as active or inert

ingredients in conventional (agricultural) pesticides . . . . . . . . . . . . . . . . . 118

Appendix E Chlorate (ClO3b) Dietary Exposure Estimates in Food . . . . . . . . . . . . . . . 121
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1.0 Executive Summary

A Human Health Risk Assessment is being conducted for Inorganic Chlorates (List D

Reregistration Case #4049). Of the inorganic chlorates listed as active ingredients in Office of

Pesticide Programs Information Network (i.e., sodium chlorate (073301), calcium chlorate

(073302), potassium chlorate (073303), and magnesium chlorate (530200)), only sodium chlorate

(073301) is present as an active ingredient in currently registered products. Sodium chlorate

(873301), calcium chlorate (875606), and potassium chlorate (900583) are present as inert

ingredients in currently registered products and will also be addressed in this risk assessment.

Chlorates are strong oxidizers used in the manufacture of dyes, explosives, matches, printing

fabric, paper pulp processing, agricultural desiccant/defoliant, weed killers, and as a weak

antiseptic, 2-3% solutions have been used in mouth washes (OEHHA, 2002). The primary

pesticidal use for sodium chlorate (073301) is as an agricultural defoliant/desiccant, primarily on

cotton, however it is also applied to a wide variety of other agricultural crops. Sodium chlorate is

also used as a precursor for chlorine dioxide generation, through a closed system, to bleach wood

pulp/paper. Only a small percentage (less than 2 percent) is used in water systems as a precursor

to chlorine dioxide generation or as a defoliant/desiccant on a number of crops to aid harvest. As

inert ingredients, sodium chlorate (873301) and potassium chlorate (900583) are present in

conventional (agricultural) pesticides used on food crops or in poultry premises. Also, as inert

ingredients, sodium chlorate (873301) and calcium chlorate (875606) are present in antimicrobial

agents used: (1) as fruit, vegetable, and egg sanitizing washes; (2) to control bacterial blotch on

mushrooms; (3) as treatment to seed used for sprouting; (4) for conditioning live oysters; (5) in

poultry drinking water; (6) in fish filleting; (7) pecan cracking/dyeing.

Understanding that sodium chlorate and sodium chlorite have common uses such as use in water

systems as precursors in chlorine dioxide generation and the potential for interconversion of

chlorate and chlorite anions in water, the environment and animals, Chemical Review Managers

(CRMs) in the Special Review and Reregistration Division (SRRD) responsible for completing the

Inorganic Chlorates Reregistration Eligibility Decision (List D Reregistration Case# 4049) and

those in the Antimicrobial Division (AD) responsible for completing the Chlorine Dioxide and

Sodium Chlorite Reregistration Eligibility Decision (List D Reregistration Case# 4023) developed

a plan to coordinate the two reregistration cases. Through a series of negotiations, it was agreed

that with regards to the Inorganic Chlorates Risk Assessments that: (1) the Inorganic Chlorates

Risk Assessments will consider residues of chlorate only; (2) the scope of the Health Effects

Division (HED) Occupational and Residential Risk Assessments will be limited to considerations

of the conventional (agricultural) uses of inorganic chlorates only; and (3) AD will address the

Occupational and Residential Assessment for the antimicrobial uses of the inorganic chlorates

using toxicological endpoints selected by HED.

We note that AD has completed an Occupational and Residential Risk Assessment for the

antimicrobial uses of the inorganic chlorates under separate cover (D312200, T. Leighton,

01/24/2005) using the appropriate toxicological endpoints selected by HED. There are no
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residential exposures associated with these uses. HED will not discuss this topic further herein

except to note that no risks above the Agency’s level of concern were identified.

We note that tolerances and/or exemptions from the requirement of a tolerance for inorganic

chlorates as active or inert ingredients in antimicrobial agents is not the purview of HED and

should be addressed by AD. HED will not discuss this topic further.

We note that since Inorganic Chlorates is a List D reregistration case, the Product Chemistry

Chapter for the Inorganic Chlorates Reregistration Eligibility Decision (RED) is the responsibility

of the Antimicrobials Division. HED will not discuss this topic in detail.

Hazard Profile

The database for the inorganic chlorates is substantially complete in terms of endpoint studies and

dose response information to characterize any potential for prenatal or postnatal risk for infants

and children. No additional FQPA or database factor is required. A 28-Day Inhalation study is

required to fulfill Guideline 870.3465.

Sodium chlorate is a thyroid toxicant producing thyroid gland follicular cell hypertrophy in rats

and mice following chronic exposures and some evidence of follicular cell tumors in rats. The

primary target of chlorate acute toxicity is rupture of red blood cell membranes with intravascular

hemolysis and the irreversible oxidation of hemoglobin to methemoglobin. Potassium chlorate has

produced renal tubular necrosis in animals. Metabolism studies in rats and dogs have shown that

chlorates are readily absorbed by the gastrointestinal tract and are excreted in the urine primarily

as chlorate (ClO3b; ca. 13% of the administered dose), chlorite (ClO2b; ca. 4% of the

administered dose), and chloride (Clb; ca. 20% of the administered dose). Using 36Cl-potassium

chlorate, peak blood concentration levels were reached after an hour of ingestion by rats. 

Elimination of the labeled chlorate from the blood was biphasic with half-lives of 6 and 36.5

hours.

In acute toxicity tests, sodium chlorate is slightly toxic by the oral (Toxicity Category IV), dermal

(Toxicity Category IV), and inhalation routes (Toxicity Category IV of a 33% aerosol). Sodium

chlorate crystals were mildly irritating to the rabbit eye (Toxicity Category III for the dry crystals

or moistened crystals), and minimal to mild dermal irritant (Toxicity Category III for the

moistened material and Toxicity Category IV for the dry crystal). Ingestion of toxic doses of

sodium chlorate by humans produce gastritis, hemolysis, methemoglobinemia, hemoglobinurea,

late toxic nephritis, and acute renal failure. Doses in excess of 100 mg/kg are generally fatal to

humans.

There are conflicting findings regarding the subchronic/chronic toxicity of sodium chlorate. In

one series of studies, rats exposed to relatively low concentrations of sodium chlorate (equivalent

to1.5 or 15 mg/kg/day) for up to 11 months exhibited decreased blood glutathione, increased

fragility of erythrocytes, inhibition of incorporation of tritiated thymidine into nuclei in rat testes,
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decreased RBC count and hematocrit and decreased body weight. In another study, exposure of

male F344 rats to 1% sodium or potassium chlorate in drinking water (654-686 mg/kg/day) for 25

weeks, the only effect reported was significant body weight reduction. Relative kidney weights

were significantly increased in potassium chlorate treated rats. Rats orally administered 10-1000

mg/kg/day sodium chlorate for 90 days did not exhibit histological or clinical chemistry treatmentrelated effects, but had lower red blood cell counts, hematocrit and hemoglobin levels, particularly

in the females. The adrenal weight was also depressed in males and females at the 1000

mg/kg/day level. In another published study in which rats were administered sodium chlorate in

the drinking water at concentrations equivalent to 512 and 800 mg/kg/day for males and females,

respectively for 90 days, final body weights were significantly lower in both sexes with some

relative organ weight changes including the adrenal glands and reduction in RBC counts and

percent hemoglobin, and prominent pituitary gland vacuolization and thyroid gland colloid

depletion in both sexes. The thyroid effects were confirmed in a recent study in rats where

subchronic treatment for 21 or 90 days with sodium chlorate in the drinking water at

concentrations up to 2,000 mg/L (225 mg/kg/day) induced a concentration dependent increase in

the incidence and severity of thyroid follicular cellular hyperplasia. Colloid depletion and

hypertrophy were the most sensitive histopathological indicators of sodium chlorate exposure,

with male rats more susceptible than females rats. Decreases in serum hormone levels

triiodothyronine (T3) and thyroxine (T4) were also reported following exposure to sodium

chlorate. Mice were less susceptible to the adverse effect from exposure to high levels of sodium

chlorate. In a subchronic exposure study in primates where sodium chlorate was administered in

drinking water for 8 weeks at 400 mg/L (58.4±27.6 mg/kg/day) to 6 male and 7 female adult

African Green Monkeys (Cercopithecus aethiops) there was no effect on the thyroid function and

the total thyroxine levels. In dogs, the only reported treatment related effect following subchronic

administration of sodium chlorate up to 360 mg/kg/day was emesis.

A 2-year bioassay to determine the potential of sodium chlorate to induce thyroid tumors in

laboratory animals (rats and mice) has been recently reported (DRAFT NTP Report 2004). In

these tests, there was some evidence of thyroid gland follicular cell carcinogenicity in male rats

which may be attributed to the imbalance of thyroid hormones (reduced T3 and T4 and elevated

TSH) seen in these studies as a result of exposure to sodium chlorate. Current EPA HED policy

states that “nonmutagenic pesticides that induce elevated levels of TSH and thyroid follicular cell

tumors in the rat should be classified as not likely to be carcinogenic to humans at doses that

do not alter thyroid hormone homeostasis” (Assessment of Thyroid Follicular Cell Tumors;

USEPA March 1998 EPA/630/R-97/002). In female mice there was equivocal and marginal

evidence of increased pancreatic islet carcinoma.

Sodium chlorate was negative in most bacterial gene mutation assays. In one assay, it showed

positive effect in the TA1535 strain in the presence of metabolic activation. It also caused DNA

damage in repair deficient E. coli strains at concentrations above 1000 ug/mL in the presence of

metabolic activation but was negative in the unscheduled DNA synthesis assay. In cytogenetics

tests, sodium chlorate was negative in the in vitro cell gene mutation assay, mammalian
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erythrocyte micronucleus assay, bone marrow cytogenetics assay and sperm head abnormality

assay.

Sodium chlorate did not cause developmental effects in rats tested at doses up to 1000 mg/kg/day

or in rabbits tested at doses up to 500 mg/kg/day. In a two generation reproductive toxicity study

in the rat, postnatal toxicity did not exceed parental toxicity. Sodium chlorate has not been

evaluated for neurotoxic effects, but acute and subchronic toxicity studies did not indicate a

neurotoxic potential. 

There are no repeated dermal toxicity or dermal absorption data available for sodium chlorate.

Based on its high water solubility and ionic nature, potential sodium chlorate (or any other

inorganic chlorate) absorption by the intact skin is considered negligible.

No increase in prenatal susceptibility of rats or rabbits was seen in developmental studies with

chlorate. No pre- or post-natal susceptibility was observed in a reproduction study in the rat.

Note: Lubbers et al (1984a, 1984b) conducted a series of studies with human volunteers which

was evaluated; however, due to the limitations of these studies, the data were not deemed useful

for dose-response evaluation and were not relied upon in the risk assessment.

Exposure and Aggregate Risk Assessment

Residue Chemistry

The residue chemistry database is not complete. New ruminant and poultry feeding studies are

required to fulfill Guideline 860.1480. These data are considered important to the risk assessment

and are needed to refine the meat/milk/poultry/egg exposure estimates in the dietary risk

assessment. Also reference standards must be submitted to the Pesticide Repository to fulfill

Guideline 860.1650.

No plant metabolism data have been submitted in support of the reregistration of sodium chlorate;

however, no new plant metabolism data are required to support the established sodium chlorate

exemptions from the requirement of a tolerance. Based on available published information

(Loomis et al., J. Am. Soc. Agron.; 25, 724 (1933)), sodium chlorate is highly soluble in water

and is expected to readily absorb and translocate throughout plants. However, given the

proposed use conditions, the means of translocation in treated plants may be substantially

disrupted. Translocation of very small amounts of chlorate ion (ClO3b) by plants (translocation of

significant amounts would be phytotoxic to plants) from the environment which may be present as

a result of inorganic chlorate pesticide uses may occur. Terminal residues are expected to be

primarily surface residues.

Since sodium chlorate is a strong oxidizing agent, depending on environmental factors, it is

expected to be easily reduced to chloride and possibly chlorite in plants. Total redox conversion
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to these reduced species is not expected; hence, the terminal residues of sodium chlorate in/on

plants are likely chlorate (ClO3b), chlorite (ClO2b), and chloride (Clb). By agreement within

OPP, the residue of concern is the chlorate anion.

No ruminant, swine, or poultry metabolism or feeding data have been submitted in support of the

reregistration of sodium chlorate; however, no new animal metabolism data are required to

support the established sodium chlorate exemptions from the requirement of a tolerance. Based

on published rat metabolism data (Abdel-Rahman et al, 1982, 1984b and 1985), terminal residues

of sodium chlorate in animal tissues are expected to be chlorate (ClO3b), chlorite (ClO2b), and

chloride (Clb). Chlorate is readily absorbed from the digestive tract and is excreted as chlorate,

chlorite, and chloride in urine primarily and feces. Within 72 hours, about 40% of the

administered dose was excreted in the urine as chlorate (ca. 13%), chlorite (ca. 4%), and chloride

(ca. 20%) and about 2-4% was excreted in the feces in the same time period. Less than 1% of the

administered dose was found in any of the tissues analyzed including kidney, liver, and skin. By

agreement within OPP, the residue of concern is the chlorate anion.

Although some previous residue chemistry reviews for specific exemptions from the requirement

of a tolerance have concluded that there is no reasonable expectation of transfer of residues to

meat, milk, poultry or eggs in specific cases, re-evaluation of the available crop field trial data

taken as a whole, indicate that there is the possibility of detectable residues of sodium chlorate on

animal feedstuffs at harvest. Hence, secondary residues of concern in meat, milk, poultry, and

eggs are possible and; therefore, new ruminant and poultry feeding data are hereby required to

support the reregistration of sodium chlorate. These data are considered confirmatory.

The analytical method used to support the established exemptions from the requirement of a

tolerance is a non-specific colorimetric method (Branderis, J. Sci. Food Agric., 16, 558 (1965)),

deemed acceptable for data collection. The method was originally developed to estimate residual

chlorate concentrations in soil and as a rapid diagnostic test for chlorate toxicity in plants. 

Briefly, the method involves acid extraction, clean-up by shaking with activated charcoal, and

filtration. A solution of ortho-toluidine in HCl is then added to the concentrated extract and the

resulting color is measured at 448 nm for low concentrations and at 490 nm for higher

concentrations of dye. The method is not specific for chlorate since it measures any oxidizing

agent capable of oxidizing chloride ion to free chlorine. A standard curve is prepared with sodium

chlorate for comparison. The lowest limit of quantitation of the method is estimated at 1 ppm

based on available fortification data from field trials. Chloride does not interfere with the method

but residues of chlorite, which might be present, may also be detected with this method. This

method is hereby deemed adequate for enforcement of sodium chlorate exemptions from the

requirement of a tolerance. A more selective HPLC method (“Determination of Residues of

Sodium Chlorate in Potatoes”, Method #S57023, 4/2/91) is available for the detection of sodium

chlorate residues in or on raw agricultural commodities (RACs). 

Only crop field trial data have been submitted to support the reregistration of sodium chlorate. 

No storage stability or processing data are available. The available crop field trial data have been
Page 6 of 141

re-evaluated herein. No additional plant magnitude of the residue or storage stability data are

required to support the reregistration of sodium chlorate.

Exemptions from the requirement of tolerances are appropriate for sodium chlorate when used as

defoliant or desiccant on beans (dry), corn, cotton, cowpeas, flax, guar, peppers (non-bell),

potatoes, rice, safflower, sorghum (grain), soybeans, sunflower, and wheat since no enforcement

action can be anticipated given the extremely low levels of chlorate expected in food commodities

(most of the residues are on the surface), limitations of the enforcement method, and possible

interconversion between chlorate and chlorite in the environment making misuse determinations

difficult.

Sodium chlorate exemptions under 40 CFR 180.1020(a) from the requirement of a tolerance

should be amended as follows to (1) specify defoliant and desiccant use only, (2) specify use on

crops rather than raw agricultural commodities, (3) and include wheat:

40 CFR 180.1020(a) Sodium chlorate is exempt from the requirement of a tolerance for residues

when used as a defoliant or desiccant in accordance with good agricultural practice on the

following crops: Bean (dry), Corn, Cotton, Cowpea, Flax, Guar, Pepper (non-bell), Potato, Rice,

Safflower, Sorghum (grain), Soybean, Sunflower, and Wheat.

Exemptions from the requirement of a tolerance are needed for sodium chlorate (873301) and

potassium chlorate (900583) as inert ingredients in conventional pesticides under 40 CFR 180.920

and 40 CFR 180.930, respectively.

Environmental Fate

Sodium chlorate is used as a desiccant/defoliant because it is a strong oxidizer. As a strong

oxidizing agent, chlorate (ClO3b, oxidation state V) gets reduced to chlorine species in lower

oxidation states, such as the oxyanions chlorite (ClO2b, oxidation state III) and hypochlorite 

(ClOb, oxidation state I), chlorine dioxide (oxidation state IV), and chloride (oxidation state -I).

Thus, at least some and possibly substantial reduction of the applied chlorate is likely to occur in

the field prior to any runoff to surface water. Under environmental (terrestrial field) redox

conditions and based on chemical equilibria alone, the thermodynamically favored, end reduction

product of chlorate in soil and in water is the chloride anion. Any intermediate chlorine dioxide

that may form under environmental conditions will undergo photochemical reactions when

exposed to sunlight. The chlorine oxyanions chlorite and hypochlorite (other possible more

reduced intermediates in the ultimate reduction of chlorate to chloride) are strong oxidizers in

themselves and thus, they are also reduced and/or undergo disproportionation reactions. Although

reduction reactions of chlorate, chlorite, and hypochlorite are said to occur “very fast”, how fast

they occur is not known (i.e., the actual rate constants in the environment are not known).

Therefore, at any given time the distribution of reduced species (type and concentration) cannot

be estimated. However, it is unlikely that a single reduced species would be present. 

Dietary - Food Only
Page 7 of 141

Dietary exposure (food only) to inorganic chlorates as the chlorate ion (ClO3b) may be expected

from the following dietary exposure routes: (1) from sodium chlorate (073301) as an active

ingredient in conventional (agricultural) pesticides used on food crops; (2) from sodium chlorate

(873301) and potassium chlorate (900583) as inert ingredients in conventional pesticides used on

food crops or in poultry premises; (3) from secondary residues in meat/milk/poultry/eggs due to

residues on animal feedstuffs; (4) from sodium chlorate (873301) and calcium chlorate (875606)

as inert ingredients in antimicrobial agents used as fruit, vegetable, and egg sanitizing washes, on

mushrooms to control bacterial blotch, as treatments to seed used for sprouting, for conditioning

live oysters, in poultry drinking water, in fish filleting, and in pecan cracking/dyeing; (5) as a

potential redox of chlorine dioxide and sodium chlorite in conventional and antimicrobial

pesticides; (6) from degradation of hypochlorites in antimicrobial agents used as fruit and

vegetable washes; and, (7) from translocation of very small amounts of chlorate ion (ClO3b) by

plants (translocation of significant amounts would be phytotoxic to plants) from the environment

which may be present as a result of inorganic chlorate pesticide uses.

A chronic Population Adjusted Dose (cPAD) of 0.03 mg chlorate/kg/day was used in the chronic

(non-cancer and cancer) dietary risk assessment based on a chronic rat study (DRAFT NTP

Report 2004) with sodium chlorate which found increased thyroid gland follicular cell

hypertrophy and follicular cell mineralization. A NOAEL was not identified in this study. 

Therefore, a bench mark dose (BMD) analysis was performed. Using the BMDL as an

approximation of the NOAEL (0.9 mg chlorate/kg/day) and an uncertainty factor of 30x (3x for

interspecies extrapolation and 10x for intraspecies extrapolation), the cPAD was calculated at

0.03 mg chlorate/kg/day.

In the same chronic study (DRAFT NTP Report 2004) there was some evidence of thyroid gland

follicular cell carcinogenicity in male rats which may be attributed to changes of thyroid hormones

(reduced T3 and T4 and elevated TSH) as a result of exposure to high doses of sodium chlorate. 

Current EPA HED policy states that “nonmutagenic pesticides that induce elevated levels of TSH

and thyroid follicular cell tumors in the rat should be classified as not likely to be carcinogenic

to humans at doses that do not alter thyroid hormone homeostasis” (Assessment of Thyroid

Follicular Cell Tumors; USEPA March 1998 EPA/630/R-97/002). In female mice there was

equivocal and marginal evidence of increased pancreatic islet carcinoma. Therefore, a cancer

dietary risk assessment was conducted using an MOE approach and the BMDL as an

approximation of the NOAEL (0.9 mg chlorate/kg/day). The level of concern for the Margin of

Exposure was 30. (The cancer risk assessment is the same as the chronic (non-cancer) risk

assessment for the U. S. General Population.)

A chronic (non-cancer and cancer) dietary risk assessment for food only were conducted using the

Dietary Exposure Evaluation Model-FCIDTM software with the Food Commodity Intake

Database (DEEM-FCIDTM Version 2.03) and food and water consumption data from the United

States Department of Agriculture’s (USDA’s) Continuing Surveys of Food Intakes by Individuals

(CSFII) from 1994-1996 and 1998. No food monitoring data are available for this risk

assessment; only limited, chemical-specific field trial data are available. Exposure estimates in
Page 8 of 141

food were based on field trial data or, in the case of fruit/vegetable/other washes, was derived

from a film thickness model. No chemical-specific livestock metabolism or feeding data are

available; exposure estimates in meat, milk, poultry, and eggs were derived from rat metabolism

data, field trial data, and livestock reference information concerning feed consumption, tissue

weights, and milk production. In some cases, due to raw data limitations, food exposure

estimates are calculated as sodium chlorate. Default concentration factors (no chemical-specific

processing data are available), percent crop treated data, and the effects of washing after foliar

treatments were also incorporated into the risk assessments.

The chronic (non-cancer and cancer) dietary risk assessment for food only is below the Agency’s

level of concern for the General U.S. Population and all subgroups. The highest exposed

population subgroup, Children 1-2 years of age, was 28% of the chronic Population Adjusted

Dose (cPAD).

Dietary - Drinking Water Only

Levels of chlorate ion (ClO3b) found in finished drinking water are more likely a consequence of

drinking water treatment with chlorine dioxide or hypochlorite than from possible source water

contamination due to inorganic chlorate pesticide uses and/or discharge from pulp mills which use

inorganic chlorates in their bleaching process. Chlorate ion (ClO3b) is a disinfection by-product

(DBP) of water treatment which can be formed during the on-site generation of chlorine dioxide

(ClO2), the decomposition of chlorine dioxide in the water treatment system, the decomposition of

hypochlorite feedstock during storage, and the interaction of chlorite ion and free chlorine. 

Chlorate ion (ClO3b) may also be present in drinking water resulting from the use of sodium

chlorate (073301) in water systems as a precursor to chlorine dioxide generation due to

incomplete reaction of sodium chlorate in the formation of chlorine dioxide resulting in unreacted

chlorate ion in the chlorine dioxide feed stream.

Data are available concerning the levels of chlorate ion (ClO3b) found in finished drinking water

collected from water treatment facilities which use chlorine dioxide or hypochlorite to treat

drinking water. No data are available concerning the levels of chlorate ion (ClO3b) in finished

drinking water collected from the small number of water treatment facilities which use sodium

chlorate as a precursor for chlorine dioxide generation, through a closed system, to treat drinking

water. 

While EPA Office of Ground Water and Drinking Water (OGWDW) has not established a

Maximum Contamination Level (MCL) for chlorate, data concerning the occurrence of chlorate

ion (ClO3b) in drinking water have been collected under the Information Collection Rule (ICR). 

Under the ICR, large water treatment systems (those serving more than 100,000 customers) that

use chlorine dioxide or hypochlorite for disinfection were required to monitor levels of chlorate

over an 18-month period. Data were collected from 66 water treatment systems (90 water

treatment plants) which use chlorine dioxide or hypochlorite for disinfection. Data from these

systems are presented separately and combined in Table 6.2.2.2.1. Concentrations of chlorate ion

(ClO3b) in finished water from these treatment facilities ranged from <0.020 mg/L to 2.2 mg/L. 
Page 9 of 141

The average concentrations of chlorate ion (ClO3b) in the distribution systems from these

treatment facilities ranged from <0.020 mg/L to 0.69 mg/L; the 90th Percentile was 0.24 mg/L and

the median was 0.11 mg/L.

The American Water Works Association Research Foundation (AwwaRF (1995)) sponsored a

project to study how water systems could minimize ClO3b formation in the hypochlorite solutions

they use for disinfection. As part of the data gathering effort, they obtained information from 185

water treatment systems concerning their use of hypochlorite solutions. Samples of source water,

hypochlorite solution, and finished drinking water from 111 of the water systems were analyzed

for ClO3b. Only one set of samples was collected for each system. Concentrations of chlorate

ion (ClO3b) in finished water from these treatment facilities ranged from <0.010 mg/L to 9.2

mg/L (ca. 9 mg/L); the 90th Percentile was 1.160 mg/L (ca. 1.2 mg/L) and the median was 0.161

mg/L (ca. 0.2 mg/L).

Based on the available occurrence data (essentially at the tap) from the ICR AUX1 Database

(USEPA, 2000d) and the AwwaRF (1995) study, the following estimated concentrations of

chlorate ion (ClO3b) in drinking water are deemed appropriate for inclusion in the dietary risk

assessments for inorganic chlorates:

• The highest annual average concentration of chlorate ion (ClO3b) in drinking water is

estimated at 0.69 mg/L and is based on the ICR AUX1 Database (USEPA, 2000d). 

• The 90th percentile average concentration of chlorate ion (ClO3b) in drinking water is

estimated at 0.24 mg/L and is based on the ICR AUX1 Database (USEPA, 2000d). 

• The treated system average concentration of chlorate ion (ClO3b) in drinking water is

estimated at 0.11 mg/L and is based on the ICR AUX1 Database (USEPA, 2000d). 

Use of the ICR AUX1 database could underestimate concentrations in drinking water since higher

levels of chlorate ion (ClO3b) in drinking water were found at the small water treatment utilities

sampled in the AwwaRF (1995) project than at the large water treatment plants included in the

ICR AUX1 Database (USEPA, 2000d). However, the AwwaRF (1995) study is a less robust

data set consisting of only one sample per utility and, therefore, the ICR AUX1 Database

(USEPA, 2000d) was considered the more appropriate source for estimating averages from

individual water treatment plants.

Chronic (non-cancer and cancer) dietary (water only) risk assessments were conducted using the

Dietary Exposure Evaluation Model-FCIDTM software with the Food Commodity Intake

Database (DEEM-FCIDTM Version 2.03) and food and water consumption data from the United

States Department of Agriculture’s (USDA’s) Continuing Surveys of Food Intakes by Individuals

(CSFII) from 1994-1996 and 1998. Available ICR monitoring data essentially at the tap were

used to estimate chlorate concentrations in drinking water. Exposures were single point

estimates.
Page 10 of 141

The chronic (non-cancer) dietary (water only) risk assessment for chlorate in drinking water,

using the highest annual average concentration estimated at 0.69 mg/L, is below the Agency’s

level of concern for the General U.S. Population and all subgroups except all infants <1 year of

age. The highest exposed population subgroup, all infants <1 year of age, was 159% of the

chronic Population Adjusted Dose (cPAD). Using the 90th percentile annual average

concentration estimated at 0.24 mg/L, the chronic (non-cancer) dietary (water only) risk for all

infants <1 year of age was 55% of the cPAD and 25% of the cPAD using the median annual

average concentration estimated at 0.11 mg/L. 

No separate cancer dietary risk assessment for chlorate in drinking water was conducted. The

estimated cancer dietary risk for the General U.S. Population is based on the chronic (non-cancer)

dietary risk, and is below the Agency’s level of concern (i.e., % cPAD is less than the level of

concern of 100%). 

Residential Exposure

All residential (non-occupational) risk estimates for inorganic chlorates, as active or inert

ingredients in conventional pesticide products used in residential environments, are below the

Agency’s level of concern (i.e., Margin of Exposures are greater than the Level of Concern of

100). These uses are considered to be short-term only due to the episodic uses associated with

homeowner products. Since the episodic nature of residential exposure is inconsistent with the

mechanism of chlorate carcinogenicity, a residential cancer risk assessment was not conducted.

There is the potential for exposure to sodium chlorate by residential handlers in outdoor

residential settings during application of conventional pesticide products containing sodium

chlorate (073301) as the active ingredient. Sodium chlorate (073301) can be used as a nonselective herbicide in outdoor residential environments as a spot treatment/edging treatment to

driveway cracks and crevices, around foundations, and underneath and around wood decks as

required. Although there is the potential for dermal exposure, sodium chlorate is an inorganic

salt, therefore, significant absorption of sodium chlorate through intact skin is not expected.

There is the potential for postapplication exposure in outdoor residential settings from entering

areas previously treated by professional handlers with conventional pesticide products containing

sodium chlorate (873301) as an inert ingredient. Although there is the potential for dermal

exposure, sodium chlorate is an inorganic salt, therefore, significant absorption of sodium chlorate

through intact skin is not expected. Also, postapplication inhalation exposure for sodium chlorate

is not expected due to negligible vapor pressure.

Aggregate Risk

Evaluation of the hazard and exposure (food, water, and residential) components for inorganic

chlorates indicates the need to estimate potential risks for the following scenarios: short-term

inhalation, chronic (non-cancer) dietary (food + water), and cancer dietary (food + water).
Page 11 of 141

The short-term aggregate risks, from residential (non-occupational) exposures (including

background, chronic dietary (food + water)) are below the Agency’s level of concern for the

Margins of Exposure (i.e., Margin of Exposures are greater that the Level of Concern of 100).

The chronic (non-cancer) dietary (food + water) risk assessment, using the highest annual average

concentration estimated at 0.69 mg/L for drinking water, is below the Agency’s level of concern

for the General U.S. Population and all subgroups except all infants <1 year of age and Children

1-2 years. The highest exposed population subgroup, all infants <1 year of age, was 174% of the

chronic Population Adjusted Dose (cPAD). Using the 90th percentile annual average

concentration estimated at 0.24 mg/L, the chronic (non-cancer) dietary (food + water) risk for all

infants <1 year of age was 70% of the cPAD. As previously indicated, there is some concern that

the exposure estimates for water may be underestimates.

The cancer dietary (food + water) risk assessment is below the Agency’s level of concern and is

based on the chronic (non-cancer) dietary (food + water) risk assessment for the general

population. 

Occupational Exposure and Risk Assessment for Inorganic Chlorates in Conventional

Pesticides

With the addition of PPE (dust/mist respirator) or engineering controls (enclosed cockpits or

cabs), all occupational handler scenarios for the use of inorganic chlorates as an active or inert

ingredient in conventional pesticides are below the Agency’s level of concern (i.e., Margin of

Exposures are greater than the Level of Concern of 100). Exposure durations are short- and

intermediate-term only. Since the exposure durations for occupational handlers are inconsistent

with the mechanism of chlorate carcinogenicity, an occupational cancer risk assessment was not

conducted.

There is potential for occupational handler exposure to inorganic chlorates from: (1) the

application of sodium chlorate (073301) as the active ingredient in conventional pesticide

products used on both agricultural and commercial (non-agricultural) sites (i.e., mixer/loaders,

applicators, flaggers, and mixer/loader/applicators); (2) the application of sodium chlorate

(873301) as an inert ingredient in conventional pesticide products used on both agricultural and

commercial (non-agricultural) sites (i.e., mixer/loaders, applicators, flaggers, and

mixer/loader/applicators); and (3) the application of potassium chlorate (900583) as an inert

ingredient in conventional pesticide products used in poultry premises. Only the inhalation route

of exposure needs to be included in the occupational handler risk assessment.

There are no dermal toxicity or dermal absorption data available for inorganic chlorates. Although

the potential for dermal exposures exists for occupational handler, based on its high water

solubility and ionic nature, significant absorption of inorganic chlorates through intact skin is not

expected.
Page 12 of 141

Postapplication scenarios do not need to be included in the occupational risk assessment for

inorganic chlorates. Although dermal and inhalation exposures are possible, these exposures are

expected to be negligible due to the physical and chemical characteristics of inorganic chlorates. 

Significant absorption of inorganic chlorates through intact skin is not expected. Postapplication

inhalation exposure is not expected based on the negligible vapor pressure of sodium chlorate.
Page 13 of 141

2.0 Ingredient Profile

Sodium chlorate is a non-selective herbicide, considered phytotoxic to all green plant parts. 

Sodium chlorate is absorbed rapidly by the plant through both roots and leaves causing cell death. 

Its oxidizing action may disrupt normal respiratory functioning leading to a buildup to toxic

peroxides and greater production of ethylene which causes leaf abscission. It is 30-50 times more

toxic to plants than sodium chloride. It has a soil-sterilant effect.

Sodium chlorate has a salty taste and is palatable to livestock. Animals may feed on enough

freshly treated areas to become poisoned.

With respect to pesticidal uses, most sodium chlorate is used as an on-site precursor to chlorine

dioxide generation for wood pulp bleaching; other uses include herbicides and water treatment. It

is used as a defoliant and desiccant on a number of crops and as spot treatments on non-crop

areas to control weeds. Agricultural products are all formulated as soluble concentrates/liquids;

non-crop products are formulated as soluble concentrates/liquids and granules or pellets/tablets.

2.1 Summary of Registered/Proposed Conventional Uses of the Active Ingredient

Sodium Chlorate (073301) Under Discussion

Table 2.1.1. Summary of Food/Feed Agricultural Uses of Sodium Chlorate as a Defoliant/Desiccant

Applic. Timing,

Type, and

Equip.

Formulation Applic.

Rate

(lb ai/A)

Max. No.

Applic.

per

Season

Max. Seasonal

Applic. Rate

(lb ai/A)

PHI (days) PGI (days)

Dry Beans, Corn, Flax, Guar, Rice, Safflower, Sorghum, Southern Peas (i.e., Cowpeas), Soybeans, Sunflower

Preharvest

Spray

Aircraft/Ground

SC 7.5 1 7.5 14 (Corn)

7 (All others)

14

Cotton

Preharvest

Spray

Aircraft/Ground

SC 7.5 2 15 7 14

Wheat (Proposed Use Rate)

Preharvest

Spray

Aircraft/Ground

SC 6 1 6 3 ??

Chili peppers, Potatoes

Preharvest

Spray

Aircraft/Ground

SC 12.5 1 12.5 10 (Chili peppers)

7 (Potatoes)

14
Page 14 of 141

Table 2.1.2. Summary of Non Food/Feed Agricultural Uses of Sodium Chlorate as a Defoliant/Desiccant

Applic. Timing,

Type, and

Equip.

Formulation Applic.

Rate

(lb ai/A)

Max. No.

Applic.

per

Season

Max. Seasonal

Applic. Rate

(lb ai/A)

PHI (days) PGI (days)

Ornamental gourds, Cucurbits (grown for seed), Fallow land

Preharvest

Spray

Aircraft/Ground

SC 6 1 6

Table 2.1.3. Summary of Industrial and Other Non-Crop Uses of Sodium Chlorate as non-selective

Herbicide

Use Site Formulations Application Equipment Application Rates 1

(lbs ai/A 2)

Industrial/Non-Crop Sites: rightsof-way areas, building perimeters,

ditch banks, bleachers, airport

runways, vacant lots, fire hydrants,

or as a pre-paving treatment.

Soluble

concentrate/liquid

rights-of-way sprayer, handgun

sprayer, groundboom, lowpressure handwand

1032

523

132

Granular or

pellet/tablet

belly grinder, push-type

spreader, tractor-drawn

spreaders

523

240

161

1

 Application rates are presented as ranges to reflect different product labels.

2

 Although area treated on most product labels is expressed as lbs ai/ft2, application rates have been calculated by

the reviewer (M. Crowley HED/RRB4) as lbs ai/A consistent with the standard expression for application rates

used for calculation and comparison purposes. 

Table 2.1.4. Summary of Residential Uses of Sodium Chlorate as non-selective Herbicide

Use Site Formulations Application Equipment Application Rates

Spot treatment/edging treatment: 

driveway cracks and crevices,

around foundations, and

underneath and around wood

decks.

Not labeled for broadcast on

residential lawns or ornamentals.

Liquid RTU sprinkler can 0.27 lb ai/gallon

Liquid low-pressure handwand,

sprinkler can

23.7 lb ai/1000 ft2

Liquid trigger-pump sprayer 0.196 lb ai/gallon

Granular belly grinder, push-type

spreader, hand

12 lb ai/1000 ft2
Page 15 of 141

2.2 Summary of Registered Conventional Uses of the Inert Ingredients Sodium

Chlorate (873301) and Potassium Chlorate (900583) Under Discussion

Sodium chlorate (873301) as an inert ingredient in herbicide formulation products can be applied

professionally to agricultural (corn, guava, macadamia nuts, sorghum grain, sugarcane, wheat),

commercial (non-agricultural), and residential sites. These conventional pesticide products

contain < 1 % sodium chlorate and can be applied at rates no greater than 0.07 lb (as sodium

chlorate) per acre.

Potassium chlorate (900583) as an inert ingredient in airborne fungicide products can be applied

in poultry premises. These conventional pesticide products contain < 20% potassium chlorate and

can be applied at rates not greater than 0.01 lb ( as potassium chlorate) per 500 ft3.

2.3 Summary of Uses of the Inert Ingredients Sodium Chlorate (873301) and

Calcium Chlorate (875606) in Antimicrobial Agents Under Discussion Due to

Dietary Concerns Only

Sodium chlorate (873301) and calcium chlorate (875606) as inert ingredients in antimicrobial

products are used: (1) as fruit, vegetable, and egg sanitizing washes; (2) to control bacterial

blotch on mushrooms; (3) as treatment to seed used for sprouting; (4) for conditioning live

oysters; (5) in poultry drinking water; (6) in fish filleting; (7) pecan cracking/dyeing. These

products contain <2% sodium chlorate or calcium chlorate and the maximum use rate is 500 ppm

total available chlorine in the sanitizing wash water; exposure time is 1-2 minutes.
Page 16 of 141

2.4 Chemical Formula and Nomenclature

Table 2.4. Chemical Formula and Nomenclature

Sodium Chlorate - NaClO3

Common name Sodium Chlorate

IUPAC name Sodium Chlorate

CAS name Sodium Chlorate

CAS# 7775-09-9

Current Food/Feed Site Registration dry beans, corn, cotton, flax, guar, peppers (chili type), rice,

safflower, sorghum (grain), southern peas (i.e., cowpeas),

soybeans, sunflowers, wheat (Section 18 Registration)

Proposed Food/Feed Site Registration wheat

Calcium Chlorate - CaCl2O6

Common name Calcium Chlorate

IUPAC name Calcium Chlorate

CAS name Calcium Chlorate

CAS# 10137-74-3

Current Food/Feed Site Registration None

Potassium Chlorate - KClO3

Common name Potassium Chlorate

IUPAC name Potassium Chlorate

CAS name Potassium Chlorate

CAS# 3811-04-9

Current Food/Feed Site Registration None

Magnesium Chlorate - MgCl2O6

Common name Magnesium Chlorate

IUPAC name Magnesium Chlorate

CAS name Magnesium Chlorate

CAS# 10326-21-3

Current Food/Feed Site Registration None
Page 17 of 141

2.5 Physical and Chemical Properties

Sodium chlorate is a white, odorless, crystalline solid that looks like common table salt (sodium

chloride) and is highly water soluble. It is a strong oxidant, not combustible buts reacts violently

with combustible and reducing materials. Vapor pressure is low (EXTOXNET lists vapor

pressure as Zero).

HED is not responsible for the Product Chemistry Chapter for the Inorganic Chlorates

Reregistration Eligibility Decision (RED); hence detailed physical and chemical properties of

sodium chlorate, calcium chlorate, potassium chlorate, and magnesium chlorate are not provided

herein.

3.0 Metabolism Assessment

By agreement within OPP, the residue of concern for inorganic chlorates is the chlorate anion. 

Discussions concerning residues to be included in the tolerance expression are not relevant here

since residues of concern are not and will not be specified in the exemptions from the requirement

of a tolerance for sodium chlorate used on crops.

3.1 Comparative Metabolic Profile

Since there are no livestock metabolism data, no comparison can be made. Based on published

rat metabolism data (Abdel-Rahman et al, 1982, 1984b and 1985), terminal residues of sodium

chlorate in animal tissues are expected to be chlorate (ClO3b), chlorite (ClO2b), and chloride

(Clb). Chlorate is readily absorbed from the digestive tract and is excreted as chlorate, chlorite,

and chloride in urine and feces. Within 72 hours, about 40% of the administered dose was

excreted in the urine as chlorate (ca. 13%), chlorite (ca. 4%), and chloride (ca. 20%) and about 2-

4% was excreted in the feces in the same time period. Less than 1% of the administered dose was

found in any of the tissues analyzed including kidney, liver, and skin.

3.2 Nature of the Residue in Foods

3.2.1 Description of Primary Crop Metabolism

No plant metabolism data have been submitted in support of the reregistration of sodium chlorate;

however, no new plant metabolism data are required to support the established sodium chlorate

exemptions from the requirement of a tolerance. Based on available published information

(Loomis et al., J. Am. Soc. Agron.; 25, 724 (1933)), sodium chlorate is highly soluble in water

and is expected to readily absorb and translocate throughout plants. However, given the

proposed use conditions, the means of translocation in treated plants may be substantially

disrupted. Translocation of very small amounts of chlorate ion (ClO3b) by plants may occur

(translocation of significant amounts would be phytotoxic to plants). Terminal residues are

expected to be primarily surface residues.
Page 18 of 141

Since sodium chlorate is a strong oxidizing agent, depending on environmental factors, it is

expected to be easily reduced to chloride and possibly chlorite in plants. Total redox conversion

to these reduced species is not expected; hence, the terminal residues of sodium chlorate in/on

plants are likely chlorate (ClO3b), chlorite (ClO2b), and chloride (Clb).

3.2.2 Description of Livestock Metabolism

No ruminant, swine, or poultry metabolism or feeding data have been submitted in support of the

reregistration of sodium chlorate; however, no new animal metabolism data are required to

support the established sodium chlorate exemptions from the requirement of a tolerance. 

Although some previous residue chemistry reviews for specific exemptions from the requirement

of a tolerance have concluded that there is no reasonable expectation of transfer of residues to

meat, milk, poultry or eggs in specific cases, re-evaluation of the available crop field trial data

taken as a whole, indicate that there is the possibility of detectable residues of sodium chlorate on

animal feedstuffs at harvest. Hence, secondary residues of concern in meat, milk, poultry, and

eggs are possible and; therefore, new ruminant and poultry feeding data are required to support

the reregistration of sodium chlorate. These data are considered confirmatory.

3.2.3 Description of Rotational Crop Metabolism

Considering the phytotoxic nature of sodium chlorate, planting crops soon after treatment of

primary crops would not seem likely. Rotational crop tolerances or plant back restrictions are not

necessary. Translocation of very small amounts of chlorate ion (ClO3b) by plants (translocation

of significant amounts would be phytotoxic to plants) from the environment which may be present

as a result of inorganic chlorate pesticide uses may occur.

3.3 Environmental Degradation

Sodium chlorate is used as a desiccant/defoliant because it is a strong oxidizer. As a strong

oxidizing agent, chlorate (ClO3 b, oxidation state V) gets reduced to chlorine species in lower

oxidation states, such as the oxyanions chlorite (ClO2b, oxidation state III) and hypochlorite 

(ClOb, oxidation state I), chlorine dioxide (oxidation state IV), and chloride (oxidation state -I).

Thus, at least some and possibly substantial reduction of the applied chlorate is likely to occur in

the field prior to any runoff to surface water. Under environmental (terrestrial field) redox

conditions and based on chemical equilibria alone, the thermodynamically favored, end reduction

product of chlorate in soil and in water is the chloride anion. Any intermediate chlorine dioxide

that may form under environmental conditions will undergo photochemical reactions when

exposed to sunlight. The chlorine oxyanions chlorite and hypochlorite (other possible more

reduced intermediates in the ultimate reduction of chlorate to chloride) are strong oxidizers in

themselves and thus, they are also reduced and/or undergo disproportionation reactions. Although

reduction reactions of chlorate, chlorite, and hypochlorite are said to occur “very fast”, how fast

they occur is not known (i.e., the actual rate constants in the environment are not known).
Page 19 of 141

Therefore, at any given time the distribution of reduced species (type and concentration) cannot

be estimated. However, it is unlikely that a single reduced species would be present. 

4.0 Hazard Characterization/Assessment

4.1 Hazard and Dose-Response Characterization

4.1.1 Database Summary

4.1.1.1 Studies available and considered (animal, human,

general literature)

Subchronic - Oral 90-day rat, 90-day mouse and 90-day dog

Repro/developmental - rat and rabbit developmental; 2- generation reproductive rat

Chronic/cancer - Two-year drinking water studies in rats and mice

Other - mutagenicity screens; metabolism in the rat; many published studies included in this

hazard and dose response characterization.

4.1.1.2 Mode of action, metabolism and toxicokinetic data

Sodium chlorate is a thyroid toxicant producing thyroid gland follicular cell hypertrophy in rats

and mice following chronic exposures and some evidence of follicular cell tumors in rats. The

primary target of chlorate acute toxicity is rupture of red blood cell membranes with intravascular

hemolysis and the irreversible oxidation of hemoglobin to methemoglobin. Potassium chlorate has

produced renal tubular necrosis in animals. 

Metabolism studies in rats and dogs have shown that chlorates are readily absorbed by the

gastrointestinal tract and in rats are excreted in the urine as chlorate (ca. 13% of the administered

dose), chlorite (ca. 4% of the dose) and chloride (ca. 20% of the dose).

Using 36Cl-potassium chlorate, peak blood concentration levels were reached after an hour of

ingestion by rats. Elimination of the labeled chlorate from the blood was biphasic with half-lives

of 6 and 36.5 hours.

4.1.1.3 Sufficiency of studies/data

Data are sufficient for each exposure scenario and for FQPA evaluation. Data are sufficient for

endpoint selection.

4.1.2 Toxicological Effects

The toxicology profile for sodium chlorate is presented in tables 4.1a and 4.1b. In acute toxicity

tests, sodium chlorate is slightly toxic by the oral (Toxicity Category IV), dermal (Toxicity

Category IV), and inhalation routes (Toxicity Category IV of a 33% aerosol). Sodium chlorate

crystals were mildly irritating to the rabbit eye (Toxicity Category III for the dry crystals or

moistened crystals), and minimal to mild dermal irritant (Toxicity Category III for the moistened

material and Toxicity Category IV for the dry crystal). Ingestion of toxic doses of sodium

chlorate by humans produce gastritis, hemolysis, methemoglobinemia, hemoglobinurea, late toxic
Page 20 of 141

nephritis, and acute renal failure. An acute or cumulative dose of 7.5-35 grams is lethal in adults. 

Ingestion of 1 g amounts of potassium chlorate was reported to be fatal in infants. 

There are conflicting findings regarding the subchronic/chronic toxicity of sodium chlorate. In

one series of studies, rats exposed to relatively low concentrations of sodium chlorate (equivalent

to1.5 and 15 mg/kg/day) for up to 11 months exhibited decreased blood glutathione, increased

fragility of erythrocytes, inhibition of incorporation of tritiated thymidine into nuclei in rat testes,

decreased RBC count and hematocrit and decreased body weight. In another study, male F344

rats were exposed to 1% sodium or potassium chlorate in drinking water (654-686 mg/kg/day)

for 25 weeks and the only effect reported was significant body weight reduction. Relative kidney

weights were significantly increased in potassium chlorate treated rats. Rats orally administered

10-1000 mg/kg/day sodium chlorate for 90 days did not exhibit histological or clinical chemistry

treatment-related effects, but had decreased red blood cell counts, hematocrit and hemoglobin

levels, particularly in the females. Adrenal weights were also depressed in males and females at

the 1000 mg/kg/day level. In another published study in which rats were administered sodium

chlorate in the drinking water at concentrations equivalent to 512 and 800 mg/kg/day for males

and females, respectively for 90 days, final body weights were significantly lower in both sexes

with some relative organ weight changes including the adrenal glands and reduction in RBC

counts and percent hemoglobin, and prominent pituitary gland vacuolization and thyroid gland

colloid depletion in both sexes. The thyroid effects were confirmed in a recent study in rats where

subchronic treatment for 21 or 90 days with sodium chlorate in the drinking water at

concentrations up to 2,000 mg/L (225 mg/kg/day) induced a concentration dependent increase in

the incidence and severity of thyroid follicular cellular hyperplasia. Colloid depletion and

hypertrophy were the most sensitive histopathological indicators of sodium chlorate exposure,

with male rats more susceptible than females rats. Decreases in serum hormone levels of

triiodothyronine (T3) and thyroxine (T4) were also reported following exposure to sodium

chlorate. Mice were less susceptible to the adverse effect from exposure to high levels of sodium

chlorate. In dogs, the only reported treatment related effect following subchronic administration

of sodium chlorate up to 360 mg/kg/day was emesis.

A 2-year study to determine the potential of sodium chlorate to cause tumors in laboratory

animals (rats and mice) has been recently reported (NTP 2004). A final report of this study is

expected during 2005. In these tests, there was some evidence of thyroid gland follicular cell

carcinogenicity in male rats which may be attributed to the imbalance of thyroid hormones

(reduced T3 and T4 levels and elevated TSH) seen in these studies as a result of exposure to

sodium chlorate. Current EPA HED policy states that “nonmutagenic pesticides that induce

elevated levels of TSH and thyroid follicular cell tumors in the rat should be classified as not

likely to be carcinogenic to humans at doses that do not alter thyroid hormone

homeostasis” (Assessment of Thyroid Follicular Cell Tumors; USEPA March 1998 EPA/630/R97/002). In female mice there was equivocal and marginal evidence of increased pancreatic islet

carcinoma.
Page 21 of 141

Sodium chlorate was negative in most bacterial gene mutation assays. In one assay (Ames test), it

showed positive effect in the TA1535 strain in the presence of metabolic activation. It also caused

DNA damage in repair deficient E. coli strains at concentrations above 1000 ug/mL in the

presence of metabolic activation but was negative in the unscheduled DNA synthesis assay. In

cytogenetics tests, sodium chlorate was negative in the in vitro cell gene mutation assay,

mammalian erythrocyte micronucleus assay, bone marrow cytogenetics assay and sperm head

abnormality assay.

Sodium chlorate did not cause developmental effects in rats tested at doses up to 1000 mg/kg/day

or in rabbits tested at doses up to 500 mg/kg/day. In a two generation reproductive toxicity study

in the rat, postnatal toxicity did not exceed parental toxicity. Sodium chlorate has not been

evaluated for neurotoxic effects, but acute and subchronic toxicity studies did not indicate a

neurotoxic potential.

There are no repeated dermal toxicity or dermal absorption data available for sodium chlorate. 

Based on its high water solubility and ionic nature, potential sodium chlorate (or any other

inorganic chlorate) absorption by the intact skin is considered negligible.

4.1.3 Dose-response

Subchronic, developmental and reproductive studies were considered. An endpoint of concern

attributable to a single dose was not identified, and therefore an acute RfD is not established. The

oral endpoints for other durations were based on subchronic and chronic studies in rats. The

toxic effects seen in the subchronic study were on the pituitary (vacuolization) and thyroid gland

(colloid depletion), body weight decrease and organ weight changes and reduction in erythrocyte

counts and hemoglobin content. In the chronic drinking water study in rats, an endpoint of

toxicity was derived on the basis of thyroid follicular cell hypertrophy. There were no dermal

toxicity studies available. Sodium chlorate is an inorganic salt and its dermal absorption is

unlikely. Therefore, a toxicity endpoint for dermal exposure is not selected. There were no

inhalation studies available suitable for assessment of inhalation risks. For the risk assessment of

inhalation exposure from sodium chlorate, the endpoint of oral toxicity for short and intermediate

exposures is used with a 100% absorption factor. 
Page 22 of 141

Table 4.1a. Acute Toxicity Profile - Sodium Chlorate

Guideline No./ Study

Type

Study Type MRID

No.

Results Toxicity

Category

870.1100 Acute oral -Rats 41819901 $5000 mg/kg (rat) IV

870.1200 Acute dermal - Rabbits 41819902

42497601

LD50 = > 2000 mg/kg (dry crystal)

LD50 = > 2000 mg/kg (moistened)

IV

IV

870.1300 Acute inhalation - Rats 41819903 LC50 = 5.59 mg/L IV

870.2400 Acute eye irritation - Rabbit 00085090 

00102998

41819904

mildly irritating

mildly irritating

III

III

870.2500 Acute dermal irritation -

Rabbit 

41819905

42497602

non-irritating (dry crystal)

minimally irritating (moistened)

IV

III

870.2600 Skin sensitization - guinea

pigs

41819906 not a dermal sensitizer NA
Page 23 of 141

Table 4.1b Subchronic, Chronic and Other Toxicity Profile: Sodium Chlorate

Guideline No./

Study Type

MRID No. (year)/

Classification /Doses

Results

870.3100

90-Day oral toxicity 

(Sprague-Dawley

Rats)

40444801(1987)

Acceptable/guideline

0, 10, 40, 100 or 1000 

mg/kg/day, oral gavage

NOAEL = 100 mg/kg/day

LOAEL = 1000 mg/kg/day based on hematological effects

(hemoglobin concentration, hematocrit, RBC counts were

statistically significantly decreased, and reticulocyte count

was statistically significantly increased in females. In

males, only the hematocrit was statistically significantly

decreased. The adrenal weight was depressed in both males

and females.

Non-Guideline

25-week tumor

promotion toxicity

study (Male F344

Rats)

Kurokawa et al, 1985

1% NaClO3 or KClO3 in

drinking water(654-686

mg/kg/day) for 25 weeks

following 2-week

initiation with 0.05% Nethyl-Nhydroxyethylnitrosamine

LOAEL = 654-686 mg/kg/day (only dose tested). 

Significant decrease in mean body weights compared to the

controls. This dose was the maximum tolerated dose based

on a 6-week screening study at 0.25, 0.5, 1 and 2% doses in

drinking water. Relative kidney weights of the chlorate

treated rats were significantly increased over the control

group. NaClO3 or KClO3 showed no promoting effect in rat

renal carcinogenesis

Non-Guideline

90-Day oral toxicity

(Sprague-Dawley

Rats)

McCauley et al, 1995

SD rats (10/sex/group) 

NaClO3 in the drinking

water 3.0, 12.0, or 48

mM for 90 days

M: 30, 100 and 512

mg/kg/day (chlorate)

F: 42, 158, and 800

mg/kg/day (chlorate)

NOAEL = 30 and 42 mg chlorate/kg/ day in males and

females.

LOAEL = 100 mg chlorate/kg/day in males and 150

mg/kg/day in females, based on the pituitary effects

(vacuolization) and thyroid gland effects (colloid depletion),

the body weight decrease and organ weight changes and

reduction in erythrocyte counts and hemoglobin content.

Non-Guideline

90-Day oral toxicity

(F344 rats and

B6C3F1 mice)

Hooth et al, 2001

NaClO3 in drinking water

at 0, 0.125, 0.25, 0.5, 1.0

or 2 g/L for 21 days or 90

days in rats (14, 28, 56,

112, 225 mg/kg/day in

males; 20, 40, 80, 160 or

320 mg/kg/day in

females).

Additional groups of

male rats at 0, 0.001,

0.01, 0.1, 1.0, 2.0 and

females at 0, 0.5, 1.0,

2.0, 4.0, 6.0 g/L for 90-

105 days. Groups of

mice were also treated.

NOAEL = 0.25 g/L (28 mg/kg/day for males)

LOAEL = 1.0 g/L based on colloid depletion and follicular

cell hyperplasia, (112 mg/kg/day for males). Females were

less susceptible to the chlorate toxicity.

Total serum triiodothyronine (T3) and thyroxine (T4)

concentrations were decreased significantly and TSH levels

increased significantly in male and female rats after 4 days

of treatment with 1.0 or 2.0 g/L and after 21 days of

treatment with 2.0 g/L. TSH levels also increased

significantly in male rats after 21 days of treatment with 1.0

g/L. Serum T3 and T4 levels were comparable to controls in

male and female rats after 90 days of treatment, but TSH

levels were increased in both sexes.

Follicular cell hyperplasia was not present in male or

female mice. 
Table 4.1b Subchronic, Chronic and Other Toxicity Profile: Sodium Chlorate

Guideline No./

Study Type

MRID No. (year)/

Classification /Doses

Results

Page 24 of 141

Non-Guideline

11-month oral

toxicity -Rats

Abdel-Rahman et al.

1984

chlorine dioxide (0, 1,

10, 100, 1000 mg/L) and

its conversion products

chlorite and chlorate (10,

100 mg/L) in drinking

water (1.5, 15

mg/kg/day)

LOAEL =1.5 mg/kg/day (lowest dose tested). At 9 months

the osmotic fragility of RBCs was decreased in all treatment

groups, while a decreased blood glutathione was only

observed in the chlorite/chlorate groups. At 2, 4 and 6

months, no significant hematologic changes were noted in

treated rats compared to control. After 9 month RBC

counts, hematocrit and Hb were decreased in all treatment

groups. The incorporation of 3

H-thymidine into nuclei of

testes was inhibited in all treated groups, also in the liver of

the chlorite groups and in the kidney of 100 mg/L chlorine

dioxide treatment. The incorporation in small intestinal

nuclei was increased in 10 and 100 mg/L chlorine dioxide

and in 10 mg/L chlorite groups. Rat body weight was

decreased in all groups after 10 and 11 months 

870.3150

90-Day oral toxicity 

(Beagle Dogs)

MRID 40460402 (1987)

Acceptable/Guideline

oral gavage 0, 30, 60 or

360 mg/kg/day for 90 d

NOAEL = 360 mg/kg/day (HDT)

LOAEL = greater than 360 mg/kg/day based on lack of

detectable adverse effects. Higher dose levels were not

possible due to occurrence of emesis at higher doses.

Non-Guideline

subacute study in

dogs

Heywood et al, 1972

doses of 200 to 326

mg/kg/day of sodium

chlorate administered

daily by intubation as 50

ml of 6% solution to 8

dogs for 5 days

LOAEL = 200 mg/kg/day (LDT). Sodium chlorate caused

reduction of packed cell volume, hemoglobin and red blood

cells. A consistent increase in plasma urea concentration

was also observed. Two animals that received 308 or 326

mg/kg/day suffered appetite loss, body weight decline and

appearance of blood in their urine or feces. One of the

animals died after 4 days of exposure. Postmortem

examination of both animals revealed typical signs of

chlorate poisoning, including cyanotic kidney surface and

evidence of necrosis and hemolysis in the kidney. Five of

the 8 animals displayed tissue pathology indicative of

hemolysis such as Kupffer cells containing brown pigment. 

Non-Guideline

21 day oral toxicity

study (B6C3F1

mice)

NTP Study (2004)

10/sex/dose: 0, 125, 250,

500, 1000 or 2000 mg/L

M: 20, 45, 90, 175 or 350

mg/kg/day F: 0, 20, 45, 

95, 190 or 365 mg/kg/day

NOAEL = 350/360 mg/kg/day (HDT). Sodium chlorate

had no effect on survival, body weights, clinical signs,

water consumption, hematology parameters,

methemoglobin concentration, or organ weights of either

sex. There were no gross or microscopic lesions that were

considered to be due to sodium chlorate treatment.
Table 4.1b Subchronic, Chronic and Other Toxicity Profile: Sodium Chlorate

Guideline No./

Study Type

MRID No. (year)/

Classification /Doses

Results

Page 25 of 141

Non-Guideline

21 day oral toxicity

study (Fisher 344

rats)

NTP Study (2004)

10/sex/dose: 0, 125, 250,

500, 1000 or 2000 mg/L

M: 0, 20, 35, 75, 170,

300 mg/kg/day

F: 0, 20, 40, 75, 150 or

340 mg/kg/day

NOAEL/LOAEL unclear from study summary. Sodium

chlorate had no effect on survival, body weights, clinical

signs or water consumption. A moderate to severe

neutropenia was observed in both sexes on day 4 and 22. 

Very mild decreases in erythrocyte counts, hemoglobin, and

hematocrit were considered not to be biologically

significant. The only gross or microscopic lesion that was

considered to be treatment related was a minimal to mild

follicular cell hyperplasia of the thyroid gland seen in males

at 500 mg/L or greater and in females at 250 mg/L or

greater.

870.3200

21/28-Day dermal

toxicity

Not required. Sodium chlorate has very low acute dermal toxicity. Dermal absorption is

also unlikely due to its ionic nature and high water solubility.

870.3250

90-Day dermal

toxicity

Not required. Sodium chlorate has very low acute dermal toxicity. Dermal absorption is

also unlikely due to its ionic nature and high water solubility.

870.3465

90-Day inhalation

toxicity

NA

870.3700a

Prenatal

developmental

(rats) 

MRID 40460401(1987)

Acceptable/Guideline

oral gavage 

0, 10, 100 or 1000

mg/kg/d on GD 6-15

Maternal NOAEL = 1000 mg/kg/day (HDT)

LOAEL = >1000 mg/kg/day.

Developmental NOAEL = 1000 mg/kg/day (HDT)

LOAEL = >1000 mg/kg/day based on lack of effects

870.3700b

Prenatal

developmental

(Rabbits)

NTP (2002)

Acceptable/Guideline

0, 100, 250, or 475

mg/kg/d on GD 6-29.

Range finding study: 0,

100, 250, 500, 750 or

1000 mg/kg/d

Maternal NOAEL = 475 mg/kg/day (HDT)

LOAEL = 500 mg/kg/day based on mortality in range

finding study.

Developmental NOAEL = 475 mg/kg/day (HDT)

LOAEL = >475 mg/kg/day
Table 4.1b Subchronic, Chronic and Other Toxicity Profile: Sodium Chlorate

Guideline No./

Study Type

MRID No. (year)/

Classification /Doses

Results

Page 26 of 141

870.3800

Reproduction and

fertility effects

(Rats)

MRID 46524001(2004)

Acceptable/Guideline

0, 10, 70 or 500

mg/kg/day (gavage)

Parental/Systemic NOAEL = 10/70 (M/F) mg/kg/day

LOAEL = 70/500 (M/F) mg/kg/day based on lower BW

gain and food consumption (F1 M), decreased RBC counts

and hemoglobin (P males and females), increased absolute

and relative thyroid weight (F1 males), increased incidence

of slight to moderate hyperactivity of the thyroid glands (P

and F1 males and females) (only in P and F1 males at 70

mg/kg/day).

Reproductive NOAEL = 500 mg/kg/day (HDT)

Offspring NOAEL = 70 mg/kg/day

LOAEL = 500 mg/kg/day based on increased relative

thyroid weight (F1 and F2 males).

870.4100a

Chronic toxicity

rodents

A 2-year NTP bioassay (2004) to determine the potential of sodium chlorate to induce

thyroid tumors in laboratory animals (rats and mice) has been reported in a draft form. 

F344 rats (50/sex/group) were exposed to drinking water at 0, 125, 1,000, or 2,000 mg/L

sodium chlorate for 2 years (5, 35, and 75 mg/kg /day in males and 5, 45, and 95

mg/kg/day in females). T4 and T3 were significantly reduced in 1,000 and 2,000 mg/L

on day 4 and in 2,000 mg/L males and females at week 3. TSH was significantly

increased in 1,000 and 2,000 mg/L males on day 4 and at week 3, in 1,000 and 2,000

mg/L females on day 4, in 2,000 mg/L females at week 3, and in 2,000 mg/L males and

females at week 13. There were positive trends in the incidences of thyroid gland

follicular cell carcinoma in male rats (0/47, 0/44, 0/43, 4/47) and of thyroid gland

follicular cell adenoma or carcinoma (combined) in males (1/47, 0/44, 0/43, 6/47) and

females (1/47, 0/47, 1/43, 4/46). The incidences of thyroid gland follicular cell

hypertrophy were significantly increased in all exposed groups of males (4/47, 13/44,

33/43, 40/47) and in 1,000 and 2,000 mg/L females (3/47, 7/47, 27/43, 42/46). Thyroid

gland focal follicle mineralization occurred in most 1,000 and 2,000 mg/L female rats.

The incidences of hematopoietic cell proliferation in the spleen of 2,000 mg/L males

(2/48, 6/49, 4/49, 11/50) and bone marrow hyperplasia in 1,000 and 2,000 mg/L males

(28/48, 35/48, 41/50, 40/49) were significantly greater than those in the controls. The

LOAEL for non neoplastic effects derived from this study is 125 mg/L (5 mg/kg/day)

based on increased thyroid gland follicular cell hypertrophy and follicular cell

mineralization. The NOAEL is less than 5 mg/kg/day. 

B6C3F1 mice 950/sex/group) were exposed to drinking water at 0, 500, 1,000, or 2,000

mg/L sodium chlorate for 2 years (40, 80, and 160 mg/kg/day to male mice and 30, 60,

and 120 mg/kg/day to female mice). There was a positive trend in the incidences of

pancreatic islet cell adenoma or carcinoma (combined) in female mice (0/46, 2/47, 2/49,

4/49). Thyroid gland follicular cell hypertrophy was significantly increased in 2,000

mg/L females (3/48, 2/50, 5/49, 14/50). The incidences of bone marrow hyperplasia

were significantly increased in all exposed groups of females (14/50, 28/50, 29/50,

31/50). 
Table 4.1b Subchronic, Chronic and Other Toxicity Profile: Sodium Chlorate

Guideline No./

Study Type

MRID No. (year)/

Classification /Doses

Results

Page 27 of 141

870.4100b

Chronic toxicity

dogs

Not available

870.4200

Carcinogenicity rats

A 2-year NTP bioassay to determine the potential of sodium chlorate to induce thyroid

tumors in laboratory animals (rats and mice) has been reported in a draft form (2004). 

In these tests, there was some evidence of thyroid gland follicular cell carcinogenicity in

male rats which may be attributed to the imbalance of thyroid hormones (reduced T3 and

T4 and elevated TSH) seen in these studies as a result of exposure to sodium chlorate. 

Current EPA HED policy considers nonmutagenic pesticides that induce elevated levels

of TSH and thyroid follicular cell tumors in the rat should as not likely to be

carcinogenic to humans at doses that do not alter thyroid hormone homeostasis.

870.4300

Carcinogenicity

mice

NTP 2004 Study. A 2-year NTP bioassay to determine the potential of sodium chlorate

to induce thyroid tumors in laboratory animals (rats and mice) has been reported in a

draft form (2004). In female mice there was equivocal and marginal evidence of

increased pancreatic islet carcinoma. 

Gene Mutation

870. 5100

870.5500 Bacterial

DNA

damage/Repair

MRID 41256201 (1989)

Acceptable/Guideline

Moriya et al, 1983

Eckhardt et al, 1982

Olivier and Marzin 1987

NTP, 2004

MRID 41256204 (1989)

Acceptable/Guideline

Sodium chlorate was negative for inducing reverse gene

mutation in Ames (bacterial) strains of Salmonella typhimurium

exposed with or without activation up to 5000 ug/plate (limit

dose).

Sodium chlorate was negative for inducing reverse gene

mutation in Ames (bacterial) strains of Salmonella typhimurium

exposed with or without activation up to 5000 ug/plate (limit

dose).

Sodium chlorate showed mutagenic activity in the TA1535

strain +S9

Potassium chlorate was not mutagenic in the SOS chromotest

using E. coli strain PQ37 without metabolic activation tested at

1-6000 nM/ml.

Sodium chlorate tested up to 10,000 ug/plate was negative in

strains TA97, TA98, TA100, TA102, TA1535 with or without

S9

Sodium chlorate caused DNA damage in repair deficient E. 

coli strains at concentrations above 1000 ug/mL in the presence

or absence of S9 fractions. It was tested up to 10000 ug/mL.
Table 4.1b Subchronic, Chronic and Other Toxicity Profile: Sodium Chlorate

Guideline No./

Study Type

MRID No. (year)/

Classification /Doses

Results

Page 28 of 141

Cytogenetics 

870.5300, in vitro

mammalian cell

gene mutation assay

MRID 41256202 (1989)

Acceptable/Guideline

Sodium chlorate was negative for inducing forward gene

mutation at the hypoxanthine-guanine phosphoribosyl

transferase (HGPRT) locus in the Chinese hamster lung

(V79) cells (HGPRT +

, -) Exposed in activated (+s9) or

non-activated (-S9) culture tested up to the limit dose of

5000 ug/mL.

870.5395 

Mammalian

erythrocyte

micronucleus test

MRID 41256203 (1989)

Acceptable/Guideline

Sodium chlorate was negative (not clastogenic) for inducing

micronuclei in polychromatic erythrocytes of male mice

with single oral doses of 200, 1000 or 5000 (limit dose)

mg/kg. 

870.5395 

Mammalian

erythrocyte

micronucleus test

NTP, 2004 Sodium chlorate did not increase the number of

micronucleated erythrocytes in B6C3F1 mice treated in the

drinking water with 20, 45, 95, 190, or 365 mg/kg/day for 3

weeks.

micronucleus test Eckhardt et al, 1982 Sodium chlorate did not induce chromosomal damage.

micronucleus test Meier et al, 1985 Sodium chlorate did not increase the number of

micronucleated polychromatic erythrocytes in CD-1 mice

treated by gavage with 8, 20 or 40 mg/kg/day for 5 days.

870.5385

Bone marrow

cytogenetics assay

Meier et al, 1985 Sodium chlorate did not cause structural or numerical

chromosomal aberrations in mice treated by gavage with 8,

20 or 40 mg/kg/day for 5 days.

Sperm head

abnormality assay

Meier et al, 1985 Sodium chlorate did not induce sperm head abnormalities

in B6C3FA male mice treated by gavage with 8, 20 or 40

mg/kg/day for 5 days.

Other Effects 

870.5550,

Unscheduled DNA

Synthesis

MRID412546205

Acceptable/Guideline

Sodium chlorate was negative for unscheduled DNA

synthesis (UDS) in human cells (HeLa-S3) exposed up to

10,000 ug/mL, with or without metabolic activation. The

incorporation of thymidine was decreased in a dosedependent manner between doses of 100 and 10,000 ug/mL

indicating cytotoxicity.

870.5275 recessive

lethal: Drosophila

Eckhardt et al, 1982 Sodium chlorate was mutagenic in this system.

870.6200a

Acute neurotoxicity screening battery Not required for this chemical
Table 4.1b Subchronic, Chronic and Other Toxicity Profile: Sodium Chlorate

Guideline No./

Study Type

MRID No. (year)/

Classification /Doses

Results

Page 29 of 141

870.6200b

Subchronic neurotoxicity screening battery Not required for this chemical

870.6300

Developmental neurotoxicity NA

870.7485

Metabolism and

pharmacokinetics

Abdel-Rahman et al,

1982, 984b, 1985-rats

Non-Guideline

National Research

Council, 1980 - dogs

(OEHHA, 2002)

Non-Guideline

There are no guideline studies available. However,

published studies provide reasonable information on the

pharmacokinetics and metabolism of the chlorate ion in the

rat and the dog. Chlorate is readily absorbed from the

digestive tract and is excreted in urine mainly and feces. In

dogs the excretion is entirely as chlorate and is complete

after 72 hours. In rats, about 40% of the administered dose

was excreted after 72 hours and it is excreted as chloride,

chlorite and chlorate. In Cl36 labeled potassium-chlorate

studies in rats, Cl36 radioactivity was detected at the end or

72 hours after the initial oral treatment in several tissues. 

Although the chlorites and the chlorates are structurally

related, their pharmacokinetics is different. 

870.7600

Dermal penetration

Not required It is not required for sodium chlorate. Acute dermal

toxicity is low and sodium chlorate is very polar being an

inorganic salt would not be readily absorbed through the

skin.

Special studies Beinfeld (1994)

Mintz et al (1994)

Sodium chlorate is in vitro inhibitor of ATP-sulfurylase and

protein sulfation

Special Studies Roy et al (1988) Sodium chlorate did not affect bile production from isolated

perfused guinea pig livers suggesting that it is not a general

liver poison

4.2 FQPA Hazard Considerations

The database with respect to the standard guideline studies is adequate to characterize potential

for prenatal or postnatal risk for infants and children. No increase in prenatal susceptibility of rats

or rabbits was seen in developmental studies with chlorate, and no increase in pre- or postnatal

susceptibility was evident in a 2-generation reproduction study in rats. Based on this, there are no

residual uncertainties from guideline studies and the special FQPA safety factor is reduced to 1X. 

There is, however, need for additional data on potential neuroendocrine effects on the developing

young based on chlorate-induced thyroid effects.

4.2.1 Adequacy of the Toxicity Data Base

The toxicity data base is complete with respect to the normal complement of guideline studies

except for a 21/28 day inhalation study. Because the inorganic chlorates affect the thyroid gland
Page 30 of 141

in rats and dogs, there is concern for potential neuroendocrine pre- and postnatal effects to

developing young and a comparative thyroid study in which T4, T3 and TSH are analyzed in

adults and in neonates is required to address this concern.

4.2.2 Evidence of Neurotoxicity

Sodium chlorate did not show neurotoxic effects in acute, subchronic testing.

4.2.3 Developmental Toxicity Studies

DEVELOPMENTAL - RAT

In a developmental toxicity study (MRID 40460401), 24 pregnant Sprague-Dawley CD rats per

group were administered technical grade sodium chlorate (100% a.i., white granular solid) by oral

gavage at 0 (distilled water) 10, 100, or 1000 mg/kg/day on gestation days (GD) 6-15, inclusive. 

On GD 20, all dams were sacrificed and all fetuses were examined for external, visceral, and

skeletal malformations/variations. All animals survived until scheduled sacrifice except for one

control that died prior to terminal sacrifice. No adverse clinical signs were reported. There were

no dose or treatment related effects detected in the dams or embryos/fetuses. Maternal body

weights, food consumption were comparable to controls. Necropsy of treated animals did not

reveal any treatment related effect. There was no treatment related effect on pregnancy rate,

corpora lutea, implantation sites, viable fetuses, dead fetuses, resorptions or fetal weights. Fetal

examinations did not reveal any anomalies attributed to treatment. The LOAEL derived from this

study for maternal and developmental toxicity in the rat is >1000 mg/kg/day and the NOAEL is at

least 1000 mg/kg/day. This study is considered Acceptable/guideline.

DEVELOPMENTAL - RABBIT

There are no registrant guideline studies available. There is an NTP study reported in 2002,

where 24 timed naturally mated female New Zealand rabbits/ dose were dosed by gavage with

sodium chlorate at 0 (deionized distilled water), 100, 250, or 475 mg/kg/day on gestation days 6

through 29. The study was conducted in a two replicate design where 12 rabbits/dose were dosed

in each replicate. The doses were selected on the basis of a range finding study conducted at 0,

100, 250, 500, 750, or 1000 mg/kg/day. In this range finding study, excessive maternal toxicity

(morbidity and mortality) resulted in termination of the groups treated with 750 and 1000

mg/kg/day by gestation day 24. One maternal death occurred in the 500 mg/kg/day group and

one doe was lethargic with respiratory distress. Clinical signs were minimal in the 100 and 250

mg/kg/day groups. These included animals with discolored urine (red, orange, orange/white or

brown). Body weights were decreased during treatment only at doses higher than 500 mg/kg/day.

Developmental toxicity was not evident at doses up to 500 mg/kg/day. In the final study,

transient changes in maternal food intake, urinary color (orange or brown) and /or urine output

were noted at 100 mg/kg/day and greater, but clear evidence of toxicity occurred only at doses

greater than 475 mg/kg/day as observed in the range finding study. According to the study

authors, comparison of the results from the range finding study and the developmental toxicity

study suggests that the dose-effect curve for maternal effects is very steep as demonstrated by

mortality at 500 mg/kg/day on the range finding study, but not at the 475 mg/kg/day in the final
Page 31 of 141

study. No significant treatment related developmental toxicity attributable to sodium chlorate

occurred under the conditions of this study. It was concluded that the maternal and

developmental toxicity NOAELs were equal to or greater than 475 mg/kg/day (the HDT). The

LOAEL for maternal toxicity is 500 mg/kg/day based on mortality observed in the range finding

study. This study satisfies guideline requirements and is acceptable/guideline.

4.2.4 Reproductive Toxicity Study

In an Acceptable/Guideline 2-generation reproduction study (MRID 46524001), sodium chlorate

(99.68% a.i.; batch/lot 1E012IUM) was administered to 25 Sprague-Dawley rats of each sex per

dose by gavage at dose levels of 0, 10, 70, or 500 mg/kg/day. P males were exposed to the test

material for 10 weeks prior to mating and after mating until the pups were weaned; P females

were exposed for 10 weeks prior to mating and then throughout gestation and lactation. 

Selection of parents (4 males and 4 females per litter) for the F1 generation was made when the

pups were 4 days of age. F1 parents were exposed in the same manner as P parents.

Oral administration of sodium chlorate resulted in parental toxicity at 70 and 500 mg/kg/day.

Treatment-related effects at 500 mg/kg/day consisted of slightly lower body weight gain and food

consumption (F1 males); decreased red blood cell counts (P males and females); decreased

hemoglobin concentration (P males and females); increased absolute and relative thyroid weight

(F1 males); increased incidence of slight to moderate follicular hyperplasia (P and F1 males and

females); and increased incidence of slight to moderate hyperactivity of the thyroid glands (P and

F1 males and females). The thyroid gland appeared to be the target organ. 

At 70 mg/kg/day, treatment-related effects consisted of a marginal increased incidence of

hyperactivity of the thyroid glands (P and F1 males). Based on these results, a NOAEL of 10

mg/kg/day for males (LOAEL 70 mg/kg/day) was established. In females a NOAEL of 70

mg/kg/day and a LOAEL of 500 mg/kg/day was established. 

For offspring, exposure to sodium chlorate resulted in toxicity at 500 mg/kg/day. Treatmentrelated effects at 500 mg/kg/day consisted of increased relative thyroid weight in F1 and F2 males. 

The offspring LOAEL is 500 mg/kg/day, based on increased relative thyroid weight. The

offspring NOAEL is 70 mg/kg/day. 

There were no treatment-related reproductive effects observed at any dose level for either

generation. Consequently, the reproductive NOAEL is 500 mg/kg/day. 

4.2.5 Additional Information from Literature Sources

In a case control study evaluating chlorination by-products in drinking water and adverse

pregnancy outcomes in Italy (Aggazzotti et al, 2004), no association was found between preterm

births and exposure to chlorination by products (trihalomethanes, chlorites and chlorates), but

there was a weak association between small weight gestational term (weighing less than the

lowest 10th percentile) and high levels of trihalomethanes ($30 ug/L drinking water) and chlorites

and chlorates ($200 ug/L drinking water).
Page 32 of 141

In a subchronic exposure study in primates where sodium chlorate was administered in drinking

water for 8 weeks at 400 mg/L (58.4±27.6 mg/kg/day) to 6 male and 7 female adult African

Green Monkeys (Cercopithecus aethiops) there was no effect on the thyroid function and the

total thyroxine levels (Bercz et al, 1982). Based on this study the NOAEL for sodium chlorate

thyroid effects in the monkey would be at least 58 mg/kg/day. 

4.2.6 Pre-and/or Postnatal Toxicity

Prenatal toxicity of sodium chlorate has been evaluated in developmental toxicity studies in the rat

and the rabbit. In both species, prenatal toxicity was not observed at the highest doses tested

(1000 mg/kg/day in the rat, and 475 mg/kg/day in the rabbit). In a 2-generation reproduction test

in the rat, there were thyroid effects to the offspring at the highest dose tested - 500 mg/kg. No

other offspring effects were noted in the study,

4.2.6.1 Determination of Susceptibility

Based on the developmental studies in rats and rabbits and the reproductive toxicity study in rats,

fetal or neonatal toxicity from administration of sodium chlorate did not occur at doses lower than

doses causing effects in parental animals.

4.2.6.2 Degree of Concern Analysis and Residual Uncertainties

for Pre and/or Post-natal Susceptibility

No increase in prenatal susceptibility of rats or rabbits was seen in developmental studies, and no

pre- or postnatal susceptibility was observed in a reproduction study in the rat. Based on this,

there are no residual uncertainties that indicate the need for a special safety factor. The hazard

factor is thus 1X.
Page 33 of 141

4.2.7 Recommendation for a Developmental Neurotoxicity Study

4.2.7.1 Evidence that supports requiring a Developmental

Neurotoxicity study

There is no evidence for requiring such a study. Sodium chlorate did not show neurotoxic effects

in acute, subchronic testing. 

4.2.7.2 Evidence that supports not requiring for a

Developmental Neurotoxicity study

No neurotoxic effects were seen in acute, subchronic studies with sodium chlorate.

4.3 Safety Factor for Infants and Children.

There was no pre- or postnatal sensitivity or susceptibility observed in the submitted

developmental studies in rats and rabbits and the 2-generation reproduction study in rats. 

However, there is a concern for developing offspring because of the effects of inorganic chlorate

on thyroid function in rats and dogs. The thyroid hormone system plays a critical role in

development, and it is therefore important to understand whether the thyroid hormone system in

the developing young differs in response to thyroid toxicants compared to adults. There exists

therefore a database uncertainty for information on comparative thyroid response in young vs

adult rats; however, a database factor reflecting the uncertainty in comparative response is not

necessary and the default 10X FQPA factor can be removed.

The rationale for removal of the factor lies in the comparative thyroid physiology of rats vs.

humans (see further discussion of the differences in physiology under the chronic RfD). As a

consequence of these dynamic differences, rats are much more sensitive to thyroid toxicants such

as chlorate than humans and non-human primates. As discussed in section 4.4.3 below, the

chronic RfD for inorganic chlorates is 0.03 mg/kg/day based on thyroid hypertrophy in adult rats. 

There is a study of the effects of chlorate on adult monkeys (Bercz et al, 1982), in which the

NOAEL for effects on blood thyroxine levels was 58 mg/kg/day. If the NOAEL from the monkey

study were used to derive a chronic RfD with uncertainty factors of 10X for interspecies

extrapolation and 10X for intraspecies variability and an FQPA factor of 10x reflecting

uncertainties in effects to the young, the chronic RfD would be 0.06 mg/kg/day. The chronic RfD

selected by the risk assessment team of 0.03 mg/kg/day derived from the chronic rat NTP study is

therefore protective of thyroid effects in primates (including a 10X factor for uncertainty with

respect to developing young) without the necessity of an additional uncertainty factor applied to

the rat data.

4.4 Hazard Identification and Toxicity Endpoint Selection

4.4.1 Acute Reference Dose (aRfD) - Females age 13-49

An acute RfD for females age 13-49 was not identified from the available developmental toxicity

studies in rats and rabbits.
Page 34 of 141

4.4.2 Acute Reference Dose (aRfD) - General Population

An endpoint of concern attributable to a single dose was not identified although several studies

were considered. The developmental NTP study in rabbits discussed above provided a NOAEL

for maternal toxicity of 475 mg/kg/day based on maternal morbidity and mortality at 500

mg/kg/day in a range finding study. In a subacute toxicity study, 200 to 326 mg of sodium

chlorate/kg administered daily for 5 days to a total of 8 dogs, all dogs experienced toxicity

including death at the higher dose. However, in a guideline study (MRID 40460402) sodium

chlorate administered to dogs by oral gavage daily for 90 days did not exert any toxicity at the

highest dose tested of 360 mg/kg/day. None of these studies provided an endpoint of toxicity

attributable to a single exposure. An acute RfD for the general population is not established.

The published literature provides numerous references to sodium chlorate poisoning in humans. 

Doses in excess of 100 mg/kg (7 grams for a 70 kg adult and 0.5 grams for a 5 kg child) are

generally fatal (Warrington 2002, Cosmetic Ingredient Review Panel 1995). Pesticide incident

data are not used for establishing dietary endpoints, but the chlorate incident data indicate that

there is a concern for direct ingestion of chlorate formulations.

4.4.3 Chronic Reference Dose (cRfD)

A chronic study with sodium chlorate in rats has been completed in 2004 and reported in a draft

form (NTP 2004). In this NTP study, groups of 50 male and 50 female F344 rats were exposed

to drinking water containing 0, 125, 1,000, or 2,000 mg/L sodium chlorate for 2 years (equivalent

to average daily doses of approximately 5, 35, and 75 mg/kg per day in male rats and 5, 45, and

95 mg/kg per day in female rats). Survival of exposed rats was similar to that of the control

groups. Mean body weights of all exposed groups were similar to those of the control groups

throughout the study. Water consumption by exposed rats was generally similar to that by

controls throughout the study (14-17 g of water/male rat/day and 10.6-13.2 g of water/female

rat/day). Serum concentrations of thyroxine (T4) and triiodothyronine (T3) were significantly

reduced in 1,000 and 2,000 mg/L males and females on day 4 and in 2,000 mg/L males and

females at week 3. Serum concentrations of thyroid stimulating hormone (TSH) were

significantly increased in 1,000 and 2,000 mg/L males on day 4 and at week 3, in 1,000 and 2,000

mg/L females on day 4, in 2,000 mg/L females at week 3, and in 2,000 mg/L males and females at

week 13. All special study rats in the 1,000 and 2,000 mg/L groups had thyroid gland follicular

cell hypertrophy at 3 and 13 weeks. There were positive trends in the incidences of thyroid gland

follicular cell carcinoma in male rats (0/47, 0/44, 0/43, 4/47) and of thyroid gland follicular cell

adenoma or carcinoma (combined) in males (1/47, 0/44, 0/43, 6/47) and females (1/47, 0/47,

1/43, 4/46). The incidences of thyroid gland follicular cell hypertrophy were significantly

increased in all exposed groups of males (4/47, 13/44, 33/43, 40/47) and in 1,000 and 2,000

mg/L females (3/47, 7/47, 27/43, 42/46). Thyroid gland focal follicle mineralization occurred in

most 1,000 and 2,000 mg/L female rats (25/47, 26/47, 40/43, 44/46). The incidences of

hematopoietic cell proliferation in the spleen of 2,000 mg/L males (2/48, 6/49, 4/49, 11/50) and

bone marrow hyperplasia in 1,000 and 2,000 mg/L males (28/48, 35/48, 41/50, 40/49) were

significantly greater than those in the controls. The LOAEL for non neoplastic effects derived

from this study is 125 mg/L (5 mg/kg/day) based on increased thyroid gland follicular cell
Page 35 of 141

hypertrophy and follicular cell mineralization. A NOAEL for non neoplastic effects cannot be

derived from this study. Therefore a bench mark dose (BMD) analysis was performed and a

BMDL of 28 mg/L as sodium chlorate (22 mg/L as chlorate) was obtained (See Memorandum

from Becky Daiss to Abdallah Khasawinah, Jan. 26, 2005). This corresponds to 0.9 mg

chlorate/kg/day oral dose. Using the BMDL as an approximation of the NOAEL, the oral RfD

using a composite 30 X uncertainty factor (3X for interspecies and 10X for intraspecies) is:

The usual interspecies uncertainty factor is 10X, but there are several important quantitative

dynamic differences between rats and humans with respect to thyroid function that permit an

interspecies factor of less than 10X for a thyroid toxicant like chlorate. The half-life of T4 in rats

is approximately 12 hours, whereas in humans, the half-life is 5-9 days (Dohler et al., 1979). The

shorter half-life in rats is likely related to a high-affinity binding globulin for thyroxin that is

present in humans, but absent in rodents. Specifically, binding of the hormone to thyroxin binding

globulin accounts for slower metabolic degradation and clearance in humans. Increased turnover

and hepatic clearance of T3 and T4 renders the basal activity of the thyroid gland markedly more

active in rats compared to humans. In the absence of a functional thyroid gland, a rat requires

approximately 10-times more T4 than an adult human for full reconstitution (Dohler, et al., 1979).

Constitutive TSH levels are nearly 25-times higher in rats than in humans, reflecting the increased

activity of the thyroid-pituitary axis in rats (Dohler et al., 1979; McClain, 1992). Therefore, the

10X interspecies factor (which is subdivided into 3X for differences in toxicokinetics and 3X for

differences in toxicodynamics) can be reduced to 3X based on dynamic considerations.

The BMDL of 0.9 mg/kg/day for chlorate based on thyroid effects in the rat, the most sensitive

species for such an effect, will be protective of any other toxicity produced by chlorate.

4.4.4 Incidental Oral Exposure (short and intermediate durations: 1

day - 6 months)

There are three 90-day toxicity studies in rats available for selecting the endpoint to assess this

exposure. In MRID 40444801, the NOAEL was 100 mg/kg/day based on hematological effects

(hemoglobin concentration, hematocrit, RBC counts were statistically significantly decreased, and

reticulocyte count was statistically significantly increased in females at 1000 mg/kg/day. In males,

only the hematocrit was statistically significantly decreased. The adrenal weight was depressed in

both males and females. In the McCauley et al, 1995 study, the NOAEL was 30 and 42

mg/kg/day (as chlorate) for males and females, respectively, based on the pituitary effects

(vacuolization) and thyroid gland effects (colloid depletion), the body weight decrease and organ

weight changes and reduction in erythrocyte counts and hemoglobin content at the LOAEL of

100 and 150 mg/kg/day in males and females, respectively. In the third study (Hooth et al, 2002),

the NOAEL was 28 and 40 mg/kg/day in males and females, respectively, based on thyroid colloid

Chronic RfD = 0.9 mg/kg/day (BMDL) = 0.03 mg/kg/day

 30 (UF)
Page 36 of 141

depletion and follicular cell hyperplasia, at 112 & 160 mg/kg/day for males and females,

respectively. Based on these subchronic studies with sodium chlorate, an appropriate endpoint

would be 30 mg/kg/day as chlorate (McCauley study). For the incidental oral exposure, the 30

mg/kg/day dose is appropriate for this risk assessment and is selected for the toxic endpoint with

an MOE of 100.

4.4.5 Dermal Absorption

There are no dermal absorption studies available for sodium chlorate. Based on its high water

solubility and ionic nature, sodium chlorate absorption by the intact skin is considered negligible.

4.4.6 Dermal Exposure (Short, Intermediate and Long Term)

There are no subchronic dermal toxicity studies available. Because sodium chlorate is unlikely to

be absorbed by the skin, a risk assessment for dermal exposure is not needed. 

4.4.7 Inhalation Exposure (Short and Intermediate Term)

There are no subacute or subchronic inhalation studies available for sodium chlorate. The toxic

endpoint from the subchronic oral rat study discussed above with a NOAEL of 30 mg/kg/day is

used for assessing the risks from the inhalation exposure to sodium chlorate and the 100% default

absorption factor for using an oral dose is applied.

4.4.8 Margins of Exposure

The Margin of Exposure is 100 for all occupational and residential exposure scenarios.

4.4.9 Recommendation for Aggregate Exposure Risk Assessments

As per FQPA of 1996, when there are potential residential exposures to the pesticide, aggregate

risk assessment must consider exposures from residues in food commodities and drinking water,

as well as exposures arising from non-dietary sources (incidental oral, dermal and inhalation

exposures) from the residential scenarios.

4.4.10 Classification of Carcinogenic Potential

A 2-year NTP bioassay to determine the potential of sodium chlorate to induce thyroid tumors in

laboratory animals (rats and mice) has been recently reported in a draft form (NTP, 2004). A final

report of this study is expected during 2005. In these tests, there was some evidence of thyroid

gland follicular cell carcinogenicity in male rats which may be attributed to changes of thyroid

hormones (reduced T3 and T4 and elevated TSH) seen in these studies as a result of exposure to

high doses of sodium chlorate. Current EPA HED policy states that “nonmutagenic pesticides

that induce elevated levels of TSH and thyroid follicular cell tumors in the rat should be classified

as not likely to be carcinogenic to humans at doses that do not alter thyroid hormone

homeostasis” (Assessment of Thyroid Follicular Cell Tumors; USEPA March 1998 EPA/630/R97/002). In female mice there was equivocal and marginal evidence of increased pancreatic islet

carcinoma. 
Page 37 of 141

Table 4.4. Summary of Toxicological Doses and Endpoints for Chlorate per se for Use in Human

Risk Assessments for Inorganic Chlorates

Exposure

Scenario

Dose (as chlorate)

per se Used in

Risk Assessment,

UF 

Special FQPA SF*

and Level of Concern

for Risk Assessment

Study and Toxicological Effects

Chronic Dietary

(all populations)

BMDL** =0.9

mg/kg/day

UF = 30

1X Chronic Study in rats (NTP, 2004).

The LOAEL= 5 mg/kg/day based on

increased thyroid gland follicular cell

hypertrophy and follicular cell

mineralization. 

Incidental Oral

Short-Term

(1 - 30 days)

NOAEL =30

mg/kg/day

MOE = 100

1X Subchronic study in rats McCauley et

al, 1995. Pituitary effects

(vacuolization) and thyroid gland

effects (colloid depletion), the body

weight decrease and organ weight

changes and reduction in erythrocyte

counts and hemoglobin content at the

LOAEL of 100 and 150 mg/kg/day in

males and females, respectively

Incidental Oral

Intermediate-Term

(1 - 6 months)

NOAEL =30

mg/kg/day

MOE = 100

1X McCauley et al, 1995

Dermal 

all durations

Not required: dermal absorption is unlikely due to the ionic nature and water solubility

of sodium chlorate

Inhalation 

Short-Term

(1 - 30 days)

NOAEL =30

mg/kg/day

UF = 100

1X McCauley et al, 1995

Inhalation 

Intermediate-Term

(1 - 6 months)

NOAEL =30***

mg/kg/day

UF = 100

1X McCauley et al, 1995
Table 4.4. Summary of Toxicological Doses and Endpoints for Chlorate per se for Use in Human

Risk Assessments for Inorganic Chlorates

Exposure

Scenario

Dose (as chlorate)

per se Used in

Risk Assessment,

UF 

Special FQPA SF*

and Level of Concern

for Risk Assessment

Study and Toxicological Effects

Page 38 of 141

Cancer (oral,

dermal, inhalation)

Classification: A 2-year NTP bioassay to determine the potential of sodium chlorate

to induce thyroid tumors in laboratory animals (rats and mice) has been recently

reported in a draft form (NTP, 2004). A final report of this study is expected during

2005. There was some evidence of thyroid gland follicular cell carcinogenicity in male

rats which may be attributed to the imbalance of thyroid hormones (reduced T3 and T4

and elevated TSH) seen in these studies as a result of exposure to high doses of sodium

chlorate. Current EPA HED policy states that “nonmutagenic pesticides that induce

elevated levels of TSH and thyroid follicular cell tumors in the rat should be classified

as not likely to be carcinogenic to humans at doses that do not alter thyroid

hormone homeostasis” (Assessment of Thyroid Follicular Cell Tumors; USEPA

March 1998 EPA/630/R-97/002). In female mice there was equivocal and marginal

evidence of increased pancreatic islet carcinoma.

UF = uncertainty factor, FQPA SF = Special FQPA safety factor, NOAEL = no observed adverse effect level,

LOAEL = lowest observed adverse effect level, PAD = population adjusted dose (a = acute, c = chronic) RfD =

reference dose, MOE = Margin of Exposure, LOC = level of concern, NA = Not Applicable

* Refer to Section 4.5

** A NOAEL was not identified in this study. Therefore a bench mark dose (BMD) analysis was performed and a

BMDL of 28 mg sodium chlorate/L (22 mg chlorate/L) was calculated. This corresponds to 0.9 mg

chlorate/kg/day oral dose. 

*** A 100% absorption factor is used for using an oral endpoint of toxicity.
Page 39 of 141

4.5 Endocrine disruption

EPA is required under the FFDCA, as amended by FQPA, to develop a screening program to

determine whether certain substances (including all pesticide active and other ingredients) “may

have an effect in humans that is similar to an effect produced by a naturally occurring estrogen, or

other such endocrine effects as the Administrator may designate.” Following recommendations of

its Endocrine Disruptor and Testing Advisory Committee (EDSTAC), EPA determined that there

was a scientific basis for including, as part of the program, the androgen and thyroid hormone

systems, in addition to the estrogen hormone system. EPA also adopted EDSTAC’s

recommendation that the Program include evaluations of potential effects in wildlife. For

pesticide chemicals, EPA will use FIFRA and, to the extent that effects in wildlife may help

determine whether a substance may have an effect in humans, FFDCA authority to require the

wildlife evaluations. As the science develops and resources allow, screening of additional

hormone systems may be added to the Endocrine Disruptor Screening Program (EDSP).

The available toxicity studies on sodium chlorate, demonstrate the thyroid gland to be its target of

toxicity.

When additional appropriate screening and/or testing protocols being considered under the

Agency’s EDSP have been developed, sodium chlorate may be subjected to further screening

and/or testing to better characterize effects related to endocrine disruption.
Page 40 of 141

5.0 Public Health Data

Sodium chlorate has been documented to cause irritation to skin, eyes, and mucous membranes of

the upper respiratory tract. Death can occur from ingestion of substantial quantities, almost

always due to suicide. Doses in excess of 100 mg/kg are generally fatal to humans.

5.1 Incident Reports

Available sources of incident data in humans were reviewed for the active ingredients Sodium

Chlorate (073301) and Calcium Chlorate (073302). Data were available from the following

sources: OPP Incident Data System (IDS) consisting of reports submitted to EPA by registrants,

other federal and state health and environmental agencies and the public since 1992, Poison

Control Centers (1993-2001), California Department of Pesticide Regulation for pesticide

poisoning since 1982, National Pesticide Telecommunications Network (NPTN) for ranking of

the top 200 active ingredients for which phone calls were received during calender years 1984-

1991, and National Institute of Occupational Safety and Health’s Sentinel Event Notification

System for Occupational Risks (NIOSH SENSOR) from 1998-2002.

A total of 21 cases were located in Poison Control Center records from 1993 through 2001. 

Seven reported minor symptoms and two reported moderate medical outcomes, primarily due to

dermal effects such as swelling and rash. It is difficult to draw any conclusions on such a small

number of cases.

Detailed descriptions of 36 cases submitted to the California Pesticide Illness Surveillance

Program (1982-2002) were reviewed. However, in just four of these cases was sodium chlorate

determined to be the primary cause of illness and all four occurred in an agricultural setting (three

in cotton fields, one unknown). Two of these cases were classified as systemic and one each

involved skin or eye effects. The two systemic cases involved applicators; one with nausea and

the other with nausea, headache, and itching skin after spraying for one week. Both of these

cases were classified as possibly due to sodium chlorate. The skin case involved a worker

exposed to drift from an adjacent field and the eye case occurred when a worker bumped into a

spray nozzle while getting off the tractor and was splashed in the face. The skin case was

classified as probably, and the eye case as definitely due to sodium chlorate.

5.2 Other

A number of suicidal ingestions of sodium chlorate have been reported in the literature. Many of

these have led to death and were summarized by Clarkson (2001). The following is taken from

Clarkson’s review:

Accidental and Intentional Poisoning The majority of deaths caused by sodium

chlorate have been the result of suicide (Mengele et al., 1969; Motin et al., 1970; Oliver

et al., 1972; Timperman and Maes, 1966). The chance of ingesting a fatal dose

accidentally is small unless the compound is mistaken for a drug and taken purposely, as
Page 41 of 141

occurred when the potassium salt mistakenly was substituted for potassium chloride

(Cochran and Smith, 1940). However, completely typical, near-fatal poisoning occurred

when a 13-year-old boy “tasted” crystals of this weed killer which he found in his

father’s shed. In spite of intensive treatment, recovery did not begin until about the 15th

day and required a little over 40 days (Starvou et al., 1978).

Dermal absorption associated with agricultural use of sodium chlorate is not sufficient to

cause systemic poisoning. Even by mouth, a large dose is required to produce illness. A

6.35% solution of potassium chlorate was long used as a gargle, or a 300-mg tablet was

allowed to dissolve slowly in the mouth to treat pharyngitis before modern antibiotics

became available. The toxicities of the sodium and potassium salts are similar. It was

considered that a dose of 10,000 mg was fatal (Cochrane ad Smith, 1940; Sollman,

1957). The smallest recorded fatal dose was 7500 mg (Bernstein, 1930). However,

vigorous treatment saved one person who had ingested about 40,000 mg (Knight et al.,

1967).
Page 42 of 141

6.0 Exposure Characterization/Assessment

6.1 Dietary Exposure/Risk Pathway

Dietary exposure (food only) to inorganic chlorates as the chlorate ion (ClO3b) may be expected

from the following dietary exposure routes: (1) from sodium chlorate (073301) as an active

ingredient in conventional (agricultural) pesticides used on food crops; (2) from sodium chlorate

(873301) and potassium chlorate (900583) as inert ingredients in conventional pesticides used on

food crops or in poultry premises; (3) from secondary residues in meat/milk/poultry/eggs due to

residues in animal feedstuffs; (4) from sodium chlorate (873301) and calcium chlorate (875606) as

inert ingredients in antimicrobial agents used as fruit, vegetable, and egg sanitizing washes, on

mushrooms to control bacterial blotch, as treatments to seed used for sprouting, for conditioning

live oysters, in poultry drinking water, in fish filleting, and in pecan cracking/dyeing; (5) as a

potential redox of chlorine dioxide and sodium chlorite in conventional and antimicrobial

pesticides; (6) from degradation of hypochlorites in antimicrobial agents used as fruit and

vegetable washes; and, (7) from translocation of very small amounts of chlorate ion (ClO3b) by

plants (translocation of significant amounts would be phytotoxic to plants) from the environment

which may be present as a result of inorganic chlorate pesticide uses.

No food monitoring data are available for this risk assessment; only limited, chemical-specific field

trial data are available. Exposure estimates in food were based on field trial data or, in the case of

fruit/vegetable/other washes, was derived from a film thickness model. No chemical-specific

livestock metabolism or feeding data are available; exposure estimates in meat, milk, poultry, and

eggs were derived from rat metabolism data, field trial data, and livestock reference information

concerning feed consumption, tissue weights, and milk production. In some cases, due to raw

data limitations, food exposure estimates are calculated as sodium chlorate. Default concentration

factors (no chemical-specific processing data are available), percent crop treated data (chronic

(non-cancer) and cancer assessments only), and the effects of washing after foliar treatments were

also incorporated into the risk assessments.

6.1.1 Residue Profile

Sodium chlorate is currently registered for preharvest and foliar applications as a defoliant or

desiccant to the following food/feed crops: dry beans, corn, cotton, flax, guar, chili peppers,

potatoes, rice, safflower, sorghum (grain), southern peas (i.e., cowpeas), soybeans, and

sunflowers. For food/feed uses, sodium chlorate is formulated as a soluble concentrate (SC) with

the active ingredient ranging from 18% to 47.2%. Sodium chlorate may be applied using aircraft

or ground spray equipment, including high and low volume equipment.

Uses of sodium chlorate as a defoliant or desiccant on cauliflower, cucurbit vegetables, and okra

grown for seed only are considered non-food uses. Uses of sodium chlorate on ornamental

gourds and fallow lands are also considered non-food uses. These non-food uses will not be

discussed further with regards to residue chemistry or dietary exposure/risk considerations.
Page 43 of 141

Under 40 CFR 180.1020 (a) Sodium chlorate is exempt from the requirement of a tolerance for

residues in or on the following raw agricultural commodities when used as a defoliant, desiccant,

or fungicide in accordance with good agricultural practice: beans (dry, edible), corn (fodder), corn

(forage), corn (grain), cottonseed, flaxseed, flax (straw), guar beans, peas (southern), peppers

(chili), potatoes, rice, rice (straw), safflower (grain), sorghum (grain), sorghum (fodder), sorghum

(forage), soybeans and sunflower seed.

Under 40 CFR 180.1020 (b) A time-limited exemption from the requirement of a tolerance is

established for residues of the defoliant/desiccant in connection with use of the pesticide under

section 18 emergency exemptions granted by EPA. This exemption has been granted for wheat

and will expire on 12/31/04. As requested by the Registration Division (Sodium Chlorate Use

Closure Memo Amendment; J. Guerry; dated 11/15/2004) the use of sodium chlorate on wheat is

also addressed herein with the intention to convert the time-limited exemption status to a

permanent exemption from the requirement of a tolerance under 40 CFR.1020 (a). The proposed

use rate is for a single application of sodium chlorate to wheat at 6 lbs ai/A with a 3-day PHI.

No plant metabolism data have been submitted in support of the reregistration of sodium chlorate;

however, no new plant metabolism data are required to support the established sodium chlorate

tolerance exempts. Based on available published information (Loomis et al., J. Am. Soc. Agron.;

25, 724 (1933)), sodium chlorate is highly soluble in water and is expected to readily absorb and

translocate throughout plants. However, given the proposed use conditions, the means of

translocation in treated plants may be substantially disrupted. Translocation of very small

amounts of chlorate ion (ClO3b) by plants (translocation of significant amounts would be

phytotoxic to plants) from the environment which may be present as a result of inorganic chlorate

pesticide uses may occur. Terminal residues are expected to be primarily surface residues.

Since sodium chlorate is a strong oxidizing agent, depending on environmental factors, it is

expected to be easily reduced to chloride and possibly chlorite in plants. Total redox conversion

to these reduced species is not expected; hence, the terminal residues of sodium chlorate in/on

plants are likely chlorate (ClO3b), chlorite (ClO2b), and chloride (Clb).

No ruminant, swine, or poultry metabolism or feeding data have been submitted in support of the

reregistration of sodium chlorate; however, no new animal metabolism data are required to

support the established sodium chlorate exemptions from the requirement of a tolerance. Based

on published rat metabolism data (Abdel-Rahman et al, 1982, 1984b and 1985), terminal residues

of sodium chlorate in animal tissues are expected to be chlorate (ClO3b), chlorite (ClO2b), and

chloride (Clb). Chlorate is readily absorbed from the digestive tract and is excreted as chlorate,

chlorite, and chloride in urine primarily and feces. Within 72 hours, about 40% of the

administered dose was excreted in the urine as chlorate (ca. 13%), chlorite (ca. 4%), and chloride

(ca. 20%) and about 2-4% was excreted in the feces in the same time period. Less than 1% of the

administered dose was found in any of the tissues analyzed including kidney, liver, and skin.
Page 44 of 141

Although some previous residue chemistry reviews for specific exemptions from the requirement

of a tolerance have concluded that there is no reasonable expectation of transfer of residues to

meat, milk, poultry or eggs in specific cases, re-evaluation of the available crop field trial data

taken as a whole, indicate that there is the possibility of detectable residues of sodium chlorate on

animal feedstuffs at harvest. Hence, secondary residues of concern in meat, milk, poultry, and

eggs are possible and; therefore, new ruminant and poultry feeding data are hereby required to

support the reregistration of sodium chlorate. These data are considered confirmatory.

The analytical method used to support the established exemptions from the requirement of a

tolerance is a non-specific colorimetric method (Branderis, J. Sci. Food Agric., 16, 558 (1965)),

deemed acceptable for data collection. The method was originally developed to estimate residual

chlorate concentrations in soil and as a rapid diagnostic test for chlorate toxicity in plants. 

Briefly, the method involves acid extraction, clean-up by shaking with activated charcoal, and

filtration. A solution of ortho-toluidine in HCl is then added to the concentrated extract and the

resulting color is measured at 448 nm for low concentrations and at 490 nm for higher

concentrations of dye. The method is not specific for chlorate since it measures any oxidizing

agent capable of oxidizing chloride ion to free chlorine. A standard curve is prepared with sodium

chlorate for comparison. The lowest sensitivity of the method is estimated at 1 ppm based on

available fortification data from field trials. Chloride does not interfere with the method but

residues of chlorite, which might be present, may also be detected with this method. This method

is hereby deemed adequate for enforcement of sodium chlorate exemptions from the requirement

of a tolerance. [Note: If needed, a more selective HPLC method (“Determination of Residues of

Sodium Chlorate in Potatoes”, Method #S57023, 4/2/91) is available for the detection of sodium

chlorate residues in or on raw agricultural commodities (RACs).] 

New reference standards must be supplied to the EPA National Pesticide Standards Repository.

Only crop field trial data have been submitted to support the reregistration of sodium chlorate. 

No storage stability or processing data are available. The available crop field trial data have been

re-evaluated herein. No additional plant magnitude of the residue or storage stability data are

required to support the reregistration of sodium chlorate. Available crop field trial data deemed

the primary sources of information to support the reregistration of sodium chlorate are briefly

discussed below and summarized in Table C.5. All other available crop field trial data are

considered supplemental and will not be discussed further.

The subject data, except the potato tuber data, were all collected using the colorimetric method

(Branderis, J. Sci. Food Agric., 16, 558 (1965)), deemed acceptable for data collection and

enforcement of the established sodium chlorate exemptions from the requirement of a tolerance. 

The potato tuber data were collected with a more selective HPLC method (“Determination of

Residues of Sodium Chlorate in Potatoes”, Method #S57023, 4/2/91) deemed adequate for data

collection. The lowest limits of quantitation (LOQs) of these methods is estimated at 1 ppm.
Page 45 of 141

Based on the available flax, guar, southern pea, soybean, and sunflower field trial data no

detectable residues of sodium chlorate (<1 ppm) are expected in/on dry beans, guar beans,

southern peas, soybeans, flaxseed, safflower seed, and sunflower seed at the point of harvest from

the maximum use rate of sodium chlorate on dry beans, guar, southern peas, soybeans, flax,

safflower, and sunflower (1 application; 7.5 lbs ai/A; 7-day PHI). Furthermore, no detectable

residues of sodium chlorate (<1 ppm) are expected in/on cottonseed at the point of harvest from

the maximum use rate of sodium chlorate on cotton (2 applications, 7.5 lbs ai/A/application; 7-day

PHI). Any residues which might be detected at the point of harvest are expected to be primarily

surface residues which would be substantially removed prior to the point of consumption. 

Based on the available chili pepper field trial data, it is possible that detectable residues of sodium

chlorate (ca. 13 ppm) might be found on the surface of unwashed chili peppers treated with

sodium chlorate at the maximum use rate of sodium chlorate on chili peppers (1 application; 12.5

lbs ai/A/application; 10-day PHI). However, these residues are primarily surface residues present

at the point of harvest which would be substantially removed by washing (<1 ppm) prior to the

point of consumption.

Based on the available potato field trial data, no detectable residue of sodium chlorate (<1 ppm)

are expected in/on potato tubers at the point of harvest from the maximum use rate of sodium

chlorate on potatoes (1 application; 12.5 lbs ai/A; 7-day PHI). As demonstrated by the chili

pepper field trial data, any residues present at harvest are expected to be primarily surface

residues which would be substantially removed by washing prior to the point of consumption.

Based on the available oat, rice, sorghum, and wheat field trial data, it is possible that detectable

residues of sodium chlorate (ca. 70 ppm (maximum) as demonstrated by sorghum grain) might be

found on the surface of cereal grains retaining their outer hulls at harvest (such as oats and

sorghum) from the maximum use rate of sodium chlorate on rice and sorghum (1 application; 7.5

lbs ai/A; 7-day PHI) and wheat (1 application; 6 lbs ai/A; 3-day PHI). However, once the outer

hulls are removed (either at harvest or during processing), no detectable residues of sodium

chlorate (<1 ppm) are expected in/on cereal grains such as rice and wheat (as demonstrated by

rice w/out hulls and wheat grain data).

Based on the available sorghum field trial data alone, maximum residues in/on sorghum grain

harvested 7-14 days after treatment with sodium chlorate at the maximum use rate for sorghum (1

application; 7.5 lbs ai/A; 7-day PHI) are not expected to exceed 70 ppm. On average, residues

in/on sorghum grain harvested 7-14 days after treatment with sodium chlorate at the maximum

use rate on sorghum (1 application; 7.5 lbs ai/A; 7-day PHI) are not expected to exceed 40 ppm.

Translating the available sorghum field trial data to corn, residues of sodium chlorate are not

expected to exceed 20 ppm (ca. 10 ppm on average) in/on corn grain at the point of harvest from

the maximum use rate of sodium chlorate on corn (1 application, 7.5 lbs ai/A; 14-day PHI). As

demonstrated by the chili pepper field trial data, any residues present at harvest are expected to be

primarily surface residues which would be substantially removed by washing prior to the point of
Page 46 of 141

consumption. Hence, residues of sodium chlorate in/on sweet corn after washing and prior to

consumption would not be expected to exceed 1 ppm.

Based on the available straw (flax, oat, wheat, rice) and forage (guar plants, sorghum stalks,

soybean forage) data, maximum residues of sodium chlorate in/on straw and forage livestock

feedstuffs harvested 3-7 days after treatment with sodium chlorate at the maximum use rate

permitted on forage crops (1 or 2 applications; 7.5 lbs ai/A/application) are not expected to

exceed 300 ppm at the point of harvest. On average, residues in/on straw and forage livestock

feedstuffs should not exceed 100 ppm when harvested 7-14 days after foliar treatment with

sodium chlorate at the maximum use rate permitted on forage crops (1 or 2 applications; 7.5 lbs

ai/A/application).

The highest average residues of chlorate (excluding percent crop treated data) in meat,

poultry, and eggs are expected to be <4 ppm and in milk are expected to be <0.5 ppm based

on the following information and assumptions:

• The highest average theoretical dietary burden for livestock is 175 ppm for cattle feed on a

dry wt. basis

• Cattle eat a maximum of 9.1 kg of feed per day on a dry wt. basis (Update of Livestock

Feed Consumption, 1993); hence, the highest average theoretical dietary exposure for

sodium chlorate to livestock is 1600 mg per day 

• Based on the available rat metabolism data, <1% of the initial dose of chlorate is expected

to be incurred in animal tissues 72 hours after exposure (Abdel-Rahman et al, 1982, 1984b

and 1985); hence <16 mg is expected to be incurred in any livestock tissue of interest

• Assuming that kidneys have the lowest weight of the organs/tissues of interest (other than

milk) in livestock (i.e., compared to meat, liver, fat, and eggs)

• Assuming that the average weight of cattle kidneys is about 4 kg (Update of Livestock

Feed Consumption, 1993; cattle kidneys weigh 3.6-4.5 kg)

• Assuming that the average milk production per day is about 30 kg (Frank, 2002; milk

production is 50-90 lb milk/cow/day) 

Calculations:

(Highest Average Theoretical Dietary Exposure (1600 mg) x Percent of Dietary Exposure Expected in Organs (< 1%)

Average Weight of the Organ/Tissue of Interest (Kidney at 4 Kg or Milk at 30 Kg)

Highest Average Residue Estimate in Meat, Poultry, and Eggs = <4 ppm

Highest Average Residue Estimate in Milk = <0.5 ppm

The maximum residues of chlorate (excluding percent crop treated data) in meat, poultry,

and eggs are expected to be <12 ppm and in milk are expected to be <2 ppm based on the

following information and assumptions:
Page 47 of 141

• The maximum theoretical dietary burden for livestock is 500 ppm for cattle feed on a dry

wt. basis

• Cattle eat a maximum of 9.1 kg of feed per day on a dry wt. basis (Update of Livestock

Feed Consumption, 1993); hence, the highest average theoretical dietary exposure for

sodium chlorate to livestock is 4600 mg per day 

• Based on the available rat metabolism data, <1% of the initial dose of chlorate is expected to

be incurred in animal tissues 72 hours after exposure (Abdel-Rahman et al, 1982, 1984b and

1985); hence <46 mg is expected to be incurred in any livestock tissue of interest

• Assuming that kidneys have the lowest weight of the organs/tissues of interest (other than

milk) in livestock (i.e., compared to meat, liver, fat, and eggs)

• Assuming that the average weight of cattle kidneys is about 4 kg (Update of Livestock Feed

Consumption, 1993; cattle kidneys weigh 3.6-4.5 kg)

• Assuming that the average milk production per day is about 30 kg (Frank, 2002; milk

production is 50-90 lb milk/cow/day)

Calculations:

(Maximum Theoretical Dietary Exposure (4600 mg) x Percent of Dietary Exposure Expected in Organs (< 1%)

Average Weight of the Organ/Tissue of Interest (Kidney at 4 Kg or Milk at 30 Kg)

Maximum Residue Estimate in Meat, Poultry, and Eggs = <12 ppm

Maximum Residue Estimate in Milk = <2 ppm
Page 48 of 141

6.1.2 Chronic (non-cancer) Dietary (food only) Exposure and Risk

A chronic (non-cancer) dietary risk assessment was conducted for all potential chlorate dietary

exposure routes, using the Dietary Exposure Evaluation Model-FCIDTM software with the Food

Commodity Intake Database (DEEM-FCIDTM Version 2.03) and food consumption data from the

United States Department of Agriculture’s (USDA’s) Continuing Surveys of Food Intakes by

Individuals (CSFII) from 1994-1996 and 1998. In this analysis the chronic dietary exposure and

risk estimates resulting from food intake were determined for the general U.S. population and

various population subgroups.

No food monitoring data are available for this risk assessment; only limited, chemical-specific field

trial data are available. Exposure estimates in food were based on field trial data or, in the case of

fruit/vegetable/other washes, was derived from a film thickness model. No chemical-specific

livestock metabolism or feeding data are available; exposure estimates in meat, milk, poultry, and

eggs were derived from rat metabolism data, field trial data, and livestock reference information

concerning feed consumption, tissue weights, and milk production. In some cases, due to raw data

limitations, food exposure estimates are calculated as sodium chlorate. Default concentration

factors (no chemical-specific processing data are available) and the effects of washing after foliar

treatments were also incorporated into the risk assessment. Percent crop treated data were used in

this analysis. Exposures were single point estimates.

The chronic (non-cancer) dietary (food only) risk assessment is below the Agency’s level of concern

for the General U.S. Population and all subgroups. The highest exposed population subgroup,

Children 1-2 years of age, was 28% of the chronic Population Adjusted Dose (cPAD). See Table

6.1.2 below for details.

Table 6.1.2. Summary of Chronic (non-cancer) Dietary (food only) Exposure and Risk for Inorganic

Chlorates

Population Subgroup cPAD a

mg/kg/day % cPAD

General U.S. Population

0.03

9

All Infants (< 1 yr) 15

Children 1-2 yrs 28

Children 3-5 yrs 23

Children 6-12 yrs 14

Youth 13-19 yrs 8

Adults 20-49 yrs 7

Adults 50+ yrs 6

Females 13-49 yrs 7

a

 The BMDL is 0.9 mg chlorate/kg/day. The level of concern for the Margin of Exposure (MOE) is 30.
Page 49 of 141

6.1.3 Cancer Dietary (food only) Exposure and Risk

A cancer dietary risk assessment was conducted for all potential chlorate dietary exposure routes,

using the same dietary (food only) exposure estimates used in the chronic (non-cancer) dietary risk

assessment for the U. S. Population, with a 9% cPAD.

Note: Sodium chlorate is a thyroid toxicant producing thyroid gland follicular cell hypertrophy in

rats and mice following chronic exposures and some evidence of follicular cell tumors in rats. The

lack of mutagenicity indicates that the thyroid tumors are induced by a non-mutagenic mechanism. 

Therefore, for the purposes of this risk assessment, the Margin of Exposure (MOE) approach is

used to estimate inorganic chlorate cancer risk. Children are not expected to be more susceptible to

chlorate-induced thyroid effects than adults and the endpoint selected for the thyroid effects is

protective for all populations, including children.

6.2 Water Exposure/Risk Pathway

6.2.1 Environmental Fate

Sodium chlorate is used as a desiccant/defoliant because it is a strong oxidizer. As a strong

oxidizing agent, chlorate (ClO3b, oxidation state V) gets reduced to chlorine species in lower

oxidation states, such as the oxyanions chlorite (ClO2b, oxidation state III) and hypochlorite 

(ClOb, oxidation state I), chlorine dioxide (oxidation state IV), and chloride (oxidation state -I).

Thus, at least some and possibly substantial reduction of the applied chlorate is likely to occur in the

field prior to any runoff to surface water. Under environmental (terrestrial field) redox conditions

and based on chemical equilibria alone, the thermodynamically favored, end reduction product of

chlorate in soil and in water is the chloride anion. Any intermediate chlorine dioxide that may form

under environmental conditions will undergo photochemical reactions when exposed to sunlight. 

The chlorine oxyanions chlorite and hypochlorite (other possible more reduced intermediates in the

ultimate reduction of chlorate to chloride) are strong oxidizers in themselves and thus, they are also

reduced and/or undergo disproportionation reactions. Although reduction reactions of chlorate,

chlorite, and hypochlorite are said to occur “very fast”, how fast they occur is not known (i.e., the

actual rate constants in the environment are not known). Therefore, at any given time the

distribution of reduced species (type and concentration) cannot be estimated. However, it is

unlikely that a single reduced species would be present. 

6.2.2 Drinking Water
Page 50 of 141

6.2.2.1 Sources and Control of Chlorate Ion

Chlorate ion (ClO3b) is primarily present in drinking water as a result of the use of chlorine dioxide

or hypochlorite solutions for oxidation/disinfection in the treatment process. It may also be present

in the untreated source water, but the ClO3b concentrations contributed to drinking water by

ambient water are generally much lower than those resulting from the treatment process.

The American Water Works Association (AWWA) Disinfection Systems Committee tracks

disinfection practices in US community water systems. Their most recent comprehensive survey

(completed in 1998) estimated that approximately 20% of the systems serving populations greater

than 10,000 use sodium hypochlorite (2% generated it on-site), 8% use chlorine dioxide, and <1%

use calcium hypochlorite. (AWWA, 2000a) For systems serving populations less than 10,000, the

survey estimated that approximately 34% use sodium hypochlorite, none use chlorine dioxide, and

at least 4.5% use calcium hypochlorite. (AWWA, 2000b)

Chlorine Dioxide: The use of chlorine dioxide can introduce ClO3b into the finished water by

several routes. Drinking water plants generally use sodium chlorite as a starting material in the

production of chlorine dioxide. Chlorate ion may be present as a contaminant in the feedstock

material (usually less than four percent of the active chlorite is chlorate). A typical range of ClO3b

carryover to the finished water from chlorite feedstock contamination is about 50 μg/L for a 1-

mg/L dose of chlorine dioxide. (Gates, 1998) Technology to generate chlorine dioxide using

sodium chlorate is now available to the drinking water industry, which introduces the possibility of

ClO3b carryover to the finished water from the chlorate feedstock.

Chlorate ion may also be produced due to inefficient generation of chlorine dioxide. Excess

chlorine will favor the production of ClO3b over chlorine dioxide, as will keeping the generator

mixtures at highly alkaline (pH > 11) or acidic (pH < 3) conditions. If the concentrations of

feedstock reactants are too low or too much dilution water is added during the reaction, ClO3b

formation is also favored.

Chlorite ion (ClO2b) is a major degradation product resulting from the reaction of chlorine dioxide

with inorganic and organic constituents in the water. When free chlorine is used after the

application of chlorine dioxide in the treatment process, ClO2b is oxidized to ClO3b. This

conversion will continue over time as the water travels through the distribution system. Chlorate

ion is also formed by photodecomposition of chlorine dioxide when treated water is exposed to

bright sunlight in open basins.

The primary ways in which water systems can control the levels of ClO3b in the finished water is

through high efficiency operation of their chlorine dioxide generators and by reducing ClO2b

concentrations prior to the addition of free chlorine. Careful control of the generation process

minimizes ClO3

-

 formation. Ferrous ion, which is a coagulant aid, can be used to convert ClO2b to

chloride ion and thus prevent it from reacting with free chlorine to form ClO3b. 
Page 51 of 141

Hypochlorite: Some water systems use sodium hypochlorite or calcium hypochlorite as their source

of free chlorine. Chlorate ion can be formed in these products during the manufacturing process,

but the decomposition of hypochlorite solutions during storage is the more significant source of

ClO3b in systems using hypochlorite. Sodium hypochlorite is usually purchased as a solution, and

ClO3b concentrations increase between the time of manufacture and delivery to the water plant. 

Calcium hypochlorite is a solid, and thus ClO3b concentrations don’t increase until calcium

hypochlorite solutions are prepared for use at the water treatment plant.

The rate at which hypochlorite ion (OClb) disproportionates to ClO3b is influenced by

concentration of OClb, pH, and temperature. The rate of decomposition increases as the

concentration of OClb increases, so water systems can use dilution as one control strategy. The pH

should be in the 12 to 13 range to minimize decomposition; a pH below 11 greatly increases the rate

of decomposition. Hypochlorite solutions should be protected from high temperatures and sunlight. 

Storage time should be minimized; both from the time of manufacture to delivery and from the time

of delivery to use.

6.2.2.2 Chlorate Ion Occurrence Data

Data on the occurrence of ClO3b in drinking water are available from two primary sources: the

Information Collection Rule (ICR) Auxiliary 1 Database, Version 5.0 (USEPA, 2000) and the

AwwaRF research study on the control of ClO3b in hypochlorite solutions (Gordon et al, 1995). 

Information Collection Rule: The most extensive data on the occurrence of ClO3b in drinking

water is from the ICR (USEPA, 1996). Source water and drinking water were monitored for

ClO3b between July 1997 and December 1998. Water systems serving a population of at least

100,000 were required to monitor for ClO3b at treatment plants using chlorine dioxide or

hypochlorite solutions in the treatment process. Plants using chlorine dioxide collected monthly

samples of the source water entering the plant, the finished water leaving the plant, and at three

sample points in the distribution system (near the first customer, an average residence time and a

maximum residence time). Plants using hypochlorite solutions were only required to collect

quarterly samples of the water entering and leaving the plant. If chlorine dioxide or hypochlorite

solutions were used intermittently at a plant, ClO3b samples were only required in sample periods in

which they were in use.

Chlorine dioxide was used by 22 water systems (29 treatment plants) during at least one of the 18

monthly ICR sampling periods. Data from 413 samples collected at the entry point to the

distribution system showed ClO3b concentrations ranging from < 20 μg/L to 1,600 μg/L. The

ClO3b concentrations ranged from < 20 μg/L to 2,200 μg/L in the 1084 samples collected in the

distribution system. The distribution of average ClO3b concentrations calculated for each treatment

plant and sample point are summarized in Table 6.2.2.2.1. The distribution system average

concentrations determined for each water plant by averaging the data from the three distribution

system sample points are summarized in the last column of Table 6.2.2.2.1. The median distribution

system average concentration is 129 μg/L with a range from < 20 μg/L to 691 μg/L.
Page 52 of 141

Sodium hypochlorite solutions were in use in 44 water systems (61 treatment plants) during the six

quarterly ICR sampling periods. (None of the systems reported using calcium hypochlorite as the

source of their chlorine solutions.) Data from 312 samples were reported with concentrations

ranging from < 20 μg/L to a maximum of 1,400 μg/L. The average ClO3b concentration in the

finished drinking water for each treatment plant ranged from < 20 μg/L to 502 μg/L with a median

concentration of 99 μg/L. The table below summarizes the distribution of average ClO3b

concentrations calculated for each plant. 

Table 6.2.2.2.1. Chlorate Concentrations1 (μg/L) - ICR Data

Hypochlorite

Plants Chlorine Dioxide

Plants

Combined Hypochlorite

and Chlorine Dioxide

Plants 

10th Percentile 23 56 24

20th Percentile 37 77 53

50th Percentile 99 119 108

80th Percentile 155 195 179

90th Percentile 239 226 242

Maximum 502 687 691

# WTPs 61 29 90

# PWSs 44 22 66

1

The average chlorate concentration was calculated for each sample point at each water treatment

plant (WTP) over the entire ICR monitoring program. The distribution of these averages is

presented in this table.

2

The distribution system average chlorate concentration was calculated for each WTP using the

three distribution system sample points. The distribution of these averages is presented in this

column.

AwwaRF Hypochlorite Project: The American Water Works Association Research Foundation

sponsored a project to study how water systems could minimize ClO3b formation in the

hypochlorite solutions they use for disinfection. As part of the data gathering effort, they obtained

information from 185 water systems concerning their use of hypochlorite solutions. Samples of

source water, hypochlorite solution, and finished drinking water from 111 of the water systems

were analyzed for ClO3b. Only one set of samples was collected for each system.

Background information on the subset of 111 water systems that provided samples was not

reported separately from the 185 systems who answered the questionnaire. Therefore, the ClO3b
Page 53 of 141

concentrations cannot be directly related to the size of the water system or type of hypochlorite

solution in use. However, 73.5 % of the systems who responded to the questionnaire served

populations less than 100,000 with a subset of 66% serving populations less than 10,000. There is

a possibility that a few systems using calcium hypochlorite were sampled in the AwwaRF project,

since 13% of the 185 systems reported using calcium hypochlorite and 85% reported using sodium

hypochlorite.

The ClO3b concentrations reported in the finished water are summarized in Table 2. The median

concentration in the finished water is 161 μg/L. The distribution of ClO3b is shown below in

Table 6.2.2.2.2. The ClO3b concentrations in the hypochlorite solutions used to treat the water

ranged from 0.03 to 113 g/L.

Table 6.2.2.2.2. Chlorate Concentrations - AwwaRF Project (PWSs using

Hypochlorite Solutions)1

Finished Water Chlorate Concentration (μg/L)

Minimum <10

10th Percentile 15

20th Percentile 41

50th Percentile 161

80th Percentile 611

90th Percentile 1,160

Max 9,180

# PWSs 111

# States 13

1

 A single sample was collected from each of the public water systems (PWSs) in the survey.

6.2.2.3 Chronic Exposure to Chlorate Ion

The ICR data were collected from systems suspected of having ClO3b contamination due to the

treatment process in use. It is reasonable to assume that there were not significant ClO3b levels in

the systems in the same size category that were not sampled. This is based on earlier drinking

water studies that found ClO3b concentrations in source water were too low to impact the levels in

drinking water on the same scale as treating the water with either chlorine dioxide or hypochlorite

(Bolyard et al, 1993). 
Page 54 of 141

The ICR data confirm the presence of ClO3b in source water (75 of 744 samples of water entering

the treatment plants contained measurable ClO3b), but also demonstrate that the concentrations are

generally very low, can vary considerably over time at the same sample site, and are minor

compared to those observed from chlorine dioxide or hypochlorite use. Data were reported from

105 treatment plant influent sample points in the ICR and samples from 33 of those sites contained

ClO3b concentrations of 20 μg/L or greater. Chlorate concentrations were reported in influent

samples from both surface and ground water sources. Samples from fifteen of the 33 sites

contained measurable ClO3b in more than one sampling period, but with one exception, the

concentrations were all #120 μg/L; 70% were between 20 and 50 μg/L. One influent water had a

ClO3b concentration of 944 μg/L in one sample period, but the concentrations were # 100 μg/L in

the other sample periods. Three influent waters contained a high ClO3b concentration (1,300 to

1,600 μg/L) in one sample period and none in the other sample periods. The ICR data indicate

that the influence of source water ClO3b (as reflected by the influent samples) on the

concentrations in finished drinking water is minimal compared to the contribution from using

chlorine dioxide or hypochlorite solutions in the treatment process.

The ICR data set provides the best available estimate of long term exposure to ClO3b from

drinking water, because multiple samples were collected over an 18 month period. Only systems

serving populations of at least 100,000 were sampled during the ICR. Even though this size

category includes roughly one percent of the total number of drinking water systems in the United

States, it serves almost 60 percent of the population. During the ICR, there were 296 water

systems in this size category; 7% used chlorine dioxide and 15% used hypochlorite solutions.

When chlorine dioxide is the source of ClO3b in drinking water, it is appropriate to use the average

concentration in the distribution system to estimate exposure. This is because the concentration is

expected to change within the system due to the conversion of ClO2b to ClO3b in the presence of

chlorine. Fifty percent of the chlorine dioxide plants had average distribution system ClO3b

concentrations of #129 μg/L. Ninety percent had concentrations #264 μg/L.

The average ClO3b concentration at the entry point to the distribution system can be used to

estimate exposure when hypochlorite solutions are the source of the ClO3b contamination. No

additional ClO3b is expected to be formed in the distribution system. Fifty percent of the plants

using hypochlorite solutions had finished water ClO3b concentrations of #99 μg/L. Ninety percent

had concentrations #239 μg/L.

The AwwaRF data set is much smaller than the ICR data set, because the 111 systems from 13

states were only sampled once. Low levels of ClO3b were measured in almost 20% of the source

waters with 90 percent of the samples having concentrations less than 35 μg/L. (Over 30% of the

source waters sampled during the ICR contained measurable concentrations of ClO3b with 90

percent having concentrations less than 23 μg/L.) The finished water ClO3b concentrations

measured in the AwwaRF study are generally higher than those observed in the ICR. This

difference could be the result of a number of factors such as: 1) The AwwaRF data represents a

single point in time while the ICR data reflects an average over 18 months; 2) Most of the
Page 55 of 141

AwwaRF samples were collected from utilities that served population of less than 100,000, while

all of the ICR samples were from utilities serving at least 100,000; and 3) Hypochlorite treatment

practices may have changed between when the AwwaRF samples were collected (1993) and the

ICR samples were collected (1997-98).

Section 6.2.2.1 explains the mode of conversion of hypochlorite ion (OCl-

) to ClO3

-

 for systems

using hypochlorite as their source of free chlorine. The conversion is influenced by the solution

concentration, pH, and ambient temperature. For systems using chlorine dioxide, ClO3

-

 level in the

finished water depends on concentration of chlorate ion in the feedstock, the efficiency of chlorine

dioxide generation, and subsequent disinfection techniques. Awareness of these factors is critical

in controlling chlorate concentrations in finished water. Smaller systems using chlorine dioxide or

hypochlorite, those serving fewer than 100,000, may be more likely to have finished water with

higher levels of chlorate due to smaller budgets and, consequently, fewer resources to devote to

running their systems or training their staff. An untrained staff may not know, for example, that

when free chlorine is used after the application of chlorine dioxide, that ClO2

-

 is oxidized to ClO3

-

.

Both the AwwaRF study and the ICR data reveal high concentrations of chlorate ion to be a local

problem affecting a relatively small number of systems. Section 6.2.2.1 outlines simple measures

that systems of any size can use to maintain low levels of chlorate ion in finished drinking water. 

6.2.2.4. Estimated Concentrations of Chlorate Ion Deemed

Appropriate for Inclusion in the Dietary Risk

Assessment(s)

Based on the available occurrence data (essentially at the tap) from the ICR AUX1 Database

(USEPA, 2000d) and the AwwaRF (1995) survey study, which are discussed above, the following

estimated concentrations of chlorate ion (ClO3b) in drinking water are deemed appropriate for

inclusion in the dietary risk assessment for inorganic chlorates:

• The highest annual average concentration of chlorate ion (ClO3b) in drinking water is

estimated at 0.69 mg/L and is based on the ICR AUX1 Database (USEPA, 2000d). 

• The 90th percentile average concentration of chlorate ion (ClO3b) in drinking water is

estimated at 0.24 mg/L and is based on the ICR AUX1 Database (USEPA, 2000d). 

• The treatment system median average concentration of chlorate ion (ClO3b) in drinking

water in tested large treatment systems is estimated at 0.11 mg/L and is based on the ICR

AUX1 Database (USEPA, 2000d). 

Use of the ICR AUX1 database could underestimate concentrations in drinking water since higher

levels of chlorate ion (ClO3b) in drinking water were found at the small water treatment utilities

sampled in the AwwaRF (1995) project than at the large water treatment plants included in the

ICR AUX1 Database (USEPA, 2000d). However, the AwwaRF (1995) survey study is a less

robust data set consisting of only one sample per utility and, therefore, the ICR AUX1 Database
Page 56 of 141

(USEPA, 2000d) was considered the more appropriate source for estimating averages from

individual water treatment plants.

Chronic (non-cancer) dietary and cancer dietary risk assessments for water only were conducted

using the Dietary Exposure Evaluation Model-FCIDTM software with the Food Commodity Intake

Database (DEEM-FCIDTM Version 2.03) and food and water consumption data from the United

States Department of Agriculture’s (USDA’s) Continuing Surveys of Food Intakes by Individuals

(CSFII) from 1994-1996 and 1998. Available ICR and AwwaRF monitoring data were used to

estimate chlorate concentrations in drinking water. Exposures were single point estimates.

The chronic (non-cancer) dietary risk assessment for chlorate in drinking water (highest annual

average concentration estimated at 0.69 mg/L) is below the Agency’s level of concern for the

General U.S. Population and all subgroups, except all infants (< 1 year of age). The highest

exposed population subgroup, all infants <1 year of age, was 159% of the chronic Population

Adjusted Dose (cPAD). See Table 6.2.2.4 below for details.

Table 6.2.2.4. Summary of Estimated Chronic (non-cancer and cancer) Dietary (water only) Exposure and

Risk for Inorganic Chlorates by Average Annual Concentration in Large Drinking Water

Systemsa

Population Subgroup b cPAD

mg/kg/dayc

% cPAD

Water Estimated

at the 

Highest Annual

Average 

(0.69 mg/L)

Water Estimated

at the 

90th Percentile

Annual Average 

(0.24 mg/L)

Water

Estimated at

the Median

Annual

Average

(0.11 mg/L)

General U.S. Population

0.03

49 17 8

All Infants (< 1 yr) 159 55 25

Children 1-2 yrs 72 25 12

Children 3-5 yrs 67 23 11

Children 6-12 yrs 47 16 7

Youth 13-19 yrs 35 12 6

Adults 20-49 yrs 45 16 7

Adults 50+ yrs 48 17 8

Females 13-49 yrs 45 16 7

a The estimated exposures and risks are based on the ICR data (multiple data points per water system). Higher

concentrations of chlorate ion (ClO3

-

) in drinking water were reported in the AwwaRF data set (only a single data

point per water system), which sampled smaller water systems. 

b

 The values for the population with the highest risk for each type of risk assessment are bolded.

C The BMDL is 0.9 mg chlorate/kg/day. The level of concern for the Margin of Exposure (MOE) is 30.

The Office of Water characterizes the population included in the ICR data as follows:
Page 57 of 141

o “EPA collected data required by the Information Collection Rule (ICR) to support future

regulation of microbial contaminants, disinfectants, and disinfection byproducts. The systems

represented in the ICR database serve 60% of the US population.

o “Included in the ICR are levels of chlorate ion concentrations in the finished water of these

systems. The agency’s level of concern for chlorate ion is 370 ppb. During the ICR, four water

treatment plants had average chlorate ion levels above the agency’s level of concern and

represented 0.5% of the ICR population (621,000 persons). 

o “One treatment plant serving 218,000 persons had average chlorate ion concentrations of 0.69

mg/L. This corresponds to 0.17% of the ICR population; 98 percent of this ICR population

received finished water with average chlorate ion concentrations at or below 0.2 mg/L; 93 percent

received finished water with average chlorate ion concentration at or below 0.1 mg/L; and over 99

percent receives finished water below the Agency’s level of concern of 0.37 mg/L.

o “1 percent of the ICR population (1,260,000 persons) is exposed to chlorate concentrations at

or greater than the 90th percentile concentration of 0.24 mg/L, while, 6.5 percent (8,490,000

persons) is exposed to chlorate concentrations at or greater than the median concentration of 0.11

mg/L. 

o “The best way for these systems to lower the level of chlorate ion in their finished water is to

implement the simple measures explained above.” 

No separate cancer dietary risk assessment for chlorate in drinking water (lifetime average

concentration estimated at 0.1 mg/L) was conducted. The cancer dietary risk assessment is based

on the chronic (non-cancer) dietary risk assessment for the General U.S. Population The cancer

dietary risk assessment for chlorate in drinking water is below the Agency’s level of concern (i.e., %

cPAD less than 100).
Page 58 of 141

6.3 Residential (Non-Occupational) Exposure/Risk Pathway - Conventional

Pesticides

All residential (non-occupational) risk estimates for inorganic chlorates, as active or inert

ingredients in conventional pesticide products used in residential environments, are below the

Agency’s level of concern (i.e., Margin of Exposures (MOEs) are greater than the Level of Concern

(LOC) of 100). These uses are considered to be short-term only due to the episodic uses associated

with homeowner products. Since the episodic nature of residential exposure is inconsistent with the

mechanism of chlorate carcinogenicity, a residential cancer risk assessment was not conducted.

6.3.1 Home Uses

6.3.1.1 Sodium Chlorate (073301) as an active ingredient in

conventional pesticide products - Short-Term Residential

Handler Exposure via Inhalation Route only

There is the potential for exposure to sodium chlorate by residential handlers in outdoor residential

settings during the application of conventional pesticide products containing sodium chlorate

(073301) as the active ingredient. Sodium chlorate (073301) can be used as a non-selective

herbicide in outdoor residential environments as a spot treatment or edging treatment around patios,

along fence lines, lawn edges, around foundations, underneath or around wood decks, and in cracks

and crevices of driveways. Residential handler exposure scenarios are considered to be short-term

only due to the episodic uses associated with homeowner products. Although there is the potential

for dermal exposure by residential handlers, sodium chlorate is an inorganic salt, therefore,

significant absorption of sodium chlorate through intact skin is not expected. Hence, a short-term

risk assessment for residential handlers via the inhalation exposure route was conducted for sodium

chlorate as the active ingredient in conventional pesticide products.

Although there is the potential for exposure to sodium chlorate in outdoor residential settings from

entering areas previously treated with sodium chlorate (073301), as the active ingredient in

conventional pesticide products, a residential postapplication exposure risk assessment for sodium

chlorate was not conducted because:

• Although there is the potential for postapplication dermal exposure in residential settings,

sodium chlorate is an inorganic salt, therefore, significant dermal absorption of sodium chlorate

through intact skin is not expected.

• Postapplication inhalation exposure for sodium chlorate is not expected due to negligible vapor

pressure.

• Postapplication exposure assessments for residential settings are not typically performed for

spot treatments.

A series of assumptions and exposure factors served as the basis for completing the residential

handler risk assessment. Each assumption and factor is detailed below. In addition to these factors,
Page 59 of 141

unit exposures were used to calculate risk estimates. Unit exposures were taken from PHED,

ORETF studies, and one proprietary study. [Note: Several of the assumptions and factors used for

the assessment are similar to those used in the occupational assessment presented under Section

9.1. As such, only factors that are unique to the residential scenarios are presented here.] The

assumptions and factors used in the risk calculations include:

C Due to the lack of chemical specific data, exposures from a scenario deemed similar might be

used. As an example, mixer/loader/applicator data for hose-end sprayers were used to assess

sprinkler can applications. These application methods are believed to be similar enough to

bridge the data.

C HED always considers the maximum application rates allowed by labels in its risk assessments. 

If additional information such as average or typical rates are available, these values also may be

used to allow risk managers to make a more informed risk management decision.

C Residential risk assessments are based on estimates of what homeowners would typically treat,

such as the size of a lawn, or the size of a garden. The factors used for the sodium chlorate

assessment were from the Health Effects Division Science Advisory Council for Exposure

Policy 12: Recommended Revisions To The Standard Operating Procedures For Residential

Exposure Assessment which was completed on February 22, 2001 and on professional

judgement. The daily volumes handled and area treated, used in each residential scenario,

include: 

• 1000 square feet when mixing/loading/applying liquids as a spot treatment with a lowpressure handwand and sprinkler cans;

• 1 gallon when applying with a RTU sprinkler can and trigger pump sprayer; and,

• 1000 square feet for granular formulation spot treatments.

Short-term risks for residential handlers via the inhalation exposure route are presented below in

Table 6.3.1.1. All risks are below the Agency’s level of concern (i.e, Margin of Exposures (MOEs)

are greater than the Level of Concern (LOC) of 100). The scenarios assessed represent worse-case

exposures and risks. It should also be noted that there were many other scenarios where medium to

low PHED quality data were used to complete the assessment. Data quality should be considered

in the interpretation of the uncertainties associated with each risk value presented.
Page 60 of 141

Table 6.3.1.1. Sodium Chlorate (073301) - Short Term Residential Inhalation Exposure1

Exposure Scenario (Scenario #) Daily Area Treated2 Crop/Target3 Application Rate4 

Mixer/Loader/Applicators, Loader/Applicators, & Applicators

M/L/A liquids with a Low Pressure HandwandSprayer (1)

1000 Spot/edging

treatment

23.7 

L/A RTU liquid with a Trigger Pump Sprayer (2) 1 Spot/edging

treatment

0.196 

M/L/A liquids with a Sprinkler Can (3) 1000 Spot/edging

treatment

23.7 

Applying liquid with a RTU Sprinkler Can (4) 1 Spot/edging

treatment

0.27 

Applying granules by Hand (5) 1000 Spot/edging

treatment

12 

L/A granules with a Belly Grinder (6) 1000 Spot/edging

treatment

12 

L/A granules with a Push-type Spreader (7) 1000 Spot/edging

treatment

12 

1 Residential exposures assessments do not include PPE.2 Amount treated is presented in ft2/day, except for Scenario #s 2 and 4 which are presented in gallons/day. (Standard EPA/OPP/HED values).3 Crops and use patterns are from label extractions (Appendix 1), BEAD’s LUIS reports, and the Sodium Chlorate Use Closure Memo (J. Guerry, 84 Ranges of application rates are based on values from label extractions (Appendix 1), BEAD’s LUIS reports, and the Sodium Chlorate Use Closur

10/13/04; 11/15/04). Application rates upon which the analysis is based are presented as lb ai/1000 ft2, except for Scenario #s 2 and 4 which are p

5 Inhalation MOE = Oral NOAEL (30 mg/kg/day) / Daily Inhalation Dose. HED LOC for MOE is 100.
Page 61 of 141

6.3.1.2 Sodium Chlorate (873301) as an inert ingredient in conventional

pesticide products - Short-Term Residential Postapplication

Exposure via Incidental Oral Route only

There is the potential for postapplication exposure in outdoor residential settings from entering

areas previously treated with conventional pesticide products containing sodium chlorate (873301)

as an inert ingredient. Hence, a residential postapplication risk assessment was conducted. 

However, since these products are professionally applied, residential handler exposure is not of

concern.

Sodium chlorate (873301) as an inert ingredient in herbicide formulation products can be applied

professionally to residential sites. These conventional pesticide products contain < 1 % sodium

chlorate and can be applied at rates no greater than 0.07 lb (as sodium chlorate) per acre.

As an inert ingredient in herbicide formulations broadcast on residential sites, there is potential for

children to have incidental oral exposures (hand-to-mouth (HTM), object-to-mouth(OTM), and soil

ingestion (SI)); however, residential postapplication exposures via dermal and inhalation routes are

not of concern because:

• Although there is the potential for postapplication dermal exposure in residential settings,

sodium chlorate is an inorganic salt, therefore, significant dermal absorption of sodium chlorate

through intact skin is not expected.

• Postapplication inhalation exposure for sodium chlorate is not expected due to negligible vapor

pressure.

A series of assumptions and exposure factors served as the basis for completing the residential

postapplication risk assessments. Each assumption and factor is detailed below.

• Residential exposure and risk estimates are conducted assuming no personal protective

equipment (i.e., short-sleeved shirt, shorts, shoes/socks, and no respirator).

• Residential postapplication exposures are assessed on the day of pesticide application.

• 15 kg represents the body weight of a toddler (3 year old).

• 5% of the application rate has been used to calculate the day-zero residue levels used for

assessing risks from HTM behaviors.

• 20% of the application rate has been used to calculate the day-zero residue levels used for

assessing risks from OTM behaviors.

• 100% of the application rate has been used to calculate the day-zero soil residue levels used

for assessing risks from SI.

• Hand-to-mouth exposures are based on a frequency of 20 events/hour and a surface area per

event of 20 cm2

 representing the palmar surfaces of three fingers;

• 50% saliva extraction factor for HTM exposures.

• OTM exposures are based on a 25 cm2

 surface area.

• Exposure durations are expected to be 2 hours.
Page 62 of 141

• Soil residues are contained in the top 1 centimeter and soil density is 0.67 cm3/gram.

 Table 6.3.1.2 below shows the risk estimates for incidental oral exposures to sodium chlorate

(877301) for children playing in treated areas following its application.

Table 6.3.1.2. Short-term Residential Postapplication Risk Estimates for Sodium Chlorate (873301)

Population Subgroup Scenario Route MOE Combined MOE

Child

Hand-to-Mouth Oral 29000

Object-to-Mouth Oral 110000 23000

Soil Ingestion Oral 8600000

6.3.2 Recreational Uses

Recreational exposures are expected to be similar to, or in many cases, less than, those evaluated in

Section 6.3.1 Home Uses; therefore, a separate recreational exposure assessment was not

conducted.

6.3.3 Other (Spray Drift, etc.)

Spray drift is always a potential source of exposure to residents nearby to spraying operations. This

is particularly the case with aerial application, but, to a lesser extent, could also be a potential

source of exposure from the ground application method employed for sodium chlorate. The

Agency has been working with the Spray Drift Task Force, EPA Regional Offices and State Lead

Agencies for pesticide regulation and other parties to develop the best spray drift management

practices. On a chemical by chemical basis, the Agency is now requiring interim mitigation

measures for aerial applications that must be placed on product labels/labeling. The Agency has

completed its evaluation of the new data base submitted by the Spray Drift Task Force, a

membership of U.S. pesticide registrants, and is developing a policy on how to appropriately apply

the data and the AgDRIFT computer model to its risk assessments for pesticides applied by air,

orchard airblast and ground hydraulic methods. After the policy is in place, the Agency may impose

further refinements in spray drift management practices to reduce off-target drift with specific

products with significant risks associated with drift.
Page 63 of 141

7.0 Aggregate Risk Assessments and Risk Characterization

Evaluation of the hazard and exposure (food, water, and residential) components for inorganic

chlorates indicates the need to estimate potential risks for the following scenarios: Short-term

inhalation, screening level acute dietary (food + water), chronic (non-cancer) dietary (food +

water), and cancer dietary (food + water).

7.1 Short-Term Aggregate Risk - Residential Handler Inhalation plus background

(chronic dietary (food + water))

Table 7.1. Short-Term Aggregate Risk Calculations

Population Target Aggregate

MOE 1

MOE

food+water 2

MOE inhalation 3 Aggregate MOE

(food+water and residential) 4

Adult 100 1715 400 324

1 Inhalation MOE = Oral NOAEL (30 mg/kg/day) / Daily Inhalation Dose. HED LOC for MOE is 100.

2

 MOE food+water = [( Short-Term oral NOAEL = 30 mg/kg/day)/(chronic dietary exposure food + water)

Chronic dietary exposure food + water = 0.002730mg/kg/day(food) + 0.01476mg/kg/day(water) = 0.01749mg/kg/day

3

 MOE inhalation = [(Short-Term inhalation NOAEL = 30 mg/kg/day)/(high-end inhalation residential exposure)]

4

 Aggregate MOE (food+water and residential) = 1÷[ [(1÷MOE food+water) + (1÷MOE inhalation)]]

7.2 Chronic (non-cancer) Dietary Risk - Food + Water

Table 7.2. Summary of Chronic (non-cancer) Dietary (food + water) Exposure and Risk for Inorganic

Chlorates

Population Subgroup a cPAD

mg/kg/day

% cPAD

Food + Water

Estimated at the 

Highest Annual

Average 

(0.69 mg/L)

Food + Water

Estimated at the 

90th Percentile

Annual Average 

(0.24 mg/L)

Food+Water

Estimated at

the Median

Annual

Average

(0.11 mg/L)

General U.S. Population

0.03

58 26 17

All Infants (< 1 yr) 174 70 40

Children 1-2 yrs 100 53 39

Children 3-5 yrs 90 47 34

Children 6-12 yrs 60 30 21

Youth 13-19 yrs 43 20 14

Adults 20-49 yrs 52 23 14

Adults 50+ yrs 54 23 14

Females 13-49 yrs 52 23 14

a

 The values for the population with the highest risk for each type of risk assessment are bolded.
Page 64 of 141

b

 The BMDL is 0.9 mg chlorate/kg/day. The level of concern for the Margin of Exposure (MOE) is 30.

7.3 Cancer Dietary Risk - Food + Water

No separate cancer dietary (food + water) risk assessment was conducted. The chronic (food +

water) dietary risk assessment is protective for cancer for the General U. S. Population. (See Table

7.2.) The estimated risk does not exceed our level of concern (less than 100% cPAD).

Note: Sodium chlorate is a thyroid toxicant producing thyroid gland follicular cell hypertrophy in

rats and mice following chronic exposures and some evidence of follicular cell tumors in rats. The

lack of mutagenicity indicates that the thyroid tumors are induced by a non-mutagenic mechanism. 

Therefore, for the purposes of this risk assessment, the Margin of Exposure (MOE) approach is

used to estimate inorganic chlorate cancer risk. Children are not expected to be more susceptible to

chlorate-induced thyroid effects than adults and the endpoint selected for the thyroid effects is

protective for all populations, including children.
Page 65 of 141

8.0 Cumulative Risk Characterization/Assessment

Unlike other pesticides for which EPA has followed a cumulative risk approach based on a common

mechanism of toxicity, EPA has not made a common mechanism of toxicity finding as to inorganic

chlorates and any other substances. However, available data indicate that there may be some

interconversion between chlorate and chlorite in water, in the environment, and in the gut.

For the purposes of this tolerance action, EPA has not assumed that inorganic chlorates have a

common mechanism of toxicity with other substances. For information regarding EPA’s efforts to

determine which chemicals have a common mechanism of toxicity and to evaluate the cumulative

effects of such chemicals, see the policy statements released by EPA’s Office of Pesticide Programs

concerning common mechanism determinations and procedures for cumulating effects from

substances found to have a common mechanism on EPA’s website at

http://www.epa.gov/pesticides/cumulative/.
Page 66 of 141

9.0 Occupational Exposure/Risk Pathway - Conventional Pesticide Products Only

9.1 Short/Intermediate/Long-Term Handler Risk

There is potential for occupational handler exposure to inorganic chlorates from: (1) the application

of sodium chlorate (073301) as the active ingredient in conventional pesticide products used on

both agricultural and commercial (non-agricultural) sites (i.e., mixer/loaders, applicators, flaggers,

and mixer/loader/applicators); (2) the application of sodium chlorate (873301) as an inert

ingredient in conventional pesticide products used on both agricultural and commercial (nonagricultural) sites (i.e., mixer/loaders, applicators, flaggers, and mixer/loader/applicators); and (3)

the application of potassium chlorate (900583) as an inert ingredient in conventional pesticide

products used in poultry premises.

With the addition of PPE (dust/mist respirator) or engineering controls (enclosed cockpits or cabs),

all occupational handler scenarios for the use of inorganic chlorates as an active or inert ingredient

in conventional pesticides are below the Agency’s level of concern (i.e., Margin of Exposures

(MOEs) are greater than the Level of Concern (LOC) of 100). Exposure durations are short- and

intermediate-term only. Since the exposure durations for occupational handlers are inconsistent

with the mechanism of chlorate carcinogenicity, an occupational cancer risk assessment was not

conducted.

9.1.1 Sodium chlorate (073301) as the active ingredient in conventional pesticide

products - Short-/Intermediate-Term Occupational Handler Exposure via

Inhalation Route only

There is potential for occupational handler exposure to sodium chlorate from the application of

sodium chlorate (073301) as the active ingredient in conventional pesticide products used on both

agricultural and commercial (non-agricultural) sites (i.e., mixer/loaders, applicators, flaggers, and

mixer/loader/applicators). Occupational handler scenarios were identified for which exposure to

sodium chlorate is expected (see Table 9.1.1).

Sodium chlorate is an agricultural defoliant/desiccant and a commercial herbicide. Use patterns

vary from short- to intermediate-term exposure durations. Occupational handlers may be exposed 

dermal and inhalation routes; however, sodium chlorate is an inorganic salt, therefore, significant

absorption of sodium chlorate through intact skin is not expected. Hence, only short- and

intermediate-term sodium chlorate risk assessment for occupational handlers via the inhalation

exposure route was conducted.

 

Risk for most occupational handler baseline (without a respirator) inhalation exposure scenarios do

not exceed the Agency’s level of concern (i.e., Margin of Exposures (MOEs) are greater than the

Level of Concern (LOC) of 100). However, occupational handler risks for some of the high end

application rates (1032 and 523 lb ai/A) did exceed the Agency’s level of concern at baseline. Risk

mitigation for these scenarios was accomplished with the addition of a dust/mist respirator (with an
Page 67 of 141

80% reduction factor), or, for certain scenarios, with engineering controls (enclosed cabs or

cockpits).

No chemical-specific handler exposure data are available and, therefore, the following data and

assumptions were used to assess the subject handler exposures and risks:

C Occupational handler exposure estimates were based on surrogate data from: (1) the Pesticide

Handlers Exposure Database (PHED), and (2) Outdoor Residential Exposure Task Force

(ORETF).

C Average body weight of an adult handler is 70 kg because the toxicity endpoint values used for

the assessments are appropriate for average adult body weight representing the general

population. This is the case because none of the effects identified in the selected toxicity studies

were sex specific.

C Exposure factors used to calculate daily exposures to handlers are based on applicable data if

available. For lack of appropriate data, values from a scenario deemed similar enough by the

assessor might be used. As an example, for sodium chlorate handler exposures, ORETF data

for hose-end sprayer equipment were used to assess sprinkling can applications. The nature of

these application methods are believed to be similar enough to bridge the data. 

C HED always considers the maximum application rates allowed by labels in its risk assessments. 

If additional information such as a different range of rates are available, these values also may be

used to allow risk managers to make a more informed risk management decision.

C The typical occupational workday is assumed to be 8 hours. 

C The daily area treated was defined for each handler scenario (in appropriate units) by

determining the amount that can be reasonably treated in a single day (e.g. acres, square feet, or

gallons per day). When possible, the assumptions for daily areas treated is taken from ExpoSAC

SOP #9: Standard Values for Daily Acres Treated in Agriculture which was completed on July

5, 2000. Assumptions for these scenarios, including further refinements based on HED

estimates, are listed below.

Agricultural Scenarios

S Aerial applications: 350 acres (typical field crop assumption) for guar beans, southern peas,

chili peppers (for processing only), potatoes, ornamental gourds, and cucurbits (grown for

seed); 1200 acres (high acreage crop assumption) for cotton, corn, rice, dry beans, sorghum,

flax, safflower, sunflower, soybeans, wheat, and fallow land.

S Groundboom: 80 acres (typical field crop assumption) for guar beans, southern peas, chili

peppers (for processing only), potatoes, ornamental gourds, and cucurbits (grown for

seeds); 200 acres (high acreage crop assumption) for cotton, corn, rice, dry beans, sorghum,

flax, safflower, sunflower, soybeans, wheat and fallow land.
Page 68 of 141

S Flaggers: 350 acres.

Refinements into “typical field” and “high acreage” crops was performed with help from HED

crop expert Bernard Schneider (email from B. Schneider, 5/24/04).

Industrial/Non-Crop Sites

S Rights-of-Way Sprayer and Handgun Sprayer: 5 acres per day;

S Low Pressure Handwand Sprayer: 2 acres per day;

Note: Although assessments for applications involving rights-of-way sprayers and low

pressure handwands typically use a volume-based approach for amount handled/treated per

day (1000 gallons and 40 gallons, respectively, from ExpoSAC Policy #9), label-specific

application rates and their respective dilution factors for larger application settings are better

represented by a daily unit area treated than a volume based approach. For example, the

label-specific application of 8 pints per 100 square feet [EPA Reg. No. 7701-34] yields the

application rate of 1032 lb ai in 2196 gallons of solution per acre. At this rate, the volumebased approach of 1000 gallons per day would have a worker treating approximately 1⁄2

acres per day. Because a rights-of-way sprayer would likely treat more than 1⁄2 acre per day,

a daily unit area of 5 acres was used as more appropriate estimate.

S Belly grinder: 1 acre per day.

S Push-type spreader: 5 acres per day

S Groundboom and Tractor-drawn Spreader: 40 acres per day.
Page 69 of 141

Table 9.1.1. Sodium Chlorate (073301): Short- and Intermediate-Term Occupational Inhalation Exposure

Exposure Scenario (Scenario #) Daily Area Treated1 Crop/Target2 Application Rate3 Inhala

Mixer/Loader

Mixing/Loading liquids for Aerial

application (1a)

1200

Cotton, Corn, Rice, Dry Beans, Grain Sorghum, Flax,

Safflower, Sunflower, Soybeans 7.5 

Fallow Land, Wheat 6 

350

Chili Peppers (for processing only), Potatoes 12.5 

Ornamental Gourds, Cucurbits (grown for seed) 6 

Guar Beans, Southern Peas 7.5 

Mixing/Loading liquids for

Groundboom application (1b)

200

Cotton, Corn, Rice, Dry Beans, Grain Sorghum, Flax,

Safflower, Sunflower, Soybeans 7.5 

Fallow Land, Wheat 6 

80

Chili Peppers (for processing only), Potatoes 12.5 

Ornamental Gourds, Cucurbits (grown for seed) 6 

Guar Beans, Southern Peas 7.5 

40 Industrial/Non-Crop Sites

1032 

523 132 

Mixing/Loading liquids for Rights-ofWay Sprayer application (1c) 5 Rights-of-Way & Industrial/Non-Crop Sites

1032 

523 132 

Loading granules for Tractor-drawn

Spreader application (2) 40 Industrial/Non-Crop Sites

523 240 161 

Applicator
Table 9.1.1. Sodium Chlorate (073301): Short- and Intermediate-Term Occupational Inhalation Exposure

Exposure Scenario (Scenario #) Daily Area Treated1 Crop/Target2 Application Rate3 Inhala

Page 70 of 141

Aerial spray applications (3a)

1200

Cotton, Corn, Rice, Dry Beans, Grain Sorghum, Flax,

Safflower, Sunflower, Soybeans 7.50 

Fallow Land, Wheat 6 

350

Guar Beans, Southern Peas 7.5 

Chili Peppers (for processing only), Potatoes 12.5 

Ornamental Gourds, Cucurbits (grown for seed) 6 

Groundboom spray applications (3b)

1200

Cotton, Corn, Rice, Dry Beans, Grain Sorghum, Flax,

Safflower, Sunflower, Soybeans 7.5 

Fallow Land, Wheat 6 

350

Guar Beans, Southern Peas 7.5 

Chili Peppers (for processing only), Potatoes 12.5 

Ornamental Gourds, Cucurbits (grown for seed) 6 

40 Industrial/Non-Crop Sites

1032

523

132

Rights-of-Way Sprayer Applications

(3c)

5 Rights-of-Way & Industrial/Non-Crop Sites

1032 

523 132 

Tractor-drawn Spreader Applications

(4) 40 Industrial/Non-Crop Sites

523240 
Table 9.1.1. Sodium Chlorate (073301): Short- and Intermediate-Term Occupational Inhalation Exposure

Exposure Scenario (Scenario #) Daily Area Treated1 Crop/Target2 Application Rate3 Inhala

Page 71 of 141

161
Table 9.1.1. Sodium Chlorate (073301): Short- and Intermediate-Term Occupational Inhalation Exposure

Exposure Scenario (Scenario #) Daily Area Treated1 Crop/Target2 Application Rate3 Inhala

Page 72 of 141

Flagger

Flagging for Aerial Spray applications

(5) 350 Various Agricultural Crops 12.5 

Mixer/Loader/Applicators & Loader/Applicators

M/L/A liquids with a Low Pressure

Handwand Sprayer (6) 2 Industrial/Non-Crop Sites

1032 

523 132 

M/L/A liquids with a Handgun Sprayer

(7) 5 Industrial/Non-Crop Sites

1032 

523 132 

L/A granules with a Belly Grinder (8) 1 Industrial/Non-Crop Sites

523 240 161 

L/A granules with a Push-type

Spreader (9) 5 Industrial/Non-Crop Sites

523 240 161 

1 Amount treated is presented in acres/day. (Standard EPA/OPP/HED values).2 Crops and use patterns are from label extractions (Appendix 1), BEAD’s LUIS reports, and the Sodium Chlorate Use Closure Memo (J. Guerry, 8/5/04; 10/3 Ranges of application rates are based on values from label extractions (Appendix 1), BEAD’s LUIS reports, and the Sodium Chlorate Use Closure Memo (J

11/15/04). Application rates upon which the analysis is based are presented as lb ai/acre.

4 Inhalation MOE = Oral NOAEL (30 mg/kg/day) / Daily Inhalation Dose. HED LOC for MOE is 100.5 Mitigation LevelsBaseline: No respiratorPPE - 80% R: Dust/mist respirator with an 80% reduction factorEngineering Control: Closed cockpit or cab
Page 73 of 141

9.1.2 Sodium chlorate (873301) as an inert ingredient in conventional pesticide

products - Short-/Intermediate-Term Occupational Handler Exposure via

Inhalation Route only

There is potential for occupational handler exposure to chlorate from the application of sodium

chlorate (873301) as an inert ingredient in conventional pesticide products used on both

agricultural and commercial (non-agricultural) sites (i.e., mixer/loaders, applicators, flaggers, and

mixer/loader/applicators). Occupational handler scenarios were identified for which exposure to

sodium chlorate is expected (see Table 9.1.2).

Herbicide formulations containing < 1% sodium chlorate (873301) as an inert ingredient may be

professionally applied to agricultural and commercial (non-agricultural) sites at the maximum use

rate of 0.07 lb (as sodium chlorate) per acre. Use patterns vary from short- to intermediate-term

exposure durations. Occupational handlers may be exposed dermal and inhalation routes;

however, sodium chlorate is an inorganic salt, therefore, significant absorption of sodium chlorate

through intact skin is not expected. Hence, only short- and intermediate-term sodium chlorate

risk assessment for occupational handlers via the inhalation exposure route was conducted.

No chemical-specific handler exposure data are available and, therefore, the following data and

assumptions were used to assess the subject handler exposures and risks:

C Assumptions for daily area treated are taken from ExpoSAC SOP #9: Standard Values for

Daily Acres Treated in Agriculture (July 5, 2000) or from professional judgement.

C Unit exposures are from the PHED Surrogate Exposure Guide (August, 1998) or data

from the Outdoor Residential Exposure Task Force (ORETF).

C Baseline personal protective equipment (PPE) represents (in terms of inhalation exposure

and risk) a worker without a respirator.

C Average body weight of an adult handler is 70 kg because the toxicity endpoint values

used for the assessments are appropriate for average adult body weight representing the

general population. This is the case because none of the effects identified in the selected

toxicity studies were sex specific.
Page 74 of 141

Table 9.1.2. Short-/Intermediate-Term Occupational Inhalation Exposure Risk Estimates for Sodium Chlorate (873301) as an Inert Ingredient in H

Exposure Scenario Unit Exposure Daily Area Treated Crop/Target Application Rate 

Mixer/Loader

Mixing/Loading liquids for Aerial application 0.0012 1200 Agricultural crops 0.07 

Mixing/Loading liquids for Groundboom application 0.0012 350 Agricultural crops 0.07 

Mixing/Loading liquids for Rights-of-Way Sprayer

application 0.0012 5 Non-agricultural sites 0.07 

Mixing/Loading liquids for Handgun Sprayer application 0.0012 100 Residential sites 0.07 

Applicator

Aerial spray applications 0.000068 1200 Agricultural crops 0.07 

Groundboom spray applications (open cab) 0.00074 350 Agricultural crops 0.07 

Rights-of-Way Sprayer Applications 0.0039 5 Non-agricultural sites 0.07 

Flagger

Flagging for Aerial Spray applications 0.00035 350 Agricultural Crops 0.07 

Mixer/Loader/Applicators

M/L/A liquids with a Low Pressure Handwand Sprayer 0.03 1 Residential sites 0.07 

M/L/A liquids with a Handgun Sprayer 0.0018 5 Residential sites 0.07 

M/L/A liquids with a Backpack Sprayer 0.03 1 Residential sites 0.07 
Page 75 of 141

9.1.3 Potassium chlorate (900583) as an inert ingredient in conventional pesticide

products - Short-/Intermediate-Term Occupational Handler Exposure via

Inhalation Route only

There is potential for occupational handler exposure to potassium chlorate from the application of

potassium chlorate (900583) as an inert ingredient in conventional pesticide products used in

poultry premises. Occupational handler scenarios were identified for which exposure to

potassium chlorate is expected (see Table 9.1.3).

Potassium chlorate (900583) as an inert ingredient in airborne fungicide products can be applied

in poultry premises. These conventional pesticide products contain < 20% potassium chlorate and

can be applied at rates not greater than 0.01 lb ( as potassium chlorate) per 500 ft3.

Use patterns vary from short- to intermediate-term exposure durations. Occupational handlers

may be exposed dermal and inhalation routes; however, potassium chlorate is an inorganic salt,

therefore, significant absorption of potassium chlorate through intact skin is not expected. Hence,

only short- and intermediate-term potassium chlorate risk assessment for occupational handlers

via the inhalation exposure route was conducted.

No chemical-specific handler exposure data are available and, therefore, the following data and

assumptions were used to assess the subject handler exposures and risks:

C This risk calculation is assumed to be a very conservative estimate. It assumes that all the

potassium chlorate (no greater than 0.01 lb) is present in the air, and available for

inhalation, following application of the airborne fungicide.

C Baseline PPE represents (in terms of inhalation exposure and risk) a worker without a

respirator.

C Exposure duration is estimated to be 1 minute per day.

C Adult inhalation rate for light activity is 16.6 l/min.

C Average body weight of an adult handler is 70 kg because the toxicity endpoint values

used for the assessments are appropriate for average adult body weight representing the

general population. This is the case because none of the effects identified in the selected

toxicity studies were sex specific.

Table 9.1.3. Short-/Intermediate-Term Occupational Inhalation Exposure Risk Estimates for Potassium

Chlorate (900583) as an Inert Ingredient Used in Airbourne Fungicides

Exposure Scenario Application

Rate

Maximum Potential

Airborne Concentration 

(mg KClO3/l)

Non-Cancer

MOE

Mitigation Level

Airborne Application of

Fungicide

0.01 lb/500 ft3 0.32 400 Baseline
Page 76 of 141

9.2 Short/Intermediate/Long-Term Postapplication Risk

Postapplication exposures do not need to be included in the occupational risk assessment for

inorganic chlorates. Although dermal and inhalation exposures are possible, these exposures are

expected to be negligible due to the physical and chemical characteristics of inorganic chlorates.

10.0 Data Needs and Label Requirements

10.1 Toxicology

870.3465 28-Day Inhalation Study

These data are needed to refine the need for additional PPE (dust/mist respirator) or

engineering controls (enclosed cockpit or cabs) to protect occupational handlers from

potential inhalation exposure resulting from conventional agricultural use of sodium

chlorate.

10.2 Residue Chemistry

860.1480 Magnitude of the Residue - Meat, Milk, Poultry, Eggs

New ruminant and poultry feeding studies are required.

860.1650 Submittal of Analytical Reference Standards

Submission of a reasonable amount of the analytical reference standards for sodium

chlorate to the Pesticide Repository is required and replenishment of standards as

requested by the repository.

10.3 Occupational and Residential Exposure

Sodium chlorate (073301) end-use product labels should be amended, as necessary, to include

application rates in terms of lbs/acre treated for clarification.

Unpublished References:

Benchmark Dose Analysis of Sodium Chlorate FCH Response in Rats: No DP Barcode, B. Daiss,

01/26/2005.

Chlorate Ion in Drinking Water, memo from Patricia Fair (Office of Ground Water and Drinking

Water Technical Support Center) to Jacqueline Guerry (OPPTS/OPP/SRRD/RB3), dated

08/10/2005.

Drinking Water Assessment of Sodium Chlorate as a Desiccant/Defoliant on Food/Feed

Terrestrial Uses: D303556, S. Termes, 01/05/2005.
Page 77 of 141

Incident Report: D310573, J. Blondell, 03/31/2005.

Inorganic Chlorates Dietary Exposure Assessment for the Reregistration Eligibility Decision:

D303555. T. Morton, 01/26/2006.

Occupational and Residential Exposure Assessment for Sodium Chlorate (073301) as an Active

Ingredient in Conventional Pesticides: D307365, M. Crowley, 06/13/2005.

Occupational and Residential Exposure Assessment for Inorganic Chlorates in Antimicrobial

Pesticides: D312200, T. Leighton, 01/24/2005.

Occupational and Residential Exposure Assessment for Inorganic Chlorates as Inert Ingredients in

Conventional Pesticides: D318045, M. Crowley, 06/13/2005.

Response to Sodium Chlorate Preliminary Risk Assessment, memo of OW to Jacqueline Guerry,

SRRD, 10/20/2005.

Note: Residue Chemistry Considerations are addressed under Appendix C.

Published References:

AWWA Water Quality Division Disinfection Systems Committee, Committee Report:

Disinfection at Large and Medium-Size Systems, May 2000a, p 32-43.

AWWA Water Quality Division Disinfection Systems Committee, Committee Report:

Disinfection at Small Systems, May 2000b, p 24-31.

Bolyard, M., Fair, P.S., and Hautman, D.P. “Sources of Chlorate Ion in US Drinking Water,”

Journal AWWA Vol 85(9) 81-88, 1993.

Dohler, K. D., Wong, C. C., Von Zur Muhlen, A. (1979) The rat as a model for the study of

drug effects on thyroid function: Consideration of methodological problems. Pharmacol. Ther. 5,

305-318

Gates, D.J. The Chlorine Dioxide Handbook. American Water Works Association, Denver, CO,

1998.

Gordon, G.G., Adam, L., and Bubnis, B. Minimizing Chlorate Ion Formation in Drinking Water

When Hypochlorite Ion is the Chlorinating Agent. American Water Works Association Research

Foundation, Denver, CO, 1995.
Page 78 of 141

McClain, R. M. (1992). Thyroid gland neoplasia: non-genotoxic mechanisms. Toxicol. Lett. 

64/65, 397-408.

USEPA, 1996. National Primary Drinking Water Regulation: Monitoring Requirements for

Public Drinking Water Supplies: Cryptosporidium, Giardia, Viruses, Disinfection Byproducts,

Water Treatment Plant Data and Other Information Requirements. Final Rule. FR 61:94:24354-

24388 (May 14, 1996).

USEPA, 2000. ICR Auxiliary 1 Database. EPA 815-C-00-002. Office of Water, Cincinnati,

OH, April 2000.
Page 79 of 141

APPENDIX A TOXICOLOGY DATA REQUIREMENTS

Test Technical

Required Satisfied

870.1100 Acute Oral Toxicity ...................... 870.1200 Acute Dermal Toxicity .................... 870.1300 Acute Inhalation Toxicity .................. 870.2400 Primary Eye Irritation .................... 870.2500 Primary Dermal Irritation .................. 870.2600 Dermal Sensitization .....................

yes

yes

yes

yes

yes

yes

yes

yes

yes

yes

yes

yes

870.3100 Oral Subchronic (Rodent) ....................

870.3150 Oral Subchronic (Non-Rodent) ................

870.3200 21-Day Dermal ............................

870.3250 90-Day Dermal ............................

870.3465 28-Day Inhalation .........................

yes

yes

no

no

yes

yes

yes

-

-

no

870.3700a Developmental Toxicity (Rodent) ............. 870.3700b Developmental Toxicity( Non-rodent) ...........

870.3800 Reproduction ..............................

yes

yes

yes

yes

yes*

yes**

870.4100a Chronic Toxicity (Rodent) ................. 870.4100b Chronic Toxicity (Non-rodent) .............. 870.4200a Oncogenicity (Rat) ...................... 870.4200b Oncogenicity (Mouse) .................... 870.4300 Chronic/Oncogenicity ....................yes

yes

yes

yes

yes

yes*

yes***

yes*

yes*

yes*

870.5100 Mutagenicity—Gene Mutation - bacterial ........ 870.5300 Mutagenicity—Gene Mutation - mammalian ..... 870.5395 Mutagenicity— Erythrocyte Micronucleus ....... 870.5385 Mutagenicity— Bone Marrow Cytogenetics ...... 870.5550 Mutagenicity—Unscheduled DNA Synthesis ..... 870.5275 Mutagenicity— Recessive lethal in Drosophila ....yes

yes

yes

yes

yes

yes

yes

yes

yes*

yes*

yes

yes*

870.6100a Acute Delayed Neurotox. (Hen) .............. 870.6100b 90-Day Neurotoxicity Hen) ................. 870.6200a Acute Neurotoxicity. Screening Battery (Rat) ..... 870.6200b 90 Day Neurotoxicity Screening Battery (Rat) ..... 870.6300 Develop. Neurotoxicity ...................no

no

no

no

no

-

-

-

-

-

870.7485 General Metabolism ..................... 870.7600 Dermal Penetration ...................... yes

no

yes*

-

Special Studies for Ocular Effects . . . . . . . . . . . . . . . . . . . . . . .

Acute Oral (Rat) . . . . . . . . . . . . . . . . . . . . . . . . . . .

Subchronic Oral (Rat) . . . . . . . . . . . . . . . . . . . . . . .

Six-month Oral (Dog) . . . . . . . . . . . . . . . . . . . . . . .

no

no

no

-

-

-

- Not Applicable

*

 Chlorate published study

** Chlorite published study

*** The 2-year NTP (DRAFT NTP Report 2004) study in the rat satisfies this requirement. No toxicity was seen in

the subchronic study in dogs administered sodium chlorate by oral gavage except for emesis at the highest dose of

360 mg/kg/day.

APPENDIX B TOXICOLOGY STUDIES

The executive summaries of tox studies presented in the sodium chlorate toxicology profile are provided below.
Page 80 of 141

Acute Toxicity

The acute oral LD50 of potassium chlorate has been reported to be 1870 mg/kg in rats and the

lowest oral lethal dose in rats was 7000 mg/kg, in rabbits 2000 mg/kg and in dogs 1200 mg/kg

(Cosmetic Ingredient Review Panel, 1995)

The published literature provides numerous references to sodium chlorate poisoning. In one

report (Helliwell & Nunn, 1979), 14 cases of deliberate and accidental sodium chlorate poisonings

in individuals (males and females) ranging in age from 3- 55 years old are described. In one case a

48 year old female died after 20 hours of accidentally ingesting 15 g of sodium chlorate. Death is

described occurring from massive intra vascular hemolysis and acute renal failure. Recovery from

sodium chlorate poisoning was low even with medical intervention. The clinical features of

sodium chlorate poisonings in these cases were nausea and vomiting, cyanosis, abdominal pain,

diarrhea, dyspnea. In the patients who died, a “constant necropsy finding was a chocolate

discoloration of the blood and viscera due to staining by bilirubin and methemoglobin”.

The acute toxic effects of potassium chlorate are summarized in the 1995 Cosmetic Ingredient

Review Panel, 1995. The toxic dose of potassium chlorate is often reported to be 5 g with the

lethal adult dose being 15-35 g. Mortality of a child has been reported after ingestion of 1 g of

potassium chlorate. Human chlorate ingestion can produce gastritis, a late toxic nephritis,

hemolysis, methemoglobinemia, hemoglobinuria and acute renal failure. The toxic effects of

potassium chlorate appear cumulative because of the slow excretion of the chlorate ion; repeated

1 g ingestions have been fatal. Dermal irritation and burns have been reported in industrial uses.

Use of potassium chlorate in toothpastes may have caused inflammation and bleeding of the gums.

In a case of severe chlorate poisoning of a 26 year old female who ingested 150-200 grams of

sodium chlorate, methemoglobinaemia was described as the early symptom of intoxication

(Steffen and Seitz, 1981). Methemoglobin was converted to hematin. The patient was deeply

cyanotic when admitted to hospital approximately 5 hours after ingesting the material. After

extensive gastric lavage and administration of methylene blue and ascorbic acid intravenously, 7.4

grams of sodium chlorate were excreted in the urine. The patient voided clear urine initially,

turning dark brown becoming muddy before it completely subsided, the result of renal failure. 

After the renal failure, the patient required several weeks of hemodialysis. Renal function was

absent for 10 days and recovered slowly and the patient was discharged after 3 months. Liver

function was only moderately disturbed. Serum tranasaminases were elevated during the first 10

days. Bilirubin was only slightly elevated for 3 weeks. 

Subchronic Toxicity 

870.3100 90-Day Oral Toxicity - Rat

In a subchronic oral toxicity study (MRID 40444801), Sprague-Dawley CD rats (15/sex/group)

were dosed with technical grade sodium chlorate (100% a.i., white granular solid) gavage at 0
Page 81 of 141

(distilled water), 10, 40, 100, or 1000 mg/kg/day for 90 consecutive days. Body weight gain was

lower in females of all dosed groups compared to controls which had abnormal body weight gain.

The body weights of males were minimally lower (not statistically significant) in the two highest

dose groups. The most notable effects of sodium chlorate dosing were on the hematological

parameters. At the 1000 mg/kg/dose, hemoglobin concentration, hematocrit, red blood cell

counts were statistically significantly decreased, and reticulocyte count was statistically

significantly increased in females. In males, only the hematocrit was statistically significantly

decreased at the highest dose tested (HDT). The adrenal weight was depressed in both males and

females at the HDT. Histological lesions were detected in all groups but with no apparent dose

relationship. The LOAEL derived from this study was 1000 mg/kg/day based on the

hematological effects and the NOAEL was 100 mg/kg/day. This study is considered

Acceptable/guideline.

In a published study (Kurokawa et al, 1985) it was reported that administration of 1% sodium or

potassium chlorate in the drinking water (654-686 mg/kg/day) to male F344 rats for 25 weeks

produced significant decrease in mean body weights compared to the controls. This dose was the

maximum tolerated dose based on a 6-week screening study at 0.25, 0.5, 1 and 2% doses in

drinking water. Relative kidney weights of the potassium chlorate treated rats were significantly

increased over the control group, suggesting renal toxicity.

Studies were conducted to determine the toxicity of chlorine dioxide (0, 1, 10, 100, 1000 mg/L)

and its conversion products chlorite and chlorate (10, 100 mg/L) in drinking water in rats. After 9

month treatment the osmotic fragility of the red blood cells (RBC) was decreased in all treatment

groups, while a decreased blood glutathione was only observed in the chlorite/chlorate groups. 

At 2, 4 and 6 months, no significant hematologic changes were noted in treated rats compared to

control. After 9 month RBC counts, hematocrit and Hb were decreased in all treatment groups. 

Chlorine dioxide, chlorite and chlorate administered chronically in drinking water for 3 months

inhibited the incorporation of 3

H-thymidine into nuclei of rat testes. This inhibition was observed

in the liver of the chlorite groups and in the kidney of 100 mg/L chlorine dioxide treatment. The

incorporation in small intestinal nuclei was increased in 10 and 100 mg/L chlorine dioxide and in

10 mg/L chlorite groups. Rat body weight was decreased in all groups after 10 and 11 months 

(Abdel-Rahman et al. 1984) 
Page 82 of 141

EPA/PATHOLOGY ASSOCIATES Study

In a published study conducted by USEPA Risk Reduction Engineering

Laboratory/Environmental Monitoring Systems Laboratory in Cincinnati, Ohio and by Pathology

Associates in Ohio (McCauley et al, 1995), Sprague Dawley rats (10/sex/group) were exposed to

sodium chlorate in the drinking water at concentrations of 0 (distilled water control), 48 mM

saline (sodium chloride) control, 3.0 mM sodium chlorate, 12 mM sodium chlorate or 48 mM

sodium chlorate for 90 days. The final sodium concentration was 48.0 mM for each group except

for the distilled water control. At the end of 90 day exposure animals were sacrificed and organs

were collected for gross pathological and histopathological examination. Blood was collected for

clinical and hematological evaluation.

During the course of chlorate exposure, no behavioral or clinical abnormalities were noted and

there were no compound related deaths. The water consumption was 100 g/kg/day for the

distilled water control group males and the mid-dose group males. The other male groups

consumed 20 to 30% more. The water consumption for the females was 133, 167, 172, 163, and

200 g/kg/day for the distilled water control, saline control, low-, mid- and high-dose groups,

respectively. Based on the water consumption, the mean delivered doses were calculated to be

0.36 mM (30 mg), 1.2 mM (100 mg), and 6.14 mM (510 mg) chlorate/kg/day for the low-, midand high- dose males and 0.5 (42 mg), 1.9 (158 mg), and 9.6 mM (797 mg) chlorate/kg/day for

the low-, mid- and high- dose females, respectively. Treatment-related effects were conspicuous

in the high dose group. These included significant body weight reduction throughout the

exposure group in both sexes, significant decreases in male relative organ weights of the heart,

kidneys and liver with relative brain and testes weights increased, significant declines in female

relative weights of adrenals, thymus and spleen with significant brain weight increased, significant

decreases in clinical chemistry parameters: ALT, AST, calcium, creatine, and phosphorus and an

increase in the serum cholesterol. Calcium and creatinine also declined in the mid-dose group,

serum BUN levels were decreased in the low dose females. The biological relevance of the

clinical chemistry changes in all chlorate groups was considered doubtful, since most of the values

were within the normal reference ranges. There was a significant decrease in hematocrit

concentration and red and white blood cell counts in the high dose animals while females of this

group exhibited a trend towards decreased erythrocyte and hematocrit values. 

Histopathologically, thyroid colloid depletion was noted in both control and treated animals in a

dose related manner and was characterized by an increased number of smaller follicles which were

lined by a prominent cuboidal epithelium but devoid of colloid. The control group had an

incidence of 30% with a minimal to mild severity while those in the mid and high dose groups

exhibited a 100% incidence level with a moderate to marked severity. The authors cite a

published study (Harrington and Shertzer, 1985) which demonstrates the effects of chlorine

dioxide on the bioavailability of iodide in drinking water and diet. In that paper, it was concluded

that chlorine dioxide in drinking water oxidizes iodide to a reactive form which binds to tissues of

the digestive tract while with dietary chow it converts iodide to a less easily absorbed by

organification to dietary constituents. According to current study authors “these findings suggest

a possible mechanism by which chlorate, a by-product of chloride dioxide degradation, may
Page 83 of 141

accentuate colloid depletion due to this anti-thyroid effect of reducing iodide availability”. The

study authors concluded that based on the biologically significant changes noted in the mid and

high dose groups of both sexes (thyroid colloid depletion) and hematological effects at the high

dose, the LOAEL is 1.20 mM (100 mg chlorate)/kg bw/day in males and 1.9 mM (158 mg

chlorate)/kg bw/day for females and the NOAEL is 0.36 mM (30 mg chlorate/kg bw/day in

males) and 0.50 mM (42 mg chlorate/kg bw/day for females).

EPA/NTP Studies

In a 21 day oral toxicity study (NTP 1999a and 1999b), B6C3F1 mice and Fisher 344 rats

(10/sex/dose) were exposed to sodium chlorate in the drinking water at 0, 125, 500, 1000 or 2000

mg/L . Measured consumption was 0, 22, 43, 173 or 348 mg/kg/day for male mice, 0, 20, 44,

94, 192 or 363 mg/kg/day for female mice; 0, 20, 36, 77 or 170 mg/kg/day for male rats and 0,

21, 38, 73, 152 or 338 mg/kg/day for female rats. In mice, sodium chlorate had no effect on

survival, body weights, clinical signs, water consumption, hematology parameters, methemoglobin

concentration, or organ weights of either sex. There were no gross or microscopic lesions that

were considered to be due to sodium chlorate treatment. In rats, sodium chlorate had no effect

on survival, body weights, clinical signs or water consumption. A moderate to severe neutropenia

was observed in both sexes on day 4 and 22. Very mild decreases in erythrocyte counts,

hemoglobin, and hematocrit were considered not to be biologically significant. The only gross or

microscopic lesion that was considered to be treatment related was a minimal to mild follicular

cell hyperplasia of the thyroid gland seen in males at 500 mg/L or greater and in females at 250

mg/L or greater. The thyroid gland was considered to be a target organ for sodium chlorate

toxicity in the rat.

In a published study conducted by USEPA National Health and Environmental Effects Research

Laboratory and the NTP National Institute of Environmental Health Sciences in North Carolina

(Hooth et al, 2001), to evaluate development of thyroid lesions in rodents exposed to sodium

chlorate in the drinking water, male and female F344 rats and B6C3F1 mice (10/group) were

exposed to sodium chlorate in drinking water at 0, 0.125, 0.25, 1 or 2 g/L for 21 days (NTP

study) . In another test, male and female rats (10/group) were exposed at 0, 0.125, 1 or 2 g/L for

4, 21 or 90 days (NTP study). Additional male rats (10/group) were exposed to 0, 0.001, 0.01,

0.1, 1 or 2 g/L for 90 days (EPA study). Mean compound consumption at these water

concentrations was estimated by the reviewer to be 0.112, 1.12, 11.2, 112, and 225 mg/kg/day for

the males and 0.16, 1.6, 16.0, 160, 320 mg/kg/day for the females based on water consumption

values reported in the McCauley et al, 1995 article. Additional female rats and female mice

(6/group) were exposed to 0, 0.500, 1, 2, 4, or 6 g/L for 105 days (EPA study) (82, 165, 330,

660, 990 estimated mg/kg/day). Animals were observed daily and moribund animals were

necropsied. Prior to necropsy, a blood sample was collected from animals treated for 4, 21 or 90

days and the serum was separated and frozen (NTP study). Complete necropsies were performed

on all animals and tissues of interest were removed, examined macroscopically, and fixed in 10%

neutral buffered formalin. Fixed thyroid tissues were processed by routine methods to 5 um

paraffin sections and stained with hematoxylin and eosin for histological examination by light
Page 84 of 141

microscopy. The thyroids were examined for the presence of colloid depletion, follicular cell

hypertrophy, and follicular cell hyperplasia. 

Total serum triiodothyronine (T3) and thyroxine (T4) concentrations were determined as well as

the thyroid stimulating hormone (TSH) concentrations. Serum T3 and T4 levels were decreased

significantly and TSH levels increased significantly in male and female rats after 4 days of

treatment with 1.0 or 2.0 g/L sodium chlorate and after 21 days of treatment with 2.0 g/L. TSH

levels also increased significantly in male rats after 21 days of treatment with 1.0 g/L. Serum T3

and T4 levels were comparable to controls in male and female rats after 90 days of treatment, but

TSH levels were increased in both sexes.

Thyroid alterations were initially diagnosed using standard published methods. According to this

method, follicular cell hyperplasia and severe colloid depletion were present in all male and female

F344 rats following 21 days of treatment with 1.0 g/L treatment of sodium chlorate or greater. 

The severity of the lesions was the same in all animals. The present study utilized a “novel”

method of diagnosis detailed in the article. According to this diagnosis colloid depletion and

hypertrophy were present in male and female rats treated with 0.125 g/L or greater, but were

statistically significant (p<0.05) at 0.5 g/L treatments. In males, the incidence and severity of

thyroid alterations was greater at 1.0 g/L Sodium chlorate than 2.0 g/L, but in females, it was the

opposite. After 90 days of treatment, significant colloid depletion was diagnosed in most treated

male F344 rats but the incidences were similar in all groups. Colloid depletion was more

significant in female rats treated with 1.0 or 2.0 g/L sodium chlorate for 21 days than for 105

days. Significant colloid depletion was diagnosed in female F344 rats treated for 105 days at

sodium chlorate concentrations of 2.0 g/L or greater. 

Follicular cell hypertrophy was present in most male and female rats after 21 or 90 days of sodium

chlorate treatment, but the incidence did not increase in a concentration dependent manner. The

incidence of follicular cell hypertrophy was higher in female rats treated with 1.0 or 2.0 g/L

sodium chlorate for 21 days than for 105 days. At 105 days, 6.0 g/L of sodium chlorate caused a

significant increase in the incidence of follicular cell hypertrophy. Complex papillary infolding or

branching was more frequent in thyroid tissue from male rats at the 1.0 and 2.0 g/L

concentrations. The area of the thyroid tissue affected in male rats increased in a concentration

dependent manner following 90 days of treatment. Thyroid alterations were not present in

male or female mice. 

It was concluded by the study authors that sodium chlorate treatment induced a concentration

dependent increase in the incidence and severity of thyroid follicular cell hyperplasia. Colloid

depletion and hypertrophy were the most sensitive histopathological indicators of sodium chlorate

exposure in male F344 rats at 21 and 90 days, although the hypertrophy response was variable

when concentration dependency was evaluated. Male rats were more sensitive to the effects of

sodium chlorate treatment than female rats. Decreases in serum hormone levels observed in the

present study may suggest that sodium chlorate has the potential to induce acute detrimental

neurodevelopmental effects. Hormone and histological alterations may reflect a transient
Page 85 of 141

physiologic response of the thyroid to sodium chlorate exposure. It is not known whether the

histological effects of sodium chlorate are reversible following cessation of chemical exposure. 

Alternatively, the concentration dependent increase in incidence and severity of thyroid follicular

cell hyperplasia may indicate an increased likelihood of the lesions progressing to cancer. The

study authors did not provide a NOAEL for the effects of sodium chlorate treatment in rats, but

based on the article, a NOAEL may be derived at 0.5 g/L (28 mg/kg/day in males and 40

mg/kg/day in females) based on colloid depletion and follicular cell hyperplasia at a LOAEL of

1.0 g/L (112 mg/kg day for males and 160 mg/kg/day for females) sodium chlorate after 90 days

of exposure. Chlorate is related in structure to bromate and perchlorate, both are thyroid

toxicants and chemical oxidants.

870.3150 90-Day Oral Toxicity - Dog

In a subchronic oral toxicity study (MRID 40460402), beagle dogs (4/sex/group) were dosed with

technical grade sodium chlorate (100% a.i., white granular solid) by oral gavage at dose levels of

0 (distilled water), 30, 60, or 360 mg/kg/day for 90 consecutive days. All dogs survived the

treatment. Clinical signs were sporadic, one female in the high dose group exhibited emesis

during the first three weeks of dosing and two other females developed yellow/brown watery

stool. There were no effects on hematological parameters, clinical chemistry (including

methemoglobin), opthalmology or histopathology. Urinalysis was not conducted. The adrenal,

and spleen weights, and organ/body weight ratios in males were increased at the HDT. Only the

spleen weights in females were increased at the HDT. Hypercellularality of the bone marrow of

males appeared to increase in severity and number of animals responding as the dose was

increased. The effect was less pronounced in females. None of these effects are sufficiently

adverse to establish an effect level. The dose levels used in this study were too low to detect

unequivocal toxicity. At higher dose levels in a range-finding study, emesis occurred, and it was

stated that emesis would have precluded a study at higher dose levels. The LOAEL derived from

this study is >360 mg/kg/day and the NOAEL is 360 mg/kg/day (the HDT). This study is

considered Acceptable/guideline (The study was originally classified supplementary because of

missing data regarding incomplete histopathological examination of mammary tissues, and number

of animals examined opthalmologicaly was not stated. These do not impact the acceptability of

the study).

In a sub-acute exposure study in dogs, doses of 200 to 326 mg/kg/day of sodium chlorate

administered daily by intubation as 50 ml of 6% solution to 8 dogs for 5 days caused reduction of

packed cell volume, hemoglobin and red blood cells (Heywood et al, 1972 cited in the Final Draft

Drinking Water Criteria, Clement International Corp., 1994). A consistent increase in plasma

urea concentration was also observed, suggesting some compromise of renal function. Two

animals that received 308 or 326 mg/kg/day suffered appetite loss, body weight decline and

appearance of blood in their urine or feces. One of the animals (not specified) died after 4 days of

exposure. Postmortem examination of both animals revealed typical signs of chlorate poisoning,

including cyanotic kidney surface and evidence of necrosis and hemolysis in the kidney. Five of

the 8 animals displayed tissue pathology indicative of hemolysis such as Kupffer cells containing
Page 86 of 141

brown pigment. Hematological values of red blood cells were reduced in all animals. The highest

methemoglobin concentrations was seen in the animal that died. Methemoglobinemia was not

correlated with changes in the other hematological parameters.

870.4100a Chronic Toxicity - Mouse

In the NTP (DRAFT NTP Report 2004) study presented in a draft form, Groups of 50 male and

50 female B6C3F1 mice were exposed to drinking water containing 0, 500, 1,000, or 2,000 mg/L

sodium chlorate for 2 years (equivalent to average daily doses of approximately 40, 80, and 160

mg/kg per day to male mice and 30, 60, and 120 mg/kg per day to female mice). Survival of

exposed mice was similar to that of the control groups. Mean body weights of exposed females

were generally less (88-90% of controls in all treated females at week 104) than those of the

control groups after week 84 of the study. Water consumption by exposed mice was generally

similar to that by controls throughout the study (3.4-4.2 g/male/day; 2.5-3.6 g/female/day). There

was a positive trend in the incidences of pancreatic islet cell adenoma or carcinoma (combined) in

female mice (0/46, 2/47, 2/49, 4/49). Thyroid gland follicular cell hypertrophy was significantly

increased in 2,000 mg/L females (3/48, 2/50, 5/49, 14/50). The incidences of bone marrow

hyperplasia were significantly increased in all exposed groups of females (14/50, 28/50, 29/50,

31/50). 

Carcinogenicity

870.4200a Carcinogenicity Study - rat

A 2-year bioassay to determine the potential of sodium chlorate to induce thyroid tumors in

laboratory animals (rats and mice) has been recently reported in a draft form. A final report of

this study is expected during 2005. In the NTP (2004) study summarized in Section 4.4.3 of the

main body of this memo, there was some evidence of thyroid gland follicular cell carcinogenicity

in male rats which may be attributed to the imbalance of thyroid hormones (reduced T3 and T4 and

elevated TSH) seen in these studies as a result of exposure to high doses of sodium chlorate. 

Current EPA HED policy considers nonmutagenic pesticides that induce elevated levels of TSH

and thyroid follicular cell tumors in the rat as not likely to be cargencogenic to humans at doses

that do not alter rat thyroid hormone homeostasis.

In a published study, sodium chlorate and potassium chlorate were tested for potential promoting

effect in a two stage rat renal carcinogenesis assay (Kurokawa et al, 1985). In this assay three

groups of 15 male F344 rats were given N-ethyl-N-hydroxyethylnitrosamine (EHEN) at 0.05%

concentration in the drinking water for the first 2 weeks during the initiation phase. Subsequently,

one group of the initiated rats was treated with 1% sodium chlorate, second group with 1%

potassium chlorate and the third group with distilled water for 25 weeks. Three other groups

(controls) were treated similarly, except that distilled water was given in the initiation phase.
Page 87 of 141

These doses were selected on the basis of 6 week study where male F344 rats were administered

the test compounds in the drinking water at 0, 0.25%, 1% or 2% concentrations and found that

1% concentration was the maximum tolerated concentration for both test compounds. All

animals survived the treatment in the main study. The mean final body weight in the sodium

chlorate and potassium chlorate groups with or without initiation were significantly lower (p

<0.05-0.01) than the controls. The mean intake of drinking water (water consumption) in rats

treated with sodium chlorate or potassium chlorate was slightly lower than the controls and it

ranged from 19.2 - 22.1 ml/day/rat. The mean consumption of sodium chlorate was 654-686

mg/kg/day for sodium chlorate and 667 to 675 mg/kg/day for the potassium chlorate. At the end

of promotion phase, rats were sacrificed and kidneys examined histopathologically for renal

neoplastic lesions which were classified as dysplastic foci and renal cell tumors. The mean

absolute kidney weights were comparable in all groups, but the mean relative kidney weights

given the sodium chlorate or potassium chlorate with or without initiation were significantly

(p<0.01-0.05) lower than the control group. There were no statistically significant differences in

the incidences in the mean number of the types of the kidney lesions between the test compounds

and the distilled water treated rats initiated with EHEN, it was concluded that sodium chlorate

and potassium chlorate did not have a promoting effect in rat renal carcinogenesis assay

(Kurokawa et al, 1985). 

870.4200b Carcinogenicity (feeding) - Mouse

A 2-year bioassay to determine the potential of sodium chlorate to induce thyroid tumors in

laboratory animals (rats and mice) has been recently reported in a draft form (DRAFT NTP

Report 2004). A final report of this study is expected during 2005. As summarized above, there

was a positive trend in the incidences of pancreatic islet cell adenoma or carcinoma (combined) in

female mice (0/46, 2/47, 2/49, 4/49). This finding was considered to be equivocal evidence.

870.7485 Metabolism - Rat

The pharmacokinetics of chlorite ion and chlorate ion was studied in rats (Abdel-Rahman et al,

1982, 1984b and 1985). Two groups of male Sprague-Dawley rats (4/group) were administered

orally 36Cl- labeled potassium chlorate or potassium chlorite at concentrations of 10 mg/L. In one

group, blood samples were collected at selected times between 5 minutes and 48 hours after

dosing and assayed for 36Cl- activity and at 72 hours, the rats were killed and the tissue

distribution of 36Cl- activity was determined. In the other group, expired air, urine, and fecal

samples were obtained for up to 72 hours and assayed for 36Cl- activity. Maximum blood 36Clconcentrations occurred 2 hours after dosing with potassium chlorite and 1 hour after treatment

with potassium chlorate. Potassium chlorate elimination from the blood was biphasic, with half 

lives of 6 hours for the first phase and 36.7 hours for the second phase. Potassium chlorite

elimination was monophasic with a half life of 35 hours. After 72 hours, 36Cl- activity was

highest in whole blood following potassium chlorite administration and highest in plasma

following potassium chlorate administration. The highest measured radioactivity after the plasma

in the chlorate treated rats was in the whole blood followed by stomach, testes, lungs, kidneys,
Page 88 of 141

skin, duodenum, spleen, brain, packed cells, ileum, carcass, liver, and bone marrow. 36Clconcentration in the plasma was 2 ng/g, and in bone marrow was less than 0.5 ng/g. Significantly

high levels of 36Cl- activity after dosing with both compounds were found in the testes. Seventy

two hours after dosing with potassium chlorite, 35 percent of the dose was eliminated in the urine

and 5% in the feces. Approximately 43% of the potassium chlorate dose was eliminated by the

urinary and feces routes. 36Cl- was not detected in exhaled air after dosing with either compound. 

The administered chlorate was eliminated as chlorate (ca. 13% of the administered dose), chlorite

(ca. 4% of the administered dose) and chloride (ca. 20% of the administered dose). The authors

suggest that the high levels of 36Cl- activity in the testes after 72 hours suggest possible

pharmacological action at this site.

870.7485 Metabolism - Dog

A metabolism study in dogs is reported in the National Research Council 1980 report on Drinking

Water and Health and is summarized in California EPA/OEHHA 2002 Report (OEHHA, 2002). 

In this study, when seven female dogs were given 500 mg/kg doses of chlorate in 500 mL water,

55-70 % of the dose was excreted in the urine in the first 6 hours. By 24 to 48 hours, 76-99% of

the dose had been excreted unchanged in urine. The chlorate concentration in the blood peaked

at 2 hours and decreased to little or none by 24 hours. 
Page 89 of 141

Special/Other Studies

Sodium Chlorate as an Inhibitor of Protein Sulfation

Sodium chlorate has been described as a non-toxic inhibitor of tyrosine sulfation (Beinfeld, 1994). 

This property is utilized by biochemists to study peptide and protein synthesis, regulation of

protein secretion and function (Beinfeld, 1994; Mintz et al, 1994). Sodium chlorate is an in vitro

inhibitor of ATP-sulfurylase, the first enzyme in the biosynthesis of 3'-phosphoadenosine 5'-

phosphosulfate which is the ubiquitous co-substrate for sulfation (Baeuerle and Huttner, 1986). 

Treatment of hybridoma derived cells and rat pheochromocytoma cell cultures with 1 mM sodium

chlorate in a medium low in sulfate and sulfur-containing amino acids resulted in more than 95%

inhibition of protein sulfation as well as tyrosine and carbohydrate sulfation, but did not inhibit

protein synthesis even after prolonged incubation. The authors concluded from this study that

sodium chlorate “provides powerful tool for studying the biological significance of protein

sulfation” (Baeuerle and Huttner, 1986). The sulfation of polyethylene glycol 200 by the isolated

perfused guinea pig liver was inhibited to about 60% by 10 mM of sodium chlorate in the plasma

of the perfusate when the concentration of the sulfate ion was 1.18 mM, but in a low sulfate

medium (0.1mM), the inhibition was almost complete (94%) (Roy et al, 1988). Bile production

from isolated perfused livers was not affected by the presence of sodium chlorate in this test,

suggesting that chlorate is not a general liver poison according to the authors of this article (Roy

et al, 1988). When bovine aorta endothelial cells were cultured in a medium containing 3

Hglucosamine, 35S-sulfate and various concentrations of sodium chlorate, cell growth and viability

was not affected by 10mM chlorate and slight inhibition at 30 mM (Humphries and Silbert, 1988). 

Chlorate concentrations of 10 mM and greater resulted in significant inhibition of sulfation of

chondroitin. With 30 mM chlorate the inhibition was 90% for chondroitin and 65% for heparin,

but 3H-glucosamine incorporation was not inhibited. Removal of chlorate from the cell culture

medium restored the rapid resumption of sulfation.

Chlorate Toxicity in Humans

In a series of studies by Lubbers et al (1984a, 1984b), investigating the physiological impact of

human ingestion of chlorine dioxide and its water breakdown byproducts (chlorite and chlorate),

reported no effects attributable to the daily consumption of water treated with these products for

periods extending to 12 weeks. In these studies normal healthy adult male volunteers (21-35

years of age) divided into groups (10/group) drank daily 500 mL of water containing 5 ppm of

chlorite, or chlorate or distilled water (control) for 12 weeks. Subjects were monitored weekly

during the 12 week treatment and for 8 additional weeks by conducting physical medical

examination, checking vital signs. Special chemical tests for thyroid function, antibody formation,

hepatoglobin and methemoglobin concentrations, and blood morphology were repeated regularly

to assess physiological functions in areas “suspected to be most sensitive to oxidative challenge”. 

Subjective evaluations of the palatability of the water disinfectant solutions were recorded at

regular intervals. A total of 47 quantitative chemical parameters derived from an extensive

battery of blood and urine testing were recorded regularly. Abnormalities in the qualitative blood

and urine analysis were few and appeared to be randomly distributed. In several cases,
Page 90 of 141

statistically significant trends (mean corpuscular hemoglobin levels) were associated with

treatment, but “none of these were judged to have physiological consequence”. The authors

concluded that the possibility that these trends might achieve proportions of clinical importance

cannot be ruled out, but “within the limits of the study, the relative safety of oral ingestion of

chlorine dioxide, and its metabolites, chlorite and chlorate, was demonstrated”. In their second

study (Lubbers et al, 1984b), 3 male healthy adult volunteers deficient in glucos-6-phosphate

dehydrogenase and receiving 500 mL of water containing 500 ppm of sodium chlorite did not

experience any adverse effects demonstrating the safety of this chemical to a susceptible group of

the human population.

These data were not deemed useful for dose-response evaluation and were not relied upon in the

risk assessment.

Chlorates Mechanism of Toxicity

The mode of action in sodium chlorate poisoning in humans is summarized by Smith and Oehme

(1991) in their review article. The chlorate ion initially reacts with thiol groups on the red blood

cells and may cause it to lyse, similar to nitrite ions, converting the hemoglobin to methemoglobin. 

The chlorate ion is a strong oxidizer, and it oxidizes the ferrous ion of the hemoglobin molecule to

ferric ion to result in methemoglobin formation. With chlorate, in contrast to nitrite, a

concentration dependent lag phase was seen before methemoglobin was formed (Singelmann et

al, 1984). Sodium chlorate ranked the least potent among six direct-acting methemoglobin agents

(French et al, 1995). These were (most to least) p-dinitrobenzene > o-dinitrobenzene > copper =

nitrite > chlorite > chlorate. The ranking was based on linear regression analysis of dose-response

data, the calculated dose expected to induce a given amount of methemoglobin formation and the

calculated percentage methemoglobin response induced by mmole/L of the agent in Dorset sheep

erythrocytes. Calbarese et al, 1995 also investigated the potency of sodium chlorate to produce

methemoglobin in mink erythrocytes and it was the least potent among six other chemicals (anaphthol>nitrite>copper>p-dinitrobenzene>chlorite>o-dinitrobenzene> chlorate). 

Potassium chlorate incubated with washed erythrocytes from human venous blood (0.1 to 6.0

mmol/L) caused a dose-related increase in glutathione activity and mechanical fragility with a

parallel increase in Heinz body formation (Hopkins and Tudhope, 1974). There was also a close

relationship between increased mechanical fragility and increased inhibition of glutathione

peroxidase. Spontaneous hemolysis in this test was less than 10%.

The mechanism of chlorate poisoning was explored in a set of in vitro and in vivo experiments by

Steffen and Wetzel (1993). They found that incubation of human erythrocytes with 5 mM sodium

chlorate oxidized hemoglobin to methemoglobin after a lag period of approximately 60 minutes. 

When after different periods of contact with the 30 mM chlorate, samples of erythrocytes were

washed free of the chlorate and incubated with methylene blue, reduction of methemoglobin was

only partial during the first hour of incubation (8%) but became nil after 2 hours of incubation. 
Page 91 of 141

The catalytic reduction of methemoglobin by methylene blue was found to be dependent on the

availability of NADPH formed in the pentose phosphate cycle. Therefore, an intact enzyme

system in erythrocytes is required. Incubation of homeliest erythrocytes with 5 mM sodium

chlorate showed that glucose-6-phosphate dehydrogenase and glyceraldehyde -3-phosphate

dehydrogenase were most sensitive, whereas glutathione reductase was very stable. When human

erythrocyte membranes (devoid of hemoglobin) were incubated with 5 mM sodium chlorate, there

was a rapid inactivation of glyceraldehyde -3-phosphate dehydrogenase when hemoglobin was

added, but not in its absence. This suggests that sodium chlorate does not inactivate the

membane-bound glyceraldehyde -3-phosphate dehydrogenase, the key enzyme in the NADPHdependent methemoglobin reduction. Nearly all membrane proteins were affected by the

hemoglobin catalyzed oxidation. Earlier work by Heubner and Jung, 1941 (cited by Steffen and

Wetzel, 1993) demonstrated that methemoglobin formation by chlorate was an autocatalytic

reaction. Both the lag period and the rate were dependent on the actual methemoglobin

concentration. 

Steffen and Wetzel (1993) also explored the in vitro effects of chlorate on rabbit erythrocytes and

compared them to the in vivo effects on methemoglobin formation in rabbits. It was discovered in

1888 by Cahn (cited by Steffen and Wetzel, 1993) that rabbits do not develop methemoglobine

anemia after chlorate administration. When rabbit erythrocytes were incubated with sodium

chlorate at concentrations ranging from 7.5 to 75 mM, methemoglobin was formed in a dose

dependent manner. Higher concentrations of the chlorate were needed for rabbit erythrocytes

than for the human erythrocytes. No methemoglobin was formed after the oral administration of

sodium chlorate (1000 mg/kg body weight) in 50 mL water. The serum concentration of the

chlorate was 10 - 20 mM for at least 12 hours. The highest concentration of the chlorate in the

serum was reached after 90 minutes (16±4.3 mM) and in the urine after 6 hours (246±99 mM). 

The elimination half-life was 20 hours. During 7 days of observation period there were no

changes in serum values of urea, creatinine, aspartate and alanine aminotransferases. When the

animals were killed at the end of the 7 day observation period and kidneys examined

histologically, there were no pathologic findings detected, indicating lack of nephrotoxicity in the

treated rabbits.
Page 92 of 141

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Heywood, R, Sortwell, RJ, Kelly, PJ, Street, AE. 1972. Toxicity of sodium chlorate to the dog.

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Subchronic Sodium Chlorate Exposure in Drinking Water Results in a Concentration-Depndent

Increase in Rat Thyroid Follicular Cell Hyperplasia. Toxicologic Pathology. 29(2):250-259.

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formation, glutahione proxidase inhibition, and changes in mechanical fragility. Br. J. Clin

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effect of sodium chlorate and potassium chlorate in two-stage rat renal carcinogenesis. J Am Coll

Toxicol 4:331-337.

Li, F.X., Byrd, D.M., Deyille, G.M., Sesser, D.E., Skeels, M.R., Katkowsky, S.R., Lamm, S.H.

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Teratology 62:429-431.

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Thyroxine Level and Perchlorate in Drinking Water. 42:200-205.

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chlorine dioxide, chlorite and chlorate to normal healthy adult male volunteers. J Environ Pathol

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chlorite to glucose-6-phosphate dehydrogenase deficient healthy adult male volunteers. J Environ

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397-408.

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exposure in Sprague-Dawley rats. Drug and Chemical Toxicology 18(2,3):185-199. 

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tyrosine sulfation on bone sialoprotein synthesis by a rat osteoblast like cell line (UMR 106-01

BSP). JBiol. Chem. 269(7): 4845-4852.

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Page 98 of 141

APPENDIX C RESIDUE CHEMISTRY CONSIDERATIONS

for Sodium Chlorate (073301) as an active ingredient in conventional

(agricultural) pesticides

Preface: Through a series of negotiations between members of SRRD and AD to coordinate

Inorganic Chlorates and Chlorine Dioxide and Sodium Chlorite, with regards to the risk

assessment for Inorganic Chlorates, the residue of concern from sodium chlorate exposures is

chlorate by agreement. See Section 1.0 Executive Summary above.

Sodium chlorate is currently registered for preharvest and foliar applications as a defoliant or

desiccant to the following food/feed crops: dry beans, corn, cotton, flax, guar, chili peppers,

potatoes, rice, safflower, sorghum (grain), southern peas (i.e., cowpeas), soybeans, and

sunflowers. For food/feed uses, sodium chlorate is formulated as a soluble concentrate (SC) with

the active ingredient ranging from 18% to 47.2%. Sodium chlorate may be applied using aircraft

or ground spray equipment, including high and low volume equipment.

Uses of sodium chlorate as a defoliant or desiccant on cauliflower, cucurbit vegetables, and okra

grown for seed only are considered non-food uses. Uses of sodium chlorate on ornamental

gourds and fallow lands are also considered non-food uses. These non-food uses will not be

discussed further with regards to residue chemistry or dietary exposure/risk considerations.

Under 40 CFR 180.1020 (a) Sodium chlorate is exempt from the requirement of a tolerance for

residues in or on the following raw agricultural commodities when used as a defoliant, desiccant,

or fungicide in accordance with good agricultural practice: beans (dry, edible), corn (fodder), corn

(forage), corn (grain), cottonseed, flaxseed, flax (straw), guar beans, peas (southern), peppers

(chili), potatoes, rice, rice (straw), safflower (grain), sorghum (grain), sorghum (fodder), sorghum

(forage), soybeans and sunflower seed.

Under 40 CFR 180.1020 (b) A time-limited exemption from the requirement of a tolerance is

established for residues of the defoliant/desiccant in connection with use of the pesticide under

section 18 emergency exemptions granted by EPA. This exemption has been granted for wheat

and will expire on 12/31/04. As requested by the Registration Division (Sodium Chlorate Use

Closure Memo Amendment; J. Guerry; dated 11/15/2004) the use of sodium chlorate on wheat is

also addressed herein with the intention to convert the time-limited exemption status to a

permanent exemption from the requirement of a tolerance under 40 CFR.1020 (a). The proposed

use rate is for a single application of sodium chlorate to wheat at 6 lbs ai/A with a 3-day PHI.

No plant metabolism data have been submitted in support of the reregistration of sodium chlorate;

however, no new plant metabolism data are required to support the established sodium chlorate

tolerance exempts. Based on available published information (Loomis et al., J. Am. Soc. Agron.;

25, 724 (1933)), sodium chlorate is highly soluble in water and is expected to readily absorb and

translocate throughout plants. However, given the proposed use conditions, the means of

translocation in treated plants may be substantially disrupted. Translocation of very small
Page 99 of 141

amounts of chlorate ion (ClO3b) by plants (translocation of significant amounts would be

phytotoxic to plants) from the environment which may be present as a result of inorganic chlorate

pesticide uses may occur. Terminal residues are expected to be primarily surface residues.

Since sodium chlorate is a strong oxidizing agent, depending on environmental factors, it is

expected to be easily reduced to chloride and possibly chlorite in plants. Total redox conversion

to these reduced species is not expected; hence, the terminal residues of sodium chlorate in/on

plants are likely chlorate (ClO3b), chlorite (ClO2b), and chloride (Clb).

No ruminant, swine, or poultry metabolism or feeding data have been submitted in support of the

reregistration of sodium chlorate; however, no new animal metabolism data are required to

support the established sodium chlorate exemptions from the requirement of a tolerance. Based

on published rat metabolism data (Abdel-Rahman et al, 1982, 1984b and 1985), terminal residues

of sodium chlorate in animal tissues are expected to be chlorate (ClO3b), chlorite (ClO2b), and

chloride (Clb). Chlorate is readily absorbed from the digestive tract and is excreted as chlorate,

chlorite, and chloride in urine primarily and feces. Within 72 hours, about 40% of the

administered dose was excreted in the urine as chlorate (ca. 13%), chlorite (ca. 4%), and chloride

(ca. 20%) and about 2-4% was excreted in the feces in the same time period. Less than 1% of the

administered dose was found in any of the tissues analyzed including kidney, liver, and skin.

Although some previous residue chemistry reviews for specific exemptions from the requirement

of a tolerance have concluded that there is no reasonable expectation of transfer of residues to

meat, milk, poultry or eggs in specific cases, re-evaluation of the available crop field trial data

taken as a whole, indicate that there is the possibility of detectable residues of sodium chlorate on

animal feedstuffs at harvest. Hence, secondary residues of concern in meat, milk, poultry, and

eggs are possible and; therefore, new ruminant and poultry feeding data are hereby required to

support the reregistration of sodium chlorate. These data are considered confirmatory.

The analytical method used to support the established exemptions from the requirement of a

tolerance is a non-specific colorimetric method (Branderis, J. Sci. Food Agric., 16, 558 (1965)),

deemed acceptable for data collection. The method was originally developed to estimate residual

chlorate concentrations in soil and as a rapid diagnostic test for chlorate toxicity in plants. 

Briefly, the method involves acid extraction, clean-up by shaking with activated charcoal, and

filtration. A solution of ortho-toluidine in HCl is then added to the concentrated extract and the

resulting color is measured at 448 nm for low concentrations and at 490 nm for higher

concentrations of dye. The method is not specific for chlorate since it measures any oxidizing

agent capable of oxidizing chloride ion to free chlorine. A standard curve is prepared with sodium

chlorate for comparison. The lowest sensitivity of the method is estimated at 1 ppm based on

available fortification data from field trials. Chloride does not interfere with the method but

residues of chlorite, which might be present, may also be detected with this method. This method

is hereby deemed adequate for enforcement of sodium chlorate exemptions from the requirement

of a tolerance. [Note: If needed, a more selective HPLC method (“Determination of Residues of
Page 100 of 141

Sodium Chlorate in Potatoes”, Method #S57023, 4/2/91) is available for the detection of sodium

chlorate residues in or on raw agricultural commodities (RACs).] 

New reference standards must be supplied to the EPA National Pesticide Standards Repository.

Only crop field trial data have been submitted to support the reregistration of sodium chlorate. 

No storage stability or processing data are available. The available crop field trial data have been

re-evaluated herein. No additional plant magnitude of the residue or storage stability data are

required to support the reregistration of sodium chlorate.
Page 101 of 141

Table C.1. Residue Chemistry Science Assessment for Reregistration of Sodium Chlorate (073301) 

as an active ingredient in conventional (agricultural) pesticides

GLN Data Requirements

Current

Tolerances

(ppm)

[§180.1020]

Additional

Data Needed? Citations 1

860.1200: Directions for Use NA No

860.1300: Nature of the Residue - Plants NA No 00062497, 00066805

860.1300: Nature of the Residue - Animals NA No None

860.1340: Residue Analytical Method NA No

00049610, 00066802,

00066804, 00066808,

00066809, 00066810,

00123747, 00124680,

00135224

860.1360: Multiresidue Method NA No None

860.1380: Storage Stability Data NA No None

860.1400: Magnitude of the Residue - Water,

Fish and Irrigated Crops None No None

860.1460: Magnitude of the Residue - Food

Handling None No None

860.1480: Magnitude of the Residue - Meat, Milk, Poultry, Eggs

- Cattle fat, meat, and meat byproducts

None Yes 2 None

- Goat fat, mean and meat byproducts

- Horse fat, meat and meat byproducts

- Sheep fat, meat and meat byproducts

- Milk

- Eggs and the Fat, Meat and Meat

Byproducts of Poultry

860.1500: Crop Field Trials 3

- Beans (dried, edible) Exempt No

- Corn (fodder, forage, grain) Exempt No

- Cottonseed Exempt No

- Flaxseed and Flax (straw) Exempt No 00136326

- Guar beans Exempt No 00136388
Table C.1. Residue Chemistry Science Assessment for Reregistration of Sodium Chlorate (073301) 

as an active ingredient in conventional (agricultural) pesticides

GLN Data Requirements

Current

Tolerances

(ppm)

[§180.1020]

Additional

Data Needed? Citations 1

Page 102 of 141

-Peas (southern) Exempt No 00128727

- Peppers (chili) Exempt No 00116554

- Potatoes Exempt No 42464201, 42930601

- Rice and Rice straw Exempt No 00159210

- Safflower (grain) Exempt No None

- Sorghum (grain, fodder, forage) Exempt No 00123727

- Soybeans Exempt No 00128727

- Sunflower seed Exempt No 00135224

- Wheat Exempt No 00136326

860.1520: Processed Food/Feed NA No None

860.1850: Confined Accumulation in

Rotational Crops NA No None

860.1650: Submittal of Analytical Reference

Standards NA Yes 4 None

860.1900: Field Accumulation in Rotational

Crops NA No None

1

 Only data considered primary sources of information to support the reregistration of sodium chlorate are

included here. All other available data are considered supplemental. 2

 New ruminant and poultry feeding studies are required.

3

 Sodium chlorate is exempt from the requirement of a tolerance for residues in or on the listed raw

agricultural commodities when used as a defoliant, desiccant, or fungicide in accordance with good

agricultural practice [40 CFR 180.1020] 4

 Replenish standards as requested by the repository.

860.1300 Nature of the Residue - Plants

No plant metabolism data have been submitted in support of the reregistration of sodium chlorate;

however, no new plant metabolism data are required to support the established sodium chlorate

tolerance exempts. Based on available published information (Loomis et al., J. Am. Soc. Agron.;

25, 724 (1933)), sodium chlorate is highly soluble in water and is expected to readily absorb and

translocate throughout plants. However, given the proposed use conditions, the means of
Page 103 of 141

translocation in treated plants may be substantially disrupted. Translocation of very small

amounts of chlorate ion (ClO3b) by plants (translocation of significant amounts would be

phytotoxic to plants) from the environment which may be present as a result of inorganic chlorate

pesticide uses may occur. Terminal residues are expected to be primarily surface residues.

Since sodium chlorate is a strong oxidizing agent, depending on environmental factors, it is

expected to be easily reduced to chloride and possibly chlorite in plants. Total redox conversion

to these reduced species is not expected; hence, the terminal residues of sodium chlorate in/on

plants are likely chlorate, chlorite, and chloride.

860.1300 Nature of the Residue - Livestock

No ruminant, swine, or poultry metabolism or feeding data have been submitted in support of the

reregistration of sodium chlorate; however, no new animal metabolism data are required to

support the established sodium chlorate exemptions from the requirement of a tolerance. Based

on published rat metabolism data (Abdel-Rahman et al, 1982, 1984b and 1985), terminal residues

of sodium chlorate in animal tissues are expected to be chlorate (ClO3b), chlorite (ClO2b), and

chloride (Clb). Chlorate is readily absorbed from the digestive tract and is excreted as chlorate,

chlorite, and chloride in urine primarily and feces. Within 72 hours, about 40% of the

administered dose was excreted in the urine as chlorate (ca. 13%), chlorite (ca. 4%), and chloride

(ca. 20%) and about 2-4% was excreted in the feces in the same time period. Less than 1% of the

administered dose was found in any of the tissues analyzed including kidney, liver, and skin.

Metabolism - Rat

The metabolism and distribution of chlorine dioxide (ClO2), chlorite ion (ClO2b), and chlorate ion

(ClO3b) were studied in rats (Abdel-Rahman et al, 1982, 1984b, 1985). Three groups of male

Sprague-Dawley rats (4/group) were administered a single oral (gavage) dose of one of the

compounds which were 36Cl-radiolabeled. Expired air, fecal and urine samples were collected

over 72 hours. The 36Cl- activity in these samples was measured and the radioactivity in the urine

was identified as chlorate (ca. 13% of the administered dose), chlorite (ca. 4% of the administered

dose) and chloride (ca. 20% of the administered dose). At 72 hours, the rats were killed and the

distribution of 36Cl- activity in tissues was determined (see Table C.2). Total radioactivity in each

of the tissues examined was <1% of the initial dose.
Page 104 of 141

Table C.2. Distribution of radioactivity in rat tissues after dosing with 36Cl-labeled chlorine dioxide,

potassium chlorite, or potassium chlorate.

Tissue

Percentage of initial dose 1

Chlorine dioxide (36ClO2) Chlorite (36ClO2b) Chlorate (36ClO3b)

Plasma 0.72 ± 0.02 0.55 ± 0.038 0.68 ± 0.09

Packed cells -- 2 0.63 ± 0.11 0.23 ± 0.02

Whole blood -- 0.64 ± 0.01 0.57 ± 0.05

Kidney 0.81 ± 0.15 0.30 ± 0.06 0.42 ± 0.07

Lung 0.74 ± 0.15 0.37 ± 0.04 0.45 ± 0.07

Stomach 0.70 ± 0.15 0.43 ± 0.07 0.46 ± 0.05

Duodenum 0.29 ± 0.07 0.31 ± 0.01 0.34 ± 0.04

Ileum 0.48 ± 0.09 0.17 ± 0.03 0.21 ± 0.02

Liver 0.38 ± 0.09 0.06 ± 0.03 0.20 ± 0.03

Spleen 0.25 ± 0.04 0.22 ± 0.02 0.29 ± 0.04

Bone marrow 0.16 ± 0.03 0.09 ± 0.03 0.15 ± 0.03

Testes -- 0.39 ± 0.04 0.45 ± 0.07

Skin -- 0.38 ± 0.06 0.42 ± 0.10

Carcass -- 0.25 ± 0.04 0.21 ± 0.02

1

 Value represents the mean ± SE as percentage of the initial dose from four rats per treatment after 72 hr.

2

 Not Determined

860.1340 Residue Analytical Methods

The analytical method used to support the established exemptions from the requirement of a

tolerance is a non-specific colorimetric method (Branderis, J. Sci. Food Agric., 16, 558 (1965)),

deemed acceptable for data collection. The method was originally developed to estimate residual

chlorate concentrations in soil and as a rapid diagnostic test for chlorate toxicity in plants. 

Briefly, the method involves acid extraction, clean-up by shaking with activated charcoal, and

filtration. A solution of ortho-toluidine in HCl is then added to the concentrated extract and the

resulting color is measured at 448 nm for low concentrations and at 490 nm for higher

concentrations of dye. The method is not specific for chlorate since it measures any oxidizing

agent capable of oxidizing chloride ion to free chlorine. A standard curve is prepared with sodium

chlorate for comparison. The sensitivity of the method is estimated at 1 ppm based on available

fortification data from field trials. Chloride does not interfere but residues of chlorite, which

might be present, may also be detected with this method. This method is hereby deemed adequate
Page 105 of 141

for enforcement of sodium chlorate exemptions from the requirement of a tolerance. A more

selective HPLC method (“Determination of Residues of Sodium Chlorate in Potatoes”, Method

#S57023, 4/2/91) is available for the detection of sodium chlorate residues in or on raw

agricultural commodities (RACs).

860.1360 Multiresidue Methods

It does not appear that the registrant has submitted multiresidue method studies. Sodium chlorate

is not listed in the FDA PESTDATA database dated 11/01 (PAM Volume I, Appendix I). 

However, sodium chlorate would not be expected to be recovered by the PAM I multiresidue

methods. No additional multiresidue methods data are required to support the reregistration of

sodium chlorate.

860.1380 Storage Stability

No storage stability data have been submitted in support of the reregistration of sodium chlorate. 

However, the available data continue to uphold the established sodium chlorate exemptions from

the requirement of a tolerance, and therefore, no new storage stability data are required to

support the reregistration of sodium chlorate.

860.1400 Water, Fish, and Irrigated Crops

Sodium chlorate is not presently registered for direct use on water and aquatic food and feed

crops other than as a desiccant on rice. Since sodium chlorate is used to desiccate green foliage

and weeds present in rice fields to increase harvest efficiency, residues of concern are not

expected to be occurred in water, fish, and irrigated crops from the use of sodium chlorate as a

desiccant on rice. Therefore, no residue chemistry data are required under these guideline topics.

860.1460 Food Handling

Sodium chlorate is not presently registered for use in food-handling establishments; therefore, no

residue chemistry data are required under these guideline topics.

860.1480 Meat, Milk, Poultry, and Eggs

No ruminant, swine or poultry feeding studies have been submitted in support of the reregistration

of sodium chlorate. Although some previous residue chemistry reviews for exemptions from the

requirement of a tolerance have concluded that there is no reasonable expectation of transfer of

residues to meat, milk, poultry or eggs in specific cases, re-evaluation of the available crop field

trial data taken as a whole, indicate that there is the possibility of detectable residues of sodium

chlorate on animal feedstuffs at harvest. Hence, secondary residues of sodium chlorate in meat,

milk, poultry, and eggs are possible and; therefore, new ruminant and poultry feeding data are

hereby required to support the reregistration of sodium chlorate.
Page 106 of 141

Table C.3. Calculation of the highest average and maximum theoretical dietary burden for

beef/dairy cattle and poultry from the maximum registered use rates of sodium chlorate

(073301) as an active ingredient in conventional (agricultural) pesticides.

Feed

Commodity

% Dry

Matter

%

Diet

Residue Estimate

(ppm)

Dietary

Contribution 1

(ppm)

Max. Feed

Per Day on

a Dry Wt.

Basis (Kg)

Dietary Exposure

Estimate

(mg)

Highest

Ave

Max Highest

Ave

Max Highest

Ave

Max

Beef and Dairy Cattle

Cowpea forage 30 40 100 2 300 2 133 400

Cowpea hay 86 20 100 2 300 2 23 70

Sorghum grain 86 40 40 3 70 3 19 33

Total Burden 175 500 9.1 5 1600 4600

Poultry

Sorghum grain Not

Used 1

80 40 3 70 3 32 56

Rice bran 20 40 4 70 4 8 14

Total Burden 40 70

1

 Dietary Contribution for Cattle = (Residue Estimate in ppm ÷ %DM) x %Diet

 Dietary Contribution for Poultry = Residue Estimate in ppm x %Diet

2

 Based on the available straw (flax, oat, wheat, rice) and forage (guar plants, sorghum stalks, soybean forage)

data, maximum residues of sodium chlorate in/on straw and forage livestock feedstuffs harvested 3-7 days after

treatment with sodium chlorate at the maximum use rate permitted on forage crops (1 or 2 applications; 7.5 lbs

ai/A/application) are not expected to exceed 300 ppm at the point of harvest. On average, residues in/on straw and

forage livestock feedstuffs should not exceed 100 ppm when harvested 7-14 days after foliar treatment with sodium

chlorate at the maximum use rate permitted on forage crops (1 or 2 applications; 7.5 lbs ai/A/application). 

3

 Based on the available sorghum field trial data alone, maximum residues in/on sorghum grain harvested 7-14

days after treatment with sodium chlorate at the maximum use rate for sorghum (1 application; 7.5 lbs ai/A; 7-day

PHI) are not expected to exceed 70 ppm. On average, residues in/on sorghum grain harvested 7-14 days after

treatment with sodium chlorate at the maximum use rate on sorghum (1 application; 7.5 lbs ai/A; 7-day PHI) are

not expected to exceed 40 ppm.

4

 Translated from sorghum grain estimate.

5

 Cattle eat a maximum of 9.1 kg of feed per day on a dry wt. basis (Update of Livestock Feed Consumption, 1993)
Page 107 of 141

The highest average residues of chlorate (excluding percent crop treated data) in meat,

poultry, and eggs are expected to be <4 ppm and in milk are expected to be <0.5 ppm based

on the following information and assumptions:

• The highest average theoretical dietary burden for livestock is 175 ppm for cattle feed on a

dry wt. basis

• Cattle eat a maximum of 9.1 kg of feed per day on a dry wt. basis (Update of Livestock

Feed Consumption, 1993); hence, the highest average theoretical dietary exposure for

sodium chlorate to livestock is 1600 mg per day 

• Based on the available rat metabolism data, <1% of the initial dose of chlorate is expected

to be incurred in animal tissues 72 hours after exposure (Abdel-Rahman et al, 1982, 1984b

and 1985); hence <16 mg is expected to be incurred in any livestock tissue of interest

• Assuming that kidneys have the lowest weight of the organs/tissues of interest (other than

milk) in livestock (i.e., compared to meat, liver, fat, and eggs)

• Assuming that the average weight of cattle kidneys is about 4 kg (Update of Livestock

Feed Consumption, 1993; cattle kidneys weigh 3.6-4.5 kg)

• Assuming that the average milk production per day is about 30 kg (Frank, 2002; milk

production is 50-90 lb milk/cow/day) 

Calculations:

(Highest Average Theoretical Dietary Exposure (1600 mg) x Percent of Dietary Exposure Expected in Organs (< 1%)

Average Weight of the Organ/Tissue of Interest (Kidney at 4 Kg or Milk at 30 Kg)

Highest Average Residue Estimate in Meat, Poultry, and Eggs = <4 ppm

Highest Average Residue Estimate in Milk = <0.5 ppm
Page 108 of 141

The maximum residues of chlorate (excluding percent crop treated data) in meat, poultry,

and eggs are expected to be <12 ppm and in milk are expected to be <2 ppm based on the

following information and assumptions:

• The maximum theoretical dietary burden for livestock is 500 ppm for cattle feed on a dry

wt. basis

• Cattle eat a maximum of 9.1 kg of feed per day on a dry wt. basis (Update of Livestock

Feed Consumption, 1993); hence, the highest average theoretical dietary exposure for

sodium chlorate to livestock is 4600 mg per day 

• Based on the available rat metabolism data, <1% of the initial dose of chlorate is expected to

be incurred in animal tissues 72 hours after exposure (Abdel-Rahman et al, 1982, 1984b and

1985); hence <46 mg is expected to be incurred in any livestock tissue of interest

• Assuming that kidneys have the lowest weight of the organs/tissues of interest (other than

milk) in livestock (i.e., compared to meat, liver, fat, and eggs)

• Assuming that the average weight of cattle kidneys is about 4 kg (Update of Livestock Feed

Consumption, 1993; cattle kidneys weigh 3.6-4.5 kg)

• Assuming that the average milk production per day is about 30 kg (Frank, 2002; milk

production is 50-90 lb milk/cow/day)

Calculations:

(Maximum Theoretical Dietary Exposure (4600 mg) x Percent of Dietary Exposure Expected in Organs (< 1%)

Average Weight of the Organ/Tissue of Interest (Kidney at 4 Kg or Milk at 30 Kg)

Maximum Residue Estimate in Meat, Poultry, and Eggs = <12 ppm

Maximum Residue Estimate in Milk = <2 ppm
Page 109 of 141

860.1500 Crop Field Trials

Available crop field trial data deemed the primary sources of information to support the

reregistration of sodium chlorate are briefly discussed below and summarized in Table C.5. All

other available crop field trial data are considered supplemental and will not be discussed further.

No additional crop field trial data are required to support the reregistration of sodium chlorate.

The subject data, except the potato tuber data, were all collected using the colorimetric method

(Branderis, J. Sci. Food Agric., 16, 558 (1965)), deemed acceptable for data collection and

enforcement of the established sodium chlorate exemptions from the requirement of a tolerance. 

The potato tuber data were collected with a more selective HPLC method (“Determination of

Residues of Sodium Chlorate in Potatoes”, Method #S57023, 4/2/91) deemed adequate for data

collection. The lowest limits of quantitation (LOQs) of these methods is estimated at 1 ppm.

Based on the available flax, guar, southern pea, soybean, and sunflower field trial data no detectable

residues of sodium chlorate (<1 ppm) are expected in/on dry beans, guar beans, southern peas,

soybeans, flaxseed, safflower seed, and sunflower seed at the point of harvest from the maximum

use rate of sodium chlorate on dry beans, guar, southern peas, soybeans, flax, safflower, and

sunflower (1 application; 7.5 lbs ai/A; 7-day PHI). Furthermore, no detectable residues of sodium

chlorate (<1 ppm) are expected in/on cottonseed at the point of harvest from the maximum use rate

of sodium chlorate on cotton (2 applications, 7.5 lbs ai/A/application; 7-day PHI). Any residues

which might be detected at the point of harvest are expected to be primarily surface residues which

would be substantially removed prior to the point of consumption. 

Based on the available chili pepper field trial data, it is possible that detectable residues of sodium

chlorate (ca. 13 ppm) might be found on the surface of unwashed chili peppers treated with sodium

chlorate at the maximum use rate of sodium chlorate on chili peppers (1 application; 12.5 lbs

ai/A/application; 10-day PHI). However, these residues are primarily surface residues present at the

point of harvest which would be substantially removed by washing (<1 ppm) prior to the point of

consumption.

Based on the available potato field trial data, no detectable residue of sodium chlorate (<1 ppm) are

expected in/on potato tubers at the point of harvest from the maximum use rate of sodium chlorate

on potatoes (1 application; 12.5 lbs ai/A; 7-day PHI). As demonstrated by the chili pepper field

trial data, any residues present at harvest are expected to be primarily surface residues which would

be substantially removed by washing prior to the point of consumption.

Based on the available oat, rice, sorghum, and wheat field trial data, it is possible that detectable

residues of sodium chlorate (ca. 70 ppm (maximum) as demonstrated by sorghum grain) might be

found on the surface of cereal grains retaining their outer hulls at harvest (such as oats and

sorghum) from the maximum use rate of sodium chlorate on rice and sorghum (1 application; 7.5

lbs ai/A; 7-day PHI) and wheat (1 application; 6 lbs ai/A; 3-day PHI). However, once the outer

hulls are removed (either at harvest or during processing), no detectable residues of sodium chlorate
Page 110 of 141

(<1 ppm) are expected in/on cereal grains such as rice and wheat (as demonstrated by rice w/out

hulls and wheat grain data).

Based on the available sorghum field trial data alone, maximum residues in/on sorghum grain

harvested 7-14 days after treatment with sodium chlorate at the maximum use rate for sorghum (1

application; 7.5 lbs ai/A; 7-day PHI) are not expected to exceed 70 ppm. On average, residues

in/on sorghum grain harvested 7-14 days after treatment with sodium chlorate at the maximum use

rate on sorghum (1 application; 7.5 lbs ai/A; 7-day PHI) are not expected to exceed 40 ppm.

Translating the available sorghum field trial data to corn, residues of sodium chlorate are not

expected to exceed 20 ppm (ca. 10 ppm on average) in/on corn grain at the point of harvest from

the maximum use rate of sodium chlorate on corn (1 application, 7.5 lbs ai/A; 14-day PHI). As

demonstrated by the chili pepper field trial data, any residues present at harvest are expected to be

primarily surface residues which would be substantially removed by washing prior to the point of

consumption. Hence, residues of sodium chlorate in/on sweet corn after washing and prior to

consumption would not be expected to exceed 1 ppm.

Based on the available straw (flax, oat, wheat, rice) and forage (guar plants, sorghum stalks,

soybean forage) data, maximum residues of sodium chlorate in/on straw and forage livestock

feedstuffs harvested 3-7 days after treatment with sodium chlorate at the maximum use rate

permitted on forage crops (1 or 2 applications; 7.5 lbs ai/A/application) are not expected to exceed

300 ppm at the point of harvest. On average, residues in/on straw and forage livestock feedstuffs

should not exceed 100 ppm when harvested 7-14 days after foliar treatment with sodium chlorate at

the maximum use rate permitted on forage crops (1 or 2 applications; 7.5 lbs ai/A/application). 

Chili peppers: MRID 00116554

Chili pepper plants were treated with a single application of sodium chlorate at 8 or 16 lb ai/A. 

Chili pepper samples were collected 7-21 days after treatment. Residues of chlorate in/on chili

pepper samples were <0.1 to 13 ppm. After washing the treated chili peppers with water, residues

of chlorate were all <0.1 ppm.

Flax, Oats, Wheat: MRID 00136326

Flax, oats, and wheat plots were treated with a single application of sodium chlorate at 6 or 12 lbs

ai/A. Grain and straw samples were collected 3-10 days after treatment. Residues of chlorate in/on

flax grain/straw, wheat grain/straw and oat straw samples were <2 ppm. Residues of chlorate in/on

oat grain samples treated at 6 and 12 lbs ai/A were 10-36 ppm (20 ppm average) and <2-125 ppm

(80 ppm average), respectively.

Guar: MRID 00136388

Guar plots were treated with a single application of sodium chlorate at 6 or 12 lbs ai/A. Seed and

plant samples were collected 2-14 days after treatment. Residues of chlorate in/on seed samples

<10 ppm. Residues of chlorate in/on plant samples were 18-266 ppm.
Page 111 of 141

Potatoes: MRID 42464201 (Chromatograms - MRID 42930601)

Potato plants were treated with a single application of sodium chlorate at 9 lbs ai/A. Potato tubers

were collected 7-10 days after treatment. Residues of chlorate in/on potato tubers were <1.0 ppm.

Rice: MRID 00159210

Rice plots were treated with a single application of sodium chlorate at 6 or 12 lbs ai/A. Grain w/out

hulls, grain with hulls, and straw samples were collected 2-9 days after treatment.

While residues of chlorate in/on grain with hulls collected 8 days after treatment were 7-160 ppm,

residues in/on grain w/out hulls collected 7 days after treatment were essentially nil (reported as 0.0

ppm). Detectable residues (0.0-30 ppm) were reported in/on grain w/out hulls collected 2 days

after treatment at 12 lbs ai/A.

Residues of chlorate in/on straw samples ranged from <1 ppm to 44 ppm from treatment at 6 lbs

ai/A and from <1 ppm to 438 ppm from treatment at 12 lbs ai/A.

Sorghum: MRID 00123727

Sorghum plots were treated with a single application fo sodium chlorate at 3, 6, and 12 lbs ai/A.

Grain and stalk samples were collected 2-14 days after application.

Residues of chlorate in/on grain samples collected 7 and 14 days after treatment at 6 lbs ai/A were

44-69 ppm (59 ppm average) and 8-21 ppm (13 ppm average), respectively. Residues of chlorate

in/on grain samples collected 7 and 14 days after treatment at 12 lbs ai/A were 83-132 ppm (106

ppm average) and 13-40 ppm (30 ppm average), respectively.

Residues of chlorate in/on stalk samples collected 7-14 days after treatment at 6 lbs ai/A were 

essentially nil (0.0 ppm) to 51 ppm (21 ppm average). Residues of chlorate in/on stalk samples

collected 7-14 days after treatment at 12 lbs ai/A were essentially nil (0.0 ppm) to 352 ppm (117

ppm average).

Southern Peas (cowpeas): MRID 00128727

Southern pea plots were treated with a single application of sodium chlorate at 6 lbs ai/A. Shelled

pea samples were collected 4 or 5 days after treatment. Some of the raw shelled peas were

processed into frozen peas. Residues of sodium chlorate were <0.3 ppm in/on all samples.

Soybeans: MRID 00128727

Soybean plots were treated with a single application of sodium chlorate at 6 or 12 lbs ai/A. 

Soybean and foliage samples were collected 2-14 days after treatment. Residues of chlorate in/on

soybeans collected 7-14 days after treatment were <5.0 ppm. Residues of chlorate in/on soybean

foliage collected 7 days after treatment at 6 or 12 lbs ai/A were as high as 153 ppm and 526 ppm,

respectively. Residues of chlorate in/on soybean forage collected 14 days after treatment at 6 or 12

lbs ai/A were as high as 100 ppm and 318 ppm, respectively.
Page 112 of 141

Sunflower Seeds: MRID 00135224

Sunflower plots were treated with a single application of sodium chlorate at 3, 6, or 12 lbs ai/A. 

Seed samples were collected 2-14 days after treatment. Residues of sodium chlorate in/on all

samples were essentially nil (reported as 0 ppm) except 1 seed sample collected 4 days after

treatment at 12 lbs ai/A which showed residues of 10 ppm (average of 3 replicates; one replicate

showed residues of 30 ppm).
Page 113 of 141

Table C.4. Summary of available crop field trial data. Note: Guar, rice, sorghum, soybean, and

sunflower data are truncated in this table. Data, except wheat grain data, collected less

than 7 days after treatment have been intentionally excluded in this table but may be

included in the brief discussions above.

Matrix Crop Application

Rate

(lbs ai/A)

PHI

(days)

Residues (ppm)

Maximum 1 Estimated

Average 2

Vegetable Chili pepper (raw) 8 or 16 7-21 13 Not

Calculated

Chili pepper (washed) <0.1 <0.1

Potato tuber 9 7-10 <1 <1

Seed/Bean Flax 6 10 <2 <2

Guar 7 <10 <10

Southern pea 4-5 <0.3 <0.3

Soybean 7-14 <5 <5

Sunflower 7-14 essentially

nil (zero)

essentially

nil (zero)

Flax 12 10 <2 <2

Guar 7-14 <10 <10

Soybean 7-14 <5 <5

Sunflower 7-14 essentially

nil (zero)

essentially

nil (zero)

Cereal Grain Oat 6 8 36 20

Rice w/out hulls 7-9 essentially

nil (zero)

essentially

nil (zero)

Rice with hulls 8 13 9.7

Sorghum 7 69 59

14 21 13

Wheat 3-9 <2 <2

Oat 12 8 125 80

Rice w/out hulls 7-9 essentially

nil (zero)

essentially

nil (zero)

Rice with hulls 8 160 93
Page 114 of 141

Sorghum 7 132 106

14 40 30

Wheat 3-9 <2 <2

Straw Flax, Oat, Wheat 6 or 12 3-10 <2 <2

Rice 6 7-9 44 11

12 7-9 438 75

Forage Guar plants 6 7 58 40

12 7-14 106 70

Sorghum stalk 6 7-14 51 21

12 7-14 352 117

Soybean forage 6 7 153 Reviewer

Cannot

Determine 14 100

12 7 526

14 318

1

 Maximum residue as reported in the data submission.

2

 Estimated Average calculated by the reviewer.

860.1520 Processed Food and Feed

No processing data have been submitted regarding residues of sodium chlorate in/on processed

food/feed commodities (corn, cotton, flaxseed, potato, rice, safflower, sorghum, and wheat).

However, since no significant residues were found in the raw agricultural commodities subject to

processing, it is unlikely that significant residues will occur in the processed fractions.

860.1650 Submittal of Analytical Reference Standards

As of 8/11/04, an analytical reference standard for sodium chlorate is not available at the EPA

National Pesticide Standards Repository. 

860.1850 Confined Accumulation in Rotational Crops

No data have been submitted regarding residues of sodium chlorate in/on confined accumulation

in rotational crops.
Page 115 of 141

860.1900 Field Accumulation in Rotational Crops

No data have been submitted regarding residues of sodium chlorate in/on field accumulation in

rotational crops.
Page 116 of 141

RESIDUE CHEMISTRY REFERENCES

Studies Considered Primary Sources of Information and Used in the Assessment

PUBLISHED 

Abdel-Rahman MS, Couri D, Bull RJ. 1982. Metabolism and pharmacokinetics of alternate

drinking water disinfectants. Environ Health Perspect. 46:19-23.

Abdel-Rahman MS, Couri D, Bull RJ. 1984b. The Kinetics of Chlorite and Chlorate in the Rat. 

Journal of the American College of Toxicology, 3(4): 261-267.

Abdel-Rahman MS, Couri D, Bull RJ. 1985. The kinetics of chlorite and chlorate in rats. J

Environ Pathol Toxicol Oncol. 6(1):97-103.

Frank, G. 2002. Cost of Milk Production per Hundredweight Equivalent in Milk Sold per Cow

Ranges. Wisconsin Dairy Data. Fact Sheet 2002-01. Center for Dairy Profitability. Univ.

Wisconsin Extension Service. Oct. 2002.

UNPUBLISHED 

49610 Rhone-Poulenc Chemical Company (1959) Method of Analysis for Chlorates. 

(Unpublished study received Jan 4, 1962 under 359-400; CDL:119511-B) 

62497 Pernert, J.C. (1960) On the Possibility of Toxic Residues following Cotton Defoliation by

Chlorate. (Unpublished study received Dec 18, 1969 under 0F0926; prepared by Hooker

Chemical Corp., submitted by Fenrich-Vincent Associates, Manhasset, N.Y.; CDL: 093232-G) 

66802 Fenrich-Vincent Associates (1969) Analytical Methods and Results of Tests on the

Amount of Residue Remaining in or on Raw Cottonseed When an (Inert Ingredient) has Been

Used on the Cotton Plant. Unpublished study; 14 p. 

66804 Gauditz, I. (1959) The Results of Tests on the Amount of Residue Remaining, Including a

Description of the Analytical Methods Used: (Penco De-fol-ate). (Unpublished study received

May 30, 1970 under 0F0926; submitted by Fenrich-Vincent Associates, Manhasset, N.Y.;

CDL:091580-O) 

66805 Banderis, A. (1965) Colorimetric Determination of chlorate in soil and plant extracts. 

Journal of the Science of Food and Agriculture 16(Sep):558-564. (Also In unpublished

submission received May 30, 1970 under 0F0926; submitted by Fenrich-Vincent Associates,

Manhasset, N.Y.; CDL:091580-P)
Page 117 of 141

66808 Peniston, Q.P. (1968) Letter sent to E.H. Karr dated Jan 3, 1968: Determination of

sodium chlorate residues on cottonseed: Report # 3. (Unpublished study received May 30, 1970

under 0F0926; prepared by Food, Chemical & Research Laboratories, Inc., submitted by

Fenrich-Vincent Associates, Manhasset, N.Y.; CDL:091580-T) 

66809 Peniston, Q.P. (1968) Letter sent to E.H. Karr dated Jul 30, 1968: Determination of

sodium chlorate residues in ground cottonseed--report # 4: Lab. No. 5639. (Unpublished study

received May 30, 1970 under 0F0926; prepared by Food, Chemical & Re- search Laboratories,

Inc., submitted by Fenrich-Vincent Associates, Manhasset, N.Y.; CDL:091580-U) 

66810 Peniston, Q.P. (1969) Letter sent to E.H. Karr dated Feb 18, 1969: Further studies on

determination of sodium chlorate residues in ground cottonseed--report #5: Lab. No. 5879;

prepared by Food, Chemical & Research Laboratories, Inc. Unpublished study; 2 p. 

116554 California, Dept. of Agriculture (1971) Application of Shed-A-Leaf on Chili Peppers:

Results. (Compilation; unpublished study received Oct 13, 1972 under 2E1286; CDL:091822-A) 

123747 Banderis, A. (1965) Colorimetric determination of chlorate in soil and plant extracts. J.

Sci. Ef. Agric. 16(Sep):558. (Also In unpublished submission received 1965 under 3E1386;

submitted by Interregional Research Project No. 4, New Brunswick, NJ; CDL: 093699-B) 

124680 Roth, F. (1967) A test for chlorate residues. Bulletin of Environmental Contamination &

Toxicology 2(4):251-254. (Also In unpublished submission received Jun 23, 1972 under 2E1286;

submitted by California, Dept. of Agriculture, Sacramento, CA; CDL:094665-A) 

128727 Interregional Research Project No. 4 (1983) The Results of Tests on the Amount of

Residues Remaining in or on Southern Peas, Including a Description of the Analytical Method

Used. (Compilation; unpublished study received Jun 10, 1983 under 3E2910; CDL:071699-A) 

135224 Interregional Research Project No. 4 (1975) The Results of Tests on the Amount of

Sodium Chlorate Residue Remaining in or on Sunflower Seeds, Including a Description of the

Analytical Method Used. (Compilation; unpublished study received Jul 1, 1976 under 6E1825;

CDL:097356-A) 

136326 Interregional Research Project No. 4 (1978) The Results of Tests on the Amount of

Sodium Chlorate Residue Remaining in or on Flax, Oats, and Wheat Including a Description of

the Analytical Method Used. (Compilation; unpublished study received Oct 20, 1978 under

9E2142; CDL:097460-A) 

136388 Interregional Research Project No. 4 (1979) Results of Tests Concerning the Amount of

Sodium Chlorate Residue Remaining in or on Guar Including a Description of the Analytical

Method Used. (Compilation; unpublished study received Jun 15, 1979 under 9E2220;

CDL:098331-A) 
Page 118 of 141

159210 Kerr-McGee Chemical Corp. (1975) Sodium Chlorate on Rice: Summary of

Experimental Conditions and Data from Texas and Louisiana in 1975. Unpublished study. 12 p. 

42464201 McGaughey, R. (1992) Determination of the Magnitude of Residues of Sodium

Chlorate in Potatoes Treated with DEFOL6: Final Report: Lab Project Number: DREX-9002:

9006-010X: 04-9012. Unpublished study prepared by Compliance Services Intl. 112 p. 

42930601 McGaughey, R. (1993) Determination of the Magnitude of Residues of Sodium

Chlorate in Potatoes Treated with DEFOL 6: Lab Project Number: DREX-9002. Unpublished

study prepared by Minnesota Valley Testing Labs. 22 p.

Study Citations Considered Supplemental Sources of Information

5620 United States Borax & Chemical Corporation (1967) Residue Data. (Unpublished study

received Apr 1, 1969 under 9F0783; CDL: 091347-A) 

48007 Abernathy, J.; Miller, C.S.; Richard, J. (1975) Sodium chlorate on Sunflowers. Prepared

in cooperation with Texas A & M Univ., Agricultural Experiment Station and Iowa State Univ.,

Ames Laboratory. Unpublished study; 17 p. 

48009 Smith, D.T.; Eastin, E.F.; Wiese, A.F.; et al. (1976) Summary of Experimental Conditions

and Data from Texas and Oklahoma in 1975. (Unpublished study received Aug 12, 1980 under

2342-964; prepared in cooperation with Texas A & M Univ., Agricultural Experiment Station and

others, submitted by Kerr-McGee Chemical Corp., Oklahoma City, Okla.; CDL:243078-I) 

48064 Abernathy, J.; Scrib, J.; Miller, C.S.; et al. (1975) Sodium chlorate on Sunflowers:

Summary of Experimental Conditions and Data from Texas in 1975; prepared in cooperation with

Texas A & M Univ. Agricultural Experiment Station and Iowa State Univ., Ames Laboratory

E.R.D.A. Unpublished study; 17 p. 

48065 Smith, D.T.; Eastin, E.F.; Wiese, A.F.; et al. (1975) Summary of Experimental Conditions

and Data from Texas and Oklahoma in 1975. (Unpublished study received Aug 12, 1980 under

2342-964; prepared in cooperation with Texas A & M Univ., Agricultural Ex- periment Station

and others, submitted by Kerr-McGee Chemical Corp., Oklahoma City, Okla.; CDL:243079-E)

49609 Chipman Chemical Company, Incorporated (1962) Progress Report: Residue Data

following the Field Use of Shed-a-Leaf on Tomatoes as a Defoliant/Desiccant in California and

New York State from Applications Made Fall of 1961. (Unpublished study received Jan 4, 1962

under 359-400; submitted by Rhone-Poulenc Chemical Co., Monmouth Junction, N.J.;

CDL:119511-A)
Page 119 of 141

53626 Chipman Chemical Company, Incorporated (1961) Residue Data Sheet. (Unpublished

study received Jan 4, 1962 under 359-400; submitted by Rhone-Poulenc Chemical Co.,

Monmouth Junction, N.J.; CDL: 119510-A)

58490 Pennwalt Corporation (1975) Efficacy of Sodium chlorate--Rice. (Reports by various

sources; unpublished study, including published data, received Oct 14, 1976 under 4581-328;

CDL:232133-T) 

66803 Walaski, L.J. (1960) Residue Analysis and Reports. (Unpublished study received May 30,

1970 under 0F0926; prepared by Chipman Chemical Co., Inc., submitted by Fenrich-Vincent

Associates, Manhasset, N.Y.; CDL:091580-N) 

74958 Rhone-Poulenc Chemical Company (1964) Tests with Shed-a-leaf L. (Compilation;

unpublished study received Apr 16, 1964 under 359- 399; CDL:023331-A)

74967 Walaski, L.J. (1962) Analyses of Dry Edible Beans, Stalks, and Pods for Possible

Residues of Borate and Chlorate: BB/9/62. (Unpublished study received Dec 3, 1962 under

359-399; prepared by Chipman Chemical Co., Inc., submitted by Rhone-Poulenc Chemical Co.,

Monmouth Junction, N.J.; CDL:101365-B) 

75021 Chipman Chemical Company, Incorporated (1960) Results of Analyses for Chlorate and

Borate Residues on Cottonseed from 1959 & 1960 California Cotton Samples. (Unpublished

study received Jan 19, 1961 under 359-399; submitted by Rhone-Poulenc Chemical Co.,

Monmouth Junction, N.J.; CDL:119545-A) 

75023 Rhone-Poulenc Chemical Company (1963) Residues in Sorghum and Rice. (Compilation;

unpublished study, including letter dated Jul 1, 1963 from L.R. Reed to Commissioner of Food &

Drugs, Food & Drug Administration, Department of Health, Education, & Wel- fare, received Jul

2, 1963 under unknown admin. no.; CDL: 119636-A) 

75025 Walaski, L.J. (1963) Analysis of Potatoes for Possible Residues of Borate following

Applications of Chlorate/Sodium Metaborate Combinations for Vinekilling: BB/1/63. 

(Unpublished study received May 21, 1963 under 359-399; prepared by Chipman Chemical Co.,

Inc., submitted by Chipman Chemical Co., Bound Brook, NJ; CDL: 119640-A) 

123745 Interregional Research Project No. 4 (1973) The Results of Tests on the Amount of

Sodium Chlorate Residue Remaining on or in Grain Sorghum, Including a Description of the

Analytical Method Used. (Compilation; unpublished study received Apr 13, 1973 under 3E1386;

CDL:093698-C) 
Page 120 of 141

140109 Interregional Research Project No. 4 (1975) The Results of Tests on the Amount of

Sodium Chlorate Residue Remaining in or on Sunflower Seeds, Including a Description of the

Analytical Method Used. (Compilation; unpublished study received Jul 1, 1976 under 6E1825;

CDL:095932-A) 

140483 Interregional Research Project No. 4 (1977) The Results of Tests on the Amount of

Sodium Chlorate Residue Remaining in or on Corn Including a Description of the Analytical

Method Used. (Compilation; unpublished study received Jun 24, 1977 under 7E1972;

CDL:097261-A) 

140486 Interregional Research Project No. 4 (1976) The Results of Tests on the Amount of

Sodium Chlorate Residue Remaining on or in Rice and Rice Straw Including a Description of the

Analytical Method Used. (Compilation; unpublished study received Apr 6, 1976 under 6E1996;

CDL:097358-A) 

159211 Ladd, R. (1976) Meat and Milk Residue Study with Antor Herbicide in a Dairy Cow

[Dosing Information Only]: Project No. 76-12: IBT No. 8580-09096. Unpublished study

prepared by Industrial Bio- Test Laboratories, Inc. 21 p. 
Page 121 of 141

APPENDIX D TOLERANCE REASSESSMENT SUMMARY

For Inorganic Chlorates as active or inert ingredients in conventional

(agricultural) pesticides

NOTE: Tolerances and/or exemptions from the requirement of a tolerance for inorganic chlorates

as active or inert ingredients in antimicrobial agents is not the purview of HED and should be

addressed by AD.

Existing exemptions from the requirement of a tolerance for sodium chlorate (073301) as an

active ingredient in conventional (agricultural) pesticides listed under 40 CFR 180.1020

Sodium chlorate is currently registered for preharvest and foliar applications as a defoliant or

desiccant to the following food/feed crops: dry beans, corn, cotton, flax, guar, chili peppers,

potatoes, rice, safflower, sorghum (grain), southern peas (i.e., cowpeas), soybeans, and

sunflowers.

Under 40 CFR 180.1020 (a) Sodium chlorate is exempt from the requirement of a tolerance for

residues in or on the following raw agricultural commodities when used as a defoliant, desiccant,

or fungicide in accordance with good agricultural practice: beans (dry, edible), corn (fodder), corn

(forage), corn (grain), cottonseed, flaxseed, flax (straw), guar beans, peas (southern), peppers

(chili), potatoes, rice, rice (straw), safflower (grain), sorghum (grain), sorghum (fodder), sorghum

(forage), soybeans and sunflower seed.

Under 40 CFR 180.1020 (b) A time-limited exemption from the requirement of a tolerance is

established for residues of the defoliant/desiccant in connection with use of the pesticide under

section 18 emergency exemptions granted by EPA. This exemption has been granted for wheat

and will expire on 12/31/04. As requested by the Registration Division (Sodium Chlorate Use

Closure Memo Amendment; J. Guerry; dated 11/15/2004) the use of sodium chlorate on wheat is

also addressed herein with the intention to convert the time-limited exemption status to a

permanent exemption from the requirement of a tolerance under 40 CFR.1020 (a). The proposed

use rate is for a single application of sodium chlorate to wheat at 6 lbs ai/A with a 3-day PHI.

Sodium chlorate exemptions under 40 CFR 180.1020 (a) from the requirement of a tolerance

should be amended as follows to: (1) specify defoliant and desiccant use only, (2) specify use on

crops rather than raw agricultural commodities, (3) include wheat concomitant with the

revocation of wheat under 40 CFR 180.1020 (b).

40 CFR 180.1020 (a) Sodium chlorate is exempt from the requirement of a tolerance for

residues when used as a defoliant or desiccant in accordance with good agricultural practice on

the following crops: Bean (dry), Corn, Cotton, Cowpeas, Flax, Guar, Pepper (non-bell), Potato,

Rice, Safflower, Sorghum (grain), Soybeans, Sunflower, and Wheat.
Page 122 of 141

Table D.1. Tolerance Reassessment Summary for Sodium Chlorate Listed under 40 CFR 180.1020(a)

Commodity Current Tolerance

(ppm)

Tolerance

Reassessment

(ppm)

[Correct Definition]

Comments

beans, dry, edible Exempt Exempt [Bean (dry)]

corn, fodder Exempt Exempt [Corn]

corn, forage Exempt

corn, grain Exempt

cottonseed Exempt Exempt [Cotton]

flaxseed Exempt Exempt [Flax]

flax, straw Exempt Revoke Flax straw is not listed in Table 1 of

OPPTS 860.1000

guar beans Exempt Exempt [Guar]

peas, southern Exempt Exempt [Cowpea]

potatoes Exempt Exempt [Potato]

peppers, chili Exempt Exempt [Pepper (nonbell)]

rice Exempt Exempt [Rice]

rice, straw Exempt Exempt

safflower, grain Exempt Exempt [Safflower]

sorghum, grain Exempt Exempt [Sorghum (grain)]

sorghum, fodder Exempt

sorghum, forage Exempt

soybeans Exempt Exempt [Soybeans]

sunflower seed Exempt Exempt [Sunflower]

Wheat None Exempt [Wheat]

Concomitant with the revocation of

wheat under 40 CFR 180.1020 (b)
Page 123 of 141

Needed exemptions from the requirement of a tolerance for sodium chlorate (873301) and

potassium chlorate (900583) as inert ingredients in conventional pesticides

Sodium chlorate (873301) as an inert ingredient in herbicide formulation products can be applied

professionally to agricultural (corn, guava, macadamia nuts, sorghum grain, sugarcane, wheat),

commercial (non-agricultural), and residential sites. These conventional pesticide products

contain < 1 % sodium chlorate and can be applied at rates no greater than 0.07 lb (as sodium

chlorate) per acre.

Potassium chlorate (900583) as an inert ingredient in airborne fungicide products can be applied

in poultry premises. These conventional pesticide products contain < 20% potassium chlorate and

can be applied at rates not greater than 0.01 lb ( as potassium chlorate) per 500 ft3

.

Table D.2. Tolerance Exemption Needed

Tolerance

Exemption

Expression

PC

Code CAS Reg No. 40 CFR § Use 

(Pesticidal)

List Classification

Sodium chlorate 873301 7775-09-9 180.920 1 Stabilizer 3

Potassium chlorate 900583 3811-04-9 180.930 2 Oxidizer 3

1 Residues listed in 40 CFR §180.920 [formerly 40 CFR§ 180.100(d)] are exempted from the requirement

of a tolerance when used in accordance with good agricultural practice as inert (or occasionally active)

ingredients in pesticide formulations applied to growing crops only. 

2 Residues listed in 40 CFR §180.930 [formerly 40 CFR§ 180.100(e)] are exempted from the requirement of

a tolerance when used in accordance with good agricultural practice as inert (or occasionally active)

ingredients in pesticide formulations applied to animals. 

Codex/International Harmonization

There are no Codex maximum residue limits (MRLs) for sodium chlorate; therefore, no questions

of compatibility with U.S. tolerances exist.
Page 124 of 141

APPENDIX E CHLORATE (ClO3b) DIETARY EXPOSURE ESTIMATES in

FOOD

Exposure estimates for chlorate residues in food are considered conservative and the

dietary (food only) risk assessments are deemed upper bound estimates.

Dietary exposure (food only) to inorganic chlorates as the chlorate ion (ClO3b) may be expected

from the following dietary exposure routes: (1) from sodium chlorate (073301) as an active

ingredient in conventional (agricultural) pesticides used on food crops; (2) from sodium chlorate

(873301) and potassium chlorate (900583) as inert ingredients in conventional pesticides used on

food crops or in poultry premises; (3) from secondary residues in meat/milk/poultry/eggs due to

residues in animal feedstuffs; (4) from sodium chlorate (873301) and calcium chlorate (875606) as

inert ingredients in antimicrobial agents used as fruit, vegetable, and egg sanitizing washes, on

mushrooms to control bacterial blotch, as treatments to seed used for sprouting, for conditioning

live oysters, in poultry drinking water, in fish filleting, and in pecan cracking/dyeing; (5) as a

potential redox of chlorine dioxide and sodium chlorite in conventional and antimicrobial

pesticides; (6) from degradation of hypochlorites in antimicrobial agents used as fruit and

vegetable washes; and, (7) from translocation of very small amounts of chlorate ion (ClO3b) by

plants (translocation of significant amounts would be phytotoxic to plants) from the environment

which may be present as a result of inorganic chlorate pesticide uses. These dietary (food) routes

of exposure are discussed below. Dietary exposure estimates for food only to be incorporated

into the dietary risk assessments for inorganic chlorate are summarized in Table E.1 below.

No food monitoring data are available for this risk assessment; only limited, chemical-specific field

trial data are available. Exposure estimates in food were based on field trial data or, in the case of

fruit/vegetable/other washes, was derived from a film thickness model. No Chemical-specific

livestock metabolism or feeding data are available; exposure estimates in meat, milk, poultry, and

eggs were derived from rat metabolism data, field trial data, and livestock reference information

concerning feed consumption, tissue weights, and milk production. In some cases, due to raw

data limitations, food exposure estimates are calculated as sodium chlorate. The effects of

washing after foliar treatments and, in some cases such as meat, milk, poultry and eggs estimates,

percent crop treated data were also incorporated into these exposure estimates.
Page 125 of 141

Table E.1. Summary of Chlorate Dietary (Food) Exposure Estimates for the Dietary Risk AssessmentsFood Group Food Crop Acute Dietary

Screen - Do Not

Use % CropTreated Data inDEEM

Chronic Dietary CommentsFrom Agricultural UsesOnly

From All Uses

Exposure Estimate(ppm)

ExposureEstimate(ppm)

/ = Use

% CropTreatedData inDEEM

ExposureEstimate(ppm)

/ = Use

% CropTreatedData inDEEM 

Vegetables chili peppers 0.5 0.5 / 0.2 Maximum/Average Exposure Estimate from agricultural use: B

grain field trial data and considering the effects of washing field chili pepper washing data, residues are expected to be <1 ppm; Incorporating available sodium chlorate percent crop treated dalevel below that from sanitizing fruit and vegetable wash.Maximum/Average Exposure Estimate from sanitizing fruit and 

film thickness model developed by FDA for sanitizing non-porobe <0.3 ppm; the exposure estimate is 0.2 ppm.

potatoes 0.5 0.5 / 0.2

sweet corn 0.5 0.5 / 0.2dry beans,guar beans,southern peas,soybeans

0.5 0.5 / 0.2 Maximum/Average Exposure Estimate from agricultural use: B

as a whole, residues are expected to be <1 ppm; the exposure esavailable sodium chlorate percent crop treated data would resulthat from sanitizing fruit and vegetable wash.Maximum/Average Exposure Estimate from sanitizing fruit and 

film thickness model developed by FDA for sanitizing non-porobe <0.3 ppm; the exposure estimate is 0.2 ppm.

all others 0.2 N/A N/A 0.2 Maximum/Average Exposure Estimate from sanitizing fruit and 

film thickness model developed by FDA for sanitizing non-porobe <0.3 ppm; the exposure estimate is 0.2 ppm.
Food Group Food Crop Acute Dietary

Screen - Do Not

Use % CropTreated Data inDEEM

Chronic Dietary CommentsFrom Agricultural UsesOnly

From All Uses

Exposure Estimate(ppm)

ExposureEstimate(ppm)

/ = Use

% CropTreatedData inDEEM

ExposureEstimate(ppm)

/ = Use

% CropTreatedData inDEEM 

Page 126 of 141

Fruits guava 0.5 0.5 0.5 Maximum/Average Exposure Estimate from agricultural use: B

sodium chlorate, as an active ingredient, in conventional (agricuand considering the effects of washing field treated RACs as demdata, residues are expected to be <1 ppm; the exposure estimate treated data are currently available.Maximum/Average Exposure Estimate from sanitizing fruit and 

film thickness model developed by FDA for sanitizing non-porobe <0.3 ppm; the exposure estimate is 0.2 ppm.

citrus fruits(except peels),bananas,plantains, andcoconuts

zero N/A N/A zero Maximum/Average Exposure Estimate from sanitizing fruit and 

film thickness model developed by FDA for sanitizing non-porobe <0.3 ppm; the exposure estimate is 0.2 ppm. For citrus fruitwhich have substantial outer peels/husks which are removed pr

residues are expected to be essentially nil; the exposure estimate are estimated at 0.2 ppm.

citrus fruitpeel

0.2 0.2

all others 0.2 0.2

Seeds cottonseed,

flaxseed,safflowerseed,sunflowerseed

0.5 0.5 / 0.5 / Maximum/Average Exposure Estimate from agricultural use: B

as a whole, residues are expected to be <1 ppm; the exposure es
Food Group Food Crop Acute Dietary

Screen - Do Not

Use % CropTreated Data inDEEM

Chronic Dietary CommentsFrom Agricultural UsesOnly

From All Uses

Exposure Estimate(ppm)

ExposureEstimate(ppm)

/ = Use

% CropTreatedData inDEEM

ExposureEstimate(ppm)

/ = Use

% CropTreatedData inDEEM 

Page 127 of 141

Cerealgrains

rice 0.5 0.5 / 0.5 / Maximum/Average Exposure Estimate from agricultural use: B

residues in/on rice w/out outer hulls, residues are expected to be ppm.

wheat 0.5 0.5 / 0.5 / Maximum/Average Exposure Estimate from agricultural use: B

field trial data, residues are expected to be <1 ppm; the exposur

corn (exceptsweet)

20 10 / 10 / Maximum/Average Exposure Estimate from agricultural use: T

maximum and average residues in/on corn grain are not expecterespectively, at the point of harvest (14-day PHI).

sorghum 70 40 / 40 / Maximum/Average Exposure Estimate from agricultural use: B

maximum and average residues in/on sorghum grain are not exprespectively, at the point of harvest (7-day PHI).

Nuts Macadamia

Nuts

0.5 0.5 0.5 Maximum/Average Exposure Estimate from agricultural use: B

sodium chlorate, as an active ingredient, in conventional (agricuresidues are expected to be <1 ppm; the exposure estimate is 0.5 data are currently available.

Pecans 0.2 N/A N/A 0.2 Maximum/Average Exposure Estimate from pecan cracking an

thickness model developed by FDA for sanitizing non-porous su<0.3 ppm; the exposure estimate is 0.2 ppm.
Food Group Food Crop Acute Dietary

Screen - Do Not

Use % CropTreated Data inDEEM

Chronic Dietary CommentsFrom Agricultural UsesOnly

From All Uses

Exposure Estimate(ppm)

ExposureEstimate(ppm)

/ = Use

% CropTreatedData inDEEM

ExposureEstimate(ppm)

/ = Use

% CropTreatedData inDEEM 

Page 128 of 141

AnimalTissues

Meat, Poultry,and Eggs

10 0.1 0.1 Maximum/Average Exposure Estimates from Agricultural uses

metabolism data that demonstrated that <1% of a single initial dincurred in any animal tissue 72 hours after oral exposure.Maximum residues are expected to be <12 ppm; the maximum based on:• Maximum theoretical dietary burden for livestock (• Maximum feed rate for livestock (9.1 kg/day)• Average weight (4 kg) of the smallest (by weight) o• Percent crop treated data is not incorporated into the Average residues are expected to be <0.2 ppm; the average expon:• Highest average theoretical dietary burden for livest• Maximum feed rate for livestock (9.1 kg/day)• Average weight (4 kg) of the smallest (by weight) o• Incorporates highest percent crop treated data (cottoMaximum/Average Exposure Estimates from sanitizing washes

agricultural uses.
Food Group Food Crop Acute Dietary

Screen - Do Not

Use % CropTreated Data inDEEM

Chronic Dietary CommentsFrom Agricultural UsesOnly

From All Uses

Exposure Estimate(ppm)

ExposureEstimate(ppm)

/ = Use

% CropTreatedData inDEEM

ExposureEstimate(ppm)

/ = Use

% CropTreatedData inDEEM 

Page 129 of 141

Milk 1 0.01 0.01 Maximum/Average Exposure Estimates from Agricultural uses

metabolism data that demonstrated that <1% of a single initial dincurred in any animal tissue 72 hours after oral exposure.Maximum residues are expected to be <2 ppm; the maximum eon:• Maximum theoretical dietary burden for cattle(500 • Maximum feed rate for cattle (9.1 kg/day)• Average milk production per day (ca. 30 kg)• Percent crop treated data are not incorporated into thAverage residues are expected to be <0.03 ppm; the average exbased on:• Highest average theoretical dietary burden for cattle • Maximum feed rate for (9.1 kg/day)• Average milk production per day (ca. 30 kg)• Incorporates highest percent crop treated data (cotto
Food Group Food Crop Acute Dietary

Screen - Do Not

Use % CropTreated Data inDEEM

Chronic Dietary CommentsFrom Agricultural UsesOnly

From All Uses

Exposure Estimate(ppm)

ExposureEstimate(ppm)

/ = Use

% CropTreatedData inDEEM

ExposureEstimate(ppm)

/ = Use

% CropTreatedData inDEEM 

Page 130 of 141

Misc. Fish fillets 0.2 N/A N/A 0.2 Maximum/Average Exposure Estimate from sanitizing fish fille

thickness model developed by FDA for sanitizing non-porous su<0.3 ppm; the exposure estimate is 0.2 ppm.

Oysters 0.2 N/A N/A 0.2 Maximum/Average Exposure Estimate from conditioning live o

thickness model developed by FDA for sanitizing non-porous su<0.3 ppm; the exposure estimate is 0.2 ppm.

Mushrooms 0.2 N/A N/A 0.2 Maximum/Average Exposure Estimate from use to control bact

derived from film thickness model developed by FDA for sanitiexpected to be <0.3 ppm; the exposure estimate is 0.2 ppm.

Sugarcane 0.5 0.5 0.5 Maximum/Average Exposure Estimate from agricultural use: B

sodium chlorate, as an active ingredient, in conventional (agricuResidues are expected to be <1 ppm; the exposure estimate is 0data are currently available.

Note: According to the Usage Report in Support of Reregistration for Sodium Chlorate (Chemical Code 073301/Case No. 4049) dated 10/27/2004, the highest average Percent Crop T

5% PCT for cotton; all others are reported as <1% PCT except processed lima beans and safflower which are reported as 2% PCT. 
Page 131 of 141

Dietary Exposure Route 1. Chlorate (ClO3b) dietary exposure estimates from sodium chlorate

(073301) as an active ingredient in conventional (agricultural) pesticides used on food crops

Sodium chlorate is currently registered for preharvest and foliar applications as a defoliant or

desiccant to the following food/feed crops: dry beans, corn, cotton, flax, guar, chili peppers,

potatoes, rice, safflower, sorghum (grain), southern peas (i.e., cowpeas), soybeans, and

sunflowers. For food/feed uses, sodium chlorate is formulated as a soluble concentrate (SC) with

the active ingredient ranging from 18% to 47.2%. Sodium chlorate may be applied using aircraft

or ground spray equipment, including high and low volume equipment.

Uses of sodium chlorate as a defoliant or desiccant on cauliflower, cucurbit vegetables, and okra

grown for seed only are considered non-food uses. Uses of sodium chlorate on ornamental

gourds and fallow lands are also considered non-food uses. These non-food uses will not be

discussed further with regards to dietary exposure/risk considerations.

Under 40 CFR 180.1020 (a) Sodium chlorate is exempt from the requirement of a tolerance for

residues in or on the following raw agricultural commodities when used as a defoliant, desiccant,

or fungicide in accordance with good agricultural practice: beans (dry, edible), corn (fodder), corn

(forage), corn (grain), cottonseed, flaxseed, flax (straw), guar beans, peas (southern), peppers

(chili), potatoes, rice, rice (straw), safflower (grain), sorghum (grain), sorghum (fodder), sorghum

(forage), soybeans and sunflower seed.

Under 40 CFR 180.1020 (b) A time-limited exemption from the requirement of a tolerance is

established for residues of the defoliant/desiccant in connection with use of the pesticide under

section 18 emergency exemptions granted by EPA. This exemption has been granted for wheat

and will expire on 12/31/04. As requested by the Registration Division (Sodium Chlorate Use

Closure Memo Amendment; J. Guerry; dated 11/15/2004) the use of sodium chlorate on wheat is

also addressed herein with the intention to convert the time-limited exemption status to a

permanent exemption from the requirement of a tolerance under 40 CFR.1020 (a). The proposed

use rate is for a single application of sodium chlorate to wheat at 6 lbs ai/A with a 3-day PHI.

Based on the available flax, guar, southern pea, soybean, and sunflower field trial data no

detectable residues of sodium chlorate (<1 ppm) are expected in/on dry beans, guar beans,

southern peas, soybeans, flaxseed, safflower seed, and sunflower seed at the point of harvest from

the maximum use rate of sodium chlorate on dry beans, guar, southern peas, soybeans, flax,

safflower, and sunflower (1 application; 7.5 lbs ai/A; 7-day PHI). Furthermore, no detectable

residues of sodium chlorate (<1 ppm) are expected in/on cottonseed at the point of harvest from

the maximum use rate of sodium chlorate on cotton (2 applications, 7.5 lbs ai/A/application; 7-day

PHI). Any residues which might be detected at the point of harvest are expected to be primarily

surface residues which would be substantially removed prior to the point of consumption. 

Based on the available chili pepper field trial data, it is possible that detectable residues of sodium

chlorate (ca. 13 ppm) might be found on the surface of unwashed chili peppers treated with
Page 132 of 141

sodium chlorate at the maximum use rate of sodium chlorate on chili peppers (1 application; 12.5

lbs ai/A/application; 10-day PHI). However, these residues are primarily surface residues present

at the point of harvest which would be substantially removed by washing (<1 ppm) prior to the

point of consumption.

Based on the available potato field trial data, no detectable residue of sodium chlorate (<1 ppm)

are expected in/on potato tubers at the point of harvest from the maximum use rate of sodium

chlorate on potatoes (1 application; 12.5 lbs ai/A; 7-day PHI). As demonstrated by the chili

pepper field trial data, any residues present at harvest are expected to be primarily surface

residues which would be substantially removed by washing prior to the point of consumption.

Based on the available oat, rice, sorghum, and wheat field trial data, it is possible that detectable

residues of sodium chlorate (ca. 70 ppm as demonstrated by sorghum grain) might be found on

the surface of cereal grains retaining their outer hulls at harvest (such as oats and sorghum) from

the maximum use rate of sodium chlorate on rice and sorghum (1 application; 7.5 lbs ai/A; 7-day

PHI) and wheat (1 application; 6 lbs ai/A; 3-day PHI). However, once the outer hulls are

removed (either at harvest or during processing), no detectable residues of sodium chlorate (<1

ppm) are expected in/on cereal grains such as rice and wheat (as demonstrated by rice w/out hulls

and wheat grain data).

Based on the available sorghum field trial data alone, maximum residues in/on sorghum grain

harvested 7-14 days after treatment with sodium chlorate at the maximum use rate for sorghum (1

application; 7.5 lbs ai/A; 7-day PHI) are not expected to exceed 70 ppm. On average, residues

in/on sorghum grain harvested 7-14 days after treatment with sodium chlorate at the maximum

use rate on sorghum (1 application; 7.5 lbs ai/A; 7-day PHI) are not expected to exceed 40 ppm.

Translating the available sorghum field trial data to corn, residues of sodium chlorate are not

expected to exceed 20 ppm (ca. 10 ppm on average) in/on corn grain at the point of harvest from

the maximum use rate of sodium chlorate on corn (1 application, 7.5 lbs ai/A; 14-day PHI). As

demonstrated by the chili pepper field trial data, any residues present at harvest are expected to be

primarily surface residues which would be substantially removed by washing prior to the point of

consumption. Hence, residues of sodium chlorate in/on sweet corn after washing and prior to

consumption would not be expected to exceed 1 ppm.

Based on the available straw (flax, oat, wheat, rice) and forage (guar plants, sorghum stalks,

soybean forage) data, maximum residues of sodium chlorate in/on straw and forage livestock

feedstuffs harvested 3-7 days after treatment with sodium chlorate at the maximum use rate

permitted on forage crops (1 or 2 applications; 7.5 lbs ai/A/application) are not expected to

exceed 300 ppm at the point of harvest. On average, residues in/on straw and forage livestock

feedstuffs should not exceed 100 ppm when harvested 7-14 days after foliar treatment with

sodium chlorate at the maximum use rate permitted on forage crops (1 or 2 applications; 7.5 lbs

ai/A/application). 
Page 133 of 141

Dietary Exposure Route 2. Chlorate (ClO3b) dietary exposure estimates from sodium chlorate

(873301) and potassium chlorate (900583) as inert ingredients in conventional (agricultural)

pesticides used on food crops or in poultry premises

Sodium chlorate (873301) as an inert ingredient in herbicide formulation products can be applied

professionally to agricultural (corn, guava, macadamia nuts, sorghum grain, sugarcane, wheat),

commercial (non-agricultural), and residential sites. These conventional pesticide products

contain < 1 % sodium chlorate and can be applied at rates no greater than 0.07 lb (as sodium

chlorate) per acre.

Taking into account the small percentage of sodium chlorate (873301) in the product(s) and the

application rate(s) of the product(s) at issue, chlorate dietary exposure estimates in/on corn,

guava, macadamia nuts, sorghum grain, sugarcane, and wheat are expected to be <1 ppm based

on the exposure estimates for sodium chlorate (073301) as an active ingredient used in

conventional (agricultural) pesticides which are used at higher rates (6-12.5 lb ai/A).

Specifically, based on the available chili pepper and potato data, residues of chlorate in/on guava,

macadamia nuts, and sugarcane are expected to be primarily surface residues leaving <1 ppm

in/on these commodities after washing and/or removal of outer surfaces prior to consumption, as

demonstrated by the available chili pepper washing data and the rice with and w/out hulls field

trial data.

Potassium chlorate (900583) as an inert ingredient in airborne fungicide products can be applied

in poultry premises. These conventional pesticide products contain < 20% potassium chlorate and

can be applied at rates not greater than 0.01 lb ( as potassium chlorate) per 500 ft3

.

No chlorate residues are expected in egg commodities from the use of potassium chlorate

(900583) as an inert ingredient in poultry premises.
Page 134 of 141

Dietary Exposure Route 3. Chlorate (ClO3b) dietary exposure estimates from secondary

residues incurred in meat, milk, poultry and eggs from consumption of feedstuffs treated with

sodium chlorate (073301 or 873301) as an active or inert ingredient in conventional (agricultural)

pesticides

The maximum residues (excluding percent crop treated data) in meat, poultry, and eggs are

estimated at 10 ppm and in milk is estimated at 1 ppm based on the following information

and assumptions:

• The maximum theoretical dietary burden for livestock is 500 ppm for cattle feed on a dry

wt. basis

• Cattle eat a maximum of 9.1 kg of feed per day on a dry wt. basis (Update of Livestock

Feed Consumption, 1993); hence, the highest average theoretical dietary exposure for

sodium chlorate to livestock is 4600 mg per day 

• Based on the available rat metabolism data, <1% of the initial dose of chlorate is expected

to be incurred in animal tissues 72 hours after exposure (Abdel-Rahman et al, 1982, 1984b

and 1985); hence <46 mg is expected to be incurred in any livestock tissue of interest

• Assuming that kidneys have the lowest weight of the organs/tissues of interest (other than

milk) in livestock (i.e., compared to meat, liver, fat, and eggs)

• Assuming that the average weight of cattle kidneys is about 4 kg (Update of Livestock

Feed Consumption, 1993; cattle kidneys weigh 3.6-4.5 kg)

• Assuming that the average milk production per day is about 30 kg (Frank, 2002; milk

production is 50-90 lb milk/cow/day)

Calculations:

(Maximum Theoretical Dietary Exposure (4600 mg) x Percent of Dietary Exposure Expected in Organs (< 1%)

Average Weight of the Organ/Tissue of Interest (Kidney at 4 Kg or Milk at 30 Kg)

Maximum Residue Estimate in Meat, Poultry, and Eggs = <12 ppm; estimated at 10 ppm

Maximum Residue Estimate in Milk = <2 ppm; estimated at 1 ppm

The highest average residues (including percent crop treated data) in meat, poultry, and

eggs are estimated at 0.1 ppm and in milk is estimated at 0.01 ppm based on the following

information and assumptions:

• The highest average theoretical dietary burden for livestock is 175 ppm for cattle feed on a

dry wt. basis (excluding percent crop treated data)

• Cattle eat a maximum of 9.1 kg of feed per day on a dry wt. basis (Update of Livestock

Feed Consumption, 1993); hence, the highest average theoretical dietary exposure for

sodium chlorate to livestock is 1600 mg per day (excluding percent crop treated data)

• The maximum percent crop treated is 5% on cotton all other feed crops are <1% (Usage

Report from A. Halvorson to B. Cropp-Kohlligian and J. Guerry dated 10/27/2004)
Page 135 of 141

hence, the highest average theoretical dietary exposure for sodium chlorate to livestock is

80 mg per day (including percent crop treated data at 5%). 

• Based on the available rat metabolism data, <1% of the initial dose of chlorate is expected

to be incurred in animal tissues 72 hours after exposure (Abdel-Rahman et al, 1982, 1984b

and 1985); hence <0.8 mg is expected to be incurred in any livestock tissue of interest

• Assuming that kidneys have the lowest weight of the organs/tissues of interest (other than

milk) in livestock (i.e., compared to meat, liver, fat, and eggs)

• Assuming that the average weight of cattle kidneys is about 4 kg (Update of Livestock

Feed Consumption, 1993; cattle kidneys weigh 3.6-4.5 kg)

• Assuming that the average milk production per day is about 30 kg (Frank, 2002; milk

production is 50-90 lb milk/cow/day) 

Calculations:

(Highest Average Theoretical Dietary Exposure (80 mg) x Percent of Dietary Exposure Expected in Organs (< 1%)

Average Weight of the Organ/Tissue of Interest (Kidney at 4 Kg or Milk at 30 Kg)

Highest Average Residue Estimate in Meat, Poultry, and Eggs = <0.2 ppm; estimated at 0.1 ppm

Highest Average Residue Estimate in Milk = <0.03 ppm; estimated at 0.01 ppm
Page 136 of 141

Dietary Exposure Route 4. Chlorate (ClO3b) dietary exposure estimates from sodium chlorate

(873301) and calcium chlorate (875606) as inert ingredients in antimicrobial agents used: (1) as

fruit, vegetable, and egg sanitizing washes; (2) to control bacterial blotch on mushrooms; (3) as

treatment to seed used for sprouting; (4) for conditioning live oysters; (5) in poultry drinking

water; (6) in fish filleting; and (7) pecan cracking/dyeing

Fruit and vegetable sanitizing washes:

Using a film thickness model, residues of chlorate in/on fruits and vegetables treated at the

maximum use rate are expected to be <0.3 ppm; estimated at 0.2 ppm. 

This estimate will also be used for seed sprouting, mushrooms, oysters, fish fillets, and pecans.

This estimate will also cover estimates on fruits and vegetables from Dietary Exposure Routes 5,

6, 7, and 8 identified below.

Since these residues are expected to be primarily surface residues in fruits which have substantial

outer peels which are removed prior to consumption, residues of chlorate in citrus fruits, bananas

and plantains are expected to be essentially nil (zero) once the peels are removed.

No chlorate residues are expected in egg commodities from surface sanitizing washes. Chlorate

residue estimates in poultry commodities from chlorate in antimicrobial agents use in poultry

drinking water are covered by the secondary residue estimates for meat/milk/poultry/egg

addressed above under Dietary Exposure Route 3. 

Calculation for percent chlorate in the sanitizing washes:

For the active ingredient(s) the maximum use rate is 500 ppm as total chlorine in the sanitizing

wash water. Exposure time is 1-2 minutes.

Percent of chlorate as an inert in the product is at most 2%.

This is equivalent to ca. <15 ppm or <0.0015% chlorate in the sanitizing wash water.

Note: The maximum or peak concentration of chlorate ion (ClO3b) in drinking water is

estimated at 9 mg/L and is based on the available AwwaRF (1995) survey study report

data.

Calculation of the surface and weight of treated fruits and vegetables:

As a model a small fruit with high surface to volume ratio such as a blueberry was selected to

represent all fruits and vegetables.

Information Provided by Cassi Walls of AD:

Diameter of one blueberry = 20 mm
Page 137 of 141

Source: Blueberry Research at the University of Georgia

http://www.ces.uga.edu/ES-pubs/RR662.htm#CPPU%20Enhances%20Fruit%20Set

Surface area of one blueberry = 12.56 cm2

Based on surface area of a sphere where A = 4Br

2

 (where r = 10mm = 1cm)

A = 4(3.14)(1 cm2

) = 12.56 cm2

Information Provided by Cassi Walls of AD:

Mass of one blueberry = 0.00136 kg (where 50 berries = 68 g or 0.068 kg)

Source: USDA’s nutrient database

http://www.nal.usda.gov/fnic/foodcomp/search/

Calculation of chlorate residues on blueberries

Information Provided by Cassi Walls of AD:

Assumes the film thickness of the sanitizing solution on the surface of the berry is 0.0023 g 

(2.3 mg) sanitizing solution/cm2

Source: Proctor and Gamble exposure assessment for ingestion of dishwashing product

residues - based on the amount of rinse water in contact with dishware surfaces

http://www.scienceinthebox.com/en_UK/safety/ingestionfromsurface_en.html

2.3 mg/cm2 (film thickness) x 12.56 cm2 (surface area) x <0.0015% chlorate in solution

 0.00136 kg blueberry

Chlorate residues on blueberry = < 0.3 ppm; estimated at 0.2 ppm
Page 138 of 141

Dietary Exposure Route 5. Chlorate (ClO3b) dietary exposure estimates from potential redox of

chlorine dioxide as the antimicrobial agent in fruit and vegetable washes and water used in poultry

processing

These dietary exposure concerns are covered by the estimates from Dietary Exposure

Routes 3 and 4 discussed above.

Under 173.300 concerning secondary direct food additives permitted in food for human

consumption chlorine dioxide (CAS Reg. No. 10049-04-4) may be safely used in food in

accordance with the following prescribed conditions: (a) The additive is generated by one of the

following methods: Treating an aqueous solution of sodium chlorite with either chlorine gas or a

mixture of sodium hypochlorite and hydrochloric acid, or treating an aqueous solution of sodium

chlorate with hydrogen peroxide in the presence of sulfuric acid. In either case, the generator

effluent contains at least 90 percent (by weight) of chlorine dioxide with respect to all chlorine

species as determined by Method 4500- ClO2 E in the ``Standard Methods for the Examination of

Water and Wastewater,'' 18th ed., 1992, or an equivalent method. Method 4500- ClO2 E is

incorporated by reference in accordance with 5 U.S.C. 552(a) and 1 CFR part 51. The additive

may be used as an antimicrobial agent in water used in poultry processing in an amount not to

exceed 3 parts per million (ppm) residual chlorine dioxide as determined by Method 4500- ClO2

E, referenced in paragraph (a) of this section, or an equivalent method. (2) The additive may be

used as an antimicrobial agent in water used to wash fruits and vegetables that are not raw

agricultural commodities in an amount not to exceed 3 ppm residual chlorine dioxide as

determined by Method 4500-ClO2 E, referenced in paragraph (a) of this section, or an equivalent

method. Treatment of the fruits and vegetables with chlorine dioxide shall be followed by a

potable water rinse or by blanching, cooking, or canning.

Dietary Exposure Route 6. Chlorate (ClO3b) dietary exposure estimates from degradation of

sodium hypochlorite or calcium hypochlorite as antimicrobial agents in fruit and vegetable washes

These dietary exposure concerns are covered by the estimates from Dietary Exposure Route

4 discussed above.

Under 40 CFR 180.2 sodium hypochlorite is generally regarded as safe

Under 40 CFR 180.1054 (a) Calcium hypochlorite is exempted from the requirement of a

tolerance when used preharvest or postharvest in solution on all raw agricultural commodities. (b)

Calcium hypochlorite is exempted from the requirement of a tolerance in or on grapes when used

as a fumigant postharvest by means of a chlorine generator pad.

Under 21 CFR 173.315 concerning secondary direct food additives permitted in food for human

consumption, chemicals used in washing or to assist in the lye peeling of fruits and vegetables ...

sodium hypochlorite ... The use of the chemicals is followed by rinsing with potable water to

remove, to the extent possible, residues of the chemical.
Page 139 of 141

Dietary Exposure Route 7. Chlorate (ClO3b) dietary exposure estimates from potential redox of

acidified sodium chlorite as an antimicrobial agent used in fruit and vegetable washes and poultry

carcass and red meat processing water

These dietary exposure concerns are covered by the estimates from Dietary Exposure

Routes 3 and 4 discussed above.

Under 21 CFR 173.325 concerning secondary direct food additives permitted in food for human

consumption, acidified sodium chlorite solutions may be safely used in accordance with the

following prescribed conditions: (a) The additive is produced by mixing an aqueous solution of

sodium chlorite (CAS Reg. No. 7758-19-2) with any generally recognized as safe (GRAS) acid.

(b)(1) The additive is used as an antimicrobial agent in poultry processing water in accordance

with current industry practice under the following conditions: (i) As a component of a carcass

spray or dip solution prior to immersion of the intact carcass in a prechiller or chiller tank; (ii) In a

prechiller or chiller solution for application to the intact carcass; (iii) As a component of a spray

or dip solution for application to poultry carcass parts; (iv) In a prechiller or chiller solution for

application to poultry carcass parts; or (v) As a component of a post-chill carcass spray or dip

solution when applied to poultry meat, organs, or related parts or trim. (2) When used in a spray

or dip solution, the additive is used at levels that result in sodium chlorite concentrations between

500 and 1,200 parts per million (ppm), in combination with any GRAS acid at a level sufficient to

achieve a solution pH of 2.3 to 2.9. (3) When used in a prechiller or chiller solution, the additive

is used at levels that result in sodium chlorite concentrations between 50 and 150 ppm, in

combination with any GRAS acid at levels sufficient to achieve a solution pH of 2.8 to 3.2. (c)

The additive is used as an antimicrobial agent in accordance with current industry practice in the

processing of red meat, red meat parts, and organs as a component of a spray or in the processing

of red meat parts and organs as a component of a dip. Applied as a dip or spray, the additive is

used at levels that result in sodium chlorite concentrations between 500 and 1,200 ppm in

combination with any GRAS acid at levels sufficient to achieve a solution pH of 2.5 to 2.9. (d)

The additive is used as an antimicrobial agent in water and ice that are used to rinse, wash, thaw,

transport, or store seafood in accordance with current industry standards of good manufacturing

practice. The additive is produced by mixing an aqueous solution of sodium chlorite with any

GRAS acid to achieve a pH in the range of 2.5 to 2.9 and diluting this solution with water to

achieve an actual use concentration of 40 to 50 parts per million (ppm) sodium chlorite. Any

seafood that is intended to be consumed raw shall be subjected to a potable water rinse prior to

consumption. (e) The additive is used as an antimicrobial agent on raw agricultural commodities

in the preparing, packing, or holding of the food for commercial purposes, consistent with section

201(q)(1)(B)(i) of the act, and not applied for use under section 201(q)(1)(B)(i)(I),

(q)(1)(B)(i)(II), or (q)(1)(B)(i)(III) of the act, in accordance with current industry standards of

good manufacturing practice. Applied as a dip or a spray, the additive is used at levels that result

in chlorite concentrations of 500 to 1200 parts per million (ppm), in combination with any GRAS

acid at levels sufficient to achieve a pH of 2.3 to 2.9. Treatment of the raw agricultural

commodities with acidified sodium chlorite solutions shall be followed by a potable water rinse, or
Page 140 of 141

by blanching, cooking, or canning. (f) The additive is used as an antimicrobial agent on processed,

comminuted or formed meat food products (unless precluded by standards of identity in 9 CFR

part 319) prior to packaging of the food for commercial purposes, in accordance with current

industry standards of good manufacturing practice. Applied as a dip or spray, the additive is used

at levels that result in sodium chlorite concentrations of 500 to 1200 ppm, in combination with

any GRAS acid at levels sufficient to achieve a pH of 2.5 to 2.9. (g) The additive is used as an

antimicrobial agent in the water applied to processed fruits and processed root, tuber, bulb,

legume, fruiting (i.e., eggplant, groundcherry, pepino, pepper, tomatillo, and tomato), and

cucurbit vegetables in accordance with current industry standards of good manufacturing

practices, as a component of a spray or dip solution, provided that such application be followed

by a potable water rinse and a 24-hour holding period prior to consumption. However, for

processed leafy vegetables (i.e., vegetables other than root, tuber, bulb, legume, fruiting, and

cucurbit vegetables) and vegetables in the Brassica [Cole] family, application must be by dip

treatment only, and must be preceded by a potable water rinse and followed by a potable water

rinse and a 24-hour holding period prior to consumption. When used in a spray or dip solution,

the additive is used at levels that result in sodium chlorite concentrations between 500 and 1,200

ppm, in combination with any GRAS acid at a level sufficient to achieve a solution pH of 2.3 to

2.9. (h) The concentration of sodium chlorite is determined by a method entitled ``Determination

of Sodium Chlorite: 50 ppm to 1500 ppm Concentration,'' September 13, 1995, developed by

Alcide Corp., Redmond, WA, which is incorporated by reference in accordance with 5 U.S.C.

552(a) and 1 CFR part 51.

Dietary Exposure Route 8. Chlorate (ClO3b) dietary exposure estimates from potential redox of

sodium chlorite as the active ingredient in conventional (agricultural) pesticides used in seed-soak

treatments

These dietary exposure concerns are covered by the estimates from Dietary Exposure Route

4 discussed above.

Under 40 CFR 180.1070, sodium chlorite is exempted from the requirement of a tolerance for

residues when used in accordance with good agricultural practice as a seed-soak treatment in the

growing of the raw agricultural commodities crop group Brassica (cole) leafy vegetables and

radishes.
Page 141 of 141

Dietary Exposure Route 9. Chlorate (ClO3b) dietary exposure estimates from translocation of

very small amounts of chlorate ion (ClO3b) by plants (translocation of significant amounts would

be phytotoxic to plants) from the environment which may be present due to inorganic chlorate

pesticide uses

These dietary exposure concerns are covered by the estimates from Dietary Exposure

Routes 1, 2, and 4 discussed above.

REFERENCES

Abdel-Rahman MS, Couri D, Bull RJ. 1982. Metabolism and pharmacokinetics of alternate

drinking water disinfectants. Environ Health Perspect. 46:19-23.

Abdel-Rahman MS, Couri D, Bull RJ. 1984b. The Kinetics of Chlorite and Chlorate in the Rat. 

Journal of the American College of Toxicology, 3(4): 261-267.

Abdel-Rahman MS, Couri D, Bull RJ. 1985. The kinetics of chlorite and chlorate in rats. J

Environ Pathol Toxicol Oncol. 6(1):97-103.

Frank, G. 2002. Cost of Milk Production per Hundredweight Equivalent in Milk Sold per Cow

Ranges. Wisconsin Dairy Data. Fact Sheet 2002-01. Center for Dairy Profitability. Univ.

Wisconsin Extension Service. Oct. 2002.